Author Topic: Лекови, дроге и терапије будућности  (Read 57992 times)

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дејан

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не'амо топик где могу да се бистре нове идеје или појаве везане за лечење или злоупотребе лекова/дрога/вакцина данас или у некој скоријој будућности.
па да почнемо са два чланка са ио9 о неуроинжињерингу:
...barcode never lies
FLA

дејан

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A Drug That Could Destroy Political Movements

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We're on the cusp of "anti-love" drugs, that could help people recover from bad love affairs. What could go wrong? A lot.


даље из чланка становите Maia Szalavitz


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Imagine families being able to inoculate their teens against crushes to improve academic performance — or spouses forcing the drug on their partners to end affairs, or even governments breaking up social networks of dissidents by chemically alienating them (which would be an interesting counterpoint to the U.S. military's wacky research into a "gay bomb" that would make enemy soldiers irresistible to each other). The dystopian potential seems endless.


или фул ствар


итд, могућности за сф писце су огромне

...barcode never lies
FLA

дејан

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Scientists Say They Need Philosophers to Continue Their Research
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At the University of Washington, researchers are pioneering a field of neuroscience called "neuroengineering," which will one day involve doing things like regulating people's moods with brain implants. In this fascinating video, they explain how their work spilled over into philosophy.

The issues that these neuroengineers are tackling are going to become increasingly important in many scientific fields that touch on the human mind. Entering the Brain Age also means that lab research will be trying to answer the same questions that people in the humanities have contemplated for thousands of years. Who are we? Do we have freewill? If somebody is controlling our minds with chemicals and medical devices, how is that different from controlling us with ideology or economic incentives?
The much-vaunted "war" between science and culture seems destined to end in a synthesis, at least in cases like these.


Art + Science = NeuroEthics
...barcode never lies
FLA

Meho Krljic

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Scientists find Achilles' heel of antibiotic resistant bacteria
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Scientists at the University of East Anglia demonstrate how the bug responsible for E. coli and salmonella builds an impenetrable wall to keep out drugs 
  The global threat of antibiotic resistance could finally be tackled after British scientists discovered a chink in the armour of deadly bacteria.   Health experts have warned that within 20 years even routine operations such as hip replacements and organ transplants could be deadly because of the risk of infection.   But now scientists at the University of East Anglia have discovered how the bug responsible for E. coli and salmonella builds an impenetrable wall to keep out antibiotics.   They believe that within a few years they could develop a drug which switches off the wall-building mechanism, making the bacteria vulnerable.   “It is a very significant breakthrough,” said Professor Changjiang Dong, from the University of East Anglia's (UAE) Norwich Medical School. 
 
 “This is really important because drug-resistant bacteria is a global health problem. Many current antibiotics are becoming useless, causing hundreds of thousands of deaths each year.
 
 “Many bacteria build up an outer defence which is important for their survival and drug resistance. We have found a way to stop that happening.
 
 "The number of superbugs are increasing at an unexpected rate. This research provides the platform for urgently-needed new generation drugs."
 
 
 The discovery, reported in the journal Nature, could pave the way to a new generation of antibiotic drugs that work by bringing down the defensive wall.
 
 Bugs such as MRSA (methicillin resistant Staphylococcus aureus) are becoming increasingly immune to "last resort" antibiotics.
 
 If the trend continues the world may see a return to the pre-antibiotic era when even a trivial scratch could prove fatal.
 
 At the heart of the breakthrough is the way "gram negative" bacterial cells transport the barrier's molecular "bricks" to the surface of the cell and form a wall.
 
 "Gram-negative" bacteria, which include Escherichia coli (E. coli) and the bugs that cause gonorrhea, cholera and Legionnaire's disease, are especially resistant to antibiotics.
 
 They can evolve a number of mechanisms to make them immune to drugs, including reducing the permeability of their outer membrane.
 
 But if the membrane barrier falls, the bacteria die - whatever other defensive ploys they may have developed.
 
 Haohao Dong, another member of the UAE team, said: "The really exciting thing about this research is that new drugs will specifically target the protective barrier around the bacteria, rather than the bacteria itself.
 
 "Because new drugs will not need to enter the bacteria itself, we hope that the bacteria will not be able to develop drug resistance in future."
 
 
 The science community and the Government said the research was a "welcome piece of news".
 
 “We are facing a difficult era in terms of antibiotic resistance; the need for new efficacious drugs to treat infectious disease is clearly an important issue,” said Mark Fielder, Professor of Medical Microbiology at Kingston University and Hon Gen Sec of the Society for Applied Microbiology.
 
 “The publication of data from the two groups is a welcome piece of news. Their findings give science an insight into some of the structures that are important in the development of a bacterial membrane.
 
 “This could be of great importance as if we fully understand the workings and construction of structures that help bacteria function as effective entities we can hopefully then exploit weaknesses therein and kill the organism.”
 
 Prof Brendan Wren, Professor of Microbial Pathogenesis, London School of Hygiene & Tropical Medicine, added: “The studies open new avenues to the design a novel class of antibiotics to disarm and kill pathogenic bacteria."
 
 Deputy Chief Medical Officer John Watson said: “Antimicrobial resistance is a hugely important issue facing the world today.
 
 “We welcome all efforts in this area and we will follow any further developments with interest.”
 

Evo i linka na sam uzveštaj (avaj, samo apstrakt može da se vidi za dž, pristup celom tekstu je brutalnih 32 dolara), ko želi da se malo udubi, pošto članak u Telegrafu brka gram-pozitivne i negativne bakterije i pravi, vele ljudi, još grešaka:
 Structural basis for outer membrane lipopolysaccharide insertion

Meho Krljic

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U jeku najnovije epidemije Ebole u Africi od koje se zarazilo i dovoljno ne-Afrikanaca da prvi svet postane zabrinut, priča se da neki Ameri dobijaju eksperimentalnu terapiju koja za sada kao da daje rezultate:


Here's Everything We Know About The 'Secret Serum' Used To Treat An American With Ebola



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Both of the Ebola-infected U.S. citizens in Liberia received a rare dose of what news reports called a "secret serum" to treat the virus before being transported to Emory University Hospital in Atlanta, according to a CNN report. And while some people do fight off the disease on their own, in the case of the two Americans, that experimental serum may have saved their lives.
As Dr. Kent Brantly and missionary Nancy Writebol waited in a Liberian hospital, someone from the National Institutes of Health reached out to Samaritan's Purse, one of the two North Carolina-based Christian relief groups the two were working with, and offered to have vials of an experimental drug called ZMapp sent to Liberia, according to CNN's unnamed source.
Although the Food and Drug Administration does allow experimental drugs to occasionally be distributed in life-threatening circumstances without approval under the expanded access or "compassionate use" conditions, it's not yet clear whether that approval was granted in this case or not.
A spokesperson for the FDA told Business Insider that federal law and FDA regulations prohibit them from commenting on specific products, as that information is considered confidential.
 An Emergency Treatment However it was approved, three frozen vials of ZMapp, a drug being developed by Mapp Biopharmaceutical, were flown to Liberia and arrived the morning of Thursday July 31.
The serum needed eight to 10 hours to thaw.
Brantly, who had been sick for nine days already, reportedly had asked that Writebol receive the first dose, as he was younger and thought he had a better chance of surviving. (It's unclear from the CNN story why the doses apparently were not all ready at the same time.)
But his condition worsened as the first dose thawed, and CNN reports that he told his doctors, "I am going to die."
He asked for the first dose and had it given to him through an IV. According to CNN's source, within an hour, he was able to breathe better and a rash on his body started to fade. The next day he was able to shower without help before boarding the air ambulance that flew him to Atlanta.
Writebol reportedly didn't respond as well to the first treatment she received, and had to be given the third vial of serum. Her second treatment seemed to improve her condition, according to CNN, and stabilized her enough that she's expected to fly to the U.S. on Tuesday, August 5.
 How It Might Have Worked The ZMapp serum itself is what's known as a "monoclonal antibody." As James Hamblin of The Atlantic explains, these substances are created by infecting an animal with the disease in question. Then, scientists harvest and use the antibodies that the animals' immune systems create to fight the virus. In this case, the antibodies were harvested from Ebola-infected mice.
Studies have tested various other blends of similar therapies against Ebola-infected monkeys before, with some efficacy — but only when the therapy is given within 48 hours of infection. As Hamblin cautions, "very little is known about the safety and effectiveness of this treatment—so little that outside of extreme circumstances like this, it would not be legal to use."
 Could Drugs Stop The Epidemic? This Ebola outbreak — the worst in history — has already killed 887 people. But promising news of an experimental serum doesn't mean that a treatment is close.
Developing a cure for a virus is complicated, and developing a treatment for Ebola has proven particularly difficult.
In this case, since health officials can't comment on a specific treatment or on the patients involved for privacy reasons, we don't know the exact status of Brantly and Writebol or how that status has been affected by the serum that they reportedly received.
Before this emergency use, ZMapp had only been tested in a small number of monkeys. The company reported that all four monkeys who received the treatment within 24 hours of being infected survived. Half of another group of four monkeys who were treated within 48 hours survived.
Brantly and Writebol had been sick much longer than that before being treated, and treatments that work in animals — especially such a small number of animals — routinely fail to work in human trials.
Standard "treatment" for Ebola usually involves trying to keep patients hydrated and alive long enough to give the immune system a chance to battle the virus. And while that approach may sound unpromising, this outbreak has had a fatality rate of about 60% so far, not close to the 90% that's often reported.
That 60% number could still rise, but survival cannot necessarily be attributed to an experimental treatment. While Ebola is highly fatal, some people do survive without any extraordinary interventions.
 A Tale Of Two Drugs: Mapp Vs. Tekmira ZMapp is not even far enough along to have entered the clinical trial phase, but it may have been chosen in this case instead of the promising experimental drug Tekmira because an ongoing Tekmira trial was just halted by the FDA.
That doesn't mean that all research on Tekmira is over, however. The ongoing trial was halted because healthy patients showed a problematic immune response. But the FDA could still approve a new trial of the drug in sick patients, as the risk-benefit equation would be changed. A potential benefit of surviving a disease that kills 60-90% of patients could outweigh the risks of many potentially problematic side effects.
CNN also reported that on July 30, the military approved additional funding for Mapp Biopharmaceutical because of their promising results so far.
If either ZMapp or Tekmira proves to be effective; testing, approving, and then producing a drug will still take time, even if the process is fast-tracked.
At this point, the best hope for stopping this outbreak is not curing it, but containing it.
Even though the virus can only be transmitted by close contact, and thus it can be contained, health officials have been completely unable to do so in West Africa due to a combination of factors including poor healthcare infrastructure, distrust of authorities, traditional burial practices, and fear of healthcare providers.
At the present rate, World Health Organization chief Margaret Chan describes the consequences of not being able to stop the disease's spread as "catastrophic."
   SEE ALSO:  Ebola Discoverer Says He Would 'Sit Next To Someone' With The Virus

Meho Krljic

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Malo širenja panike za Subotnje jutro
 Making viruses in the lab deadlier and more able to spread: an accident waiting to happen
 
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All rights come with limits and responsibilities. For example, US Supreme Court Justice Oliver Wendell Holmes famously noted that the right to free speech does not mean that one can falsely shout "fire" in a crowded theatre.
The same constraints and obligations apply to the right of scientific inquiry, a topic that has been in the news recently after researcher Yoshihiro Kawaoka of the University of Wisconsin-Madison published an article in the journal Cell Host and Microbe in June describing the construction of a new flu virus from wild-avian-flu strain genes that coded for proteins similar to those in the 1918 pandemic virus; the new virus was not only able to spread between ferrets—the best current model for human flu transmission—but was also more virulent that the original avian strains. (The 1918 Spanish Flu killed an estimated 50 million people; the molecular structure of the new strain is only three percent different than the 1918 version.)
Asked for comment by The Guardian newspaper, Robert, Lord May of Oxford, the former chief scientific advisor to the British Prime Minister and former president of the British Royal Society—one of the oldest and most prestigious scientific organizations in the world—condemned the work as "absolutely crazy," calling "labs of grossly ambitious people" a real source of danger.
As if that research were not enough to cause worry, in July a newspaper investigation asserted that Kawaoka was also conducting another controversial—but so far unpublished—study in which he genetically altered the 2009 strain of flu to enable it to evade immune responses, "effectively making the human population defenseless against re-emergence."
If true, it may be that Kawaoka has engineered a novel strain of influenza with the capability of generating a human pandemic, if it ever escaped from a laboratory. (“Pandemic” means that it occurs over a wide geographic area and affects an exceptionally high proportion of the population. In comparison, the Centers for Disease Control define an “epidemic” as merely “the occurrence of more cases of disease than expected in a given area or among a specific group of people over a particular period of time.”)
An independent risk-benefit assessment of this work conducted at the request of the journal Nature demonstrated that Kawaoka’s work did indeed meet four of the seven criteria outlined in the US Policy for Oversight on Dual Use Research of Concern (DURC) of March 29, 2012, meaning that the institution found that the research could be misused to threaten public health and would therefore require additional high-level safety measures, including a formal risk-mitigation plan.
But even with these measures in place, this research still seems like an unnecessary risk, given the danger that the bio-engineered viruses could turn into a pandemic threat, and that some experts think that there are far better and safer ways to unlock the mysteries of flu transmissibility. Claims that this work would help in the manufacture of a preventive vaccine have been strongly contradicted by Stanley Plotkin of the Center for HIV-AIDS Vaccine Immunology, among other critics.
Part of the justification behind conducting these experiments, apparently, was to develop a better understanding of the pandemic potential of influenza viruses by enhancing their properties, such as altering their host range, for example. Since the newly engineered viruses possess characteristics that their naturally found, or "wild," counterparts do not, this type of study is commonly referred to as "gain-of-function" research in virologists’ parlance.
But considering the likelihood of accidental or deliberate release of the virus created by gain-of-function experiments, the following issues should be considered before approving any such studies—and preferably they would have been taken into consideration by those attending the Biological and Toxin Weapons Convention earlier this month.
In a nutshell: The Convention’s attendees should have agreed on a common understanding requiring that all gain-of-function experiments be stopped until an independent risk-benefit assessment is carried out; the scientific community should exhaust all alternative ways of obtaining the necessary information before approving gain-of-function experiments; biosecurity education and awareness-raising should be given a priority as tools for fostering a culture of responsibility in the life sciences; and there should be a modern version of the “Asilomar process” to identify the best approaches to achieving the global public health goals of defeating pandemic disease and assuring the highest level of safety. (At Asilomar, California, in the early 1970s, researchers studying recombinant DNA met to discuss whether there were risks from their research, what the negative social implications could be, and how to contain the dangers.)
There will be another meeting of the Biological and Toxin Weapons Convention in December; one can only hope that it will consider these proposals then.
What, me worry? Sometimes, the potential for accidents is inherent in a system, making their occurrence not only able to be anticipated but inevitable, even "normal." For example,Charles Perrow’s famous account of the Three Mile Island nuclear accident contends that the very structure and organization of nuclear power plants make them accident-prone. As a result, even in the presence of sophisticated safety designs and technical fixes, multiple and unexpected interactions of failures are still bound to occur, as illustrated more recently in the Fukushima disaster.
Gain-of-function research in the life sciences is another example of the inevitable failure of overly complex, human-designed systems with multiple variables. Some of the most dangerous biological agents—anthrax, smallpox, and bird flu—have been mishandled in laboratories. As noted by the newly formed Cambridge Working Group, of which one of us —Malcolm Dando—is a member, these are far from exceptional cases; in the U.S. alone, biosafety incidents involving regulated pathogens "have been occurring on average over twice a week."
Such situations are not confined to the United States; China’s poor track record for laboratory containment means that it was "appallingly irresponsible" (in Lord May’s words) for a team of Chinese scientists to create a hybrid viral strain between the H5N1 avian influenza virus and the H1N1 human flu virus that triggered a pandemic in 2009 and claimed several thousand lives. In a July 14, 2014 statement about the creation of such pathogens, the Cambridge Working Group noted:
An accidental infection with any pathogen is concerning. But accident risks with newly created “potential pandemic pathogens” raise grave new concerns. Laboratory creation of highly transmissible, novel strains of dangerous viruses, especially but not limited to influenza, poses substantially increased risks. An accidental infection in such a setting could trigger outbreaks that would be difficult or impossible to control.
Against this backdrop, the growing use of gain-of-function approaches for research requires more careful examination. And the potential consequences keep getting more catastrophic.
High-profile examples. In April, 2014, the Daniel Perez Lab at the University of Maryland engineered an ostrich virus known as H7N1 to become “droplet transmissible”—meaning that the tiny amounts of virus contained in the minuscule airborne water droplets of a sneeze or a cough would be enough to make someone catch the illness. Hence, it could be easily transmitted from one subject to another.
So far, there has not been one laboratory-confirmed case of human infection by H7N1. It is apparently not a threat to man, unlike H5N1 and H7N9.
However, while the chance of airborne transmission of H7N1 in humans by droplet is apparently low, the test animals that it did manage to infect became very ill indeed—60 percent of ferrets infected through the airborne route died. This is a phenomenal rate of lethality; in contrast, only about two percent of humans who contracted the illness died from it during the Spanish Flu pandemic of 1918.
So it was with concern that the scientific world noted Kawaoka’s study describing the construction of a brand-new flu virus from wild-avian-flu strain genes that coded for proteins similar to those in the 1918 pandemic virus. The resulting new pathogen was not only able to spread between ferrets—the best current animal model for human flu transmission—but it was also more severe in its effects than the original avian strain. But the story does not finish here. As an article in Nature revealed, the “controversial influenza study was run in accordance with new US biosecurity rules only after the US National Institute of Allergy and Infectious Diseases (NAID) disagreed with the university’s assessments,” thus showing the real need for reform of the current system.
Avoiding a ‘normal’ accident. While biotechnology promises tremendous public health benefits, it also holds a considerable potential for catastrophe, as these gain-of-function experiments illustrate. As scientific capabilities and work involving dangerous pathogens proliferate globally, so too do the risks and the prospects for failure—whether coming from technology or arising from human error. Indeed, in assessing the rapidly evolving life-science landscape, Jose-Luis Sagripanti of the US Army Edgewood Chemical Biological Center—the nation’s principal research and development resource for chemical and biological defenses—has argued that “current genetic engineering technology and the practices of the community that sustains it have definitively displaced the potential threat of biological warfare beyond the risks posed by naturally occurring epidemics.”
Laboratories, however well equipped, do not exist in isolation but are an integral part of a larger ecological system. As such, they are merely a buffer zone between the activities carried out inside and the greater environment beyond the laboratory door. Despite being technologically advanced and designed to ensure safety, this buffer zone is far from infallible. Indeed, as researchers from Harvard and Yale demonstrated earlier this year, there is almost a 20 percent chance of a laboratory-acquired infection occurring during gain-of-function work, even when performed under conditions of the highest and more rigorous levels of containment. Addressing the rapid expansion of gain-of-function studies is therefore both urgent and mandatory.
In December 2013, the Foundation for Vaccine Research sent a letter to the European Commission calling for a “rigorous, comprehensive risk-benefit assessment of gain-of-function research” which “could help determine whether the unique risks to human life posed by these sorts of experiments are balanced by unique public health benefits which could not be achieved by alternative, safe scientific approaches.” Given the recent developments with influenza viruses, there is a need for an independent assessment of the costs and benefits of gain-of-function research. Such independent review would allow for adopting newer and better regulations and conventions, as well as help to identify policy gaps. As David Relman of the Stanford School of Medicine recently pointed out in the Journal of Infectious Diseases, the time has come for a balanced and dispassionate discussion that “must include difficult questions, such as whether there are experiments that should not be undertaken because of disproportionately high risk.”
 

Mica Milovanovic

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Vidiš da se lilith ne javlja već neko vreme.
Ko zna šta je smućkala tamo u K.und.K...
I Zosko se nešto ućutao...
Ja više ne idem u Beč...
Mica

Meho Krljic

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Ako ništa drugo, lek za ebolu koji se trenutno testira na majmunima u laboratoriji, pokazuje solidne uspehe:


Ebola Drug Saves Infected Monkeys

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ZMapp is the first treatment to completely protect animals after they show symptoms of disease


ZMapp, the drug that has been used to treat seven patients during the current Ebola epidemic in West Africa, can completely protect monkeys against the virus, research has found.
The study, published online today in Nature, comes the day after the World Health Organization (WHO) warned that the Ebola outbreak, which has killed more than 1,500 people, is worsening and could infect 20,000 people before it ends. A fifth West African nation, Senegal, reported its first case of the disease on Friday.
Public-health experts say that proven measures, such as the deployment of greater numbers of health-care workers to stricken areas, should be the focus of the response. But ZMapp, made by Mapp Pharmaceutical in San Diego, California, is one of several unapproved products that the WHO has said could be used in the outbreak.
The drug — a cocktail of three purified immune proteins, or monoclonal antibodies, that target the Ebola virus — has been given to seven people: two US and three African health-care workers, a British nurse and a Spanish priest. The priest and a Liberian health-care worker who got the drug have since died. There is no way to tell whether ZMapp has been effective in the patients who survived, because they received the drug at different times during the course of their disease and received various levels of medical care.
In the study, designed and conducted in part by Mapp Pharmaceutical scientists, 18 monkeys were given three doses of the drug starting three, four or five days after they were infected with Ebola. All animals that received the drug lived, no matter when their treatment started; three monkeys that were not treated died.
The strain of Ebola virus used in the study is not the same as the one causing the current outbreak. But researchers showed that the antibodies in ZMapp recognize the current form of the virus in cell cultures, and the parts of the virus recognized by the drug are present in the strain of Ebola that has caused the outbreak.
Advanced disease
 The findings make ZMapp the first drug shown to be highly effective against Ebola when given to monkeys that are already showing symptoms of infection, such as fever and abnormalities in proteins that aid blood clotting. That is important because unless a patient is known to have been exposed to the virus, symptoms such as fever are the first sign that he or she is infected and needs treatment.
Thomas Geisbert, a virologist at the University of Texas Medical Branch at Galveston, estimates that day 5 of infection in the monkeys studied is roughly equivalent to days 7 to 9 of a human infection. People can develop symptoms up to 21 days after they contract Ebola, although signs commonly develop between 8 and 10 days after infection.
The study authors say that ZMapp works in an “advanced” stage of the disease. The drug was able to save one monkey that had bleeding under the skin affecting more than 70% of its body, and other monkeys that had enough virus in their blood to cause severe symptoms in people, says study co-author Gary Kobinger, an infectious-disease researcher at the Public Health Agency of Canada in Winnipeg.
In humans, the large majority are unable to walk or even sit with this level, and most will die within 24 hours,” Kobinger says.
But other researchers say that the findings should be interpreted with caution, because monkeys with Ebola are not a perfect analogue for humans with the disease. “I don’t think the data support that this drug is effective, even in the animal model, in individuals with advanced Ebola disease,” says infectious-disease physician Charles Chiu at the University of California, San Francisco.
Knowing when to give the drug may help guide its use in future outbreaks. But for now, Mapp says that no more ZMapp is available and will not be for months.

Meho Krljic

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I kad smo već na ovom topiku, lepo je čuti da države u Americi koje dopuštaju marihuanu kao terapiju protiv bola imaju značajno nižu statistiku smrtnosti od jakih  opiodia:



States with Medical Marijuana Have Fewer Painkiller Deaths



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Could medical cannabis help prevent the more than 16,500 deaths each year due to opioid overdose?


In the U.S., 23 states and the District of Columbia allow their residents to legally use medical marijuana. And, according to a new study, death certificates reveal that states with a medical marijuana law have lower rates of deaths caused by narcotic painkiller overdoses than other states.  Only California, Oregon and Washington had laws effective prior to 1999, the point when the researchers began their analysis. Ten other states put laws on their books between 1999 and 2010. The researchers analyzed each state in the years after a medical cannabis law came into effect.
Overall, the states with these laws had a nearly 25 percent reduction in opioid overdose deaths. The study was published this week in JAMA Internal Medicine.
The findings could help address the nation’s growing problem with opioid overdoses—about 60 percent of deaths are people who have prescriptions for the medication. However, the study authors caution that their analysis doesn’t account for health attitudes in different states that might explain the association. They did explore whether policies addressing painkiller abuse had any effect on the decline in deaths and didn’t find a link.
Previous studies hint at why marijuana use might help reduce reliance on opioid painkillers. Many drugs with abuse potential such as nicotine and opiates, as well as marijuana, pump up the brain’s dopamine levels, which can induce feelings of euphoria. The biological reasons that people might use marijuana instead of opioids aren’t exactly clear, because marijuana doesn’t replace the pain relief of opiates.  However, it does seem to distract from the pain by making it less bothersome.



scallop

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To je, valjda, i očekivano. Pored lekovitih dejstava marihuane. O njima sam čitao još u HERBS, Eyewitness handbooks, 1994.
Never argue with stupid people, they will drag you down to their level and then beat you with experience. - Mark Twain.

Meho Krljic

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Artificial Spleen Removes Ebola, HIV Viruses and Toxins From Blood Using Magnets



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Harvard scientists have invented a new artificial spleen that is able to clear toxins, fungi and deadly pathogens such as Ebola from human blood, which could potentially save millions of lives.
Blood can be infected by many different types of organ infections as well as contaminated medical instruments such as IV lines and catheters.
When antibiotics are used to kill them, dying viruses release toxins in the blood that begin to multiply quickly, causing sepsis, a life-threatening condition whereby the immune system overreacts, causing blood clotting, organ damage and inflammation.
It can take days to identify which pathogen is responsible for infecting the blood but most of the time, the cause is not identified, while the onset of sepsis can be hours to days. Broad-spectrum antibiotics with sometimes devastating side effects are used and currently over eight million people die from the condition worldwide annually.
"Even with the best current treatments, sepsis patients are dying in intensive care units at least 30% of the time," said Dr Mike Super, senior staff scientist at Harvard's Wyss Institute for Biologically Inspired Engineering, which led the research. "We need a new approach."


To overcome this, researchers have invented a "biospleen", a device similar to a dialysis machine that makes use of magnetic nanobeads measuring 128 nanometres in diameter (one-five hundredths the width of a single human hair) coated with mannose-binding lectin (MBL), a type of genetically engineered human blood protein.
The study, An Extracorporeal Blood-Cleansing Device For Sepsis Therapy, has been published in the journal Nature Medicine.
The MBL on the nanobeads binds itself to toxins and pathogens, which can then be pulled out of the blood by the device through two hollow channels connected by a series of slits, with one channel containing flowing blood, while the other contains a saline solution that collects and removes the pathogens that travel through the slits.
The scientists tested their device by cleaning human blood that had been spiked with different pathogens and when blood flowed through a single device at the rate of 500ml to 1 litre an hour, over 90% of key pathogens were removed.
To speed up the device for human use, many devices can be linked together to clean the blood at a faster rate.
The researchers also tested the bio-spleen on rats that had been infected by toxins and viruses such as E. coli and S. aureus. After just five hours of filtering, 90% of the toxins and pathogens had been removed from the rats' bloodstreams and 90% of the treated rats survived.


"Sepsis is a major medical threat, which is increasing because of antibiotic resistance," said Donald Ingber, a professor of vascular biology at Harvard Medical School and the Vascular Biology Program at Boston Children's Hospital, as well as professor of bioengineering at SEAS.
"We're excited by the biospleen because it potentially provides a way to treat patients quickly without having to wait days to identify the source of infection and it works equally well with antibiotic-resistant organisms.
"We hope to move this towards human testing to advancing to large animal studies as quickly as possible."
Biospleens could be used in the future to treat patients suffering from viral diseases such as HIV and Ebola, where a person's survival depends on how quickly the amount of virus in the blood can be lowered to a negligible level.
The researchers plan to use pigs next to test their invention.


Meho Krljic

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People Are Yelling at Avatars to Get Rid of the Voices Inside Their Head



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Schizophrenia  is a brain disorder that affects a person’s ability to tell the difference between what is reality and fantasy. It affects an estimated one in 100 people.
 Basically, schizophrenia makes living a normal life extremely difficult. Those afflicted with it often hallucinate, think others are controlling their minds, or are plotting to harm them. Even after drugs and therapy, most sufferers have to deal with these symptoms their whole lives.
 Sadly, it’s an illness that not only ruins lives, but takes them too. We all know the story of Vince Li, who decapitated his seatmate on a Greyhound bus because the voices in his head told him to. On top of this, an estimated 40 percent of schizophrenics will attempt suicide at least once. Prescribed drugs help keep symptoms at bay, but a quarter of schizophrenics see no change after medication.
 Oddly enough, the solution to all this may lie in yelling at your computer.
 Five years ago, retired psychiatrist and professor Dr. Julian P. Leff had a radical idea. 12 years into his retirement, he decided that the best way to get rid of hallucinated voices was to meet them, and tell them off. Using patented 3D facial imaging software from Toronto, he constructs avatars with the face and voice of the patient’s tormentor. He sits in with the patient during sessions and encourages them to verbally confront their avatar on a computer screen.
 Dr. Leff is now using avatar therapy to treat patients in a 1.2 million pound study over the next three years. If he can replicate the positive results from an initial pilot study, it will mark a huge advance in psychotherapy. I reached out to him over the phone to talk about schizophrenia, avatars, and yelling at computer screens.
 VICE: Hi Dr. Leff. Tell me about this project, in your own words.
 Dr. Leff: We allow schizophrenic patients to interact with the voices in their heads as a form of therapy. Using patented 3D facial imaging software from Toronto, the being in the patient’s head comes to life on a computer screen. I encourage my patients to confront the avatar during sessions with the hope that they can gain control of the voices, or even eliminate them completely. The project started in 2009 with a small group of patients and has since grown to a much larger study with the 1.2 million pound grant we were given.
 How did you think of this? What inspired the avatar aspect?
 I was seven years out of retirement, reading books, and relaxing when the idea came to me. It was a complete shot in the dark, but I thought, Why not try this? One out of 100 people are affected by schizophrenia and one out of four people affected by schizophrenia experience no improvements with medication. So I wanted to do something, I wanted to offer treatment to these people who have their lives controlled by this devastating illness. What other forms of therapy don’t offer is the ability to put a face and a being to their voices, and I’ve found that interacting with the tormentor can have a profound impact on getting patients’ lives back on track.
 What have the results been like so far?
 The first study was a randomized control trial from 2009 to 2011 that involved 16 patients who had had no improvement with drugs. Out of the 16, three lost their voices altogether, and the others showed promising improvements. The effect size (a measurement of the strength of treatment) for other therapies treating auditory schizophrenia is between 0.2 and 0.4. For my avatar therapy, the effect size was 0.8. This means that my treatment is at least twice as effective as any other non-pharmaceutical therapy. I was not expecting such extremely effective results. I had hoped for a minor improvement, so this came as a very big surprise.
 What does a typical session look like?
 Once we’ve designed their avatar, the patient is seated front of the screen, face to face with it. I am in a separate room from the patient, and the two rooms are connected with a cable. At the first meeting with the patient, I ask what the voice habitually says. I warn the patient that in the first session the avatar will say those things, but reassure them that as the therapist I will support them against the avatar. During a session, I switch back and forth from my two voices to mediate the conversation. As the therapy goes on, I progressively allow the avatar to yield to the patient's control and eventually to cease abusing the patient and instead to offer to help and support the patient.
 How do your patients react when they first see their avatar?
 Typically they are very timid at first. A few of my patients were sexually abused so naturally the treatment was very difficult for them. We have a panic button that the patient can press at any point if they feel overwhelmed, at which point the screen changes to a beach scene and Vivaldi’s "Four Seasons" is played to relax them. It’s tough at first to look at the thing that has been controlling their life, but it very rarely gets to the point where they have to use the panic button.
 Tell me about the patients who were cured altogether.
 The one’s whose voices disappear have their lives changed. I had one patient who was tormented by a devil inside his head who controlled him and got him to make bad decisions with his money. He took the devil’s advice and lost all of his money. In the first session he came in furious and just shouted at the devil. “Go to hell and leave me alone!” he said. In the second session he came back more relaxed, and when I phoned him for a third session he said, “I don’t need it!” He thanked me for giving him his life back, and for feeling clear in his mind for the first time. He now works as a successful financial analyst in Europe.
 What does the future hold for avatar therapy?
 Right now we’re conducting a much larger study using 140 patients over the course of three years. Up to date the statistics are outstandingly strong for the treatment, and if the results of this next study compare to the first trial, this kind of thing will become applicable all over the world. We’re not yet sure how the treatment will work in other languages, so there is still a lot of work to do. But if the first study can be replicated, this is a huge advance in psychotherapy that will change lives.
 
 
 @keefe_stephen




Avatar therapy helps confront distressing voices

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Plan the perfect murder with the nocebo effect

'ноцебо' је од латинског 'повредићу' - ефекат супротан плацебу - може се наћи на кутијама цигарета (и пророчки тврдим да је већи изазивач рака и свих осталих болести него само канцер ђубре) или у разговору у било којој српској амбуланти

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Yes, you can kill someone using strategic mind control. It's called the nocebo effect.

In the 1970s, a man was told that he had advanced liver cancer and had only a few months to live. He died within a few months. An autopsy showed that he had a tumor much too small to be the cause of death. As far as they could tell, the diagnosis itself killed him.

In the 1990s doctors found a group of women four times more likely than the average woman to die of heart disease. Their one common factor was that they all believed that they were prone to heart disease.

Many people have heard of the placebo effect. Patients who believe they are taking a certain drug describe a beneficial effect from a medicine, despite the fact that they aren't actually taking it. It is so common that a false form of a medication is generally dispensed to people in drug studies, to provide a sort of ‘base' of patients with the placebo effect to measure against the patients who are actually given the drug.

The flip side of this is the ‘nocebo' effect. In latin ‘nocebo' means ‘I will harm.' The sinister name is well earned. A quick survey of nocebo effect studies provides almost a blueprint for driving someone to death or insanity. Sometimes it is as simple as telling them that they've been exposed to electromagnetic radiation. In a study, students were told that electric monitoring equipment that they put on their head would cause headaches. Two thirds of them reported headaches. Similarly, people who were told that aspirin could cause stomach pain reported stomach pain much more than those who weren't told

Once actual treatment commences, things can get more serious. Warnings about insomnia and stress are naturally more likely to induce stress and insomnia, of course, but victims of the nocebo effect report depression, fatigue, nausea, and chronic pain. Those who were told that medical procedures would be painful reported more pain than those who were told that the procedures would be relatively painless.

For those suffering from the nocebo effect, then, every step farther into the medical establishment, with its attendant warnings and consents, is a step down. Of course the difference between feeling pain, reporting pain, and feeling comfortable enough to fully report pain, not to mention depression or anxiety, is a nebulous one. Still there are those deaths. The nocebo effect seems to suggest that it's possible to talk someone to death.
...barcode never lies
FLA

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а ово је спекулација на могуће ефекте ноцеба

The Anthropocebo Effect Explains How Our Minds Can Destroy the World


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Jennifer Jacquet
Assistant Professor of Environmental Studies, NYU; Researching cooperation and the tragedy of the commons
The Anthropocebo Effect
Humans are today something we have never been before: a global geologic force. This epoch, which begins around 1800, has been called the Anthropocene and is characterized by steep line graphs that look like Mount Everest sliced in half: human population, water use, biodiversity loss, nitrogen run off, atmospheric carbon dioxide, etc.

The data irrefutably establish humans as the dominant driver of environmental change, which is something that should worry us all. But we should also be worried that framing humans as the dominant driver of change will lead to further negative change, which I am calling the "Anthropocebo Effect".

The effects of cultural framing are everywhere. The Placebo Effect (experiencing the positive effects of an inert pill) occurs only in cultures that believe taking a pill can cure an illness. The even stranger Nocebo Effect, where just mentioning the side effects makes them more likely to occur, shows the power of the mind.

The Anthropocebo Effect is then a psychological condition that exacerbates human-induced damage—a certain pessimism that makes us accept human destruction as inevitable.

Science helps shape how we see ourselves. Words also matter to perception, and perception matters to behavior.  Consider what the theory of natural selection did to our view of humans in the biological world.  We should be worried about the new era of Anthropocene—not only as a geological phenomenon, but also as a cultural frame.

сам блог на коме се налази овај текст је одличан извор антропоцеба :)



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We worry because we are built to anticipate the future. Nothing can stop us from worrying, but science can teach us how to worry better, and when to stop worrying.
WHAT SHOULD WE BE WORRIED ABOUT?
Tell us something that worries you (for scientific reasons), but doesn't seem to be on the popular radar yet—and why it should be. Or tell us something that you have stopped worrying about, even if others do, and why it should be taken off the radar.
...barcode never lies
FLA

Meho Krljic

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Ako vam se presađivanje fekalija čini kao odveć bizarna terapija, čak i ako treba da vam spase život, izgleda da imate sreće - stižu pilule punjene smrznutim fekalijama, za oralnu konzumpciju:


Feces-filled capsules treat bacterial infection

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Clostridium difficile infections kill approximately 14,000 Americans every year, often because the diarrhea-causing bacteria are highly resistant to standard antibiotics. Now, scientists have found an unusual way to combat the bugs: human feces in pill form. Doctors have used so-called fecal transplants since the 1950s to combat various types of infections. The treatment is thought to work by restoring the gut’s natural balance of bacteria, which can outcompete the invading microbes for resources. Typically, physicians insert the donor feces rectally through a colonoscopy or a plastic tube running into the nose or mouth and down to the stomach. While these procedures are both relatively safe, they are not entirely devoid of risk. In the new study, published today in The Journal of the American Medical Association, researchers show that frozen fecal matter encapsulated in clear, 1.6 g synthetic pills (not pictured) was just as safe and effective as traditional fecal transplant techniques at treating C. difficile. Within 8 weeks or less, 18 out of 20 participants saw a complete resolution of diarrhea after consuming 30 or 60 of the feces-filled capsules. “It’s probably not the best experience of your life,” says team leader Ilan Youngster, a pediatric infectious disease doctor at Harvard University. “But it beats getting a tube stuck down your throat or a colonoscopy … or having C. diff.”

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There May Be a Monumental New Finding in the Fight Against HIV/AIDS





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On Tuesday, scientists in Paris claim to have discovered the genetic mechanism that allows for a "​spontaneous cure" among a very rare group of HIV-infected patients called "elite controllers." These people belong in a fewer-than-1-percent group. They are able to keep the virus inactive in their bodies, with virtually undetectable symptoms.
 The two asymptomatic patients studied in this case were a 57-year-old man diagnosed in 1985, and a 23-year-old man infected in 2011. The scientists have stated the phenomenon isn't new. However,  they've detailed new findings in medical journal Clinical Microbiology and Infection, writing that the virus was inactive due to an altered HIV gene coding that prevented it from replicating in immune cells. This spontaneous evolution is called "endogenization." The claim states this could be the result of the stimulation of an enzyme—a method that could possibly be used for a future AIDS cure.
 "The work opens up therapeutic avenues for a cure, using or stimulating this enzyme, and avenues for identifying individuals among newly infected patients who have a chance of a spontaneous cure," they wrote. This is a different approach from previously attempted cures, which aimed to eradicate all traces of HIV from the body. The researchers believe that, instead, it may actually be the persistence of HIV DNA that could cure infected patients. To further their study, the scientists have called for "massive sequencing" of human DNA, particularly from African patients who have been exposed to HIV the longest.
 It's not a foolproof method, and we could still be far from a real AIDS cure. There are still many scientists who are dubious about the findings. For one, Jonathan Ball, molecular virology professor at University of Nottingham, has told AFP that there is no real evidence of a cure in their work. Others, like Sharon Lewis, Director of Doherty Institute for Infection and Immunity in Melbourne, say that the real battle now is finding the right protein for "crippling the virus." Only time, and a lot more research, will tell.

Meho Krljic

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Počinju klinički testovi na ljudima za verepamil, inače kardiovaskularni lek, koji je kod miševa i drugih test-sisara uspeo da, er, izleči dijabetes (doduše samo tip I). Ovo je stvarno zanimljiva vest.


In human clinical trial, UAB to test drug shown to completely reverse diabetes in human islets, mice



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New research conducted at the University of Alabama at Birmingham has shown that the common blood pressure drug verapamil completely reverses diabetes in animal models. Now, thanks to a three-year, $2.1 million grant from the JDRF, UAB researchers will begin conducting a potentially groundbreaking clinical trial in 2015 to see if it can do the same in humans.
The trial, known as “the repurposing of verapamil as a beta cell survival therapy in type 1 diabetes,” is scheduled to begin early next year and has come to fruition after more than a decade of research efforts in UAB’s Comprehensive Diabetes Center.
The trial will test an approach different from any current diabetes treatment by focusing on promoting specialized cells in the pancreas called beta cells, which produce insulin the body needs to control blood sugar. UAB scientists have proved through years of research that high blood sugar causes the body to overproduce a protein called TXNIP, which is increased within the beta cells in response to diabetes, but had never previously been known to be important in beta cell biology. Too much TXNIP in the pancreatic beta cells leads to their deaths and thwarts the body’s efforts to produce insulin, thereby contributing to the progression of diabetes.
But UAB scientists have also uncovered that the drug verapamil, which is widely used to treat high blood pressure, irregular heartbeat and migraine headaches, can lower TXNIP levels in these beta cells — to the point that, when mouse models with established diabetes and blood sugars above 300 milligrams per deciliter were treated with verapamil, the disease was eradicated.


“We have previously shown that verapamil can prevent diabetes and even reverse the disease in mouse models and reduce TXNIP in human islet beta cells, suggesting that it may have beneficial effects in humans as well,” said Anath Shalev, M.D., director of UAB’s Comprehensive Diabetes Center and principal investigator of the verapamil clinical trial. “That is a proof-of-concept that, by lowering TXNIP, even in the context of the worst diabetes, we have beneficial effects. And all of this addresses the main underlying cause of the disease — beta cell loss. Our current approach attempts to target this loss by promoting the patient’s own beta cell mass and insulin production. There is currently no treatment available that targets diabetes in this way.”
The trial will enroll 52 people between the ages of 19 and 45 within three months of receiving a diagnosis of type 1 diabetes. Patients enrolled will be randomized to receive verapamil or a placebo for one year while continuing with their insulin pump therapy. In addition, they will receive a continuous glucose monitoring system that will enable them to measure their blood sugar 24 hours a day, seven days a week.
Fernando Ovalle, M.D., director of UAB’s Comprehensive Diabetes Clinic and co-principal investigator of the study, helped develop the clinical trial and will oversee all clinical aspects of the trial, including subject recruitment, treatment, testing, and data acquisition and analysis. Recruitment for the trial will begin in early 2015.
“Currently, we can prescribe external insulin and other medications to lower blood sugar; but we have no way to stop the destruction of beta cells, and the disease continues to get worse,” Ovalle said. “If verapamil works in humans, it would be a truly revolutionary development in a disease affecting more people each year to the tune of billions of dollars annually.”
 Battling a health crisis Diabetes, which is the nation’s seventh-leading cause of death, raises risks for heart attacks, blindness, kidney disease and limb amputation. Recent federal government statistics show that 12.3 percent of Americans 20 and older have diabetes, either diagnosed or undiagnosed. Another 37 percent have pre-diabetes, a condition marked by higher-than-normal blood sugar. That is up from 27 percent a decade ago.
While a new report in the Journal of the American Medical Association showed rates at which new cases are accumulating have slowed in recent years, the numbers remain high and are still increasing overall, with 8.3 percent of adults diagnosed with the disease as of 2012. And no slowing of the disease has been seen in new cases among blacks and Hispanics or in overall rates among people with high school educations or less.
Plus, the annual cost to treat the disease is exorbitant — and rising. The American Diabetes Association reports that the disease cost the nation $245 billion in 2013.
Researchers have known for some time that beta cells are critical in type 1 and type 2 diabetes. The cells are gradually lost in both types of the disease due to programmed cell death, but the exact triggers for the deaths were previously unknown. Somewhat surprisingly, it was also noted that, after years — decades, even — of living with type 1 diabetes, where beta cells were thought to be completely destroyed early on by the autoimmune process, patients still had a measurable amount of beta cell function; it just was not enough to maintain a normal blood sugar. 



Shalev says replacing this beta cell mass by transplantation has proved more difficult and problematic than initially thought, but creating an environment that would enable beta cells to survive and possibly regenerate or become functional again does provide an attractive alternative by increasing the body’s own beta cell mass. UAB lab studies have shown verapamil to be extremely effective in this area, which has helped to make this clinical trial — funded by the JDRF, the largest charitable supporter of type 1 diabetes research — a possibility now.
JDRF is funding this study as part of its beta cell restoration research program whose goal is to restore a person’s ability to produce their own insulin — in essence, a biological cure for type 1 diabetes.
“A first step towards that goal may be the ability to improve the survival and functioning of a person’s beta cells shortly after diagnosis,” said JDRF director of Discovery Research, Andrew Rakeman, Ph.D. “This study represents the result of years of investment in basic research at JDRF. We are now at the stage of translating basic laboratory research into potential significant new therapies for type 1 diabetes and we’re excited to support Dr. Shalev’s team to test this concept in a study of people with type 1 diabetes. Finding a therapy to improve beta cell survival and functioning would put JDRF’s efforts to find a cure on a new trajectory.”
Ovalle will manage all patients with the use of insulin pumps and continuous glucose sensors and co-manage patients who are already seeing another endocrinologist remotely. UAB’s clinic team will analyze patients’ blood sugar control and their ability to produce insulin. They will also use a more complex test known as c-peptide response as a way to measure beta cell insulin production and functional beta cell mass.
One of the truly unique and different aspects of this clinical trial is that, unlike most type 1 diabetes trials, the verapamil trial does not include the use of any immunosuppressive or immune modulatory medications, which often have very severe side effects.
“This trial is based on a well-known blood pressure medication that has been used for more than 30 years and is unlikely to have any severe side effects,” Shalev said. “This study is also backed by a lot of strong mechanistic data in different mouse models and human islets, and we already know the mechanisms by which verapamil acts. Finally, unlike any currently available diabetes treatment, the trial targets the patient’s own natural beta cell mass and insulin production.”

A first step Shalev says the trial is a first step in the direction of such a novel diabetes treatment approach.
“While in a best-case scenario, the patients would have an increase in beta cells to the point that they produce enough insulin and no longer require any insulin injections — thereby representing a total cure — this is extremely unlikely to happen in the current trial, especially given its short duration of only one year,” Shalev said.
Shalev expects verapamil to have a much more subtle yet extremely important effect.
“We know from previous large clinical studies that even a small amount of the patient’s own remaining beta cell mass has major beneficial outcomes and reduces complications,” Shalev said. “That’s probably because even a little bit of our body’s own beta cells can respond much more adequately to very fine fluctuations in our blood sugar — much more than we can ever do with injections or even sophisticated insulin pumps.”
Because verapamil’s mode of action is different from current drugs or interventions, this opens up an entirely new field for diabetes drug discovery — one that UAB’s Comprehensive Diabetes Center is already engaged in with the Alabama Drug Discovery Alliance, a partnership between UAB’s School of Medicine and Southern Research Institute. The group is actively looking for small therapeutic molecules that inhibit TXNIP to protect the beta cells and treat diabetes.
“We want to find new drugs — different from any current diabetes treatments — that can help halt the growing, worldwide epidemic of diabetes and improve the lives of those affected by this disease,” Shalev said. “Finally, we have reason to believe that we are on the right track.”
Shalev says none of the research leading up to this point — nor the clinical trial itself — would have been possible without the existence of the UAB Comprehensive Diabetes Center and the continued support of the community. To fund this and other diabetes research at UAB, visit the Comprehensive Diabetes Center.

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Ovo su strahote:


Dumped drugs lead to resistant microbes



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A continual discharge of antibiotic-contaminated water has created a hotspot of bacterial antibiotic resistance in an Indian river.


High levels of antibiotic resistance have been found in bacteria that live downstream from a waste-water treatment plant in Patancheru, near Hyderabad in India1.
Two years ago, Joakim Larsson of the University of Gothenburg, Sweden, and his colleagues reported that the treatment plant released drugs in its effluent water at levels sometimes equivalent to the high doses that are given therapeutically2. The antibiotic-containing water reaching the plant came from 90 bulk pharmaceutical manufacturers in the region, near Hyderabad, they determined. The researchers wondered what might be happening to bacteria in the environment exposed to these drugs.
  Serendipitous resistance Bacteria can trade bundles of drug-resistance genes in mobile 'cassettes' carried, for example, on small circles of DNA called plasmids, which can replicate themselves independently of the bacterium's chromosome. To find these DNA snippets, Larsson and his colleagues used a DNA sequencing approach called 'shotgun metagenomics', to analyse all the DNA present in the effluent, the river water and the river sediments they had gathered in the earlier study. Postdoctoral researcher Erik Kristiansson developed a bioinformatics method to parse the information and search for evidence of known antibiotic-resistance genes.
In three sites downstream of the plant, the resistance genes made up almost 2% of the DNA samples taken there, the researchers report in  PLoS ONE1. Because only one or two genes out of the typical genome of around 5,000 genes are necessary to protect the bacterium, that's a lot of genetic resistance, says Dave Ussery, a microbiologist at the Technical University of Denmark, who was not involved in the work.
The researchers found resistance genes for a wide range of antibiotics but the relationship to the antibiotics present was not straightforward. For example, the most frequent resistance genes found were for a class of antibiotics called sulphonamides, but the researchers found no evidence of the drugs themselves. They hypothesize that this may be an instance where resistance to one group of drugs could provide resistance to others.
And despite detecting high concentrations of fluoroquinolones, a chemical class that includes the heavy-hitting antibiotic ciprofloxacin, the team found less evidence of resistance to these drugs downstream than upstream from the plant. The researchers suggest that the levels of fluoroquinolones in the downstream effluent were so high that they overpowered even the resistant bugs.
Finding resistance amid so much exposure to active drug ingredients "is not surprising," comments David Graham at Newcastle University, UK, who has studied sites in Cuba, for example, exposed to lower levels of medical waste. "But in a way, it's sort of like a beaker experiment," he says, that tests the worst-case scenario, only this is "in a natural system. That's what makes it useful".
  Round the world ticket? The spread of antibiotic-resistance genes is complicated, says Björn Olsen, an infectious-disease specialist at Uppsala University in Sweden. Olsen says resistance hotspots like the one at Patancheru could end up behaving like a volcanic eruption: "the cloud is going to drop down somewhere else, not just around the sewage plant". His team recently documented multidrug-resistant  Escherichia coli  in the faeces of birds that migrate to the Arctic3.
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   The presence of high levels of antibiotics in the river and its sediments might not actually be the factor driving the genetic resistance, warns Sheridan Haack, a microbiologist at the US Geological Survey (USGS) in Lansing, Michigan. Resistance genes already present in bacteria from human waste, or developed by the bacteria used in the plant's treatment stages to break down the sludge, could be swept along with the effluent into the river.
Whatever the reason, the high rates of resistance found by Larsson and his team are interesting, says Haack, and the team seems to be the first to combine this metagenomic approach to environmental samples with bioinformatics. She says that Larsson's team should now use more traditional, specific searches for resistance genes and for the surviving bacterial species that are carrying those genes.
Ussery cautions that even if the bacteria found are not dangerous to humans or other animals in the area, they may transfer their resistance genes to bacteria that are. "They need to know who's there," says Ussery, to identify which species are surviving and which are the sources of genetic resistance.



Antibiotics resistance: Drug firms 'to blame'


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Drug companies are partly to blame for the rise of antibiotic resistance, which threatens to make even what was once the mildest of infections deadly, one industry chief executive claims.



Doctors have usually been blamed for bacterial resistance because of over-prescribing, but Karl Rotthier, chief executive of the Dutch DSM Sinochem Pharmaceuticals, claims lax procedures at drugs companies are the real cause.
He said the industry that produced life-saving antibiotics was also fuelling a global crisis.
He said that poor waste-water management had caused some rivers in Patancheru, India, to have higher concentrations of active antibiotics than the blood of patients undergoing treatment.
Rotthier said the world risks "sleepwalking" towards the end of modern medicine and a "post-antibiotic era".
"For a couple of years now antimicrobial resistance has been rising and if we don't do anything we risk deaths of up to 10million a year by 2050," he said.
"Something once as innocuous as a throat infection could become a life-threatening condition, and treatments such as transplant surgery would become impossible.
"As medicine producers, our business is intrinsically good. But we do not always live up to the responsibility we have towards society. Irresponsible behaviour is tainting the image of our industry and puts society at risk."
The World Health Organisation echoes Rotthier's concerns and has classified antimicrobial resistance as a "serious threat" to every region of the world. It says it "has the potential to affect anyone, of any age".
Rotthier said: "Most antibiotics are now produced in China and India and I do not think it is unjust to say that the environmental conditions have been quite different in these regions.
"Poor controls mean that antibiotics are leaking out and getting into drinking water. They are in the fish and cattle that we eat, and global travel and exports mean bacteria are travelling. That is making a greater contribution to the growth of antibiotic resistance than over-prescribing."
Antibiotic resistance is estimated to contribute to more than 25000 deaths every year in Europe alone.
Penicillin, the first antibiotic, was discovered in 1928 and more than 100 compounds have been found since but, until a reported discovery earlier this month, no new class has been found since 1987.
Dame Sally Davies, the UK government's chief medical officer, has said that antibiotic resistance is "as big a risk as terrorism" and warned that Britain could return to a 19th-century world in which the smallest infection or operation could kill.
Rotthier said the responsibility was on everyone, from patients and doctors to governments and pharmaceutical companies, to take immediate steps to ensure the "legacy of antibiotics as a life-saving medicine is not squandered".
"In some countries antibiotics are readily available over the counter and they are being given to cattle and painted on to boats to prevent algae," Rotthier added.
"We need to insist on the highest standards of environmental protection methods for producing antibiotics so no waste water and sludge ends up in our lakes.
"We cannot have companies discharging untreated waste water into our environment, contributing to illness and, worse, antibacterial resistance. We cannot accept that rivers in India show higher concentrations of active antibiotic than the blood of someone undergoing treatment."
Earlier this month scientists in the US said that they had discovered the first new antibiotic in nearly 30 years, hailing it as a "paradigm shift" in the fight against growing resistance to drugs.

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ноцебо аген!
виа ио9

How The "Nocebo Effect" Can Trick Us Into Actually Dying

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Why Your Doctor Talks Like That

The nocebo effect and the attempts made to avoid it help explain the exaggeratedly bland hospital language that often exasperates patients. "This is going to hurt like hell," seems charmingly honest, but it's also something that can cause people to hurt more than they would for the comparatively disingenuous "some patients may experience some discomfort."

How The "Nocebo Effect" Can Trick Us Into Actually Dying
A few words are effective in causing or preventing pain. Patients with back pain who took a stretch test were more likely to feel pain if the doctors administering it admitted it could hurt. If the doctors just shut up and let them stretch, they tended to report no pain.

This puts doctors in a bind. There's no ethical way to practice medicine without allowing patients informed consent. Informed consent means letting a patient know about everything that could go wrong with them. By mentioning these details, all the things that could cause a patient to feel pain, to regress, or to die, a doctor could be increasing the suffering, or even hastening the death, of a person who would have been fine with less information. This puts doctors in the position of trying to give patients information while simultaneously trying to keep them from focusing on it. The practice leads to some weird quirks. One paper on the nocebo effect and surgery notes "an epidemic that "kills 1,286 people out of every 10,000" is perceived as worse than an epidemic that "kills 24.14% of the population," even though the latter kills almost twice as many people." It advises doctors to give death and complication rates in percentages, rather than numbers per thousand.
...barcode never lies
FLA

Meho Krljic

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Fekalna transplantacija agen!!!!!!!!! Ovog puta pričamoo neželjenim efektima, kao što je na primer: dobijete fekalni transplant od osobe koja ima problem sa gojaznošću - vi razvijete problem sa gojaznošću. Kod miševa se ovo do sada takođe dešavalo, a evo sad i kod ljudiju:


Woman's stool transplant leads to 'tremendous weight gain'


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A woman has dramatically gained weight after a stool transplant from her daughter, doctors report.
It is a genuine medical procedure to transplant healthy bacteria into a diseased gut, but US doctors think it may have affected her waistline.
She quickly gained 36lb (16kg) and is now classed as obese, the case report in Open Forum Infectious Diseases says.
A UK expert said the link between gut bugs and obesity was still unclear.
A faecal microbiota transplant - also referred to by some as a "transpoosion" - is like an extreme version of a probiotic yogurt.
The aim is to introduce good bacteria into the gut and it was officially backed by the UK health service last year.
 New treatment It is used when people have stubborn Clostridium difficile infection in their bowels.
This can cause vomiting, diarrhoea and abdominal pain and cannot always be treated with antibiotics.


The 32-year old woman, who has not been indentified, had an infection that could not be treated with even the most powerful antibiotics.
Dr Colleen Kelly, from the Medical School at Brown University, said the option of a faecal transplant was discussed and the woman wanted to use a relative - her daughter.
The daughter was overweight at the time and was on her way to becoming obese.
The procedure did clear the woman's infection.
But Dr Kelly told the BBC News website: "She came back about a year later and complained of tremendous weight gain.
"She felt like a switch flipped in her body - to this day she continues to have problems."
She started with a Body Mass Index of 26.  Sixteen months after the procedure she had a BMI of 33 and three years after it, a BMI of 34.5.
 Caution Previous research has shown that transplanting gut bacteria from obese people into mice led to the animals gaining weight.
Dr Kelly said limited conclusions could be drawn from a single patient, but called the case a warning as "there's not a lot on safety evidence out there".
Dr Kelly has now changed her practices and "as a result I'm very careful with all our donors don't use obese people".
Dr Andreas Karatzas, from Reading University, said: "You have to bear in mind that this person was saved.
"If you run the risk of losing a patient, you don't bother about what could happen 20 years later."
However, he said the evidence that gut bacteria affected human waistlines was still inconclusive.
"There is some evidence in animals, but we have to be careful - it is a different organism. Just because it happens in animals doesn't mean it happens in humans as well."

Doduše, već par godina se priča i o tome da bi gojazni ljudi mogli da smršaju dobijajući fekalne transplante od mršavih.


zakk

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Why shouldn't things be largely absurd, futile, and transitory? They are so, and we are so, and they and we go very well together.

Meho Krljic

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Studija poredi negativne efekte alkohola, duvana, kanabisa i drugih narkotika da bi se videlo šta je najgore. Spojlr alrt: alkohol pobeđuje.


Comparative risk assessment of alcohol, tobacco, cannabis and other illicit drugs using the margin of exposure approach



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Abstract
A comparative risk assessment of drugs including alcohol and tobacco using the margin of exposure (MOE) approach was conducted. The MOE is defined as ratio between toxicological threshold (benchmark dose) and estimated human intake. Median lethal dose values from animal experiments were used to derive the benchmark dose. The human intake was calculated for individual scenarios and population-based scenarios. The MOE was calculated using probabilistic Monte Carlo simulations. The benchmark dose values ranged from 2 mg/kg bodyweight for heroin to 531 mg/kg bodyweight for alcohol (ethanol). For individual exposure the four substances alcohol, nicotine, cocaine and heroin fall into the “high risk” category with MOE < 10, the rest of the compounds except THC fall into the “risk” category with MOE < 100. On a population scale, only alcohol would fall into the “high risk” category, and cigarette smoking would fall into the “risk” category, while all other agents (opiates, cocaine, amphetamine-type stimulants, ecstasy, and benzodiazepines) had MOEs > 100, and cannabis had a MOE > 10,000. The toxicological MOE approach validates epidemiological and social science-based drug ranking approaches especially in regard to the positions of alcohol and tobacco (high risk) and cannabis (low risk).Compared to medicinal products or other consumer products, risk assessment of drugs of abuse has been characterised as deficient, much of this is based on historical attribution and emotive reasoning1. The available data are often a matter of educated guesses supplemented by some reasonably reliable survey data from the developed nations2. Only in the past decade, have there been some approaches to qualitatively and quantitatively classify the risk of drugs of abuse. These efforts tried to overcome legislative classifications, which were often found to lack a scientific basis3. UNODC suggested the establishment of a so-called Illicit Drug Index (IDI), which contained a combination of a dose index (the ratio between the typical dose and a lethal dose) and a toxicology index (concentration levels in the blood of people who died from overdose compared with the concentration levels in persons who had been given the drug for therapeutic use)4. King and Corkery5 suggested an index of fatal toxicity for drugs of misuse that was calculated as the ratio of the number of deaths associated with a substance to its availability. Availability was determined by three separate proxy measures (number of users as determined by household surveys, number of seizures by law enforcement agencies and estimates of the market size). Gable6 provided one of the earliest toxicologically founded approaches in a comparative overview of psychoactive substances. The methodology was based on comparing the “therapeutic index” of the substances, which was defined as the ratio of the median lethal dose (LD50) to the median effective dose (ED50). The results were expressed in a qualitative score as safety margin from “very small” (e.g. heroin) to “very large” (e.g. cannabis). In a follow-up study, Gable7 refined the approach and now provided a numerical safety ratio, which allowed a rank-ordering of abused substances.
Despite these early efforts for toxicology-based risk assessments, the most common methods are still based on expert panel rankings on harm indicators such as acute and chronic toxicity, addictive potency and social harm, e.g. the approaches of Nutt et al.8,9 in the UK and of van Amsterdam et al.3 in the Netherlands. The rankings of the two countries correlated very well3,8. Similar studies were conducted by questioning drug users, resulting in a high correlation to the previous expert judgements10,11,12. The major criticism that was raised about these “panel” based approaches was the necessity of value judgements, which might depend upon subjective personal criteria and not only upon scientific facts13. The methodology was also criticized because a normalization to either the total number of users or the frequency of drug use was not conducted, which might have biased the result toward the harms of opiate use14 and may have underrepresented the harms of tobacco15. Problematic may also have been the nomenclature applied in previous studies, mixing up “hazard” and “risk” into the term “drug harm”. In chemical and toxicological risk assessment, the term “harm” is not typically used, while hazard is the “inherent property of an agent or situation having the potential to cause adverse effects when an organism, system, or (sub)population is exposed to that agent”. Risk is defined as “the probability of an adverse effect in an organism, system, or (sub)population caused under specified circumstances by exposure to an agent”16.
In the context of the European research project “Addiction and Lifestyles in Contemporary Europe – Reframing Addictions Project”, the aim of this research was to provide a comparative risk assessment of drugs using a novel risk assessment methodology, namely the “Margin of Exposure” (MOE) method. The Margin of Exposure (MOE) is a novel approach to compare the health risk of different compounds and to prioritize risk management actions. The MOE is defined as the ratio between the point on the dose response curve, which characterizes adverse effects in epidemiological or animal studies (the so-called benchmark dose (BMD)), and the estimated human intake of the same compound. Clearly, the lower the MOE, the larger the risk for humans. The BMD approach was first suggested by Crump17, and was later refined by the US EPA for quantitative risk assessment18. In Europe, the MOE was introduced in 2005 as the preferred method for risk assessment of carcinogenic and genotoxic compounds19. In the addiction field, the MOE method was never used, aside from evaluating substances in alcoholic beverages20,21 or tobacco products22,23. This study is the first to calculate and compare MOEs for other addiction-related substances.Go to:ResultsThe only toxicological threshold available in the literature for all of the compounds under study was the LD50. The LD50 values taken from the ChemIDplus database of the US National Library of Medicine and from Shulgin24 are shown in table 1. Using the method of Gold et al.25, the LD50 values were extrapolated assuming linear behaviour (as no other information on dose-response is available) to BMDL10 values. As shown in Supplementary Table S1 online, the full range of available LD50 values in different animal species is taken into account as a risk function assuming a normal distribution for BMDL10 rather than that a single value is entered into the calculation (except methamphetamine and MDMA for which only one value was available in the literature). The mean values of BMDL10 range from 2 mg/kg bodyweight (bw) for heroin and cocaine up to 531 mg/kg bw for ethanol.Table 1Table 1Toxicological thresholds selected for calculating the margin of exposureTo determine the typical range of individual daily dosage, various textbook and internet sources21,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41 were evaluated (Table 2). As no information about the most likely function for dosage distribution is available, a uniform probability distribution was entered into the calculation in this case (Supplementary Table S1).Table 2Table 2Exposure data selected for calculating the margin of exposure (see Supplementary Table S1 online for distribution functions used for calculation)The data used for calculation of population-based exposure is shown in Table 2. Prevalence data was available for all drugs except methadone; and amphetamine and methamphetamine were grouped together. For a sub-group of drugs, exposure estimation based on sewage analysis is available (Table 2) (not all drugs are available in sewage analysis due to different stabilities/degradation rates of the compounds, for details see Ref. 26). The corresponding risk functions are shown in Supplementary Table S1 online. Except for ethanol and nicotine, for which certain distributions could be fitted to the data for the European countries, uniform probability distributions were chosen in all other cases as only minimum/maximum prevalence values for Europe in total were available. The detailed calculation formulae chosen for probabilistic risk assessment are shown in Supplementary Table S2 online.
The margin of exposure values were calculated for individual exposure (Figure 1), population-based exposure calculated from prevalence data (Figure 2) and population-based exposure calculated from sewage analysis (Figure 3). The full numerical results of the MOE distributions are presented in Supplementary Table S3 online. For both individual and population-based scenarios, alcohol consumption was found to have the lowest margin of exposure. For individual exposure, heroin has the second lowest margin of exposure. However, considering worst-case scenarios (e.g. 5th percentile), heroin may have a lower MOE than alcohol (compare standard deviation bars in Figure 1). On the other end of the scale, THC or cannabis can be consistently found to have high MOE values, as well as amphetamine-type stimulants and benzodiazepines. Cocaine and nicotine/tobacco were found to have intermediary MOE values.Figure 1Figure 1Margin of exposure for daily drug use estimated using probabilistic analysis (left red bar: average; error bar: standard deviation; right gray bar: tolerant user; circle symbol (for alcohol): value based on human data).Figure 2Figure 2Margin of exposure for the whole population based on prevalence data estimated using probabilistic analysis (left red bar: average; error bar: standard deviation; right gray bar: tolerant user; circle symbol (for alcohol and cannabis): value based on ...Figure 3Figure 3Margin of exposure for the whole population based on sewage analysis estimated using probabilistic analysis (left red bar: average; error bar: standard deviation; right gray bar: tolerant user; circle symbol (for THC): value based on human.For sensitivity analysis, three different methods were applied: convergence testing during the probabilistic simulation, application of a factor to consider drug tolerance, and comparison with human toxicological thresholds for some of the agents.
Convergence was achieved for all calculated output MOE values. This means that the generated output distributions are stable and reliable. The estimated means change less than 5% as additional iterations are run during the simulation. From the model input variables, the highest influence (as expressed by rank of regression coefficients) on the results is caused by the exposure, rather than the toxicological thresholds or the bodyweights.
The sensitivity analysis data for tolerant users are additionally shown in Figure 1–3 based on the ratio between no-tolerance and high tolerance dosage as shown in Table 227,37,42,43,44,45,46,47,48,49,50,51,52,53,54. Even though the general results remain stable (i.e. especially alcohol at the top position), the ranks between opiates and cocaine change due to the high tolerance to extreme dosages that was reported for opiates. However, as the percentage of tolerant users is generally unknown, the most probable value of MOE would lie in the range between non-tolerant and tolerant users (the gray-marked area in Figures 1–3).
Finally, the sensitivity analysis results from application of human toxicity data for some of the compounds (alcohol, nicotine and THC21,55,56,57) are shown in Supplementary Table S3 online and marked in Figures 1–3. For alcohol, the human MOE results correspond closely to the ones calculated from animal LD50. For the other compounds, a discrepancy between animal and human data was detected (see discussion).Go to:DiscussionMany governments in Europe have favoured more restrictive policies with respect to illicit drugs than for alcohol or tobacco, on the grounds that they regard both illicit drug abuse and related problems as a significantly larger problem for society58. Drug rankings can therefore be useful to inform policy makers and the public about the relative importance of licit drugs (including prescription drugs) and illicit drugs for various types of harm58.
Our MOE results confirm previous drug rankings based on other approaches. Specifically, the results confirm that the risk of cannabis may have been overestimated in the past. At least for the endpoint of mortality, the MOE for THC/cannabis in both individual and population-based assessments would be above safety thresholds (e.g. 100 for data based on animal experiments). In contrast, the risk of alcohol may have been commonly underestimated.
Our results confirm the early study of Gable6 who found that the margin of safety (defined as therapeutic index) varied dramatically between substances. In contrast, our approach is not based on a therapeutic index, which is not necessarily associated with risk, but uses the most recent guidelines for risk assessment of chemical substances, which also takes the population-based exposure into account.
A major finding of our study is the result that the risk of drugs varies extremely, so that a logarithmic scale is needed in data presentation of MOE (e.g. Figures 1–3). Therefore, we think that previous expert-based approaches which often applied a linear scale of 0–3 or 0–1003,9, might have led to a form of “egalitarianism”, in which the public health impact of drugs appears more similar than it is in reality (i.e. more than 10.000-fold different as shown in our results on a population basis, e.g. Fig. 2 and ​and3).3). As expected, for an individual the difference between the impact of different drugs is not as large as for the whole society (i.e. only up to 100 fold, Fig. 1).
According to the typical interpretation of MOEs derived from animal experiments, for individual exposure the four substances alcohol, nicotine, cocaine and heroin fall into the “high risk” category with MOE < 10, the rest of the compounds except THC fall into the “risk” category with MOE < 100. On a population scale, only alcohol would fall into the “high risk” category, and cigarette smoking would fall into the “risk” category. A difference between individual and whole population MOE was confirmed by the lack of correlation between average values (linear fit: R = 0.25, p = 0.53). This result is different to the previous expert-based surveys, for which the ranking performed at the population and individual level generally led to the same ranking (R = 0.98)3. Nevertheless, we judge our results as more plausible. For an individual heavy consumer of either heroin or alcohol, the risk of dying from a heroin overdose or from alcoholic cirrhosis increased considerably in each case. However for the society as a whole, the several ten-thousands of alcohol-related deaths considerably outnumber drug overdose deaths. Hence, it is plausible that the MOE for alcohol can be lower than the one for heroin, purely because of the high exposure to alcohol in the European society (see also Rehm et al.59).
Nevertheless, as previously stressed, our findings should not be interpreted that moderate alcohol consumption poses a higher risk to an individual and their close contacts than regular heroin use14. Much of the harm from drug use is not inherently related to consumption, but is heavily influenced by the environmental conditions of the drug use2, and this additional hazard is not included in a drug ranking based on (animal) toxicology.
The first major problem of the approach is the lack of toxicological dose-response data for all compounds except alcohol and tobacco. No human dose-response data are available; also no dose-response data in animals, only LD50 values are published. Furthermore, no chronic-toxicity data (long-term experiments) are available, which are usually used for such kinds of risk assessment. Therefore, we can assess only in regards to mortality but not carcinogenicity or other long-term effects. The absence of such data is specifically relevant for compounds with low acute toxicity (such as cannabis), the risk of which may therefore be underestimated.
Additionally, the available toxicological thresholds (i.e. LD50 values) have considerable uncertainty (for example, more than a factor of 10 for diazepam in different species). However it has been previously shown that the animal LD50 is closely related to fatal drug toxicity in humans60. The sensitivity analysis based on human data for ethanol shows that the average MOE result is similar to the result based on animal LD50. Our results for ethanol are also consistent with previous MOE studies of ethanol20,21. For cannabis and nicotine, the discrepancy in the sensitivity analysis can be explained in the chosen endpoints (no dose response data on mortality in humans were identifiable in the literature). For example, the only available human toxicological endpoint for cannabis as chosen by EFSA55 was “psychotropic effects”. The rationale for choosing this endpoint was the exclusion of risk for the inadvertent and indirect ingestion of THC when hemp products are used as animal feed55. We were unable to identify dose-response information for other endpoints of cannabis (e.g. mental health problems, chronic risk, or other cannabis-constituents besides THC). We think that while it is clear that different endpoints may yield quite different results, the human MOE for cannabis based on the endpoint “psychotropic effects” can be seen as general validation of the MOE concept, because the resulting values below 1 are expected as the psychotropic effect is the desired endpoint (and hence the psychotropic threshold dose is exceeded by drug users). Similar to cannabis, the sensitivity analysis for nicotine based on human data resulted in much lower MOE values. This again is based on a different endpoint (increase of blood pressure in this case, which is expected to be more sensitive than mortality). We nevertheless think that the risks of cigarettes could have been underestimated in our modelling, because in contrast to the other agents, tobacco contains a multicomponent mixture of toxicants. Previous risk assessment of tobacco (both financed and co-authored by the tobacco industry) have looked at various compounds but not included nicotine itself22,23. From the variety of investigated compounds in tobacco smoke, the lowest MOEs were found for hydrogen cyanide (MOE 15)22 and acrolein (MOE range 2–11)23. These values are reasonably consistent with our MOE for nicotine of 7.5 (individual exposure). However, it would be advisable for future risk assessments of tobacco smoking to include modelling of a combined MOE, which considers all toxic compounds.
The second major problem is the uncertainty in data about individual and population-wide exposure due to the illegal markets. There is a scarcity of epidemiological studies of cannabis use by comparison with epidemiological studies of alcohol and tobacco use61. If population data are available, they are usually provided as “% prevalence”, but for risk assessment we need a population-wide per-capita dosage in “mg compound/person/day”.
Due to both problems (or in other words the large uncertainty in input data of exposure), we cannot calculate with point estimates. To overcome this, we are using a probabilistic calculation methodology that takes the whole distribution of the input variables into account. For example, for the exposure a random sample of the number of days of annual drug use is combined with a random sample in the range of the usual dosages of the drug to provide an estimate for dosage.
The downside of the probabilistic approach is that the output also is not a single numerical value but rather a likelihood distribution. Nevertheless, using graphical approaches (Figs. 1–3) the results for all drugs under study can be quickly compared. On the other hand, this may be an advantage, as we did not try to establish a single value “to be written in stone”. The utility of “single figure index harm rankings” has also been questioned in general62.
Our approach contains some further limitations: Drug interactions cannot be taken into account as we just do not have any toxicological data on such effects (e.g. by co-administration in animals). However, polydrug use in humans is common, especially of illicit drugs with ethanol or benzodiazepines63. Addiction potential and risk of use (e.g. unclean syringes leading to increased infection risk) are also not considered by the model, because adequate dose-response data could not be identified for these endpoints.
Aside from the limitations in data, our results should be treated carefully particularly in regard to dissemination to lay people. For example, tabloids have reported that “alcohol is worse than hard drugs” following the publication of previous drug rankings. Such statements taken out of context may be misinterpreted, especially considering the differences of risks between individual and the whole population.
A main finding of our study is the qualitative validation of previous expert-based approaches on drug-ranking (e.g. Nutt et al.9), especially in regard to the positions of alcohol (highest) and cannabis (lowest). Currently, the MOE results must be treated as preliminary due to the high uncertainty in data. The analyses may be refined when better dose-response data and exposure estimates become available. As the problem is multidimensional15, it would also make sense to establish some form of harm or risk matrix64 that may be more suitable than a single indicator. Our MOE could be one piece in the puzzle that constitutes to the establishment of a “holistic drug risk”.
Currently, the MOE results point to risk management prioritization towards alcohol and tobacco rather than illicit drugs. The high MOE values of cannabis, which are in a low-risk range, suggest a strict legal regulatory approach rather than the current prohibition approach.Go to:MethodsThe methodology for comparative quantitative risk assessment was based on a previous study conducted for compounds in alcoholic beverages20 with the exception that probabilistic exposure estimation was conducted65,66,67. The MOE approach was used for risk assessment18,19. The MOE is defined as the ratio between the lower one-sided confidence limit of the BMD (BMDL) and estimated human intake of the same compound. If the BMD as preferred toxicological threshold for MOE assessment is unavailable, no observed effect levels (NOEL), no observed adverse effect levels (NOAEL) or lowest observed adverse effect levels (LOAEL) may be applied. As none of these thresholds (neither human data nor animal data) was available for the illicit drugs, LD50 values from animal experiments were selected instead and extrapolated to BMDL. The exposure was calculated for individual scenarios of daily drug use, as well as for population based scenarios using drug prevalence data and sewage analysis data for Europe, which is a promising complementary approach for estimating the drug use in the general population.
The MOE was calculated using the software package @Risk for Excel Version 5.5.0 (Palisade Corporation, Ithaca, NY, USA). Monte Carlo simulations were performed with 100,000 iterations using Latin Hypercube sampling and Mersenne Twister random number generator. Convergence was tested with a tolerance of 5% and a confidence level of 95%. The distribution functions and detailed calculation methodology is specified in Supplementary Tables S1–S2 online.Go to:Author ContributionsD.W.L. conceived of the study, conceptualized the data analyses and performed the calculations. J.R. collected the data from WHO and provided additional data for sensitivity analysis. All authors have been involved in the drafting of the article and the interpretation of the data and in critical revisions of the content. All authors have given final approval of the version to be published.Go to:Supplementary MaterialSupplementary Information: Supplementary Tables S1-S3Click here to view.(147K, doc)Go to:AcknowledgmentsThe research leading to these results or outcomes has received funding from the European Community's Seventh Framework Programme (FP7/2007–2013), under Grant Agreement n° 266813 - Addictions and Lifestyle in Contemporary Europe – Reframing Addictions Project (ALICE RAP – www.alicerap.eu). Participant organisations in ALICE RAP can be seen at http://www.alicerap.eu/about-alice-rap/partner-institutions.html. The views expressed here reflect only the author's and the European Union is not liable for any use that may be made of the information contained therein. Support to CAMH for the salaries of scientists and infrastructure has been provided by the Ontario Ministry of Health and Long Term Care. The contents of this paper are solely the responsibility of the authors and do not necessarily represent the official views of the Ministry of Health and Long Term Care or of other funders.



Meho Krljic

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Alchajmer je na kolenima: nova terapija potpuno vraća funkciju pamćenja (kod miševa):


New Alzheimer’s treatment fully restores memory function



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Of the mice that received the treatment, 75 percent got their memories back.


Australian researchers have come up with a non-invasive ultrasound technology that clears the brain of neurotoxic amyloid plaques - structures that are responsible for memory loss and a decline in cognitive function in Alzheimer’s patients.
If a person has Alzheimer’s disease, it’s usually the result of a build-up of two types of lesions - amyloid plaques, and neurofibrillary tangles. Amyloid plaques sit between the neurons and end up as dense clusters of beta-amyloid molecules, a sticky type of protein that clumps together and forms plaques.

 Australian researchers have come up with a non-invasive ultrasound technology that clears the brain of neurotoxic amyloid plaques - structures that are responsible for memory loss and a decline in cognitive function in Alzheimer’s patients.
If a person has Alzheimer’s disease, it’s usually the result of a build-up of two types of lesions - amyloid plaques, and neurofibrillary tangles. Amyloid plaques sit between the neurons and end up as dense clusters of beta-amyloid molecules, a sticky type of protein that clumps together and forms plaques.
Neurofibrillary tangles are found inside the neurons of the brain, and they’re caused by defective tau proteins that clump up into a thick, insoluble mass. This causes tiny filaments called microtubules to get all twisted, which disrupts the transportation of essential materials such as nutrients and organelles along them, just like when you twist up the vacuum cleaner tube.
As we don’t have any kind of vaccine or preventative measure for Alzheimer’s - a disease that affects 343,000 people in Australia, and 50 million worldwide - it’s been a race to figure out how best to treat it, starting with how to clear the build-up of defective beta-amyloid and tau proteins from a patient’s brain. Now a team from the Queensland Brain Institute (QBI) at the University of Queensland have come up with a pretty promising solution for removing the former.
Publishing in Science Translational Medicine, the team describes the technique as using a particular type of ultrasound called a focused therapeutic ultrasound, which non-invasively beams sound waves into the brain tissue. By oscillating super-fast, these sound waves are able to gently open up the blood-brain barrier, which is a layer that protects the brain against bacteria, and stimulate the brain’s microglial cells to activate. Microglila cells are basically waste-removal cells, so they’re able to clear out the toxic beta-amyloid clumps that are responsible for the worst symptoms of Alzheimer’s.
The team reports fully restoring the memories of 75 percent of the mice they tested it on, with zero damage to the surrounding brain tissue. They found that the treated mice displayed improved performance in three memory tasks - a maze, a test to get them to recognise new objects, and one to get them to remember the places they should avoid.
"We’re extremely excited by this innovation of treating Alzheimer’s without using drug therapeutics," one of the team, Jürgen Götz, said in a press release. "The word ‘breakthrough’ is often misused, but in this case I think this really does fundamentally change our understanding of how to treat this disease, and I foresee a great future for this approach."
The team says they’re planning on starting trials with higher animal models, such as sheep, and hope to get their human trials underway in 2017.
You can hear an ABC radio interview with the team here.

mac

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Ovo je fenomenalno otkriće! Fizičko rešenje za kako se čini fizički problem. Doduše čovek mora povremeno da ide na terapiju, ali ne bi me čudilo da jednom naprave kućni aparat, koji ćemo svi dnevno koristiti na svojim glavama da budemo svežiji i "pametniji". I predeće nam na glavi kao neka mehanička mačka.

Pitanje je samo da li moramo da budemo zdravi (od bakterija i virusa) za ovu proceduru, pošto se tokom procedure otvara barijera krv-mozak, jer u suprotnom neki mikrob može da se provuče i napravi haos žurku u mozgu.

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što je onda zovu ''neinvazivnom'' metodom?

u svakom slučaju, đe su sve turali te sonde i čuda, može i u vugla 8-)

mac

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Pa ne otvaraju ti glavu nego ultrazvukom preko kože i kostiju utiču na razne stvari u glavi.

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sorry, ja to stvarno laički shvatam

dakle, ne bi mi dirali kožu al mogu mozak da skaše, pa to je superinvazivno 8-)

kao neće biti ožiljaka a unutra pire krompir :)

a neka antibiotska terapija iz predostrožnosti ne bi riješila stvar?

Meho Krljic

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Ovo nije ni lek ni terapija nego... bolest? Za koju se tek nadamo da će je prepoznati kao bolest i naći terapiju. Užasno zvuči:
 Joni Mitchell suffers from a disease most doctors think isn't real
 
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When Joni Mitchell was admitted to the hospital this week after being found unconscious in her Los Angeles home, a controversial affliction she has long suffered with hit the headlines again.
 
The 71-year-old singer-songwriter has often complained of her battle with Morgellons, a medical mystery that has stumped the scientific community for years.
 
"I couldn't wear clothing. I couldn't leave my house for several years," she described in her 2014 book Joni Mitchell: In Her Own Words. "Sometimes it got so I'd have to crawl across the floor. My legs would cramp up, just like a polio spasm. It hit all of the places where I had polio." (It's unclear if Morgellons was related to her recent hospitalization, but she has certainly brought attention to the issue over the years.)
 
 Morgellons involves unexplained itching sensations
 
Sufferers of Morgellons report itching, biting, and crawling sensations.  "Fibers in a variety of colors protrude out of my skin," Mitchell has said. "They cannot  be forensically identified as animal, vegetable or mineral."

They say their skin feels like it's erupting from underneath, infested by insects, worms, or mysterious fibers. Like Mitchell, they say their symptoms are debilitating: they point to lesions that won't heal, and say the biting and stinging that afflicts them every day leaves them fatigued and depressed, even affecting their memory.
 
 
Mitchell wrote in her book: "Morgellons is constantly morphing. There are times when it's directly attacking the nervous system, as if you're being bitten by fleas and lice. It's all in the tissue and it's not a hallucination. It was eating me alive, sucking the juices out. I've been sick all my life."
 
The condition was first described in the 1600s, and then named in 2001 by an American, Mary Leitao, whose son's itching couldn't be remedied or explained by modern medicine. Leitao eventually scraped his skin and examined the samples under a microscope. She found fiber-like strands, which she determined "cannot be coming out of my son's body," she told the Pittsburgh Post-Gazette.

After getting frustrated by her doctors' dismissive tones, she launched the Morgellons Research Foundation and began pressuring Congress to figure out what was going on. The movement gained traction in the United States in 2005, when lawmakers requested that the Centers for Disease Control and Prevention investigate.
 Researchers say Morgellons is a "mass-shared delusion"
For the past decade, researchers have searched for a biological cause or single underlying factor that might explain the suffering. But they have mostly concluded that Morgellons is "a psychosis or mass-shared delusion."
 
In one of the most comprehensive studies to date, published in the journal PLOS, researchers from the CDC collected detailed epidemiological information, medical histories, and skin samples from 115 Morgellons sufferers in Northern California.
 
"No parasites or mycobacteria were detected," they reported. The researchers also couldn't find any environmental explanation for patients' suffering.
 
 
The fiber-like strands on sufferers were mostly just cotton debris, probably lint from clothing. Their skin damage seemed to be caused by nothing more than sun exposure. While some patients had sores, these appeared to have arisen from chronic picking and scratching.
 
Interestingly, a large number of people in the study had a psychiatric or addictive condition, including depression and drug use. Among half of the participants in the study used drugs, but it wasn't clear whether the drugs caused the symptoms or whether they were being used to deal with the disease.

Even so, the researchers could not uncover any particular underlying medical condition or infectious source, and concluded that Morgellons is "similar to more commonly recognized conditions such as delusional infestation."
 
That last conclusion is echoed by other research on Morgellons patients. One study, out of the Mayo Clinic, concluded this way: "Although patients are convinced that their skin is infested with parasites or inanimate material," skin biopsies and specimen analyses turned up no evidence of infestation. The patients were probably suffering from delusional parasitosis — or the false belief that one is infected with parasites — the researchers determined.
 Still, many patients insist Morgellons is very real
For now, delusional parasitosis is the most common diagnosis for Morgellons sufferers, with many skeptics arguing that this is just "a cultural entity spreading mainly on the internet." (There are a few medical experts who think Morgellons is a real disease, but they are in the minority.)
 
Doctors, for their part, seem exasperated by the phenomenon. As Jeffrey Meffert, a dermatologist at the University of Texas Health Science Center in San Antonio, told Newsweek, "People with delusional parasitosis are very functional and rational except when it comes to this one issue." He continued: "Many dermatologists  would rather these patients never show up, because they don't feel they  have the time to spend. No one knows how to deal with them."
 
Still, the issue hasn't gone away. For people like Mitchell, the lack of empirical evidence doesn't diminish their suffering. They feel dismissed by most doctors and let down by modern medicine. And even though many experts feel that further research is a waste of time and money, calls to pursue the issue are unlikely to disappear.

Indeed, the online discussion — fueled by  celebrities like Mitchell — "gives the  condition a name, gives   it a  shape, and gives the sufferers a community  with which to interact  and  legitimize the condition" said Tim Caulfield, a researcher and author of  Is Gwyneth Paltrow Wrong About Everything? When Celebrity Culture and Science Clash.

That  community creates advocacy, and winds up driving the research agenda,  whether or not it's scientifically warranted. "The exposure that's created by celebrities," Caulfield continued, "can help shape the research agenda, and researchers are very savvy. As things gain exposure in popular culture, it creates  an interest in the area, and perhaps increases the chance for research funding. The Joni phenomenon is part of this."


Meho Krljic

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Kako preduprediti demenciju pod stare dane? Lako, budite gojazni!!!!!!  :-| :-| :-| :-| :-|
 
 Being overweight 'reduces dementia risk'
 
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Being overweight cuts the risk of dementia, according to the largest and most precise investigation into the relationship.
The researchers admit they were surprised by the findings, which run contrary to current health advice.
The analysis of nearly two million British people, in the Lancet Diabetes & Endocrinology, showed underweight people had the highest risk.
Dementia charities still advised not smoking, exercise and a balanced diet.
Dementia is one of the most pressing modern health issues. The number of patients globally is expected to treble to 135 million by 2050.
There is no cure or treatment, and the mainstay of advice has been to reduce risk by maintaining a healthy lifestyle. Yet it might be misguided.'Surprise'The team at Oxon Epidemiology and the London School of Hygiene and Tropical Medicine analysed medical records from 1,958,191 people aged 55, on average, for up to two decades.
Their most conservative analysis showed underweight people had a 39% greater risk of dementia compared with being a healthy weight.
But those who were overweight had an 18% reduction in dementia - and the figure was 24% for the obese.
"Yes, it is a surprise," said lead researcher Dr Nawab Qizilbash.
He told the BBC News website: "The controversial side is the observation that overweight and obese people have a lower risk of dementia than people with a normal, healthy body mass index.
"That's contrary to most if not all studies that have been done, but if you collect them all together our study overwhelms them in terms of size and precision."
 
 
Any explanation for the protective effect is distinctly lacking. There are some ideas that vitamin D and E deficiencies contribute to dementia and they may be less common in those eating more.
But Dr Qizilbash said the findings were not an excuse to pile on the pounds or binge on Easter eggs.
"You can't walk away and think it's OK to be overweight or obese. Even if there is a protective effect, you may not live long enough to get the benefits," he added.
Heart disease, stroke, diabetes, some cancers and other diseases are all linked to a bigger waistline.AnalysisBy James Gallagher, Health editor, BBC News website
These findings have come as a surprise, not least for the researchers themselves.
But the research leaves many questions unanswered.
Is fat actually protective or is something else going on that could be harnessed as a treatment? Can other research groups produce the same findings?
Clearly there is a need for further research, but what should people do in the meantime?
These results do not seem to be an excuse to eye up an evening on the couch with an extra slice of cake.
The Alzheimer's Society and Alzheimer's Research UK have both come out and encouraged people to exercise, stop smoking and have a balanced diet.Dr Simon Ridley, of Alzheimer's Research UK, said: "These new findings are interesting as they appear to contradict previous studies linking obesity to dementia risk.
"The results raise questions about the links between weight and dementia risk. Clearly, further research is needed to understand this fully."
The Alzheimer's Society said the "mixed picture highlights the difficulty of conducting studies into the complex lifestyle risk factors for dementia".
Prof Deborah Gustafson, of SUNY Downstate Medical Center in New York, argued: "To understand the association between body mass index and late-onset dementia should sober us as to the complexity of identifying risk and protective factors for dementia.
"The report by Qizilbash and colleagues is not the final word on this controversial topic."
Dr Qizilbash said: "We would agree with that entirely."
 

Meho Krljic

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Užas. Pleme u amazonskim džunglama Venecuele kontaktirano nedavno po prvi put od strane naučnika već ima bakterije u crevima koje su otporne na antibiotike.


Resistance to antibiotics found in isolated Amazonian tribe




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When scientists first made contact with an isolated village of Yanomami hunter-gatherers in the remote mountains of the Amazon jungle of Venezuela in 2009, they marveled at the chance to study the health of people who had never been exposed to Western medicine or diets. But much to their surprise, these Yanomami’s gut bacteria have already evolved a diverse array of antibiotic-resistance genes, according to a new study, even though these mountain people had never ingested antibiotics or animals raised with drugs. The find suggests that microbes have long evolved the capability to fight toxins, including antibiotics, and that preventing drug resistance may be harder than scientists thought.
The human gut harbors trillions of bacteria, collectively known as the microbiome. Several recent studies have found that people in industrialized nations host far fewer types of microbes than hunter-gatherers in Africa, Peru, and Papua New Guinea, for example. This is intriguing as the absence of diverse bacteria has been linked to obesity, diabetes, and many autoimmune disorders, such as allergies, Crohn’s disease, celiac disease, and colitis.
So, when microbiologist Maria Dominguez-Bello of the New York University School of Medicine in New York City learned that army personnel aboard a helicopter had spotted Yanomami living in an uncharted village in the mountains of southern Venezuela in 2008, she immediately requested permission to study these uncontacted people before they were exposed to Western medicines and diets and would, therefore, lose diverse microbes. “This information is important; because it will give us some light on what are the bacteria we are missing, what bacteria are we losing,” she says. “We need to get a better understanding of the microbiota in this community of hunter-gatherers before they are lost.”
The Yanomami health care workers who were the first to contact the remote villagers in a medical expedition in 2009 collected bacteria from the mouths, skin, and feces of 34 of the 54 Yanomami for the researchers. They prescribed medicines to some children with respiratory ailments but have not published the name of the village to protect these people from further contact. After 2 years of getting the proper permits and an 11-month delay when Dominguez-Bello’s lab in New York was closed by damage from Hurricane Sandy, she and her colleagues eventually sequenced the Yanomami gut bacteria RNA in their labs to compare it with samples from industrialized Americans and rural Guahibo Amerindians of Colombia and farmers from Malawi. When they compared the genetic sequences, they found that the Yanomami harbor “significantly higher diversity than other populations,” including high amounts of Prevotella, Helicobacter, Oxalobacter, and Spirochaeta, for example, that are absent or significantly reduced in industrialized humans. The medical workers also documented that although these Yanomami had high levels of parasites, they were healthy and did not suffer from autoimmune disorders, diabetes, high blood pressure, or heart disease, the team reports today in Science Advances.
Meanwhile, microbiologist Gautam Dantas of Washington University in St. Louis interrogated the Yanomami gut and oral samples for the presence of antibiotic-resistance genes. Dantas’s graduate student Erica Pehrsson cloned bacterial DNA from these samples and tested whether any of their genes could inactivate natural and synthetic antibiotics. They found that the Yanomami gut bacteria had nearly 60 unique genes that could turn on and rally to fend off antibiotics, including a half-dozen genes that could protect the bacteria from synthetic antibiotics. This is particularly troubling, Dantas says, because researchers have thought that it would take bacteria longer to evolve resistance to humanmade antibiotics not found naturally in the soil.
The medical team’s interviews with these Yanomami villagers found they were never given drugs or exposed to food or water with antibiotics. Instead, Dantas suggests that the Yanomami gut bacteria have evolved an armory of methods to fight a wide range of toxins that threaten them—just as our ancestors and other primates have done to fight dangerous microbes. For example, the Yanomami bacteria may already have encountered toxins that occur naturally in their environment that are similar in molecular structure to modern antibiotics, but have yet to be discovered by scientists. Or, gut bacteria in humans have evolved a generalized mechanism for detecting certain features shared by all antibiotics—including the synthetic ones designed by scientists—and so can mount a defense against new threats.
The discovery is troubling because it suggests that “antibiotic resistance is ancient, diverse, and astonishingly widespread in nature—including within our own bodies,” says anthropologist Christina Warinner of the University of Oklahoma in Norman, who is not a co-author. “Such findings and their implications explain why antibiotic resistance was so quick to develop after the introduction of therapeutic antibiotics, and why we today should be very concerned about the proper use and management of antibiotics in both clinical and agricultural contexts.”
Other researchers are also interested in exploring the function of the diverse bacteria found in the Yanomami, to see if these microbes train their children’s immune systems early and if they are protective against autoimmune diseases on the rise in industrialized populations. One type of gut bacteria, Oxalobacter, found in the Yanomami is already known to protect humans from the formation of kidney stones. “I think these missing microbes are at the root of many Western diseases,” says microbiologist Justin Sonnenburg of Stanford University in Palo Alto, California, co-author of the forthcoming book The Good Gut: Taking Control of Your Weight, Your Mood, and Your Long-term Health. “The big message is we in the Western world have lost the diversity in our microbiota. We have to study these groups to figure out what we lost, what these microbes do, and how we get back to a healthy microbiota.”
 

Meho Krljic

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Aderal je medikament koji lekari na dekadentnom zapadu prepisuju deci koja imaju problem sa ADHDom, dakle, hiperaktivna a sa slabom koncentracijom, jer pomaže da se bolje usredsrede. Ja sam već na neki od igračkih topika kačio reportaže o tome kako kompetitivni igrači, to jest profesionalni e-sportisti gutaju Aderal pre važnih LoL/ DotA turnira jer ih bolje fokusira. Studenti po Americi takođe ovo koriste kad treba da uče jer - bolje uče.  Međutim sad se razvija debata o tome da li korišćenje Aderala da budete bolji radnik u firmi može da dovede do hemijskog rata za radna, jelte, mesta.

Njujork Tajmz je pitao nekoliko stručnjaka za mišljenje.


Meho Krljic

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Kad smo već na Njujork tajmzu, valja pročitati ovo o pripremi zakona koji će učiniti vakcinaciju dece obaveznom:


Bill Requiring Vaccination of Children Advances in California, but Hurdles Remain



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LOS ANGELES —  A bill that would require nearly all children in California to be vaccinated by eliminating “personal belief” exemptions advanced through the State Legislature on Wednesday, though it still has several hurdles to clear. If approved, California would become one of only three states that require all parents to vaccinate their children as a condition of going to school, unless there is a medical reason not to do so.
Under the bill, introduced after a measles outbreak that began at Disneyland, parents who refuse vaccines for philosophical or religious reasons would have to educate their children at home. The legislation prompted a roiling debate in Sacramento, and last week hundreds of people protested at the Capitol, arguing that it infringed on their rights and that it would unfairly shut their children out of schools.
   
  Last Wednesday, the legislation stalled in the Senate Education Committee as lawmakers said they were concerned that too many students would be forced into home schooling. This Wednesday, however, the bill passed that committee after its authors tweaked it, adding amendments that would expand the definition of home schooling to allow multiple families to join together to teach their children or participate in independent study programs run by public school systems.


“We think we’ve struck a fair balance here that provides more options for parents who don’t want to vaccinate their children,” said Senator Ben Allen, a Democrat from Santa Monica and a co-author of the bill.
The legislation still must clear at least one other committee before coming to a vote by the full Senate. If it is approved, it would then go through several committees in the State Assembly before being considered during a floor vote.
“This bill still has a long way to go,” said Senator Carol Liu, a Democrat and chairwoman of the Senate Education Committee. Ms. Liu requested some changes to the bill last week and said she was still not “completely satisfied.”
“I do think in terms of public health it is necessary, but I am concerned about the rights of our parents,” she said.
Ms. Liu joined six other senators who voted in favor of the bill; two voted against it.
Unlike last week, there was no public comment at the committee meeting. Still, opponents of the bill stood outside the Capitol holding signs that read “Let freedom win” and “Because there is a risk we must have a choice.”
Senator Richard Pan, a physician and the lead author of the bill, said he would not agree to an amendment to allow exemptions for religious reasons, saying that they could easily be abused.
The number of personal belief exemptions has increased drastically in recent years. In 2014, there were about 535,000 kindergartners in California, and 2.5 percent had a personal belief exemption, compared with less than 1 percent in 2000. In some school districts, more than 20 percent of kindergartners received personal belief exemptions.
Mr. Pan, like other doctors, has repeatedly said that the vaccination rate has fallen so low in some communities that “herd immunity” that prevents infectious diseases from spreading has been compromised.
“Let’s not forget there are children who cannot be immunized,” Mr. Pan said. “These children deserve protection, they need to be safe.”

Ako se Amerikanci prizivaju pameti, možda ima nade i za nas?  :lol: :lol: :lol: :lol:

Meho Krljic

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I ovo možda može u ovaj topik, mada je moglo i u "Živimo SF" ali ajde da napravim het-trik. Dakle, kineski naučnici uspešno genecki modifikovali ljudski embrion. Užasne posledice ćemo sigurno videti u nekom američkom filmu za godinu-dve:



Chinese scientists genetically modify human embryos



Quote
Rumours of germline modification prove true — and look set to reignite an ethical debate.
 
In a world first, Chinese scientists have reported editing the genomes of human embryos. The results are published1 in the online journal Protein & Cell and confirm widespread rumours that such experiments had been conducted — rumours that sparked a high-profile debatelast month2, 3 about the ethical implications of such work.
In the paper, researchers led by Junjiu Huang, a gene-function researcher at Sun Yat-sen University in Guangzhou, tried to head off such concerns by using 'non-viable' embryos, which cannot result in a live birth, that were obtained from local fertility clinics. The team attempted to modify the gene responsible for β-thalassaemia, a potentially fatal blood disorder, using a gene-editing technique known as CRISPR/Cas9. The researchers say that their results reveal serious obstacles to using the method in medical applications.
"I believe this is the first report of CRISPR/Cas9 applied to human pre-implantation embryos and as such the study is a landmark, as well as a cautionary tale," says George Daley, a stem-cell biologist at Harvard Medical School in Boston, Massachusetts. "Their study should be a stern warning to any practitioner who thinks the technology is ready for testing to eradicate disease genes."


Some say that gene editing in embryos could have a bright future because it could eradicate devastating genetic diseases before a baby is born. Others say that such work crosses an ethical line: researchers warned in Nature2 in March that because the genetic changes to embryos, known as germline modification, are heritable, they could have an unpredictable effect on future generations. Researchers have also expressed concerns that any gene-editing research on human embryos could be a slippery slope towards unsafe or unethical uses of the technique.
The paper by Huang's team looks set to reignite the debate on human-embryo editing — and there are reports that other groups in China are also experimenting on human embryos.
   Problematic gene                                                            The technique used by Huang’s team involves injecting embryos with the enzyme complex CRISPR/Cas9, which binds and splices DNA at specific locations. The complex can be programmed to target a problematic gene, which is then replaced or repaired by another molecule introduced at the same time. The system is well studied in human adult cells and in animal embryos. But there had been no published reports of its use in human embryos.
Huang and his colleagues set out to see if the procedure could replace a gene in a single-cell fertilized human embryo; in principle, all cells produced as the embryo developed would then have the repaired gene. The embryos they obtained from the fertility clinics had been created for use in in vitro fertilization but had an extra set of chromosomes, following fertilization by two sperm. This prevents the embryos from resulting in a live birth, though they do undergo the first stages of development.
Huang’s group studied the ability of the CRISPR/Cas9 system to edit the gene called HBB, which encodes the human β-globin protein. Mutations in the gene are responsible for β-thalassaemia.
   Serious obstacles                                                            The team injected 86 embryos and then waited 48 hours, enough time for the CRISPR/Cas9 system and the molecules that replace the missing DNA to act — and for the embryos to grow to about eight cells each. Of the 71 embryos that survived, 54 were genetically tested. This revealed that just 28 were successfully spliced, and that only a fraction of those contained the replacement genetic material. “If you want to do it in normal embryos, you need to be close to 100%,” Huang says. “That’s why we stopped. We still think it’s too immature.”
His team also found a surprising number of ‘off-target’ mutations assumed to be introduced by the CRISPR/Cas9 complex acting on other parts of the genome. This effect is one of the main safety concerns surrounding germline gene editing because these unintended mutations could be harmful. The rates of such mutations were much higher than those observed in gene-editing studies of mouse embryos or human adult cells. And Huang notes that his team likely only detected a subset of the unintended mutations because their study looked only at a portion of the genome, known as the exome. “If we did the whole genome sequence, we would get many more,” he says.
   Ethical questions                                                            Huang says that the paper was rejected by Nature and Science, in part because of ethical objections; both journals declined to comment on the claim. (Nature’s news team is editorially independent of its research editorial team.)
He adds that critics of the paper have noted that the low efficiencies and high number of off-target mutations could be specific to the abnormal embryos used in the study. Huang acknowledges the critique, but because there are no examples of gene editing in normal embryos he says that there is no way to know if the technique operates differently in them.
Still, he maintains that the embryos allow for a more meaningful model — and one closer to a normal human embryo — than an animal model or one using adult human cells. “We wanted to show our data to the world so people know what really happened with this model, rather than just talking about what would happen without data,” he says.
But Edward Lanphier, one of the scientists who sounded the warning in Nature last month, says: "It underlines what we said before: we need to pause this research and make sure we have a broad based discussion about which direction we’re going here." Lanphier is president of Sangamo BioSciences in Richmond, California, which applies gene-editing techniques to adult human cells.
Huang now plans to work out how to decrease the number of off-target mutations using adult human cells or animal models. He is considering different strategies — tweaking the enzymes to guide them more precisely to the desired spot, introducing the enzymes in a different format that could help to regulate their lifespans and thus allow them to be shut down before mutations accumulate, or varying the concentrations of the introduced enzymes and repair molecules. He says that using other gene-editing techniques might also help. CRISPR/Cas9 is relatively efficient and easy to use, but another system called TALEN is known to cause fewer unintended mutations.
The debate over human embryo editing is sure to continue for some time, however. CRISPR/Cas9 is known for its ease of use and Lanphier fears that more scientists will now start to work towards improving on Huang's paper. “The ubiquitous access to and simplicity of creating CRISPRs," he says, "creates opportunities for scientists in any part of the world to do any kind of experiments they want.”
A Chinese source familiar with developments in the field said that at least four groups in China are pursuing gene editing in human embryos.
 Naturedoi:10.1038/nature.2015.17378

Meho Krljic

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U budućnosti možda ne bude homeopatije jer, eto, nauka veli da ona zapravo ne radi ništa...



Are We Seeing the End of Homeopathy?





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Several years ago, during a lecture on Science-Based Medicine, I noted that if there were one medical pseudoscience that was vulnerable to extinction it was homeopathy. Homeopathy is perhaps the most obviously absurd medical pseudoscience. It is also widely studied, and has been clearly shown to not work. Further, there is a huge gap in the public understanding of what homeopathy is; it therefore seems plausible that the popularity of homeopathy can take a huge hit just by telling the public what it actually is.
Further, homeopathy is in a precarious regulatory position. Homeopathic products are presented and regulated as drugs, but clearly they are not, and they are also not supplements, herbal drugs, nutrition-based, or natural products. They are simply fraudulent drugs riding a wave of ignorance.
In the last few years homeopathy has had a rough time. While the industry is still growing, there are signs of clear trouble on the horizon. Let’s review:
Some Background
Homeopathy is a 200 year old pre-scientific system of medicine based upon magical thinking. It is mostly based on two notions, the first of which is that like cures like. In other words, a substance that causes a symptom can cure that symptom in extremely low doses. There is no scientific basis for this, despite the desperate attempts by homeopaths to invoke vaccine-like analogies, or their new favorite, hormesis.
The second notion is that you make a remedy more powerful by diluting it to extreme degrees. People have fun making comparisons, such as the need to drink a solar-system’s worth of water to have a 50% chance of getting a single molecule of active ingredient. No problem, say the homeopaths, homeopathic potions contain the magical “essence” of what was previously diluted in them. It’s turtles all the way down.
Homeopaths are also hoist with their own petard when it comes to the evidence. Rigorous clinical trials of homeopathy are frustratingly (but not surprisingly) negative. Homeopaths explain this away by saying that double-blind placebo controlled trials are not really appropriate for homeopathic treatments. Such studies take a cookie-cutter approach to treatment, while real homeopathy individualizes the treatment to the patient. This argument, however, just creates two even more serious problems.
The first is that whenever homeopaths use this argument they throw the entire homeopathic industry under the bus. They are essentially saying that all over the counter (OTC) homeopathic products are useless, and even fraudulent. I would be happy to stipulate to this, and erase the entire OTC homeopathic product industry. We can then deal with homeopathic practitioners separately.
The second problem is the manner in which homeopathic treatments are individualized. This also is not based on any scientific principle or set of reliable empirical data. It’s all magic and witchcraft. Quirky traits, like whether someone is weepy, are used to determine their optimal treatment. There is also no consistency among homeopaths – see ten different homeopaths and you may get ten different treatments. This has more in common with an astrological reading than medicine. It is an elaborate system of utter nonsense.
Troubled Waters
Word that homeopathy is complete bollocks is starting to get out. In 2010 the UK House of Commons Science and Technology Committee completed a full report on homeopathy in which they concluded it is witchcraft – that it cannot work, it does not work, and support for homeopathy in the national health service should be completely eliminated. In 2015 the Australian government completed its own review, concluding that there is no evidence that homeopathy works for anything. Homeopathy is a placebo.
Homeopaths like to point to the favorable Swiss government review. However, as I have explained in detail previously, even the biased Swiss report, which was packed with homeopaths specifically to give a favorable review, could not conclude that there is rigorous evidence showing homeopathy works. They had to resort to arguing for lower quality evidence.
This was all just the beginning. The FDA and the FTC in the United States are now both receiving testimony, questioning their current regulation of homeopathy. Currently the FDA essentially doesn’t regulate homeopathy, even though the law tasks them to do so. They let the homeopathic industry regulate itself, but they are questioning this in light of the exploding OTC homeopathic product industry. This is a good thing. Any change is likely to be an improvement. Likewise, the FTC is accepting comments on how it can better regulate the advertising of homeopathic products.
There is even a possibility that the FDA will decide to do their actual job – require testing of homeopathic products to demonstrate efficacy before allowing them on the market. If they do this simple and obvious thing, the homeopathic industry in the US will vanish over night, because there is no evidence to support any homeopathic product for any indication. They will have to endure the outrage of quacks, charlatans, and the deluded, but hey, that’s their job. Suck it up.
While I hold out a sliver of hope, I am realistic about the political realities here. Doing the right thing because it is right, even when bold and courageous action is required, is a rarity in politics. Further, Congress may quickly take away any victory, even before they are enacted, by changing the law and taking away the FDAs power to regulate homeopathy. That is a fight I would love to have, however. At least it’s a fight.
Another outcome that is less than total victory but at least is an improvement is truth in labeling and advertising. Homeopathic products should be labeled so it is absolutely clear what they are – what the actual ingredients are in plain language, and in what amounts. Also, if the labels could not pretend to be real medicine, and make claims not supported by evidence, that would be a good thing.
Maybe then we could put pressure on pharmacies to stop selling them. This is also happening. The Royal Pharmaceutical Society’s chief scientist just wrote an editorial in which she writes:
 
The public have a right to expect pharmacists and other health professionals to be open and honest about the effectiveness and limitations of treatments. Surely it is now the time for pharmacists to cast homeopathy from the shelves and focus on scientifically based treatments backed by clear clinical evidence.
Some individual pharmacists at taking a stand, and throwing away their homeopathic products.
Conclusion
Homeopathy is obvious pseudoscience and magic that has no place in a modern society. It cannot work and it does not work. It is simply an expensive placebo.
All we need now is the political will to acknowledge these clear facts and regulate homeopathic products as they should be – essentially by banning them as fraudulent. Nothing short of that is honest or fulfills our duty to the public.
I would, however, welcome any partial victories that are a clear improvement over the current situation. Right now we have a clear window, with the FDA and FTC reviews. This is a good time to push public awareness of what nonsense homeopathy actually is.

zakk

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Mneee, dok ima ljudi sa problemima koje sistemska medicina ne rešava ili ne priznaje, biće i toga. Ja to ne podržavam, mislim da je to šarlatanstvo i uzimanje para bolesnima bez izbora, a ako ima boljitaka to je ili bočni efekat ili placebo.

Kod nas se doktori medicine uredno bave homeopatijom, ko sporedno ko full time. Imaš državnog homeopatu (mislim) u DZ Stari grad. Znam više ne-neozbiljnih ljudi koji se kunu da im je homeopatija pomogla gde je klasično zdravstvo zakazalo. I to je to.
Why shouldn't things be largely absurd, futile, and transitory? They are so, and we are so, and they and we go very well together.

mac

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Ni ja ne verujem u to čudo, a znam nekog ko se kune da mu je pomoglo (to jest nečijem malom detetu). Možda homeopatija ima efekta samo u slabo uređenim društvima, u kojima pritom vlada i sujeverje?

дејан

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кад смо код хомеопатије или не - имам пример у породици веома малог детета које вуче неки синдром/болес (опростите ми што сам заборавио како се зове) и код којег је класична медицина у потпуности заказала (све са чувеним - знате то се не лечи, такве ствари можемо само да пратимо и да се надамо да ће се организам некада у будућности сам изборити иако су шансе сасвим мале)
родитељи су у очају копали по интернету и налетели да се та болест веома успешно лечи хомеопатијом
они нађоше овде неку чувену др.мед. која се и званично бави хомеопатијом (све по препоруци) и жена је за 6 месеци довела дете у нормално, здраво стање.
сад тај хомео-плацебо једино да је деловао на родитеље па да су они екстрасензорно деловали на дете те је оно оздравило зато што су родитељи веровали да ће оно да оздрави...што би било још чудније од лековитог деловања хомеопатије
да се разумемо, дете је било превише мало да би било какав плацебо могао да се припише његовој свести.
едит...нисам имао мишљење о хомеопатији до овог фамилијарног случаја, сад мислим да ради пошто имам доказа за то.
...barcode never lies
FLA

zakk

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To baš i zeza: ZNAMO da je to samo šećerna kuglica, ali uprkos tome neki ljudi reše da im bude bolje. Ili kako već :)
Why shouldn't things be largely absurd, futile, and transitory? They are so, and we are so, and they and we go very well together.

mac

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Kad malo razmislim, ja samo mislim da znam nekog kome je homeopatija pomogla, ali sad ne mogu da se setim ko je to bio. Možda sam u stvari samo čuo priču o tome...

Meho Krljic

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New Letters Added to the Genetic Alphabet

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Scientists hope that new genetic letters, created in the lab, will endow DNA with new powers.

mac

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Možda je vreme za film Gattaca 2: Zagpact. Svi povlašćeni u prvom filmu na ime boljih gena bivaju zamenjeni novom klasom ljudi, i smešteni su u isti koš sa onima koji imaju loše gene. Nature's a bitch.

Nego, kad se DNK duplicira potrebno je da u okolini budu dostupni slobodni nukleotidi koji će da formiraju dva nova DNK lanca. Ako ima mnogo novih tipova nukleotida onda bara postaje mala za mnogo krokodila, i dupliciranje lanca je usporeno i otežano. Možda zato u prirodi imamo samo dva para.

Meho Krljic

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Bizarno dugačak tekst o vrlo zanimljivoj temi. A tema je... recimo, opsesija pronalaženjem leka za neke bolesti koje su za sada hronične/ neizlečive vs. traženja načina da se život sa tim bolestima učini udobnijim.

The Cure Culture



scallop

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Sad ću da lupim.
Palijativna farmacija je daleko isplativija od kurativne, koja često završi u ćorsokaku.
Never argue with stupid people, they will drag you down to their level and then beat you with experience. - Mark Twain.

Meho Krljic

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Pa, da, neki od komentara na ovaj tekst koje sam pročitao su imali sličan sentiment - da se više isplati da razvijaš medikamente koji neko stanje olakšavaju nego one koji ga izleče... I to nije ni netačno, no ovaj tekst gleda na stvari, mislim, iz drukčije perspektive.

Albedo 0

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generalno, jebeš bušenje guma, mogle bi i apoteke da se kamenuju

scallop

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Ne znam da li postoji neki zakon koji bi podsticao teška istraživanja za retke bolesti. Ne isplate se farmaceutskoj industriji. To ti je kao zakon da oni koji proizvode kifle i peciva moraju da proizvode i leba. Samo obrnuto.
Never argue with stupid people, they will drag you down to their level and then beat you with experience. - Mark Twain.

Father Jape

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Blijedi čovjek na tragu pervertita.
To je ta nezadrživa napaljenost mladosti.
Dušman u odsustvu Dušmana.

https://lingvistickebeleske.wordpress.com

Meho Krljic

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Pa, da.
 
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That’s the point. Science thrives on public debate

Meho Krljic

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Hm...
 
 Ebola vaccine trial proves 100% successful in Guinea
 
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A vaccine against Ebola has been shown to be 100% successful in trials conducted during the outbreak in Guinea and is likely to bring the west African epidemic to an end, experts say.

 
The results of the trials involving 4,000 people are remarkable because of the unprecedented speed with which the development of the vaccine and the testing were carried out.
 
Scientists, doctors, donors and drug companies collaborated to race the vaccine through a process that usually takes more than a decade in just 12 months.
 
“Having seen the devastating effects of Ebola on communities and even whole countries with my own eyes, I am very encouraged by today’s news,” said Børge Brende, the foreign minister of Norway, which helped fund the trial.
 
“This new vaccine, if the results hold up, may be the silver bullet against Ebola, helping to bring the current outbreak to zero and to control future outbreaks of this kind. I would like to thank all partners who have contributed to achieve this sensational result, due to an extraordinary and rapid collaborative effort,” he said on Friday.
 
There have been a total of 27,748 cases of Ebola in Guinea, Liberia and Sierra Leone up to 26 July, with 11,279 reported deaths, although the outcome of many cases is unknown and the toll will be significantly higher. In the week ending 26 July, there were just four new cases in Guinea and three in Sierra Leone.

 
Because of the diminishing number of Ebola cases in west Africa and the shifting nature of the epidemic, with many sudden small outbreaks occurring across the region, researchers hit on a novel design for the trial.
 
The “gold standard” approach would be to take a population at risk of Ebola and vaccinate half of them while giving the other half a placebo. Instead, the researchers used a “ring” design, similar to that which helped prove the smallpox vaccine worked in the 1970s.
 
When Ebola flared up in a village, researchers vaccinated all the contacts of the sick person who were willing – the family, friends and neighbours – and their immediate contacts. Children, adolescents and pregnant women were excluded because of an absence of safety data for them. In practice about 50% of people in these clusters were vaccinated.
 
To test how well the vaccine protected people, the cluster outbreaks were randomly assigned either to receive the vaccine immediately or three weeks after Ebola was confirmed. Among the 2,014 people vaccinated immediately, there were no cases of Ebola from 10 days after vaccination – allowing time for immunity to develop – according to the results published online in the Lancet medical journal (pdf). In the clusters with delayed vaccination, there were 16 cases out of 2,380.
 
In another precedent-breaker, the trial was sponsored by the World Health Organisation because “nobody wanted to step into this role so we took the risk”, said assistant director-general, Dr Marie-Paule Kieny.
 
Funding came from the Wellcome Trust and other partners, including the governments of Norway and Canada. Others involved included Médecins sans Frontières, whose volunteer doctors were on the front line, and the London School of Hygiene and Tropical Medicine. About 90% of the trial staff were from Guinea, a country where no clinical research had been carried out before. The vaccine is made by Merck.
 
Kieny said: “We believe that the world is on the verge of an efficacious Ebola vaccine.”
 
The trial will continue, but without randomisation, which means that in Guinea, where there have been 3,786 cases and 2,520 confirmed deaths, every contact of a person who develops Ebola – and their contacts – will be offered it. Work in Gabon has now established that the vaccine is safe for children and adolescents, so they will be offered it, too.
 
In terms of vaccines, which are usually trialled in hundreds of thousands of people, Kierny said the numbers were small but highly promising. It is likely when larger numbers are collected that efficacy will be between 75% and 100%.
 
The future of two other potential Ebola vaccines, one from GlaxoSmithKline and the other from Johnson & Johnson, is now in question, because there are too few cases of Ebola for their trials to be completed.
 
The authors of the research said the ring design made it “logistically feasible” to conduct trials even in poor countries in the middle of a fading epidemic and it was a promising strategy for the future.
 
“This trial dared to use a highly innovative and pragmatic design, which allowed the team in Guinea to assess this vaccine in the middle of an epidemic,” said Jeremy Farrar, director of the Wellcome Trust and one of the world’s leading experts on infectious disease. “It is a remarkable result which shows the power of equitable international partnerships and flexibility.

 
 “Our hope is that this vaccine will now help bring this epidemic to an end and be available for the inevitable future Ebola epidemics. This partnership also shows that such critical work is possible in the midst of a terrible epidemic. It should change how the world responds to such emerging infectious disease threats.”
 
John-Arne Røttingen, the head of infectious disease control at the Norwegian Institute of Public Health and chair of the trial’s steering group, said it had been a race against time in the most challenging circumstances.
 
“We are really pleased with the interim results,” he said. “It is really important to add the vaccine to the traditional hygiene measures we have used in the response so far. I believe this will be an important contribution to getting down to zero cases.”
 
Médecins sans Frontières said it was keen for the vaccine to be used in Sierra Leone and Liberia, where there were still cases.
 
Bertrand Draguez, MSF’s medical director, said: “In parallel with the ring vaccination we are also conducting a trial of the same vaccine on front-line workers. These people have worked tirelessly and put their lives at risk every day to take care of sick people. If the vaccine is effective, then we are already protecting them from the virus.

 
“With such high efficacy, all affected countries should immediately start and multiply ring vaccinations to break chains of transmission and vaccinate all front-line workers to protect them.”
 
Margaret Chan, the director general of of the WHO, said the vaccine trial’s success was a promising development. “The credit goes to the Guinean government, the people living in the communities and our partners in this project.”
 
The British government contributed £1m of the trial funding and has said it will increase that amount to help allow the testing to continue.
 
“Ebola has claimed thousands of lives and devastated communities across west Africa,” the international development secretary, Justine Greening, said. “The results of these UK-backed vaccine trials are hugely promising and represent a significant breakthrough in our battle against this deadly disease. The vaccine offers hope for a future where we never have to face an Ebola epidemic like this again.”
 
Trial data will now go to regulatory agencies in the hope of getting a licence for the vaccine that will allow it to be stockpiled for future Ebola epidemics. It is likely to be used only for people at risk in outbreaks and not given to whole populations.
 
The rVSV-ZEBOV vaccine is sometimes known as the Canadian vaccine as it was originally developed by the Public Health Agency of Canada before being sold to Merck to conclude the testing.
 

džin tonik

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Hm...
 
Quote
Scientists, doctors, donors and drug companies collaborated to race the vaccine through a process that usually takes more than a decade in just 12 months.

hm...

džin tonik

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ne, lijepo je to od medija, ali koliko god se trudio, zasluge ipak pripisujem sreci. nikako okolnosti da su ih nekako pokrenuli na 2 sata rada dnevno.
plus, posto smo sad dugorocno iscrpili kapacitete na nekakvoj eboli, ne znam koliko je ovo produktivno u borbi protiv virusa koji muce i velikog bijelog covjeka. da stanje bude gore, izgubili i one u padu zrakoplova nad ukrainom. bojim se da ce nas pojesti obicna gripa prije no sto ovi izadju iz burnouta ili stasaju nove generacije strucnjaka.

džin tonik

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dalje, sto je vanredno pogresno, igramo se boga u do nedavno zatvorenim primitivno-primalnim zajednicama koje opstanak osiguravaju brojnoscu, dok ih priroda na izdisaju i krajnje ocajno regulira ebolom.
i sad ce si jos nekolicina strucnjaka pripisati nekakve zasluge, otici na zasluzeni odmor, a sa bujicom migranata neka se zajebava netko drugi, sve da njihovo potomstvo ne bi zavrsilo na non-delegirajucim poslovima. dno.

Meho Krljic

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Non-invasive spinal cord stimulation gets paralyzed legs moving voluntarily again



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Five men with complete motor paralysis have regained the ability to move their legs voluntarily and produce step-like movements after being treated with a non-invasive form of spinal cord stimulation. The new treatment builds on prior work to generate voluntary movements in paralyzed people through electrical stimulation – in particular, two studies (one completed in 2011, the other in 2014) that involved surgically implanting an electrode array on the spinal cord. This time, however, the researchers found success without performing any invasive surgery.
The new treatment uses a technique called transcutaneous electrical nerve stimulation, which involves strategically placing electrodes on the skin of the lower back. While receiving stimulation, the men's legs were supported by braces that hung from the ceiling. At first their legs only moved involuntarily, if at all. But they soon found they could voluntarily extend the distance their legs moved during stimulation. They doubled their range of voluntary motion after four treatment sessions.
In an effort to further improve voluntary motion, the researchers gave the men a drug called buspirone during the final four weeks of the 18-week study. This drug mimics the neurotransmitter serotonin, and it is known to induce walking motions in mice with spinal cord injuries.
All five men had been paralyzed for more than two years prior to receiving the treatment, which lasted 45 minutes at a time and was conducted once a week for the duration of the study. But by the end of the study, after they had received the buspirone drug, they could all move their legs with no stimulation at all. This movement was comparable to what they achieved while receiving stimulation.
"It's as if we've reawakened some networks [in the nervous system]," said co-lead researcher V. Reggie Edgerton.
There appear to be connections between the brain and spinal cord even in some paralyzed people, only they have gone dormant. But electrical signals generated in the men's leg muscles during stimulation suggest this can be reversed.
Edgerton now hopes to test the non-invasive stimulation on people with partial paralysis. He also notes that, while the results here are very promising, both invasive and non-invasive forms of electrical stimulation will need to be developed further and one will likely not prove better than the other for everyone.
"All patients are going to need something slightly different," he said, "and maybe non-invasive stimulation is going to be best in some cases and epidural stimulation in others. What we need to do is maximize the clinical tool box that we have so that the physician and the patient can select a therapy that is best for them."
The study was conducted by researchers at UCLA, the University of California, San Francisco, and Russia's Pavlov Institute. A paper describing the research was published in the Journal of Neurotrauma.
The video below shows how men's leg movement improved after treatment.




http://youtu.be/lf5OMQbcJ90

Meho Krljic

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Joj, mene ovakve stvari intenzivno brinu. Namera je dobra, to je jasno, ali ove ideje mi deluju vrlo nerazborito. Mislim, wikipedija je sjajna stvar ali nije zamena za prave izbore znanja....


What is Open Source Pharma (and why should you care)?



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I’m writing this over the north Atlantic as I return from most of a week of very compelling meetings at a castle in Germany. Nominally, the subject of the discussion was something generally referred to as “open source pharma” (OSP). But more particularly, the meeting was about working towards saving the millions of lives a year that are lost either to so called “neglected diseases,” or because those stricken cannot possibly afford the price of the drugs that could provide a cure. Even though the actual cost of manufacturing the drugs they so desperately need may be only pennies a pill.What’s a neglected disease? It’s one that as much as half the world’s population is at risk of dying from, but which nevertheless doesn’t present an attractive profit target for any of the major pharmaceutical companies. Why? Because once again, those at risk can’t pay as much as patients in the developed world, and those in the developed world rarely get the disease. Diseases like malaria and drug resistant tuberculosis, which together claim millions of lives a year in developing countries. Open Source Pharma holds the promise of addressing these appalling realities, and it’s therefore imperative that it take hold in the marketplace. While the name doesn’t fully explain what OSP is, it certainly suggests what it’s all about. But before we turn to a detailed definition, let’s look at what the alternative looks like. Today, pharmaceutical development is the very epitome of a proprietary business. Research results are closely guarded, developments are immediately patented, and ingenious strategies are employed to extend that patent protection for sometimes decades after the original drug should have become generic. Yet at the same time, the great majority of actual innovation goes on in universities rather than at the big pharma’s, often funded by government and non-profit grants. When innovative new startups do pop up, they are soon purchased by the big pharmas, thereby reducing the diversity of innovation. A major reason that this system has evolved is because of the enormous cost of clinical trials and the low success rate of promising drugs once they are entered into that process. The result is that the big pharmas are constantly in search of the next blockbuster drug, and loath to lose their monopoly control over one until all options have been exhausted. At the same time, there are many hundreds of promising discoveries that never go anywhere. Perhaps the discoverer is a startup that is acquired before it gets to clinical trials and the acquirer has no interest in seeing it through, or a big pharma’s strategy changes, or there’s a staff reorganization and the project is killed in the process. When this happens, the discoveries go on the shelf, usually never to be touched again. There are also many hundreds of existing drugs that can be highly efficacious for other disease conditions. Doctors are frequently surprised when a patient makes a miraculous recovery, with the only identifiable change in their regimen being a prescription for an unrelated drug for a different malady. Most of this anecdotal evidence ends up going nowhere, because there is no easy way for overworked physicians to post and aggregate such possibly random, but occasionally very significant observations. The possibilities here are enormous, because so many of these drugs are already generic, and they have already been approved by the appropriate authorities. Such “off label” uses of very inexpensive, repurposed drugs can be immediate, and lifesaving. Proprietary practices have other pernicious effects as well. Multiple pharmas may be exploring the same drug possibilities at the same time. Worse, one company may have already learned that the line of inquiry is a dead end, either because the animal trials did not replicate in humans, or because of toxicity. Similarly, where research is not published until the patents have been filed and the drug introduced, a decade or more can pass before other researchers can benefit from and build upon it. This should begin to provide a clue as to what OSP is, and why it matters. What if, for example, all of the results of research were added into a common, publicly available database upon discovery? Unproductive pathways and toxic molecules could be avoided, saving enormous amounts of time and funding. And new fundamental discoveries could immediately become the foundation of additional research and promising new drug candidates. Proprietary pharmas would risk little by sharing failures and toxicities, and would realize significant costs savings as a result. So the first fundamental concept behind OSP, as the name suggests, is transparency of data and results, at the earliest opportunity. And especially so, where the data was derived and the discoveries made using public funds. But the concept can also be taken farther, extending to roughly incorporate the methodology of open source development. Counting in the costs of failures as well as successes, major pharmas estimate that it takes about $1.5 billion dollars to bring a new drug to market. At each step of the way, highly paid professionals and facilities are employed. But imagine, if you will, if we were to map out the entire drug development process from initial theory through research, clinical trials and regulatory approval (and there are many, many sub-steps along the way). After we’ve produced our detailed work flow model, we can then spec out the type of IT platform needed to support that end to end process, and also the type of database needed to hold and share all the resulting data. Of course the software tools we will want to use will insure that all of the data from one end to the other is in compatible formats to maximize efficiency in developing that drug, and also to permit maximum universal use of the resulting database by other researchers. The software tools comprising the resulting framework will be best of breed open source tools (many of which already exist), and to the extent that there are gaps, existing tools can be optimized, or new ones created. The work flow model will also specify exactly what number of individuals, with what skills, are needed at each step along the way. It will also identify the points at which crowd sourcing of knowledge from appropriate experts would be helpful, as well as what types of funding might be appropriate and available at which junctures. Importantly, it can also be designed in such a way as to dramatically drive down the costs at every stage, from beginning to end. The completed model can then be exposed to the database of interested professionals that have registered as being willing to provide volunteer efforts. Their rewards will be personal, but also professional, as they will receive credit for discoveries, as well as the ability to publish their results.

While so extensive an ecosystem is a long way from being fully realized, neither are we just at the starting line. Open Source Malaria is just one example of a project that is already making meaningful progress on attacking neglected diseases by expanding on open source software development techniques. The result of creating this development model, with the associated tools and professional resources, would lay the foundation from which an alternative drug development ecosystem can rise. Once it exists, additional resources can be added. Imagine, for example, a non-profit entity that would assemble and maintain the IT infrastructure and databases needed to support the entire end to end process, and make it available free of charge, provide training as and when needed. Another might provide a master insurance policy to make the clinical trials possible, as well as pull together ethical panels for hospitals in emerging countries that do not have the resources to fulfill that function internally. The likelihood of funding new projects would increase as well, as the costs of achieving real results would drop. One could imagine a billion dollar fund, made up of equal contributions from governments, foundations and even big pharmas, the latter benefiting from access to the data and selected rights in the discoveries. The results of such a model would be profound. A non-profit brought a generic drug back to market to treat a neglected disease, and expended only $26 million to do so – orders of magnitude less than the usual cost for a new drug. That’s a number that is within the reach of private foundations to provide. While this is the briefest of overviews, it should make obvious that something similar to the distributed methods used for open source software can also be used to change the way that pharmaceutical development is carried out. There are, of course, significant differences from open source software, since expensive equipment is required, and sometimes teams will need to work in the same physical lab. But these are details. After all, the Manhattan Project to develop the atomic bomb occurred at breakneck speed in scores of widely separated research facilities. And that was long before the Internet existed. But there is one dimension to OSP that is very different from the creation of software. In the years after the drugs were developed that changed HIV/Aids from a death sentence to a treatable chronic condition, more than 10 million people died of the disease in Africa alone, largely because the drugs cost $15,000 per year per patient. And yet within only a few years generic drug manufacturers were able to make a full course of treatment available for $350 per person per year, and then for under $100. But the people continued to die, ten million of them, because the big pharmas that held the patents would neither drop the price, nor permit the generic drug manufacturers to distribute the medications. Could this happen again? The only intervening change has been the adoption of an international treaty that binds countries even more tightly to respect the inviolability of drug patents than before. It was a rewarding and humbling experience to take part in this meeting, along with about 30 other people, most of whom were prominent researchers from Europe, Asia and Africa and leaders from organizations like the Tata Trusts[/url] in India, the Foundation for Neglected Disease Research[/url], Médecins Sans Frontières,  the European and Developing Countries Clinical Trials Partnership[/url], the government of India, the Centre de Recherches Interdisciplinaire[/url] and the Open Societies Foundation. It has been observed that when one person dies, it’s a tragedy, but that when a million do, it’s a statistic. Perhaps the best way to bring the reality of non-existent and over-priced medications back into focus is to quote from an essay written[/url] by James Arinaitwe, one of the members of Open Source Pharma, the (so far) loosely affiliated group of individuals and organizations that have now met for the second year to further this cause: I grew up in rural Western Uganda, where two of my siblings succumbed to measles before their fifth birthday and my father to HIV/AIDS before I turned 10. I often wondered why so many preventable and treatable diseases were still killing the world's poorest and most vulnerable people. Could it be possible that big pharmaceutical companies and big, bureaucracy-laden governments were so vertically aligned in their approach to bringing life-saving medicines to market, that they rarely saw any reason to find solidarity with the communities that would eventually benefit from their inventions and policies?
 
 My father and my baby sisters did not die because the vaccines for measles or the antiretroviral drugs for HIV were not available. They died, in large part, because life-saving vaccines and medicines were priced beyond our reach.
I hope to become more involved in furthering the cause of OSP, and as I do, I’ll continue to write about it, beginning with more detail regarding the underlying concepts. If you’d like to learn more, visit the Open Source Pharma site here.


Meho Krljic

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 Antibiotic 'last line of defence' breached in China





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Bacteria resistant to an antibiotic of last resort have been found in pigs, meat and a small number of hospital patients in China, setting off alarm bells for doctors and researchers.
Scientists discovered bacteria with a gene that makes them resistant to an old antibiotic called colistin.
"What they discovered is that by mouth it doesn't work, it doesn't get absorbed. But you could put it through your veins and it's very powerful because we haven't used that antibiotic for a very long time," Dr. Peter Lin, a family physician and medical commentator on CBC News Network, said Thursday.


For doctors, colistin is last line of defence against some infections.
"When they found this gene popping up in China in the animals and in the meats that they were testing and also in the patients, now they're worried because now this germ is now strong against this last line. And so if we don't have another antibiotic to come in, what do we do then?" Lin said.
Worse yet, the Chinese researchers found the new resistance gene, called mcr-1, was easily spread by plasmids, a portable form of DNA.
Prof. Jian-Hua Liu with the South China Agricultural University in Guangzhou and his co-authors found the mcr-1 gene had the potential to spread to bacterial species such as Klebsiella pneumoniae and Pseudomonas aeruginosa, which can cause diseases ranging from pneumonia to serious blood infections.
In Wednesday's online issue of the Lancet Infectious Diseases, the researchers report finding the gene in 166 of 804 pigs at slaughter across four provinces, and from pork and chicken sold in 30 open markets and 27 supermarkets in Guangzhou between 2011 and 2014.
It was also found in 1 per cent of 1,322 samples they tested from hospitalized patients in China, which the researchers called a relatively low proportion.


"Although currently confined to China, mcr-1 is likely to emulate other resistance genes … and spread worldwide," the researchers wrote. "There is a critical need to re-evaluate the use of polymyxins in animals and for very close international monitoring and surveillance of mcr-1 in human and veterinary medicine."
The discovery of the spreading mcr-1 resistance gene echoes the 2010 discovery of  another so-called "superbug" gene, NDM-1, which emerged in India and rapidly spread around the world.
David Paterson and Patrick Harris from Australia's University of Queensland wrote a commentary in the same journal, titled, "Colistin resistance: a major breach in our last line of defence."
The links between agricultural use of colistin, colistin resistance in slaughtered animals, colistin resistance in food, and colistin resistance in humans are now complete, the pair said.
 China leads world "There have been previous calls for curtailing the use of polymyxins in agriculture. We must all reiterate these appeals and take them to the highest levels of government or face increasing numbers of patients for whom we will need to say, 'Sorry, there is nothing I can do to cure your infection,'" Paterson and Harris wrote.
China is one of the world's largest users and producers of colistin for agriculture and veterinary use.
Worldwide demand for the antibiotic in agriculture is expected to reach almost 12,000 tonnes per year by the end of 2015, rising to 16,500 tonnes by 2021, according to a 2015 report by the QYResearch Medical Research Centre.
Lin and other doctors suggested people can do their part in curbing antibiotic resistance by only taking the drugs when prescribed, taking the full course and returning unused antibiotics to the pharmacy for proper disposal rather than fostering the spread of resistance genes among bacteria in the sewage system.



O istoj stvari:


Antibiotic resistance: New gene found in China heralds breach in last line of defence

Meho Krljic

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A Harvard professor says he can cure aging, but is that a good idea?
 
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At the gene-editing summit, you can’t miss George Church. He’s the big guy with the bushy beard and wavy hair, someone who looks like he stepped out of an 18th century painting of “natural philosophers.” Church, who is 61, is among several hundred scientists, policymakers and thinkers on hand to discuss the powerful technology known as CRISPR, a new method for editing genes. The technique was invented in the past four years, and Church is among those who can claim at least partial credit for the innovation (there’s an intense legal battle over patents — a story for another day).
 
I mentioned to Church that this is the kind of work for which Nobels are awarded. He quickly responded that there are more important things in the balance than prizes. There are cures for human diseases, he said.
 
[How George Church used gene editing to improve the likelihood of pig-to-human organ transplants]
 
Church thinks that one of the ailments he can cure is aging. When I met him early this year, in his laboratory at Harvard Medical School, where he is professor of genetics, he expressed confidence that in just five or six years he will be able to reverse the aging process in human beings.
 
“A scenario is, everyone takes gene therapy — not just curing rare diseases like cystic fibrosis, but diseases that everyone has, like aging,” he said.
 
He noted that mice die after 2.5 years but bowhead whales can live to be 180 or 200.
 
“One of our biggest economic disasters right now is our aging population. If we eliminate retirement, then it buys us a couple of decades to straighten out the economies of the world,” he said.
 
Eliminate retirement? (I briefly envisioned being on deadline in my 90s.)
 
“If all those gray hairs could go back to work and feel healthy and young,” he said, “then we’ve averted one of the greatest economic disasters in history.”
 
He went on: “Someone younger at heart should replace you, and that should be you. I’m willing to. I’m willing to become younger. I try to reinvent myself every few years anyway.”
 
So on Tuesday, I asked him if he was still on track to reversing the aging process in the next five years or so. He said yes — and that it’s already happening in mice in the laboratory. The best way to predict the future, he said, is to predict things that have already happened.
 
Even without CRISPR, genetic engineering was becoming part of the fabric of modern life (your grocery store is full of products from soybeans and corn that have been genetically modified in laboratories). The big difference with CRISPR is how cheap it is, how handy, how flexible. This will put an amazing tool in the hands of a lot more researchers. (Another co-inventor of CRISPR, Feng Zhang, told the summit attendees that soon there will be an entire “toolbox” of CRISPR-like techniques that can be used to edit genes.)
 
For most of us lay people, what’s striking here is not the way that scientists fiddle with the code of life but the mere fact that they do it at all. Awed though we may be by the skills of the experimenters, we naturally question whether this is a good idea.
 
That’s the whole point of the gene-editing summit: To find a path forward that fosters innovation but avoids crossing into ethically dubious territory. Gene-editing could be a tool for eliminating heritable diseases. But it just as easily could be used for purely cosmetic enhancements, or for something smacking of eugenics. The gravest concern is that CRISPR enables germline edits that get passed on to future generations. You’re permanently changing the human species when you do that.
 
Who calls the shots here?
 
Intellectual humility requires scientists to go slowly. Editing genes isn’t like renovating your kitchen. As  Klaus Rajewsky, of the Max Delbruck Center for Molecular Medicine, pointed out Tuesday, “We have become masters in the art of manipulating genes, but our understanding of their function and interaction is far more limited.”
 
Eric Lander, who heads the Broad Institute in Cambridge and was a leader of the effort to sequence the human genome, offered a valediction to Tuesday’s session that addressed both the enormous possibilities of the new technologies and the reasons for being extremely cautious. He said there are 4,000 to 5,000 genetic variants associated with human diseases. But these variants don’t necessarily cause those diseases; they just make them slightly more prevalent. Moreover, genes can have multiple purposes — day jobs and night jobs, as Lander put it. These are complex systems, not modules that you can pop out and replace with a better version with zero unintended consequences.
 
Lander said he could think of only a handful of human diseases that CRISPR could plausibly address at this time, and even then, he said, we should ask whether such genetic manipulation is a good idea. That’s because Nature has had millions of years to do the same experiment and has not done so.
 
“If it is such a good idea, I want to scratch my head and say why didn’t evolution try to do that, and increase that in the population?” Lander said.
 
“We largely exist in a state of limited knowledge,” he said. “Before we make permanent changes to the human gene pool, we should exercise considerable caution.”
 
Which brings us back to aging. Is it a bug, or a feature?
 

 
In reporting this item I came across a story I wrote on biotech [please forgive bad formatting] and Craig Venter, published on Nov. 29, 1998, in the Post magazine. The most surprising line came from Venter:
 
“Intelligent application of this technology is one to two centuries away.”
 
A surprising comment from one of the big boosters of synthetic biology.
 
The story ends with my quasi-neo-crypto-Luddite peroration:
 
Perfection may be a dangerous goal. Nature has feedback systems. There are microbes that adapt to our every move. We think of ourselves as the rulers of the planet; the microbes think of us as a useful host. At some level, we’re still just a bunch of meat.
Perfection may not even be a goal worth pursuing. There is something more interesting about a mortal, imperfect life. Here’s a thought: The revolutionaries of the future will be the people who keep their lives natural. They will choose to grow old. They will allow themselves to experience pain and suffering, so that their joys and triumphs will be all the more intense. They will walk in the woods and sing songs and appreciate the bounty of the planet. Two lovers might put down a blanket and have a picnic. They will fall asleep, because they still get sleepy. They will do this instead of going to the lab to be genetically reengineered.

Meho Krljic

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Ako nije bilo jasno koliko nam je potebno da izbacimo šećer iz ishrane:
 
 This guy lost 25 pounds by eating mostly fat
 
Quote

For a whole year, geneticist Jim McCarter went on a super-low-carb, high-fat diet to see what would happen.
 
He gave up sugar and high-carb foods and got 80% of his calories from fat. McCarter presented what he learned at the 2015 Quantified Self Conference.
 
Low-carb diets (think Atkins) have been one of the most common ways to treat obesity since the 1960s.
 
McCarter's method, called a ketogenic diet, or keto for short, is a diet extremely low in carbohydrates (often less than 20 grams a day) that is most commonly recommended by doctors to treat epilepsy in children. It's also typically high in fat in and low in protein.
 
According to the Mayo Clinic, side effects can include "nausea, headache, mental and physical fatigue, and bad breath." In children on the diet long term, more serious side effects, like kidney stones and brittle bones, have been observed.
 
For dieters, the idea is that reducing carbohydrate intake so dramatically will force the body to burn stored fat, a state called ketosis. This kind of eating plan has been shown in some scientific studies to control hunger and lead to weight loss.
 
In his Quantified Self talk, which we first saw on BoingBoing, McCarter said he saw similar results: He got hungry less easily, lost 25 pounds, and shed half his body fat.
 
He also reported better concentration, better stamina, and better cholesterol. (Bear in mind that these are the self-reported effects from a single person; large studies would be needed to test whether some of the effects McCarter saw are the norm.)
 
For a while though, McCarter said it took him longer to warm up for a workout. He also frequently had muscle cramps, and he got cold more easily. But he said getting about 5 grams of sodium a day had prevented these issues.
 
That level of salt is above the recommended upper limit of 2.3 grams, and he referred to a 2014 study finding that 4 to 6 grams of sodium a day could increase cardiovascular risk. But that's not putting McCarter off his ketogenic diet.
 
"I've learned that the benefits of ketosis, for me, are substantial, and they make me want to continue," McCarter said at the conclusion of the talk. "Getting rid of sugar was the easy part — more challenging has been moderating protein and getting enough fat and salt. And that requires contradicting conventional wisdom about nutrition."
 
A scientific review published this November concluded that ketogenic diets were more effective for weight loss than low-fat diets were, supporting previous studies suggesting this was the case.
 
But the Mayo Clinic advises caution: "It's not clear what kind of possible long-term health risks a low-carb diet may pose because most research studies have lasted less than a year."
 
How long people stay on a diet can matter much more than the type, since keeping weight off can be harder than losing it. That's one reason extreme diets, like some version of the ketogenic diet, don't work for many people.
 
Most important, your overall health should take priority over simply your weight. The ketogenic diet may well be a good bet for some people, but consult your doctor or a licensed dietician before dramatically changing your eating habits.
 
Watch here:
 

 

lilit

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Ako nije bilo jasno koliko nam je potebno da izbacimo šećer iz ishrane:

..trebalo bi da nam bude jasno posle ovoga? oh wait...
Some things you have to do yourself.

Meho Krljic

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Nakon mračnih tvrdnji da dve trećine svog kancera nema veze ni sa čim do sa lošom srećom, nova studija veli da su stvari ipak malo manje nasumične. Nemam ja para da to platim, pa evo samo abstrakt:
 
 Substantial contribution of extrinsic risk factors to cancer development
 
Quote
Recent research has highlighted a strong correlation between tissue-specific cancer risk and the lifetime number of tissue-specific stem-cell divisions. Whether such correlation implies a high unavoidable intrinsic cancer risk has become a key public health debate with the dissemination of the ‘bad luck’ hypothesis. Here we provide evidence that intrinsic risk factors contribute only modestly (less than ~10–30% of lifetime risk) to cancer development. First, we demonstrate that the correlation between stem-cell division and cancer risk does not distinguish between the effects of intrinsic and extrinsic factors. We then show that intrinsic risk is better estimated by the lower bound risk controlling for total stem-cell divisions. Finally, we show that the rates of endogenous mutation accumulation by intrinsic processes are not sufficient to account for the observed cancer risks. Collectively, we conclude that cancer risk is heavily influenced by extrinsic factors. These results are important for strategizing cancer prevention, research and public health.
 

lilit

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premda 100% mislim da su egzogeni faktori presudni za pojavu kancera, ova studija me ubi statistikom.

nevermind, zaključak je:

These sensitivity analyses demonstrate that our conclusions are highly robust, and that the attribution of intrinsic mutations to lifetime cancer risk through stem-cell divisions, particularly for those cancers with low risk, is rather small, even using widely different intrinsic mutation rates.
In summary, we find that a simple regression analysis cannot distinguish between intrinsic and extrinsic factors. We have provided a new framework to quantify the lifetime cancer risks from both intrinsic and extrinsic factors on the basis of four independent approaches that are data-driven and model-driven, with and without using the stem-cell estimations. Importantly, these four approaches provide a consistent estimate of contribution of extrinsic factors of 70–90% in most common cancer types. This is consistent with the overall conclusion regarding the role of extrinsic factors in cancer development.


ako neko hoće ceo rad (da se bavi :lol: ), javljajte.
Some things you have to do yourself.

Meho Krljic

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Gardasil: More Anti-Vax Nonsense Collapses Under the Gaze of Reality



Quote
I’ve been seeing an uptick in my social media feeds over the past couple of weeks about anti-vaxxers and their dangerous nonsense. As usual, they’re upset because the real world has once again contradicted their view of it.
   First, a new study has shown that, once again, the Gardasil vaccine is not causing widespread health problems.
   Gardasil is a vaccine that protects us from the human papillomavirus, or HPV, a nasty bug that causes all sorts of horrid problems like genital warts and cancer of the throat, penis, vulva, vagina, and cervix. In the United States alone, 4,000 women die every year from cervical cancer, roughly one-third of those who get it. By fighting against HPV, Gardasil can seriously cut back on the occurrence of these deaths, and all those other cancers as well. The Centers for Disease Control and Prevention recommends it for preteen girls and boys, and it is given in three separate doses spread out over time.
 
 The anti-vaxxers, of course, have gone ballistic over this, trying to tie Gardasil to all sorts of problems, including the deaths of some young girls after receiving it. But here’s the thing they miss: Gardasil has been given to tens of millions of girls. When you have a population that huge, just by random statistical chance a few girls will, sadly, die not long after the vaccination due to unrelated circumstances.
   Of course, shortly after receiving the vaccination some girls will win the lottery, and others will read a book, and a large number will get good grades in a science class. Are those due to the vaccination as well?
   Of course not. But that’s the anti-vax logic.
   Gardasil has been blamed for a lot of illnesses, and in a new study, researchers looked at the incidence of two such issues—complex regional pain syndrome and postural orthostatic tachycardia syndrome. They showed that the evidence doesn’t support any connection between these syndromes and Gardasil, and the incidence of these syndromes is just what you’d expect from chance in the age group examined.
   So once again Gardasil is falsely accused, and comes out on top. Not that this will stop anti-vaxxers, of course. If evidence goes against them, they a) ignore it, b) yell louder, and/or c) say you’re a Big Pharma shill.
   Another reason I’ve seen more anti-vax baloney is because on Facebook my brother linked (skeptically, of course) to an anti-science group saying that a young girl died after getting the Gardasil shot. That group had a link up to the Natural News site—a site so full of quackery it’s like they’re cloning ducks there—which breathlessly threw around the usual pile of anti-vax fertilizer.
   Now, the real story is tragic and awful: In 2014, a 12-year-old girl died within hours of getting a Gardasil shot. Her parents were devastated and (as reported) believed that the vaccine caused her death.
   However, what Natural News and the Facebook anti-science group didn’t report is that the medical examiner found that girl apparently died of an antihistamine overdose. To make this more clear, the examiner is quoted as saying, “There is no evidence that any vaccination caused or contributed to her death.”
   So again there you have it. It’s another typical anti-vax call to arms due to a complete and gross misunderstanding of how reality works. To them, if something happens after something else, it was caused by that first thing. This is the classic post hoc, ergo propter hoc fallacy. But the Universe doesn’t work that way.
   And this kind of bad thinking has consequences. In the U.S. alone, 79 million people are infected with HPV. That’s more than a quarter of the entire population. Fourteen million new cases crop up every year. Gardasil can substantially cut those numbers back—it’s working, and working well, in the U.S. and Australia—but not if the fearmongering falsehoods by anti-vaxxers get traction.
   As I’ve noted before, Gardasil finds itself in a weird crossfire; anti-vaxxers (who fall across the entire political spectrum) hate it reflexively, of course, but also those on the far right fight against it as well because it’s connected with women’s sexual health. In both cases, prejudice and anti-science rhetoric are supporting the needless suffering of millions of people, and the deaths of thousands.
   Anti-vax beliefs are dangerous. They certainly lead to disease outbreaks, and this can cause deaths, including the deaths of infants. Many of their claims are based on fraud, yet they still enjoy the support of talk show hosts and even Congress.
   If you wonder why I write on this topic, there you go. When anti-science rhetoric puts people in danger, it’s important to talk about it. And it’s important to put your money where your mouth is. That’s why my family is up to date on all their vaccinations, and why my own daughter got the full course of Gardasil. Vaccines save lives, and their benefits hugely, hugely outweigh their minuscule risk. It’s really just that simple.
   My thanks to the wonderful Refutations to Anti-Vaccine Memes on Facebook for the link to the Gardasil study, and to my brother Sid for the link to the Natural News baloney.
 

lilit

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Gardasil: More Anti-Vax Nonsense Collapses Under the Gaze of Reality








anti-vax shit ne mogu i neću da komentarišem, samo nekoliko detalja ako se neko još dvoumi.

hpv je prelep ovako vizuelno al rak grlića i rak grla nisu baš sjajne dijagnoze.
gardasil u sebi ima 4 tipa HPV-a, 2 nisko-onkogeno-rizična (tipovi 6 i 11) i dva visoko-onkogeno-rizična (tipovi 16 i 18).

mali problem je što na ovoj divnoj planeti imamo (dosad detektovanih) oko 140 tipova HPV od kojih smo za 10-ak sigurni (dugogodišnje studije humane populacije potvrdile rezultate in vitro eksperimenata) da su high-risk (što ne znači da još bar 20 out of 140 takođe nije), a samo za 2 (gorepomenuti tipovi 16 i 18) od tih 10-ak poznatih imamo vakcinu. sreća pa su 16 i 18 najrasprostranjeniji i odgovorni za oko 75% slučajeva obe vrste raka, te je vakcinacija pametan potez.
 
sigurno ima i neke kros-reaktivnosti sa nekim drugim tipovima (kao što je i kod influence slučaj), što je utehica za one koji upadnu u onih 25% :lol: pa se i u tim slučajevima preporučuje vakcinisanje u terapeutske svrhe.

vakcina definitivno uzrokuje neobičan osećaj kad je primite a to je zato što joj je adjuvans (stvar koja pojačava imunski odgovor) tzv. virus-like particles, a njih su ubacili jer prethodna vakcina (cervarix) nije bila previše efikasna. i na tom osećaju su građene razne horror stories kad je gardasil u pitanju.

austrija krenula da vakciniše i dečake i devojčice.
Some things you have to do yourself.

lilit

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Joj, mene ovakve stvari intenzivno brinu. Namera je dobra, to je jasno, ali ove ideje mi deluju vrlo nerazborito. Mislim, wikipedija je sjajna stvar ali nije zamena za prave izbore znanja....

What is Open Source Pharma (and why should you care)?


iz pozicije belog čoveka u beloj evropi (makar i pod vučićem! :lol: ), tvoja zabrinutost deluje logično.
međutim, neglected tropical diseases su tako bolan problem ovog shitty societyja, da meni svaka akcija deluje kao pokušaj da se pomogne. pa možda nekad nekom klikne.
ne bih da se frljam velikim rečima al odnos big farme prema svemu što nije white_man_relevant_disease je negde i zločin against humanity.
Some things you have to do yourself.

Meho Krljic

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Da, to mi isto kažu moji prijatelji koji se bave javnim zdravljem. Žalosna planeta  :cry:

Apropo HPV vakcinisanja, samo da podsetim, od raka cerviksa, najizlečivijeg kancera na svetu, koga izazivaju pomenuti tipovi HPV, u Srbiji godišnje umre 500 žena. Zato što ne mogu da makar jednom u pet godina vide ginekologa i urade papa test. Dakle kod nas je vakcinisanje zapravo način da se spasu stotine života. Ali ženskih, priznajem.

lilit

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Apropo HPV vakcinisanja, samo da podsetim, od raka cerviksa, najizlečivijeg kancera na svetu, koga izazivaju pomenuti tipovi HPV, u Srbiji godišnje umre 500 žena. Zato što ne mogu da makar jednom u pet godina vide ginekologa i urade papa test. Dakle kod nas je vakcinisanje zapravo način da se spasu stotine života. Ali ženskih, priznajem.

jeste (ako upadnu u onih 75% sa tipovima 16 i 18).
al vakcina je preskupa za srbiju (o ostatku sveta da ne pričamo) i individualno i za državu koja bi eventualno preuzela finansiranje. doza bez popusta (ako si stariji od 27 godina) je 190 evra. 3 doze neophodne.

btw, ne budimo diskriminatorski orjentisani prema muškarcima i setimo se  majkija daglasa :lol:
Some things you have to do yourself.

Meho Krljic

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Ali on je uredno išao na kontrole, dobio ranu dijagnozu i uspešno se izlečio. Naše žene previše retko idu kod ginekologa i onda ih previše umre od izlečivog kancera.

lilit

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o bre mehane, matematiko moja!  xremyb   :lol:

ako pap test u srbiji košta 10 evra (recimo) i ako to pomnožiš sa 5 godina, to znači da ti je potrebno 140 evra da ženu od 70 godina iskontrolišeš tokom života. što je 4x manje para nego da se vakcinišeš. i pouzdanije.
prisustvo high risk HPV-a ne znači da ćeš razviti kancer, kao što ne znači da ćeš vakcinacijom pokriti sve high-risk tipove (hoćeš samo 16 i 18, al nećeš 31, 33, 35, 39, 45, 51, 52, 53, 56, 58, 59, 66, 68).
plus, pap test je nezamenljiv vakcinisao se ili ne.
to što se tiče logike vezane za vakcinisanje i spašavanje života.  xfrog

a da idu retko na preglede, idu.
Some things you have to do yourself.

Meho Krljic

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Matematika je lepa nauka, ali ovde ona ne rešava osnovni problem. A taj je da žene ovde naprosto ne idu kod ginekologa i da je lakše imunizovati ih da bi ostale žive (pretpostavka, naravno da pričamo o tri čevtrtine onih koje hoće spasti imunizacija). Naravno, troškove na pap testa dodaj i trošak hirurške intervencije u slučaju pozitivne identifikacije cervikalnog kancera, a koji značajno poskupljuje celu stvar, pa tih 500 žena postaju značajno higher maintenance.

Meho Krljic

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No, naravno da treba gurati i vakcinu i redovne godišnje pap smirove.

lilit

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Odavno je poznato da je gender je bitan faktor kad pričamo o imunskom odgovoru, muškarci lakše obole od infektivnih bolesti nego žene (statistički gledano) al zato žene ginu od šireg spektra autoimunskih bolesti.

Quote
Gender has long been known to be a contributory factor in the incidence and progression of disorders associated with immune system dysregulation. More recently, evidence has accumulated that gender may also play an important role in susceptibility to infectious diseases. In general, females generate more robust humoral and cell-mediated immune responses following antigenic challenge than their male counterparts. Such sexual dimorphism would be expected to result in greater susceptibility of males to infectious disease and this appears to be supported by data for a number of bacterial and viral pathogens. However, it has been suggested that these elevated immune responses in females may also underlie the higher incidence of an array of disorders thought to be autoimmune in origin. In contrast, males have frequently been observed to mount more aggressive acute immune responses to microbial stimuli. Indeed, it is now well known that the male gender is a significant risk factor in the incidence and severity of bacterial sepsis.

Sepsis and acute disseminated viral infections appear to share many common features in their pathology and both are associated with marked elevations in monokine production. In this review we have examined the current evidence for gender-based differences in innate immune responses to both bacterial and viral pathogens. In general, the available data suggest that sentinel cells, such as macrophages, in males respond more vigorously to microbial components than their female counterparts by producing higher levels of cytokine and chemokines that are likely to play a key role in the progression of damaging inflammation.

A considerable amount of evidence indicates that estrogens and androgens can exert direct effects on immune cells via classical or nonclassical steroid hormone receptors. Furthermore, numerous studies have demonstrated that many of the gender-based differences observed in immune responses against bacterial or viral pathogens can be attributed, at least in part, to the relative levels of male and female reproductive hormones.

Sve je prepoznatija i potreba za individualnom pristupu vakcinama, nema više mantre one for all. Nisam pametna kuda će nas to odvesti kao društvo, mislim, što nešto individualnije to skuplje, sumnjam da će big farma biti filantropski raspoložena.Što se tiče HIV tretmana, u većini bolnica se ne uzima u obzir gender razlika u imunskom sistemu niti se testiranje odgovarajućih paramentara prilagođava, i to je i dalje jedan od razloga zašto HIV+ žene brže razvijaju AIDS nego muškarci.



Crno al tako mu je to.


Some things you have to do yourself.

lilit

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Twins study finds no evidence that marijuana lowers IQ in teens
http://www.sciencemag.org/news/2016/01/twins-study-finds-no-evidence-marijuana-lowers-iq-teens

te se nadajmo da će istraživanja o dejstvu CBD-a u tretmanu epilepsije koja se ne može kontrolisati lekovima postati malo ozbiljnija nego što su danas:
http://www.gwpharm.com/Clinical%20Use.aspx
Some things you have to do yourself.

lilit

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rat se nastavlja



Some things you have to do yourself.

lilit

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Does the ‘monogamy hormone’ make us better soldiers?

A hormone that seems to promote monogamy and parenting in people may also make us more likely to cooperate with others, even in risky situations.
Research in rodents shows while the hormone, called AVP (arginine vasopressin), promotes bonding, it also boosts aggression in males.
“Part of the dark side of monogamy is that an AVP-pumped-up male is more likely to behave aggressively toward intruders,” says Colin Camerer, a professor of behavioral economics at Caltech.
Camerer wanted to test the idea that AVP could help explain our species’ cooperative tendencies.
“One of the reasons humans rule the world rather than apes is that we do things that require a great deal of trust. We cooperate in large-scale groups,” Camerer says. “Where does that come from? Is it something like pair bonding but just scaled up? And if it is, what role does AVP play?”
To investigate these questions, Camerer and his colleagues administered a nasal spray containing AVP or a hormone-free nasal spray (a placebo) to 59 male volunteers, aged 19 to 32 years old. Pairs of subjects then used computers to play a so-called assurance game in which they had to choose whether or not to cooperate with another player; “assurance” comes from the fact that subjects will take a risky action if they are sufficiently assured that others will, too.
When they cooperated, both players received more points than they would have if they did not mutually cooperate. If one player chose not to cooperate but his partner made the opposite decision, the non-cooperative player received an intermediate payoff whereas the cooperative player received nothing.

“The game is designed to mimic situations in which people are willing to help, but only if everyone else helps too,” Camerer says. “Think of pitching in on a team project, or of a group of soldiers rushing the enemy. If a critical mass cooperates, then everyone else should go along. Thus it is in your best interest to help only if enough others do.”
To help ensure the players were engaged, the points they accumulated were converted into actual money at the end of the game (usually around $20).
It makes people more cooperative
The experiment showed that players who received AVP before the game were significantly more likely to cooperate than those who received the placebo.
“By targeting a specific hormonal system in the human brain, we could manipulate people’s willingness to cooperate and help them do better,” says Gideon Nave, a graduate student in Camerer’s lab and a coauthor on the study.

Using control experiments, the researchers were also able to rule out other explanations for why the subjects were cooperating. For example, one possibility is that AVP was increasing the subjects’ appetite for risks. Alternatively, the administered hormone might be amplifying their altruistic tendencies, so that they just wanted to help other people regardless of the risk to themselves.
“We found that when we asked them, ‘Do you want to just give some money to this stranger?’ they don’t do it,” Camerer says. “So AVP seems to be quite specialized to this particular type of risky cooperation.”

What brain scans show
To better understand the neural mechanism underlying AVP’s effect on risky cooperation, the researchers conducted the same experiment but this time had subjects—a separate group of 34 men—play the game while their brains were being imaged using a functional magnetic resonance imaging (fMRI) scanner.
The scans indicated that after AVP administration, a part of the brain’s reward system known as the ventral pallidum—a region that is known to have an abundance of AVP receptors—showed a change in neural activity when the players decided to cooperate.

Did drop in testosterone make humans more civilized?
“That was very encouraging, because it showed that the hormone is activating a part of the brain that is known to be rich in AVP receptors,” Camerer says.
Could the discovery that AVP increases the likelihood of risky cooperation have practical applications and be used, for example, to engender trust and foster cooperation in groups? Perhaps.
“You could imagine a high-stakes situation, such as a military operation, in which people have to trust each other to all do something difficult and it fails if anyone chickens out,” Camerer says. “In that case, you might want to administer AVP to help ensure that everyone is cooperative.”
The Center for Behavioral Brain Sciences and the Gordon and Betty Moore Foundation funded the study, which appears in the Proceedings of the National Academy of Sciences.

http://authors.library.caltech.edu/64303/
Some things you have to do yourself.

lilit

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a taman smo se ponadali da ćemo sve moći da vidimo iz jedne kapi krvi :lol:

Not Every Drop of a Person’s Blood Is the Same, a Study Says

http://mobile.nytimes.com/2016/02/23/health/not-every-drop-of-a-persons-blood-is-the-same-a-study-says.html
(science communication)

http://ajcp.oxfordjournals.org/content/144/6/885.full
(science)
Some things you have to do yourself.

džin tonik

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kvaziznastvenici: isisati pet litara krvi, konfundirati, izdvojiti kap.

Meho Krljic

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A tek ovo: šta ako je rak zapravo zarazna bolest? Dakle, ne pričamo o nečemu poput cervikalnog kancera koji se "prenosi" human papiloma virusom nego o tome da maligna ćelija iz jednog organizma pređe u drugi i tamo izazove malignitet. Tekst koji linkujem pominje vrlo retke slučajeve koji su izazvali lokalni malignitet, ali i primere iz životinjskog sveta koji su malo više zabrinjavajući. Kod pasa obrazloženje je da njihov koitus traje jako dugo. Kod tasmanijskih đavola da im je genetska raznolikost premala jer su vrsta koja živi na jako malom prostoru pa onda imunosistem i ćelije druge jedinke greškom doživi kao, jelte, domaće. No, sve to na kraju vodi do užasnog zaključka teksta koji daje primer čoveka čiji su limfni čvorovi bili puni kanceroznih ćelija ali premalih da bi pripadali njemu - da bi na kraju ispalo da su izgleda originirale iz pantljičare koju je isti nosio unaokolo i koja je sama imala rak  :cry: :cry: :cry: :cry: :cry:



Scientists mull prospect of contagious cancer



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For all its peculiar horror, cancer comes with a saving grace. If nothing else can stop a tumor's mad evolution, the cancer ultimately dies along with its host. Everything the malignant cells have learned about outwitting the patient's defenses — and those of the oncologists — is erased. The next case of cancer, in another victim, must start anew.
 Imagine if instead, cancer cells had the ability to press on to another body. A cancer like that would have the power to metastasize not just from organ to organ, but from person to person, continuing to evolve deadly new skills along the way. While there is no sign of an imminent threat, several recent papers suggest that the eventual emergence of a contagious human cancer is within the realm of medical possibility. This would not be a disease, like cervical cancer, that is triggered by the spread of viruses, but rather one in which cancer cells actually travel from one person to another and thrive in their new location.
 
  So far this is known to have happened only under the most unusual circumstances. A 19-year-old laboratory worker who pricked herself with a syringe of colon cancer cells developed a tumor in her hand. A surgeon acquired a cancer from his patient after accidentally cutting himself during an operation. There are also cases of malignant cells being transferred from one person to another through an organ transplant or from a woman to her fetus.



 On each of these occasions, the malignancy went no farther. The only known cancers that continue to move from body to body, evading the immune system, have been found in other animals. In laboratory experiments, for instance, cancer cells have been transferred by mosquitoes from one hamster to another. And so far, three kinds of contagious cancers have been discovered in the wild — in dogs, Tasmanian devils and, most recently, in soft shell crabs.
  The oldest known example is a cancer that spreads between dogs during sexual intercourse — not as a side effect of a viral or bacterial infection, but rather through direct conveyance of cancer cells. The state of the research is described in a review, "The Cancer Which Survived," published last year by Andrea Strakova and Elizabeth P. Murchison of the University of Cambridge. The condition, canine transmissible venereal tumor disease, is believed to have sprung into existence 11,000 years ago — as a single cell in a single dog — and has been circulating ever since. (Why did this happen in dogs and not, say, cats? Perhaps because of what the authors demurely call the dogs' "long-lasting coital tie" — the half an hour or so that a male and female are locked in intercourse, tearing genital tissues and providing the cancer cells with a leisurely crossing.)
  Normally a cancer evolves in a single body over the course of years or decades, accumulating the mutations that drive it to power. But to have survived for millenniums, researchers have proposed, canine cancer cells may have developed mechanisms — like those in healthy cells — to repair and stabilize their own malignant genomes.
 Early on, cancer cells typically flourish by disabling DNA repair and ramping up the mutational frenzy. Somewhere along the way, the age-old canine cells may have reinvented the device to extend their own longevity. There is also speculation that this cancer may have learned to somehow modify canine sexual behavior in ways that promote the disease's spread and survival.
  The second kind of contagious cancer was discovered in the mid-1990s in Tasmanian devils, which spread malignant cells as they try to tear off one another's faces. Though it may be hard to sympathize, devil facial tumor disease threatens the creatures with extinction. With so few examples, transmissible cancer has been easy to dismiss as an aberration. But in December, scientists at the Universities of Tasmania and Cambridge reported in Proceedings of the National Academy of Sciences that Tasmanian devils are passing around another kind of cancer — genetically distinct from the first. It's weird enough that one such cancer would arise in the species. What are the chances that there would be two?
  One theory is that the animals are unusually vulnerable. Driven so close to extinction — by climate change, perhaps, or human predators — the species is lacking in genetic diversity. The cells of another devil injected through a vicious wound may seem so familiar that they are ignored by the recipient's immune system. If some of the cells carry the mutations for the facial cancer, they might be free to flourish and develop into a new tumor.
  But the scientists also proposed a more disturbing explanation: that the emergence of contagious cancer may not be so rare after all. "The possibility," they wrote, "warrants further investigation of the risk that such diseases could arise in humans."
  Cancer has probably existed ever since our first multicellular ancestors appeared on Earth hundreds of millions of years ago. The life spans of even the longest-lived animals may be just too brief for cancers to easily evolve the ability to leap to another body. Otherwise, contagious cancer would be everywhere. For now, at least, it remains a curiosity. Consider the case of a 41-year-old man in Medellin, Colombia, who was examined by doctors in 2013 because of fatigue, fever and weight loss. His lymph nodes were clogged with cancer cells that had also spread to his lungs and liver.
 Yet the cells looked far too small and simple to be human. "This case posed a diagnostic conundrum," the doctors wrote in November in The New England Journal of Medicine.
  The solution to the puzzle came when the man was also found to be harboring a tapeworm called Hymenolepis nana. Further analysis concluded that the cancer cells had originated in the parasite and then metastasized through the man's body.
  There is no reason to think that tapeworm cancer is about to become a threat to public health. The patient's immune system had been compromised by H.I.V., and he died several months later.
  But nature is infinite in its surprises.

lilit

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bakteriofagi su mi ljubimci već decenijama  al jonathan je hilarious :lol:
premda, možda nešto i bude od ovoga.

http://www.pbs.org/wgbh/nova/next/body/phage-alzheimers-cure


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lilit

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Fascinantan rad na koji natrčah, pa da podelim.
http://science.sciencemag.org/content/348/6235/694.full


Ukratko:      Male boginje brišu kompletnu imunološku memoriju teško sticanu tokom života, tako što roknu 99% memorijskih B i T limfocita, zasad nepoznatim mehanizmom. Ekstra zanimljivo je da su uništeni samo memorijski a ne naivni (oni koji se još uvek nisu sreli s nekim antigenom) limfociti. The best of everything je: kad male boginje prođu, mislim, prođe infekcija, jedini specifični memorijski limfociti koje je moguće detektovati su oni protiv malih boginja.
Da bi se imunski sistem vratio u normalu posle infekcije, potrebno je approx. 28 meseci (statistika :lol:). Što bi dalje značilo da se vraćamo na nivo imuniteta koje ima dvogodišnje dete s tim što ono još uvek ima timus koji mu omogućava da lakše izađe na kraj sa de novo infekcijom, dok kasnije timus atrofira.
U svakom slučaju, broj smrti od drugih infekcija je takođe posledica preležanih malih boginja, slično kao sa HIVom, samo su druge ćelije target. Plus, process je reverzibilan. Samo treba preživeti prvih 28 meseci.
Tako da priče kako se kalio imunitet valja neozbiljno shvatati i vakcinisati se na vreme. Što si matoriji i dobiješ male boginje…više si ga ugasio.
Evo i  slika! :lol:
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Mica Milovanovic

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Zaista veoma zanimljivo!


Da li to znači da bi, ako eventualno zakačiš male boginje kao mator, moglo da pomogne da se ponovo vakcinišeš od svega živog, kao da si bebiron?
Ili je bolje da se dve i po godine kriješ od ljudi?  :)
Mica

Biki

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Zaista veoma zanimljivo!


Da li to znači da bi, ako eventualno zakačiš male boginje kao mator, moglo da pomogne da se ponovo vakcinišeš od svega živog, kao da si bebiron?
Ili je bolje da se dve i po godine kriješ od ljudi?  :)
To znaci da ako niste vakcinisani ili prelezali male boginje bilo bi dobro da se vakciniste.
Ja sam prosle godine primila dve doze MMRa.

Evo kakva je preporuka za vakcinaciju odraslih ovde u Kanadi

http://www.phac-aspc.gc.ca/publicat/cig-gci/p03-02-eng.php



Mica Milovanovic

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Ma, prelezao sam, na vreme... Mama mi je bila medicinska sestra, pa sam prelezao sve zivo sto se moglo prelezati... Pitam cisto iz radoznalosti...
Mica

Biki

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Ma, prelezao sam, na vreme... Mama mi je bila medicinska sestra, pa sam prelezao sve zivo sto se moglo prelezati... Pitam cisto iz radoznalosti...
:)

lilit

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Zaista veoma zanimljivo!

Da li to znači da bi, ako eventualno zakačiš male boginje kao mator, moglo da pomogne da se ponovo vakcinišeš od svega živog, kao da si bebiron?
Ili je bolje da se dve i po godine kriješ od ljudi?  :)

obe opcije su validne al druga zvuči lepše! :lol:

šalu na stranu, da, to su dva rešenja s tim što drugo jeste bolje jer ti teško možeš da se vakcinišeš protiv svega čemu si bio izložen od rođenja. i koliko god ti se činilo da one male infekcije npr. rota virusima nisu bitne i lako prođu, toliko su i one kumulativno  uticale da ti je imunski sistem iskusan i speman da pobedi i infekciju i kancer i autoimunost, etc. a onda dođu male boginje i sve što si video, ko da nisi video. selektivna lobotomija :lol: imunskog sistema koja te dovede do toga da kad prođu, on samo njih ima u sećanju. scary! :lol:

najbolje je ipak probati da ih ne zakačimo a sad me najviše zanima kojim se mehanizmom dođe do situacije gde ti se izbriše sve što je tvoj imunski sistem "video" tokom života.
plus, zanimljivo je i kako smo uopšte došli do toga da mislimo da su male boginje relativno bezopasna bolest: herd immunity je odlična stvar al loše je što zato lako zaboravljamo bolesti koje nismo u prilici da vidimo jer zaštita, koja je posledica fenomena :lol: da je većina oko tebe zaštićena, odlično šljaka.

a onda te roknu measles i praktično umreš od koinfekcije koju zakačiš. bjutiful.
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Mica Milovanovic

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Quote
a onda te roknu measles i praktično umreš od koinfekcije koju zakačiš. bjutiful.


Što ti je istraživač - daj mu boginje i sve mu je lepo... :)
Mica

lilit

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to je pre histerija prouzrokovana H2020 dedlajnom koji se neminovno približava al biće bolje posle 13.4.
EtOH je iz božije bašte izašao.
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lilit

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Sweet drug clears cholesterol, reverses heart disease—and was found by parents

Here’s how parents of kids with rare disease found what may be blockbuster drug.

 
    Addi and Cassi Fund 

Two parents’ quest to save their twin daughters’ lives from a rare, degenerative genetic disorder may end up saving and improving the lives of millions.
After digging through medical literature and fitting pieces of data together, the non-medically trained couple contacted German researchers and suggested that a chemical called cyclodextrin may be able to treat atherosclerosis—the hardening of arteries with cholesterol-rich plaques, which is a precursor to heart attack, stroke, and other cardiovascular diseases.
The researchers, Eicke Latz at the University of Bonn and colleagues, followed up on the parents’ hypothesis and found that in mice, cyclodextrin indeed blocked plaque formation, melted away plaques that had already formed in arteries, reduced atherosclerosis-associated inflammation, and revved up cholesterol metabolism—even in rodents fed cholesterol-rich diets. In petri dish-based tests, the researchers found that the drug seemed to have the same effects on human cells and plaques.
The findings, published Wednesday in Science Translational Medicine, suggest that cyclodextrin—a drug already approved for use in humans by the US Food and Drug Administration—may be highly effective at treating and preventing heart disease.
Currently, cardiovascular diseases are the leading cause of death worldwide, and around 43 percent of Americans have high cholesterol, which can lead to atherosclerosis. Typical treatments include statins and other cholesterol-lowering drugs, which are not always effective, particularly when patients don’t adhere to doctor-prescribed, low-cholesterol diets.
While Latz and co-authors stress that clinical trials are needed to validate the effects of cyclodextrin, the researchers note that it would be fairly easy to repurpose the drug to treat and prevent cardiovascular diseases.
But, while cyclodextrin’s road ahead may be clear, its path to medical treatments was oddly bumpy...

dalje...
http://arstechnica.co.uk/science/2016/04/drug-clears-cholesterol-reverses-heart-disease/


rad izasao u Sajensu:  http://stm.sciencemag.org/content/8/333/333ra50
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Meho Krljic

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BioViva’s Liz Parrish makes progress in controversial gene quest to reverse aging



Quote
The way BioViva founder Elizabeth Parrish sees it, biological aging is a disease – and she’s willing to bet her life on a cure.
Last fall, the 45-year-old Seattle-area woman underwent an experimental type of gene therapy aimed at addressing some of the big effects of aging, including loss of muscle mass and a shortening of the chromosomes’ telomeres. The procedure was reportedly done in Colombia, to get around U.S. regulations.
The idea of having gene therapy done on yourself raised eyebrows in the biotech community, but Parrish was unfazed.
“I 100 percent believe that it will work, or else I wouldn’t have done it,” Parrish told GeekWire during an interview in February. “I didn’t try to flame out in glory. The research shows that it should absolutely work.”


Now BioViva is reporting that it does seem to work, at least on Parrish’s telomeres. And that’s likely to fuel a debate over the widening scientific quest for greater longevity – conducted not only by BioViva, but by other ventures such as Human Longevity Inc. This week, Human Longevity announced a 10-year deal with AstraZeneca to analyze 500,000 DNA samples for anti-aging clues.
Parrish is already trying to follow up on a couple of clues through Bioviva USA, the privately held company she founded on Bainbridge Island last year. Bioviva announced its own deal this week with a London-based investment fund called Deep Knowledge Life Sciences.
One of BioViva’s anti-aging clues has to do with a protein called myostatin: Research suggests that genetically blocking the production of myostatin could help prevent age-related muscle loss.
The other clue has to do with telomeres, the stretches of DNA at the ends of our chromosomes that are thought to protect our genetic data from harmful mutations – much as the plastic tips on the ends of shoelaces keep them from unraveling. As we age, those telomeres become shorter, and the protective effect is gradually lost.
The gene therapy that Parrish underwent was aimed at inhibiting myostatin and building up telomeres.
In February, Parrish was reluctant to describe the effects. “There are a lot of things I could say – ‘Oh, this has happened, or that has happened’ – but it could all be due to the placebo effect,” she said. “Data is king.”
A bit of data came out this week: The Biogerontology Research Foundation reported that Parrish’s telomeres were short for her age when her white blood cells were tested last September at SpectraCell Laboratories in Houston. But when SpectraCell ran the same test on her cells in March, the telomere length went from 6,710 DNA base pairs to 7,330 base pairs.
The foundation said the lengthening implied that Parrish’s white blood cells had become biologically younger. That’s debatable, however. For one thing, the findings haven’t yet been submitted for peer-reviewed publication. For another, the connection between a change in telomere length and improved cellular function hasn’t been nailed down. Human telomere length can vary widely, from less than 5,000 to more than 15,000 base pairs.
Bottom line? Parrish is likely to continue as a human guinea pig for years to come.
   The fact that she went ahead with self-experimentation under less-than-transparent circumstances has rubbed some people the wrong way. Last October, MIT Technology Review said there’s a chance that the experiment could be remembered as “a new low in medical quackery.”
University of Washington medical researcher George Martin resigned from BioViva’s scientific advisory board after he heard what Parrish had done.
“She’s a good-hearted person, and I’m very fond of her,” Martin told GeekWire this week. “But as a physician, I felt very strongly that we had to do clinical trials and pre-clinical trials.”
Parrish herself acknowledged that she didn’t tell any of her scientific advisers about her gene therapy in advance. “They would have had to say no,” she said.
The way she sees it, she had to say yes.
“Over 100,000 people die every day of aging diseases,” she said. “Somebody told me today, they said, ‘You’re so brave.’  Maybe I am, maybe I’m not. What’s brave is knowing that there could be a cure for aging diseases, and not taking it, and deciding that you’re going to wither away. I’m not that brave.”

lilit

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BioViva’s Liz Parrish makes progress in controversial gene quest to reverse aging

da ne ulazimo u priču o telomerama i da li se tako zaista može doći do eliksira mladosti, what elizabeth parrish did, već su odradili mnogi a najpoznatiji je dobio i nobelovu nagradu
http://discovermagazine.com/2010/mar/07-dr-drank-broth-gave-ulcer-solved-medical-mystery
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lilit

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upravo čitam o uticaju sopstvenog mikrobioma (onih 1x1014 bakterijica na našim mukoznim površinama) na (pojednostavljeno :lol:) biti debeo ili mršav story. horor!
http://www.cell.com/cell-metabolism/abstract/S1550-4131%2815%2900566-5
https://www.sciencedaily.com/releases/2015/11/151124143330.htm

evo shemica kakva je biohemija kontrole apetita:


ako ova priča sa mikrobiomom pije vodu, u suštini to negde znači da bismo targetovanom izmenom mikrobioma mogli ubaciti više bakterijica koje šalju signal da nismo/jesmo gladni i tako uticati na path kojim želimo da idemo.
na stranu psihološki aspekt (jer i to je in the end: biohemija), ovo bi značilo i da ako hoćete da ostanete vitki, i partner mora da bude isti takav, inače belaj :lol:
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Meho Krljic

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To objašnjava zašto se moja žena i ja gojimo paralelno  :lol: :lol: :lol:

lilit

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teorecki, ClpB protein (šalje signal da si sit) injection i sve rešeno. :lol: tamo negde u 22. veku. ako u međuvremenu ne napalmujemo planetu.
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mac

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Ma sipaće nam taj protein u vodu, da bismo manje hrane bacali, da bi moglo više nas da postoji istovremeno, a bili zdraviji i manje na zdravstveno osiguranje trošili.

ЖивОзбиљан

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Па шта ће ми то у 22. вијеку :(

Уосталом, ја одувијек тврдим да се мрша од свињетине, и то је неки протеин
šta će mi bogatstvo i svecka slava sva kada mora umreti lepa Nirdala

lilit

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ovo je dosad potvrđeno samo na miševima pa ako ima dobrovoljaca... :)
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lilit

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s vakcinom se nije previše odmaklo al je lek protiv hepatitis C infekcije medju nama (big fajnding). jes da košta grdno al je vrlo promissing stvar posebno za ljude koji već imaju HIV.


http://mobile.aidsmap.com/Hepatitis-C-therapy-improves-quality-of-life-for-people-who-inject-drugs-but-reinfection-risk-remains/page/3054033
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lilit

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Some things you have to do yourself.

lilit

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john oliver razbio i naučne studije i nauku i istraživače :lol:

https://www.youtube.com/watch?v=0Rnq1NpHdmw
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Meho Krljic

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Da, pola slashdota ga slavi zbog ovoga. Moram da pogledam kad dođem kući.  :lol:

lilit

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priznajem da su mi tvoji "science" postovi bili u glavi kad se pričalo kako se nauka prezentuje na TV-u. oprostićeš mi što sam zlica, znam! :lol:
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Meho Krljic

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Pa, ja radim sa onim što (donekle) razumem, a pošto sam neobrazovan toga nema mnogo  :oops: :oops:  Pa je gomila toga što kačim zaista vrlo sumnjivog epistemološkog statusa, ali računam da ljudi shvataju da je u pitanju tek po koji kurio, nikako ne neka mudrost koja je nedovodljiva u pitanje i na kojoj treba da zasnuju ostatke svojih života.

lilit

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ajde mehane, znam te (još dok gojazan nisi bio!) :lol:

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Meho Krljic

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U.S. sees first case of bacteria resistant to last-resort antibiotic 
 
Quote
  U.S. health officials on Thursday reported the first case in the country of a patient with an infection resistant to a last-resort antibiotic, and expressed grave concern that the superbug could pose serious danger for routine infections if it spreads. "We risk being in a post-antibiotic world," said Thomas Frieden, director of the U.S. Centers for Disease Control and Prevention, referring to the urinary tract infection of a 49-year-old Pennsylvania woman who had not traveled within the prior five months. Frieden, speaking at a National Press Club luncheon in Washington, D.C., said the bacteria was resistant to colistin, an antibiotic that is reserved for use against "nightmare bacteria." The infection was reported Thursday in a study appearing in Antimicrobial Agents and Chemotherapy, a publication of the American Society for Microbiology. It said the superbug itself had first been infected with a tiny piece of DNA called a plasmid, which passed along a gene called mcr-1 that confers resistance to colistin. "(This) heralds the emergence of truly pan-drug resistant bacteria," said the study, which was conducted by the Walter Reed National Military Medical Center. "To the best of our knowledge, this is the first report of mcr-1 in the USA." The patient visited a clinic on April 26 with symptoms of a urinary tract infection, according to the study, which did not describe her current condition. Authors of the study could not immediately be reached for comment. The study said continued surveillance to determine the true frequency of the gene in the United States is critical.  "It is dangerous and we would assume it can be spread quickly, even in a hospital environment if it is not well contained," said Dr. Gail Cassell, a microbiologist and senior lecturer at Harvard Medical School. But she said the potential speed of its spread will not be known until more is learned about how the Pennsylvania patient was infected, and how present the colistin-resistant superbug is in the United States and globally. "MEDICINE CABINET IS EMPTY FOR SOME" In the United States, antibiotic resistance has been blamed for at least 2 million illnesses and 23,000 deaths annually. The mcr-1 gene was found last year in people and pigs in China, raising alarm. The potential for the superbug to spread from animals to people is a major concern, Cassell said. For now, Cassell said people can best protect themselves from it and from other bacteria resistant to antibiotics by thoroughly washing their hands, washing fruits and vegetables thoroughly and preparing foods appropriately. Experts have warned since the 1990s that especially bad superbugs could be on the horizon, but few drugmakers have attempted to develop drugs against them.  Frieden said the need for new antibiotics is one of the more urgent health problems, as bugs become more and more resistant to current treatments. "The more we look at drug resistance, the more concerned we are," Frieden added. "The medicine cabinet is empty for some patients. It is the end of the road for antibiotics unless we act urgently."  Overprescribing of antibiotics by physicians and in hospitals and their extensive use in food livestock have contributed to the crisis. More than half of all hospitalized patients will get an antibiotic at some point during their stay. But studies have shown that 30 percent to 50 percent of antibiotics prescribed in hospitals are unnecessary or incorrect, contributing to antibiotic resistance.  Many drugmakers have been reluctant to spend the money needed to develop new antibiotics, preferring to use their resources on medicines for cancer and rare diseases that command very high prices and lead to much larger profits.  In January, dozens of drugmakers and diagnostic companies, including Pfizer (PFE.N), Merck & Co (MRK.N), Johnson & Johnson (JNJ.N) and GlaxoSmithKline (GSK.L), signed a declaration calling for new incentives from governments to support investment in development of medicines to fight drug-resistant superbugs. (This story corrects headline, first and third paragraphs to show bacteria is resistant to last-resort antibiotic colistin, not all antibiotics) (Reporting by Ransdell Pierson; Additional reporting by Bill Berkrot; Editing by Bernard Orr)
 

lilit

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koliko vidim, našli su da je bakterija rezistentna na colistin (ima mrc-1 gen plus je taj gen u plazmidu što joj omogućava brz horizontalni prelaz sa bakterije na bakteriju) al kad su je testirali na ukupno 20 antibiotika, 6 je odradilo posao.
biće da ipak imamo još malo vremena da pronađemo nove antibiotike ili da se malo bolje pozabavimo kako da upotrebimo bakteriofage (viruse koji napadaju bakterije) u ovu svrhu.
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Meho Krljic

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 Stanford researchers ‘stunned’ by stem cell experiment that helped stroke patient walk 
 
Quote

 
Stanford researchers studying the effect of stem cells injected directly into the brains of stroke patients said Thursday that they were "stunned" by the extent to which the experimental treatment restored motor function in some of the patients. While the research involved only 18 patients and was designed primarily to look at the safety of such a procedure and not its effectiveness, it is creating significant buzz in the neuroscience community because the results appear to contradict a core belief about brain damage — that it is permanent and irreversible.
The results, published in the journal Stroke, could have implications for our understanding of an array of disorders including traumatic brain injury, spinal cord injury and Alzheimer's if confirmed in larger-scale testing.
The work involved patients who had passed the critical six-month mark when recoveries generally plateau and there are rarely further improvements. This is the point at which therapies are typically stopped as brain circuits are thought to be dead and unable to be repaired. Each participant in the study had suffered a stroke beneath the brain’s outermost layer and had significant impairments in moving their arms and-or legs. Some participants in the study had had a stroke as long as three to five years before the experimental treatment.
[Stem cell study: Up to 90 percent of cancers not ‘bad luck,’ but due to lifestyle choices, environment]
The one-time therapy involved surgeons drilling a hole into the study participants' skulls and injecting stem cells in several locations around the area damaged by the stroke. These stem cells were harvested from the bone marrow of adult donors. While the procedure sounds dramatic, it is considered relatively simple as far as brain surgery goes. The patients were conscious the whole time and went home the same day.
They suffered minimal adverse effects such as temporary headaches, nausea and vomiting. One patient experienced some fluid buildup from the procedure that had to be drained but recovered fully from the issue. The volunteers were then tested at one month, six and 12 months after surgery using brain imaging and several standard scales that look at speech, vision, motor ability and other aspects of daily functioning.
Gary Steinberg, the study's lead author and chair of neurosurgery at Stanford, said in an interview that while he is cautious about "overselling" the results of such a small study, his team has been "stunned" that seven of the 18 patients experienced significant improvement in their abilities following treatment.
[Scientists create a new type of stem cell with only half a human’s usual 46 chromosomes]
"Their recovery was not just a minimal recovery like someone who couldn't move a thumb now being able to wiggle it. It was much more meaningful. One 71-year-old wheelchair-bound patient was walking again," said Steinberg, who personally performed most of the surgeries.
He also recounted the progress of a much younger patient, age 39, who was two years post-stroke and had had such problems walking and speaking that she "did not want to get married to her boyfriend." "She was embarrassed about walking down the aisle," he explained. But after treatment, Steinberg said, "She's now walking much better and talking much better and she's married and pregnant."
Steinberg said that the study does not support the idea that the injected stem cells become neurons, as has been previously thought. Instead, it suggests that they seem to trigger some kind of biochemical process that enhances the brain's ability to repair itself.
"A theory is that they turn the adult brain into the neonatal brain that recovers well," he explained.
[Frightening images show the insidious way Zika appears to attack babies’ brains]
Sean Savitz, a professor of neurosurgery at the University of Texas, said he was encouraged by the study but said there is a lot more work to be done to try to confirm the results and figure out the mechanism for the reaction. One major question, he said, is whether there is something about the stem cells that is stimulating the changes or whether it is simply the procedure itself inducing some other sort of biological reaction or a placebo effect.
Nicholas Boulis, a neurosurgeon and researcher at Emory University, said the study appears to support the idea that there may be latent pathways in the brain that can be reactivated — a theory that has been "working its way to the surface" over the past few years.
"There is certainly reason to be enthusiastic based on the magnitude of responses from these patients," he said.
 
There are close to 7 million so-called chronic stroke patients in the United States who are living with the aftermath of the damage to their brains and bodies from stroke. While there are several treatments that can be administered within hours or days of an incident in order to improve a patient's outcome, and physical therapy that can take place for a few months after that, there is very little doctors can do after that time.
Stem cells have been among the most promising new avenues of research. Huge improvements have been shown in animal models but results of the first human tests are just starting to come in. Earlier this month researchers at the University of Miami Miller School of Medicine reported that a year-long study of 48 patients found that infusing patients with stroke with stem cells through their carotid artery appeared to be safe.
The Stanford researchers have launched a larger randomized, double-blinded multicenter trial using the same procedure and have already begun to enroll patients. They are aiming for 156 total and say they hope to have results in as soon as two years.

lilit

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moram malo da pofalim firmu :lol:

https://www.sciencedaily.com/releases/2016/06/160611125403.htm

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World’s first vaccine developed against Toxic Shock Syndrome

(Vienna, 11-06-2016) Toxic Shock Syndrome (TSS) is a severe circulatory and organ failure caused by bacterial toxins, usually triggered by bacteria from the Staphylococcus group. Researchers from MedUni Vienna's Department of Clinical Pharmacology, in collaboration with the company Biomedizinische Forschungsgesellschaft mbH in Vienna, have now developed the world's first safe and effective vaccine against this disease and successfully tested it in a Phase I trial. The promising results were recently published in the leading journal "The Lancet Infectious Diseases".

This syndrome was first described in the 1980s. General symptoms of sepsis or blood poisoning occurred in young women who had used so-called "super tampons" during their periods. This is why the syndrome was also known as "tampon disease". This subsequently led to the absorption capacity of tampons being regulated.

Staphylococci colonize nearly all of us, especially on our skin and mucous membranes. They are totally harmless to most people. "However, for people with weakened immune systems, they can cause serious diseases such as Toxic Shocks Syndrome," explains Martha Eibl, director of Biomedizinische Forschungsgesellscaft mbH and former university professor at the Institute for Immunology of the medical faculty of the University of Vienna. This affects dialysis patients, the chronically sick, people with liver diseases and people recovering after heart operations. "Nevertheless, in 50% of cases the disease is associated with menstruation in young women," says Bernd Jilma from MedUni Vienna's Department of Clinical Pharmacology.

The vaccine, which has now been found to be safe and effective – and to have practically no side effects – in a clinical Phase I trial, and has been tested on 46 young men and women, was developed from a detoxified Staphylococcus toxin. The vaccine is injected into the skin and its effect is similar to that of a tetanus vaccination, says Jilma. "Immunization with such vaccines lasts for five years or more." Once vaccinated, a person develops antibodies, which become active if the germs start to pose a threat. A blood test can show whether someone is short of antibodies. Risk groups could then be preventively vaccinated.

"We are well on the way to having a vaccine that prevents this series disease. However, it will still take some years before it is in clinical use," explains Eibl. A Phase II trial with a larger test population has now started, in order to check the initial, promising results. "We are still looking for more volunteers," says Jilma.

Service: Lancet Infectious Diseases
"Safety, tolerability, and immunogenicity of a recombinant toxic shock syndrome toxin (rTSST)-1 variant vaccine: a randomised, double-blind, adjuvant-controlled, dose escalation first-in-man-trial." M. Schwameis, B. Rappenser, C. Firbas, C. Gruener, N. Model, N. Stich, A. Roetzer, N. Buchtele, B. Jilma, M. Eibl. Lancet Infectious Diseases, June 2016, dx.doi.org/10.1016.S1473-3099(16)30115-3

Some things you have to do yourself.

lilit

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aripiprazole je najbolji lek trenutno da se ukontroliše delusional thinking, posebno kad je deluzija u kombinaciji sa emotivnom labilnošću. upravo dobih info da ga je moguće nabaviti i u srbiji.

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Aripiprazole: A New Option in Delirium.
Prommer E1.Delirium is a palliative care emergency where patients experience changes in perception, awareness, and behavior. Common features include changes in the sleep-wake cycle, emotional lability, delusional thinking, and language and thought disorders. Delirium results from neurotransmitter imbalances involving several neurotransmitters such as dopamine, glutamate, norepinephrine, acetylcholine, gamma-aminobutyric acid, and serotonin. Untreated delirium causes significant morbidity and mortality. Nonpharmacologic and pharmacologic approaches treat delirium. Current pharmacologic management of delirium involves using agents such as haloperidol or second-generation antipsychotics. Third-generation atypical antipsychotic drugs have emerged as a potential choice for delirium management. Aripiprazole is a third-generation antipsychotic with a dopamine receptor-binding profile distinct from other second-generation antipsychotics. Aripiprazole acts as partial agonist at dopamine D2 and 5-hydroxytryptamine (5-HT)1A receptors, stabilizing the dopamine receptor leading to improvement in symptoms. The article reviews the pharmacology, pharmacodynamics, metabolism, and evidence of clinical efficacy for this new antipsychotic agent.

Some things you have to do yourself.

Meho Krljic

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Zanimljivo. Ali nama to ne treba sada kad imamo Kineze.

U drugim vestima:



Depressing paper suggests cancer's an evolutionary mechanism to 'autocorrect' our gene pool



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  Two scientists have come up with a depressing new hypothesis that attempts to explain why cancer is so hard to stop.
Maybe, they suggest, cancer's not working against us. Maybe the disease is actually an evolutionary 'final checkpoint' that stops faulty DNA from being passed down to the next generation.
To be clear, this is just a hypothesis. It hasn't been tested experimentally, and, more importantly, no one is suggesting that anyone should die of cancer. In fact, it's quite the opposite - the researchers say that this line of thinking could help us to better understand the disease, and come up with more effective treatment strategies, like immunotherapy, even if a cure might not be possible.
So let's step back a second here, because why are our bodies trying to kill us? The idea behind the paper is based on the fact that, in the healthy body, there are a whole range of inbuilt safeguards, or 'checkpoints', that stop DNA mutations from being passed onto new cells.
One of the most important of these checkpoints is apoptosis, or programmed cell death. Whenever DNA is damaged and can't be fixed, cells are marked for apoptosis, and are quickly digested by the immune system - effectively 'swallowing' the problem. No mess, no fuss.
But the new hypothesis suggests that when apoptosis - and the other safeguards - don't work like they're supposed to, cancer just might be the final 'checkpoint' that steps in and gets rid of the rogue cells before their DNA can be passed on... by, uh, killing us, and removing our genetic material from the gene pool.
"Dividing cells have to be able to pass at least four crucially important checkpoints during different phases of the cell cycle," the researchers write in the paper, published in Biotechnology & Biotechnological Equipment.
Most of these four stages, like apoptosis, are checking for DNA damage, but they can occasionally miss things, and when they do, it can lead to uncontrolled cell growth, and eventually cancer. Unchecked, the researchers say, those DNA mutations could eventually be passed on - if the carrier isn't killed first.
It sounds like something out of a particularly brutal sci-fi plot, but the authors of the paper - Rumena Petkova and Stoyan Chakarov from the Scientific Technology Service and Sofia University in Bulgaria - defend their idea by explaining that old age is pretty much a similar mechanism. After all, the planet couldn't survive if we all lived forever.
"[Cancer] seems to be a key evolution mechanism similar to DNA repair and apoptosis that protects the life on Earth as we know it from being extinguished ... a kind of a supreme checkpoint to ensure replacement of generations and evolution on planet Earth," they explain.
What that means, they suggest, is that a "universal and radical" cure for cancer is unlikely to exist - but instead our best hope is to focus on finding ways to improve the lifespan and quality of life for those with the disease.
"Despite the successes of modern medicine, cancer is rarely completely cured and is likely to cause, directly or indirectly, the death of the patient," the authors write.
"Nevertheless, the medicine of today and the near future has enough potential to slow down the progression to terminal cancer so that the life expectancy and the quality of life of cancer-affected individuals may be comparable to those of healthy aged individuals."
That's obviously not an easy idea for anyone to swallow, particularly for those who are living with cancer themselves, or who have loved ones with the disease - but the good news is there's no evidence just yet to suggest that any of this is true.
Like we said before, it's just a hypothesis - and there are many out there - for why cancer has proven so challenging for modern medicine to halt. In the new paper, the researchers simply lay out scientific observations that support their hypothesis. It now needs to be tested experimentally to see if there's any evidence that it might be true.
But before we get to that point, there are already a few big holes, as Charlie Sorrel over at Fast Company points out, like the fact that cancer is more common as people get older, and therefore is most likely to kill them after reproductive age, when passing on genes is no longer an issue. 
"And if a cancer comes along to do it's clean-up after we've passed reproductive age, then it's too late to stop your defective genes from being passed along," writes Sorrel. "Not that gene heredity is that cut and dried, but, like the [hypothesis] presented here, it's an interesting thought experiment."
Ignoring cancer for a second, the bottom line of all this is really the fact that we were never meant to live forever, and the idea that our body has its own safeguards in place to make sure that doesn't happen. Whether or not that's true, it's probably time to get out there and start living, huh?
 

lilit

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Some things you have to do yourself.

Meho Krljic

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Izvinjavam se, pročitao sam post, sećam se bugarskih imena, ali sam očigledno to zaboravio kada sam naleteo na ovaj članak. Kriv sam.

lilit

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no need to be worried, imamo odličan a dostupan tretman a da nije u budućnosti!! :lol:

http://onlinelibrary.wiley.com/doi/10.1002/stem.277/full

:)
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Meho Krljic

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Prelepo. Eh, što nisam miš...

lilit

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jučerašnji dan je bio solidno uzbudljiv tako da sam noćas sanjala implante i bakterijski biofilm pa da podelim.

veštački kuk, veštačko koleno, i ostale androidne stvari koje će se možda naći u našim krhkim humanoidnim telima, sa sobom nose opasnost od bakterijske infekcije, al nije problem kad je u pitanju single infekcija već kad se bakterijice organizuju u biofilm a u biofilm se organizuju onda kad imaju odgovarajuću površinu na kojoj će da sviju gnezdo (idealno: naš veštački kuk! :lol:).
čak i taj biofilm mi se do juče nije činio kao big problem al kad sam čula da se Staphylococcus aureus žrtvuje i umire for the sake of other towns, for the sake of humanity drugih bacterija prisutnih u biofilmu, shvatila sam da smo (we, the humans), na duže staze, ugasili.

šta radi s. aureus?
recimo: imamo s. aureus biofilm, e.g. bakterijski society na našem veštačkom kuku i rana neće da zaraste. rokamo se mi antibioticima, biofilm i tu ima ne preterano loša rešenja al kad rokamo najjačim oružjima, još uvek imamo šansu da se rešimo i biofilma (dok se ne sretnemo sa velikim brojem antibiotik rezistenstnih bakterija al to je za neku drugu priču).

u momentu kad biofilm (njegov površinski matrix) shvati da je celo društvo ugroženo, taj površinski deo kreće u programirani suicide da bi tako oslobodio ekstracelularnu DNK (eDNA) koja u velikom broju slučajeva spašava ostatak bakterijske družine. eDNA stabilizuje martrix biofilma, veže prisutne antibiotike, posreduje kod horizontalnog genskog transfera (pomoć za rezistenciju), krlja urođeni imunski odgovor tako što uglavnom sprečava fagocitozu a kad nema fagocitoze nema ni imunskog sistema protiv tih mikroba...

sve u svemu, ja fascinirana. in s. aureus we trust! :lol:

evo malo non-too-scientific-literature, kad nema šta pametnije da se radi:

http://www.podiatrytoday.com/what-you-should-know-about-biofilm-and-implants

https://microbewiki.kenyon.edu/index.php/Biofilms_and_Human_Implants

http://www.ncbi.nlm.nih.gov/pubmed/22094562
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Meho Krljic

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Dakle, veštački kukovi ima da dolaze sa već ugrađenim rezervoarima joda ili već nekog drugog oksidanta. Ništa drugo mi ne pada na pamet...

lilit

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well, ne, jer tek onda nema šanse da rana zaraste.

ide se na razvoj lekova koji će da inhibiraju adheziju bakterija za implante, a radi se i na  novim neadhezivnim implant materijalima.

zanimljivo je i da su mehanizmi kojima biofilm operiše različiti u npr. kateterima i u veštačkom kolenu. onaj kateterski je uglavnom sastavljen od s. epidermidis i  cilj mu je da se što bolje prikači za kateter jer je svestan da mu života posle vađenja katetera nema a u kateteru ga ni imunski sistem ne ferma previše jer i on zna da će kateter da nas napusti jednog dana.
tako da tu osnovni mehanizam preživljavanja biofilma ide preko tzv. polisaharidnog intracelularnog adhezina (PIA) koji pojačava adheziju bakterija za kateter i omogućava formiranje biofilma.
ovi u kukićima morali su da razviju sofisticirane metode preživljavanja, eDNA je jedan takav.
ajd sve da prihvatim, al programirani suicide...e to me dirnulo! :lol:
Some things you have to do yourself.

lilit

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autoimunske bolesti su solidan shit koji može da vas strefi u životu pošto vaš savršeni imunski sistem, a koji je naučen da fajtuje raznorazne izazove okoline, ne primeti i ne ubije klon koji se okrene protiv sopstvenog. onda taj klon (limfocit) krene da posmatra sopstveno kao strano (ljudsku ćeliju kao bakteriju, simplifikovano) i napravi čudo u organizmu.
za neke autoimunske bolesti relativno dobra terapija (medikamentima) postoji, za neke ne.
dugo sam radila u ovoj oblasti i znam s kojim problemima i izazovima se susreću ljudi koji su oboleli od širokog spektra ovih bolesti.
otud, jako lepe vesti:


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Immune system autocorrect feature reverses autoimmune disease in mice

The human immune system—the powerful, complex network of cells that watches over and defends the body—just got a new weapon: autocorrect.

According to a report in Science, researchers were able to reverse an autoimmune disorder in mice by engineering certain healthy immune cells to weed out faulty ones. The method behind the treatment involves chimeric antigen receptor (CAR) T cells and is identical to the method used in an experimental therapy for certain types of leukemias and lymphomas that has so far proven successful in some small human trials. While researchers will need to do much more work to prove that the strategy holds up against autoimmune disorders in humans, the authors argue that its track record of beating cancers is reason to be optimistic.

"Our study effectively opens up the application of this anti-cancer technology to the treatment of a much wider range of diseases, including autoimmunity and transplant rejection," coauthor Michael C. Milone, of the University of Pennsylvania School of Medicine, said in a news release.

In those anti-cancer applications, engineered CAR T cells are used to fight off B cells that have become cancerous and are causing B cell-based leukemias or lymphomas. Normally, B cells are responsible for making antibodies, the Y-shaped proteins that detect germs and other invaders.

For the treatment, T cells are taken from a patient and genetically tweaked to contain an artificial detector—chimeric antigen receptor—that specifically singles out those cancerous B cells. Then researchers put the tweaked T cells back into the patient’s blood, where they track down and destroy the bad B cells.

Milone and colleagues realized this strategy might work for certain types of autoimmune disorders, particularly ones involving rogue B cells. They decided to test out the idea on a rare autoimmune disease called pemphigus vulgaris. In patients with this disease, faulty B cells pump out antibodies that attack a protein that helps skin and membrane cells stick together. The result is painful blistering in various places on the body and in the mouth and throat. The disease can be fatal without treatments, which often include powerful, immune-suppressing drugs that leave patients defenseless against life-threatening infections.

In cell experiments and in mice engineered to have the disease, CAR T cells were able to take out the faulty B cells while leaving the rest of the immune system intact. The treated mice survived and no longer developed blisters.

Next, Milone and his colleagues will test out the therapy in dogs, one of the few other animals that naturally get the disease. If the strategy holds up, they’ll move on to clinical trials and branch out to see what other autoimmune disorders CAR T cells might be able to treat.

T-limfocit je naravno lutka (elektronska mikroskopija)




ceo rad:
http://science.sciencemag.org/content/353/6295/179
Some things you have to do yourself.


lilit

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evolucija na delu?
Some things you have to do yourself.

Meho Krljic

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Nešto je to mnogo brzo za ono kako evolucija inače radi...

lilit

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hteo si da kažeš: ...za ono kako mi verujemo da evolucija inače radi? :lol: :lol: :lol:

kad sam već u the office (GB) modu, turiću ovo ovde:
http://xkcd.com/1706/
Some things you have to do yourself.

ЖивОзбиљан

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s tolkom glavudžom a ni procenat šarplaninca!
šta će mi bogatstvo i svecka slava sva kada mora umreti lepa Nirdala

lilit

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ajd da ne otvaram novu temu premda je naš imunski sistem fenomen na rubu SF-a, al oftopik volim više nego lebac  :lol:

dve lepe prezentacije: i) čime raspolažemo i ii) protiv kakvih kreatura se borimo:
http://www.inside-immunity.org/
Some things you have to do yourself.

Аксентије Новаковић

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http://antistresvodic.rs/seme-koje-sami-posadite-vas-najbolji-lekar/

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Seme koje sami posadite
VAŠ NAJBOLJI LEKAR


Mame, tate, bake, deke, tetke, stričevi… svi vi koji sadite bašte ili pripremate rasade. Evo jednog divnog i korisnog odlomka iz knjige Anastasija, Vladimira Megrea, koju su na našem jeziku izdali Zvoneći kedri Srbije

Evo kako je govorila Anastasija o semenu posađenom vašom rukom, a zapisao Vladimir Megre:
– Svako, posađeno vašom rukom seme, sadrži u sebi ogroman obim Vaseljenske informacije. Ovaj obim se ne može porediti ni po veličini, ni po tačnosti, ni sa jednim veštačkim. Pomoću ove informacije seme zna tačno, do milionitog dela sekunde, vreme kada treba da se pokrene, počne da raste, kakve sokove da uzima iz zemlje, kako da koristi zračenja kosmičkih tela – Sunca, Meseca, zvezda, u šta da raste, kakve plodove da donosi. Plodovi su namenjeni obezbeđenju čovekovog života. Ovi plodovi mogu uspešnije i snažnije od veštačkih lekova, ranije stvorenih ili budućih, da se bore i suprotstave bilo kom oboljenju ljudskog organizma. Ali, o tome, o stanju čovekovom mora da zna seme, da bi se u procesu svoga zrenja zasitio plod neophodnim odnosom supstanci za lečenje određenog čoveka, njegovih bolesti ukoliko postoje, ili postoje predispozicije za njih.

Pre sadnje. Da bi seme krastavca, paradajza ili bilo kog drugog rastinja, uzgajano na parceli, imalo takvo obaveštenje, neophodno je sledeće:
– Pre sadnje uzeti u usta jedno ili nekoliko malenih zrna, držati ih u ustima pod jezikom, ne manje od devet minuta.
– Potom ih položiti između dlanova ruku i držati ih tako tridesetak sekundi. Među dlanovima svojim semenje držeći, treba stajati bos na tom komadu zemlje, na kom će se zatim odvijati sadnja.
– Otvoriti dlanove i seme koje leži u tvojim rukama pažljivo prineti usnama i izdahnuti na seme iz svojih pluća vazduh. Ugrejati ga dahom svojim, i to što postoji u tebi, maleno seme će upoznati.
– Onda je još nužno držati otvorene dlanove tridesetak sekundi, nebeskim telima seme predstavljajući. I seme će ustanoviti trenutak svog izlaska. Planete sve će mu pomoći u tome! I za tebe će izdancima potrebnu svetlost darivati.

Zalivanje posle tri dana. Anastasija kaže da se seme nakon toga može u zemlju posaditi.
– Ni u kom slučaju ga ne treba odmah zalivati, da se ne bi sprala pljuvačka koja je obavila seme, i obaveštenje o tebi koje seme u sebe upija. Po isteku tri dana od sadnje, dozvoljeno je zalivanje.
Sadnju je neophodno sprovoditi u pogodnim danima za određeno povrće (to je svakom čoveku već poznato po mesečevom kalendaru). Ranija sadnja bez zalivanja nije tako strašna, kao prekasna.
– Ne treba spaljivati pored sadnica sav korov koji se pojavio. Treba od raznih vrsta ostaviti bar po jedan. Korov se može podrezati…

Plodovi koji su naš lek. Po rečima Anastasijinim, seme na ovaj način upija u sebe obaveštenje o čoveku, i u toku sazrevanja svog ploda do maksimuma će odabirati iz kosmosa i zemlje neophodnu energiju, upravo za tog određenog čoveka. Korov sav ne treba ukloniti zato, što i on ima svoje predodređenje. Jedan štiti biljke od bolesti, drugi daje dodatne informacije. U vreme rasta, treba dolaziti u dodir sa biljkama – barem jednom u toku njihovog sazrevanja. Poželjno je u vreme punog Meseca prilaziti im i dotaći ih.
Anastasija je tvrdila da su plodovi, uzgajani na ovaj način, ako ih upotrebljava čovek koji ih je sam negovao, kadri da ga izleče od apsolutno svih bolesti, da znatno usporavaju starenje organizma, oslobađajući ga od loših navika, da mnogo puta uveličavaju radne sposobnosti, dajući duševni mir. Plodovi će imati najdelotvorniji uticaj ukoliko se upotrebe najkasnije tri dana od branja.

Razlika ne samo u izgledu. Nije obavezno saditi na taj način cele leje. Dovoljno je da bude po nekoliko strukova.
Uzgajani na ovaj način, plodovi će se razlikovati od drugih iste sorte, ne samo po ukusu. Ukoliko se podvrgnu analizi, razlikovaće se i po odnosu supstanci u njima. Odnosi će biti potpuno različiti.
Pri polaganju sadnica obavezno je svojim rukama i prstima bosih nogu izgnječiti zemlju i pljunuti u rupu. Na pitanje, zbog čega nogama – Anastasija je pojasnila da kroz znojenje nogu iz čoveka izlaze supstance (verovatno toksini), koje sadrže obaveštenje o bolestima organizma. Tu vest će dobiti mladice. One će je preneti plodovima, koji će onda biti u stanju da se bore sa nedaćama. Anastasija je savetovala da se s vremena na vreme po parceli hoda bos.

Kakve kulture je neophodno gajiti. Anastasija je na ovo konkretno pitanje odgovarala da treba da ih bude onoliko raznorodnih koliko postoji na većini parcela: maline, ribizle, ogrozd, krastavci, paradajz, šumske jagode, bilo koja jabuka. Veoma je dobro ako postoji višnja ili trešnja, cveće. Količina, veličina parcele koja se sadi ovim kulturama, nema neki veći značaj.
Kao obavezne, bez kojih je teško zamisliti pun energetski mikroklimat, na parceli treba uvrstiti takvo rastinje kao što je suncokret (barem jedan). Neizostavno treba posejati na parceli, veličine jedan i po do dva kvadratna metra, žitne kulture – raž, pšenicu, i obavezno ostaviti ostrvce, ne manje od dva kvadratna metra, pod različitom travom. To se ostrvce ne sme sejati veštački, treba da bude prirodno. Ukoliko niste sačuvali na svojoj parceli razne trave, treba doneti iz šume busen i stvoriti takvo ostrvce uz njegovu pomoć.

Prirodni lekar. Vladimir Megre je pitao Anastasiju ima li potrebe za sadnjom kultura, koje ona smatra obaveznim, ukoliko iza ograde, nedaleko od parcele, one već postoje. Dobio je sledeći odgovor:
– Važnost ima ne samo raznovrsnost, već i način njihove sadnje, neposredno opštenje s njima, preko kog se i odvija zasićivanje obaveštenjima. Već sam ti govorila o jednom od načina sadnje – on je osnovni. Najvažnije je – zasititi obližnji deo prirode vestima o sebi. Samo je tada lekovit učinak, te će čak i imunitet tvog organizma biti znatno uvećan. Mnogo više nego od uobičajenih plodova. U divljoj, kako je vi nazivate, prirodi, a ona nije divlja, već vam je prosto nepoznata, postoji mnoštvo biljaka, uz čiju se pomoć mogu izlečiti apsolutno sve postojeće bolesti. Te biljke su zato i stvorene, ali je čovek izgubio, ili skoro sasvim izgubio sposobnost da ih prepozna.
Ispričao sam Anastasiji da kod nas postoji mnogo specijalizovanih apoteka koje trguju lekovitim travama, ima i lekara, i vidara, koji leče travama profesionalno, na šta je ona odgovorila:
– Postoji glavni lekar – tvoj organizam. On je odvajkada obdaren sposobnošću da zna, koju travu je neophodno upotrebiti i kada. Kako se uopšte hraniti, disati. On je u stanju da predupredi bolest, pre njenih spoljašnjih znakova. I niko drugi ne može da zameni tvoj organizam, jer je to tvoj lični lekar, dat lično tebi, isključivo tebi, od Boga. Objašnjavam ti kako da mu daš mogućnost da deluje u tvoju korist.
Uređeni uzajamni odnosi sa skupom bilja na tvojoj parceli lečiće te i brinuti o tebi. Samostalno će postaviti tačnu dijagnozu, i pripremiti poseban, najdelotvorniji, upravo za tebe, lek.


Аксентије Новаковић

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Лековима фармакомафије се нико није излечио, већ су људи претворени у таблетомане који, да би живели, морају свакоднедневно да гутају таблете које одржавају у функцији оболели орган.
Тако популација постаје зависна од произвођача лекова.

Сећам се времена кад људи нису гутали никакве таблете, живели су колико толико у складу са приородом и доживљавали дубоку старост.
Док су Срби гутали глог и дрен да имају здраво срце и да буду здрави ко дренови - нису гутали таблете.

Шта је са применом индустријске конопље?
Алескијев Тито је Србима забранио конопљу, од чије би производње Србија, као превасходно пољопривредна земља, могла да процвета, што због експеримената у области медицине (уље против рака, мелеми за опекотине итд итд), што због свих могућих продуката на произведених на бази конопљиног влакна, попут одеће, обуће, блокова за градњу кућа од конопље, плус би било довољно хране произведене од семенки конопље.
Просто речено, биљка створена од Бога да голог обуче, да оном без куће створи кров над главом, да болесне лечи и да гладне нахрани високопротеинском и омега мастима здравом храном.

Значи, линк који сам пре неки дан поставио има везе са лечењем помоћу биљака, и лично сведочим да семе третирано на начин описан у тексту који сам поставио даје крупнији цвет са много више латица од семена које није третирано на такав начин.

На даље, помињеш бајалице.
Не видим ништа спорно у лечењу бајалицама, јер не треба потцењивати моћ изговорене речи.

Такође, будућност не лежи у таблетама и медицинским киборг причама, већ будућност лежи у биоенергији, самоисцеливању и саморегенерацији оболелих органа, но за тако нешто је потребан и одређен ниво више свести, јер је теорија биг бенга убедила наивне да су продукт случајности, а теорија еволуције је на то надодала да су продукт и еволуцијске случајности, па такав наивко који је прогутао те приче о случајним случајностима себе не доживљава као део Свемира већ као апгрејдованог мајмуна, па никад неће ни помислити да поседује нпр. биоенергију, а о телепатији или телекинези да не говоримо...

Као што сам рекао, биоенергија представља једну од грана будуће медицине ослобођене од фармакомафије, таблета, капсула и других ствари које не лече него залечују и човека чине робом своје болести.
Охрабрујем свакога да ствар преузме у своје руке и да почне са спознајом себе.

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Bioenergija je energija zivota, doslovno "zivotna energija". Lecenje uz pomoc bioenergije je terapija koja moze uravnoteziti i uskladiti fizicko i duhovno stanje organizma. Ovakva terapija usmerena je na bioenergetska polja, energetske centre i kanale po kojima energija tece u telu. Da pokusamo da pojasnimo, svaka stanica u ljudskom telu funkcionise uz pomoc energije, emitirajuci elektricne impulse, sto zauzvrat cini elektro-magnetno bio-energetsko polje koje okruzuje nasa tela.

http://www.priroda-leci-sve.com/bioenergija.htm

mac

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Naučne teorije su upravo to zbog čega imam pojačan osećaj da sam deo veće celine. Svi atomi teži od helijuma su nastali eksplozijom zvezda. U nama je zvezdana prašina. Većinu našeg genoma smo nasledili iz davnina i sastavni smo deo biosfere. Naš predak nije došao na gotovo, nego se izborio za svoj deo Zemlje. Sve je to davno utvrđeno, pre nego što su se naši dedovi i rodili. Nema tu nikakve sumnje.

Ali hajde, igramo se, reci dakle u šta tačno sumnjaš, i naučni razlog zbog kojeg sumnjaš. Sumnja je zdrava, ali u nauci imamo sistem. Ako postoje dokazi za tvrdnju onda te dokaze moraš da opovrgneš, a ne tvrdnju. Tvrdnja je samo posledica dokaza. Navedi dokaz i navedi zašto taj dokaz tebi nije dobar.

ALEKSIJE D.

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Konoplja je zabranjena u SAD negde 1947-48 posebnim zakonom jer ima u sebi THC. Međutim, pravi razlog zabrane konoplje (ne sve, industgrijksa nije kod nas zabranjena ali je fabrike koje bi prerađivale ne postoje) počiva u tome što je jak lobi vlasnika šuma tražio da se zabrani ovaj OBNOVLJIVI izvor celuloze od koje pravio papir i tkanina, kako bi iskoristili šumska bogastva koja su posedovali.
Kada bi konoplju upotrebljavli za odeću, farmerke ili jakne, one bi trajale i po 40 godina. Papir ne bi bio problem, šume ne bi bile sečene itd.
A i T2 bi mogao da razmišlja u hladu konopljinog lista o tom njegovom imaginarnom četničkom komunizmu.

Meho Krljic

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Crispr: Chinese scientists to pioneer gene-editing trial on humans



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A team of Chinese scientists will be the first in the world to apply the revolutionary gene-editing technique known as Crispr on human subjects.

Led by Lu You, an oncologist at Sichuan University’s West China hospital in Chengdu, China, the team plan to start testing cells modified with Crispr on patients with lung cancer in August, according to the journal Nature.
Crispr is a game-changer in bioscience; a groundbreaking technique which can find, cut out and replace specific parts of DNA using a specially programmed enzyme named Cas9. Its ramifications are next to endless, from changing the color of mouse fur to designing malaria-free mosquitoes and pest-resistant crops to correcting a wide swath of genetic diseases like sickle-cell anaemia in humans.
The concept of editing human DNA has often been controversial. In the UK, genetic modification in humans remains off-limits. Peter Mills, assistant director of the UK Nuffield Council on Bioethics, has told the Guardian of the worries it raises about playing god and “designer babies”.

A study on non-viable human embryos, also conducted in China, was called off after researchers found what they described as “serious obstacles” to using the method in a clinical setting.



And in March 2015 a group of researchers published an open letter in Nature saying that there were “grave concerns” about the ethical and safety implications of editing the “germ-line” in human genes – the genetic code which is passed on.


The Sichuan University trial, it is important to note, does not edit the germ-line; its effects will not be hereditary.
What the researchers plan to do is enroll patients with metastatic non-small cell lung cancer, Nature reported, and for whom other treatment options – including chemotherapy and radiotherapy – have failed.
They will then extract immune cells from the patients’ blood and use Crispr to add a new genetic sequence which will help the patient’s immune system target and destroy the cancer. The cells will then be re-introduced into the patients’ bloodstream.
China has been at the forefront of Crispr research. In 2014, researchers at Nanjing University reported that they had successfully engineered mutations in macaques – the first reported successful use of the technique in non-human primates.
Crispr was approved for human trials in the US by a research group backed by tech billionaire Sean Parker, but if it begins on schedule in August the Sichuan University study will beat them to the punch of being the first of its kind.

Аксентије Новаковић

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  • Homo Superior
Склапао је Тито и дил са америма за памук, зато нам је конопља забрањена, иначе све речне обале су биле под конопљом.
Пре неки дан сам видео кошуљу од конопље стару 90ак година, време се на њој уопште не познаје.

@mac
Кажеш: ali u nauci imamo sistem.

Какав си ти научник, и какав си ти део било каквог научног система?
Осим ако евентуални рад у просвети не сматраш битним фактором, мислим просветари су јако битни и они штрајкују само онда када им зине дупе за паре а никако да се сете да штрајкују због лошег образовног система којим заглупљују децу.

mac

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Šta sad, ja sam kriv za nešto? Za šta sam tačno ja kriv?

I koji dokaz bi želeo da opovrgneš?

Аксентије Новаковић

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  • Homo Superior
Крив си јер у оквиру своје радне заједнице не подстрекаваш колеге на штрајк због неадекватног образовног програма са којим свакодневно радите и чијем погубном дејству излажете генерације младих Срба.
Крив си јер по форуму пишеш о револуцији, а у оквиру своје радне заједнице не позиваш ни да се штрајкује.

Дај ми доказ да хемотерапија успешно лечи рак.

mac

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Ima dokaza, naravno, pa nisu osiguravajuća društva veverice, pa da plaćaju za nešto što ne daje rezultate. Follow the money. Ali nije na meni da dokazujem nešto što je odavno utvrđeno, nego na tebi da dokažeš novu tvrdnju. Tvoja tvrdnja je novum, koji pobija ono što je ustanovljeno, znači obaveza je na tebi. Nije dovoljno samo da kažeš "ja ne verujem u hemoterapiju", potrebno je nešto jače, tipa "u poslednjih godnu dana hemoterapiju je primilo x pacijenata, projektovano izlečenje je bilo y%, a zapravo izlečenih je z%, i to z je toliko malo da ne opravdava hemoterapiju kao vid borbe protiv kancera". E to je iskaz, i kad bi rekao tako nešto, i kad bi to još bila i istina, ispao bi ljudina i čestit čovek.

Meho Krljic

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Ima ovde detaljna rasprava o ovom pitanju:



Chemotherapy doesn’t work? Not so fast…

Аксентије Новаковић

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  • Homo Superior
Ниси ми дао ниједан доказ да нешто што је направљено од заосталих нервих агенаса из другог светског рата може да излечи рак.

Да је заиста тако - не би људи ишли чак у Албанију да наточе кило петролеја којим се лече, или скупљају последњу цркавицу да им се из иностранства донесе уље од конопље.

Какв исказ, какви проценти, ти бараташ шатро бројкама, ја радим са живим људима, и свакодневно се умире од рака, проценат излечених помоћу хемотерапије је НУЛА.

Крив си јер подржаваш постојеће стање и кријеш се иза лажнних статистичких показатеља (ко несрећници у 1984) доводећи у заблуду друге којима си окружен да је све у најбољем реду.



mac

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Šta radiš sa živim ljudima? Radiš u osiguravajućem društvu, ili kao doktor u domu zdravlja, ili si konobar/taksista/novinar/policajac? Koje su ti kvalifikacije za procenu efektivnosti dejstva hemoterapije, osim što su ljudi s kojima radiš živi?

Budi čovek, teži znanju, beži od neosnovanih izjava, poput one da se poznati Kelti mogu zvati samo Bran...

Meho Krljic

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Da, to za petrolej i ulje od konoplje su nezgodne stvari. Ljudi troše ozbiljne pare na nešto što ne leči*, ali, eto, nada umire poslednja valjda.... Ja sam letos sahranio taštu koja je sve to probala, pa eto - sahranjena je. Doduše, nije je ubio rak na kraju, već embolija koja je došla kao posledica transfuzije krvi a koja joj je bila neophodna jer joj je bolest jako oslabila krvnu sliku itd... U svakom slučaju, ulje od konoplje tu nije bilo ni od kakve pomoći, pa ako su individualne priče argumenti, eto jednog...











* bar ne postoje proverljivi dokazi da leči

ЖивОзбиљан

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kad bi hemoterapija stvarno bila krivac, a ne placebo i razni eksperimentalni lijekovi koje nam podmeću, a koji nigdje nisu ranije isprobani

zato se ''elita'' i ne liječi na Balkanu nego Pariz-Njujork i te fore, a ovdje uvezu sranje od lijekova, čija je učinkovitost znatno manja
šta će mi bogatstvo i svecka slava sva kada mora umreti lepa Nirdala

lilit

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Crispr: Chinese scientists to pioneer gene-editing trial on humans

ej mehane, super da si stavio ovaj trial (premda se neće ići dalje od faze 1, znači samo safety and tolerability, i na jednom pacijentu dodatno definisanje doze) jer shvatih da dosad nismo pominjali crispr/cas9 sistem za editovanje DNK a to je big otkriće 21. veka sa velikim potencijalom za tretiranje genetskih bolesti ali i kancera, dijabetesa i sl.

http://www.youtube.com/watch?v=2pp17E4E-O8
Some things you have to do yourself.

lilit

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gud njuz, taman će je napraviti kad budem ready za penziju

Quote
FluGen Starts Clinical Trial for Universal Flu Vaccine

It took longer than FluGen planned, but a human clinical trial is now underway for the experimental universal influenza vaccine that the Madison, WI-based biotech startup is developing.

The primary goals of the trial announced Wednesday are to evaluate the safety of the vaccine, which is known as Redee Flu, and evaluate antibody and T-cell responses in study participants, the company said.

Ninety-six subjects, all between the ages of 18 and 49, will be dosed with the vaccine, FluGen said. They are broken into three groups of 32, and the dosage will increase with each group, said Paul Radspinner, FluGen’s co-founder, president, and CEO.

“We’ve already started dosing subjects in the first cohort,” Radspinner said in an interview. “Once we clear the first week of this group, then we’ll start recruiting for the second group.”

Radspinner said that researchers will be taking measurements on subjects throughout the study, but investigators must wait 28 days after a cohort has been dosed before they can collect the most vital data on subjects’ immune responses.

FluGen leaders hope to have safety and immune response data on all three cohorts in the trial by December, Radspinner said.

One benefit of a universal flu vaccine is that it could protect against strains of the virus that vary from the ones groups like the CDC and World Health Organization predict will be the predominant strain (or strains) for a given flu season.

Redee Flu is made up of a live flu virus from which a key gene, known as M2, has been deleted. The vaccine virus is able to live in the body just long enough to provoke a strong immune response, but thanks to the deleted gene it’s not able to cause disease or spread to other people, according to FluGen. Radspinner said that other companies, such as Fort Collins, CO-based Vivaldi Biosciences, are developing vaccines that have similarities to Redee Flu, but that he does not know of any that remove the M2 gene.

Radspinner said that after the current clinical trial concludes, FluGen is likely to initiate a Phase 1b trial. The goal is for that to happen sometime in 2017, he said. The company also plans to conduct a challenge study in which subjects would receive a vaccine designed to primarily protect against a particular flu strain, then be “challenged” by being dosed with a different strain of the virus. The idea is to test a vaccine’s ability to protect against “drifted or mismatched flu strains,” as FluGen termed them in a press release.

“It would mimic what happened in 2014 and 2015 when there was a mismatch between the vaccine and the prevailing strain,” Radspinner said.

FluGen has raised a total of about $20 million from investors, Radspinner said, and the company is in the process of securing additional capital commitments. He co-founded FluGen in 2007, along with Yoshihiro Kawaoka and Gabriele Neumann.

At the time FluGen closed a $3.4 million bridge financing round in June 2014, the plan was to get a vaccine into human trials in early 2015. FluGen was still working toward that goal when it raised another $9.4 million in August 2015.

Radspinner said there are a few reasons for the delay between then and now. Among them were completing preclinical studies and a FDA Good Laboratory Practice study, as well as making sure the vaccine material was manufactured in a way that meets standard FDA specifications, he said.

“And then finally, probably the most important thing was to put together the [investigational new drug] document that had to be given to the FDA,” Radspinner said. “Obviously, we had to succeed with that in order to initiate this study.”
Some things you have to do yourself.

ЖивОзбиљан

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taman da se pobije bapska priča (ili potvrdi, ko će ga znati): stalno spominju kako je nemoguće da ova regionalna ministarstva zdravlja znaju baš koji će tip gripa da navali, i baš tu vakcinu naruče te zime.

Naravno, teorija zavjere tvrdi da to neki tvoji zli laboranti ubace međ pošten svijet, dok razumnije objašnjenje jeste da se prati epidemija globalno i da se može prognozirati širenje. Samim tim se prilično pouzdano može znati koju vakcinu treba kupiti

pitanje je, dakle, da li babe griješe?
šta će mi bogatstvo i svecka slava sva kada mora umreti lepa Nirdala

lilit

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kakva bre regionalna ministarstva, oni naručuju ono što se za tu godinu proizvede a proizvodnja kreće u februaru najkasnije na osnovu preporuka epidemioloških studija za tu godinu (u australiji je zima kad je kod nas leto, da simplifikujem  xrofl )

Quote
http://www.who.int/influenza/surveillance_monitoring/en/

The WHO’s Global Influenza Programme (GIP) provides global standards for influenza surveillance. In addition GIP collects and analyzes virological and epidemiological influenza surveillance data from around the world. The regular sharing of quality influenza surveillance and monitoring data by countries allows WHO to:

  -  provide countries, areas and territories with information about influenza transmission in other parts of the world to allow national policy makers to better prepare for upcoming   
seasons;
  -  describe critical features of influenza epidemiology including risk groups, transmission characteristics, and impact;
  -  monitor global trends in influenza transmission; and
   - support the selection of influenza strains for vaccine production.

plus

Quote
The ability to identify new strains of influenza viruses and describe their circulation has expanded in recent years. National virologic data are obtained through weekly reports from ∼75 World Health Organization (WHO) and 50 National Respiratory and Enteric Virus Surveillance System laboratories. Global viral surveillance involves 115 national influenza centers in 84 countries that analyze 175,000–200,000 samples and characterize 4000–8000 viruses annually. Viruses submitted for detailed antigenic and genetic characterization to WHO centers in Atlanta, London, Melbourne, and Tokyo are used in formulating annual influenza vaccines [4]. A recent initiative to strengthen the influenza surveillance infrastructure in Asia and elsewhere is expected to lead to enhanced viral surveillance and to provide a better early-warning system for viruses with pandemic potential [5]

Some things you have to do yourself.

lilit

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pošto sam već u ofisu, još jedna gud njuz: napokon se krenulo sa long-acting lekom protiv šizofrenije (paliperidone palmitate ) - 4x godišnje - injekcija - nema zaboravljanja ili izbegavanja terapije.


Quote
Long-acting schizophrenia drug could reduce relapses

The approval of a new, very long-acting schizophrenia medication by Health Canada could encourage more patients to use injectable drugs that reduce relapses, according to a leading psychiatrist.

“Patients who are reluctant to be injected every two weeks or every four weeks would only have to take this drug once a season,” said Howard Margolese, a Montreal-based expert in the treatment of schizophrenia. “That increases acceptability of this form of treatment because it is less often and less invasive.”

Invega Trinza — paliperidone palmitate — is injected four times a year by a physician or a nurse. Previously approved injectable medications for schizophrenia are typically injected at least once a month, while oral medications are taken at least once a day, 365 days a year.

“People who respond well to (long-acting) medications don’t have to feel like a patient between visits, they don’t have to remember to take medication every day and they can focus on other goals and other aspects of their lives,” said Margolese.

Schizophrenia is a complex mental illness characterized by abnormal social behaviour, delusion and hallucinations that affects 40,000 British Columbians and 350,000 Canadians. About 80 per cent of people with schizophrenia suffer a relapse in the first five years of treatment.

An analysis of five drug-compliance studies published by the Journal of Clinical Psychiatry found that only half of patients with schizophrenia take their oral medication at least 75 per cent of the time.

Patients taking long-acting injectable medications are far less likely to relapse, which reduces the rate and duration of hospital stays particularly in patients who struggle to take daily oral medication consistently, he said.

“For a lot of patients, their symptoms interfere with their ability to take medication reliably,” said Chris Summerville, CEO of the Schizophrenia Society of Canada. “With a mental illness, it is critical that you take medication regularly.”

Patients and their families are eager for solutions, he said. There is also a strong economic case for long-acting drugs.

So-called “mirror studies” that follow patients before and after switching from daily oral medication to long-acting injectable medication show a significant reduction in hospitalizations in patients taking long-acting drugs, according to a meta-analysis of 25 studies involving 5,940 patients published in the Journal of Clinical Psychiatry.

A Canadian mirror study by Fiore Lalla and Larry Arshoff of long-acting medications involving just 19 patients who were heavy users of emergency and in-patient services noted savings of more than $1 million in hospitalization costs in one year.

Randomized control trials comparing oral and injectable medications have failed to show a difference in relapse rates, but those studies set a high bar for inclusion that would disqualify unstable patients who don’t take their medication reliably, the very people injectable meds help the most, said Margolese.

In addition to reducing hospitalization rates, longer-acting drugs may allow some patients to go longer between appointments with their psychiatrist, he said.

“The main difference with injectable drugs is that we know when patients aren’t taking it and that gives us a chance to do something about it,” said Margolese. “With oral medications, we simply don’t know if patients are taking them.”

A clinical trial found that nine per cent of patients taking Invega Trinza relapsed, compared with 29 per cent of patients taking a placebo.

http://www.calgaryherald.com/health/long+acting+schizophrenia+drug+could+reduce+relapses/12074257/story.html
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Meho Krljic

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NIH moves to lift moratorium on animal-human chimera research



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The National Institutes of Health (NIH) today announced that the agency soon expects to lift a moratorium on funding for controversial experiments that add human stem cells to animal embryos, creating an organism that is part animal, part human. Instead, these so-called chimera studies will undergo an extra layer of ethical review but may ultimately be allowed to proceed.
Although scientists who support such research welcomed the move, some were left trying to parse exactly what the draft policy will mean. It is “a step in the right direction,” says Sean Wu, a stem cell researcher at Stanford University in Palo Alto, California, who co-authored a letter to Science last year opposing the moratorium. But "we still don’t know what the outcome will be case by case,” he adds. However, some see the proposal as opening up research in some areas that had been potentially off-limits.
At issue are experiments in which scientists introduce human pluripotent stem cells—cells that can potentially turn into any kind of tissue—into very early embryos of mice and other animals and then let the animals develop. Such experiments can be used to study human development, generate disease models, and potentially grow human organs for transplantation. But the idea of such human-animal chimeras has drawn public concern, and some scientists and ethicists worry that the experiments could produce, say, a supersmart mouse.
Last September, NIH abruptly announced it was suspending funding for studies that introduce human stem cells into animal embryos while the agency considered the ethical issues. Although NIH wasn’t yet funding such research, the pause put on hold future federal support for studies by researchers who want to create pig-human or sheep-human chimeras to generate organs for transplantation. NIH then held a workshop last November to gather input, where the general consensus was that these studies are scientifically valuable.
According to two notices released today, NIH is proposing to replace the moratorium with a new agency review process for certain chimera experiments. One type involves adding human stem cells to nonhuman vertebrate embryos through the gastrulation stage, when an embryo develops three distinct layers of cells that then give rise to different tissues and organs. The other category is studies that introduce human cells into the brains of postgastrulation mammals (except rodent studies, which won’t need extra review).
These proposed studies will go to an internal NIH steering committee of scientists, ethicists, and animal welfare experts that will consider factors such as the type of human cells, where they may wind up in the animal, and how the cells might change the animal’s behavior or appearance. The committee’s conclusions will then help NIH’s institutes decide whether to fund projects that have passed scientific peer review.
NIH also wants to tighten its existing stem cell guidelines to prohibit studies that add human stem cells to primate embryos up to and including the blastocyst stage. (Current guidelines only prohibit adding human pluripotent cells to primate blastocysts.) And the agency wants to extend a current ban on breeding chimeric animals that might carry human eggs or sperm to include chimeras created with any kind of human cell, not just pluripotent stem cells.
“I am confident that these proposed changes will enable the NIH research community to move this promising area of science forward in a responsible manner,” writes NIH's associate director for science policy Carrie Wolinetz in a blog post today. In a call with reporters, she emphasized that the proposal “is not ... a prohibition” on chimera research. “It is merely an extra look.”
NIH is collecting comments on the proposed changes until 4 September, then hopes to issue a final policy and lift the moratorium by late January, Wolinetz said.
Although some scientists are holding their applause, one sees the proposed policy as an indication that NIH is relaxing its chimera policy. Neuroscientist Steve Goldman of the University of Rochester in New York, who injects human stem cells into the brains of mice, notes that even experiments that put human cells into the brains of monkeys or other primates appear to be potentially permissible. Such studies, which could be useful for studying mental illnesses, “had been a very murky zone” until now, Goldman says. The proposed changes suggest “a much more permissive environment.”


Meho Krljic

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 Measles are gone from the Americas 
Quote

The Americas are now free of measles and we have vaccines to thank, the Pan American Health Organization said earlier this week.
This is the first region in the world to be declared measles-free, despite longtime efforts to eliminate the disease entirely. The condition — which causes flu-like symptoms and a blotchy rash — is one of the world’s most infectious diseases. It’s transmitted by airborne particles or direct contact with someone who has the disease and is highly contagious, especially among small children.
To be clear, there are still people with measles in the Americas, but the only cases develop from strains picked up overseas. Still, the numbers are going down: in the US this year, there have been 54 cases, down from 667 two years ago. The last case of measles that developed in the Americas was in 2002. (It took such a long time to declare the region measles-free because of various bureaucratic issues.)
Health officials say that credit for this victory goes to efforts to vaccinate against the disease. Though the measles, mumps, and rubella (MMR) vaccine is recommended for all children and required by many states, anti-vaxxers have protested it due to since-discredited claims that vaccines can cause autism.
   To stop transmission, 90 to 95 percent of people in a given region need to be vaccinated according to Seth Berkley, who runs the nonprofit GAVI, which promotes vaccination and immunization. In the US, that number is around 90 percent, but worldwide the number is only about 80 percent. Though declaring the Americas free of measles is a big step, people should keep vaccinating to ensure the disease doesn’t come back, experts say.
 

lilit

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ma dobro, ovo je malo PR-a al lepo je da se brojke spuštaju.
Some things you have to do yourself.

lilit

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Quote
Innate Immunity and Asthma Risk in Amish and Hutterite Farm ChildrenMany genetic risk factors have been reported to modify susceptibility to asthma and allergy, but the dramatic increase in the prevalence of these conditions in westernized countries in the past half-century suggests that the environment also plays a critical role. The importance of environmental exposures in the development of asthma is most exquisitely illustrated by epidemiologic studies conducted in Central Europe that show significant protection from asthma and allergic disease in children raised on traditional dairy farms. In particular, children’s contact with farm animals and the associated high microbial exposures have been related to the reduced risk. However, the effect of these traditional farming environments on immune responses is not well defined.
To address this gap in knowledge, we designed a study that compares two distinctive U.S. farming populations — the Amish of Indiana and the Hutterites of South Dakota — that recapitulate the differences in the prevalences of asthma and allergy observed in farmers and nonfarmers in Europe. These two particular groups of farmers originated in Europe — the Amish in Switzerland and the Hutterites in South Tyrol — during the Protestant Reformation and then emigrated to the United States in the 1700s and 1800s, respectively. Both groups have since remained reproductively isolated. Their lifestyles are similar with respect to most of the factors known to influence the risk of asthma, including large sibship size, high rates of childhood vaccination, diets rich in fat, salt, and raw milk, low rates of childhood obesity, long durations of breast-feeding, minimal exposure to tobacco smoke and air pollution, and taboos against indoor pets. However, whereas the Amish practice traditional farming, live on single-family dairy farms, and use horses for fieldwork and transportation, the Hutterites live on large, highly industrialized, communal farms. Strikingly, the prevalence of asthma in Amish versus Hutterite schoolchildren is 5.2% versus 21.3% and the prevalence of allergic sensitization is 7.2% versus 33.3%, as previously reported.

mnogo lepa studija kojom su dokazali ulogu okoline na razvoj urođene imunosti (innate immunity) plus kad tu vrstu imunosti lepo stimulišemo i razvijemo, imamo i manje astme međ đecom (sve smo mi to naravno znali i ranije i primenjivali staru narodnu: pusti đecu u prašinu i daj im da jedu s poda, al ne daj da se valjaju u barama  :mrgreen: )

šalu na stranu, imamo dve etno-religijske grupe: amiše i huterite (https://en.wikipedia.org/wiki/Hutterite), zavidne genetske sličnosti (što je bitno za isključenje genetske komponente u ovoj studiji), relativno izolovane zajednice, osnovna razlika je u tome što amiši sve rade bez struje (npr. konje koriste za obradu zemlje) a huteriti se ne gade struje, pa zemlju obrađuju mašinski.
u svakom slučaju, zaključak studije je da bakterije prisutne u amiš kućama imaju molekul koji deluje protektivno na razvoj određenih delova urođene imunosti, a bakterijice u kućama huterita nemaju te karakteristike (malo pojednostavljeno).

e sad, terapija neće biti isključenje struje svima :lol: već dalja karakterizacija prašine u amiša, identifikacija protektivnih bakterija i njihovih produkata, pa možda svi mi alergičari konačno odahnemo!
sve ovo je na dugačkom štapu al bitno je da se palamudi.

evo studijica:
http://www.nejm.org/doi/full/10.1056/NEJMoa1508749#t=article

a evo i filmić. i moja mama razumela temu.  :lol: :lol: :lol:
http://www.nejm.org/do/10.1056/NEJMdo005078/full/?requestType=popUp&relatedArticle=10.1056/NEJMoa1508749
Some things you have to do yourself.

Meho Krljic

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Ako mogu tu prašinu da stave u pilulu, da se daje deci, to će biti pun pogodak  :lol: :lol: :lol:

lilit

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ja predložila da povremeno razmene decu na nekoliko meseci al su mi objasnili da to i nije tako veličanstvena ideja.  :lol:

da, da, pilula (mukoza oralno, jedini problem što ide u želudac gde se isecka i što treba i što ne treba) ili još bolje sprej (mukoza intranazalno ili konjunktivalno) bi bio pravi pogodak!
Some things you have to do yourself.

lilit

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jutros malo EPP-a za "firmu".

uvetis (https://sh.wikipedia.org/wiki/Uveitis) je solidno dosadna i gadna boleščina posebno što može da odvede do trajnog slepila. može biti posledica raznoraznih infekcija (virusi, bakterije, gljivice, paraziti) ili sekundarna manifestacija nekih sistemskih bolesti. povrede oka takođe mogu da dovedu do uveitisa a i autoimunska etiologija (ono kad se naš imunski sistem bori protiv nas samih) nije isključena.

elem, upravo je objavljena studija da ćemo, odsad pa nadalje i ubuduće, umesto lekova na bazi kortizona (širok spektar nus efekata, npr: https://www.psychologytoday.com/blog/the-athletes-way/201301/cortisol-why-the-stress-hormone-is-public-enemy-no-1), za tretman neinfektivnog uveitisa moći da koristimo Adalimumab (https://en.wikipedia.org/wiki/Adalimumab). radi se o leku koji je praktično humani imunoglobulin  (tj. monoklonsko antitelo koje se vezuje za TNFa koji je medijator upale i inhibira je) koji već koristimo za tretman nekih drugih autoimunskih bolesti.


Quote
Cortisol-free rheumatoid arthritis medication also works for rare eye disease Summary:A well-known rheumatoid arthritis medication containing the active agent adalimumab, a therapeutic human monoclonal antibody, is also effective for treating non-infectious uveitis, a rare eye disease, report scientists.

A well-known rheumatoid arthritis medication containing the active agent adalimumab, a therapeutic human monoclonal antibody, is also effective for treating non-infectious uveitis, a rare eye disease. This has now been discovered by an international research group, in which MedUni Vienna was also involved with significant participation by Talin Barisani-Asenbauer of the Center for Pathophysiology, Infectiology & Immunology and the Laura Bassi Center at MedUni Vienna. The results of the VISUAL-I study have now been published in the leading journal New England Journal of Medicine.
  "We were able to prospectively demonstrate for the very first time that non-infectious uveitis can also be successfully treated with a cortisol-free medication. That will significantly improve the management of uveitis patients who have only partially responded to corticosteroids, need a corticosteroid sparing therapy or who are unsuitable for treatment with corticosteroids," explains Barisani-Asenbauer. The biologic medication adalimumab has long been used to treat rheumatic diseases and has to be injected subcutaneously every two weeks. For sufferers, steroid-free means there are fewer side-effects, so that it can be used over a longer period of time.
In Europe, up to 5/10,000 people (Source: www.orpha.net) suffer from some form of uveitis. Non-anterior, non-infectious uveitis, which was the subject of the recent study, affects around 40% of sufferers. Uveitis is the name used for inflammatory conditions of the inner eye, in particular the uvea, which consists of the iris and the ciliary body in the front section and the choroid in the back section.
Inflammation can also affect other parts of the eye, such as the retina and the vitreous body. 70 -- 90% of sufferers are aged between 20 and 60 and are in the middle of their working lives. The first symptoms are floaters in the visual field, blurred vision, visual disturbances and photosensitivity. Potential complications of uveitis are macular oedema (accumulation of fluid in the retina), glaucoma or cataracts, for example. Uveitis can even lead to loss of vision.
 


http://www.nejm.org/doi/10.1056/NEJMoa1509852
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Meho Krljic

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Prvo marihuana, a sad, vrlo moguće i ekstazi će moći da se izdaje na recept u doglednoj budućnosti. Kao deo terapije za posttraumatski stresni poremećaj. Slutim skok u samodijagnostikovanom PTSD za jedno pola decenije  :lol: :lol:  :
 
 
 
 FDA’s OK on trial opens possibility of prescription ecstasy in five years

lilit

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ima preporuka da se ekstazi koristi i kod delusional disorders, a moj seal of approval bi dobili odmah! sreća pa se ne pitam. :lol:
Some things you have to do yourself.

Palmer Eldrič

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Još jedna iz niza psihoaktivnih supstanci za koje se preispituje mogućnost korišćenja u terapijske svrhe: psilocibin.


https://www.theguardian.com/society/2016/dec/01/magic-mushroom-ingredient-psilocybin-can-lift-depression-studies-show


A single dose of psilocybin, the active ingredient of magic mushrooms, can lift the anxiety and depression experienced by people with advanced cancer for six months or even longer, two new studies show.

Researchers involved in the two trials in the United States say the results are remarkable. The volunteers had “profoundly meaningful and spiritual experiences” which made most of them rethink life and death, ended their despair and brought about lasting improvement in the quality of their lives.

The results of the research are published in the Journal of Psychopharmacologytogether with no less than ten commentaries from leading scientists in the fields of psychiatry and palliative care, who all back further research. While the effects of magic mushrooms have been of interest to psychiatry since the 1950s, the classification of all psychedelics in the US as schedule 1 drugs in the 1970s, in the wake of the Vietnam war and the rise of recreational drug use in the hippy counter-culture, has erected daunting legal and financial obstacles to running trials.

“I think it is a big deal both in terms of the findings and in terms of the history and what it represents. It was part of psychiatry and vanished and now it’s been brought back,” said Dr Stephen Ross, director of addiction psychiatry at NYU Langone Medical Center and lead investigator of the study that was based there.

Tiny minority of people with depression get treatment, study finds

 
Read moreAround 40-50% of newly diagnosed cancer patients suffer some sort of depression or anxiety. Antidepressants have little effect, particularly on the “existential” depression that can lead some to feel their lives are meaningless and contemplate suicide.
The main findings of the NYU study, which involved 29 patients, and the larger one from Johns Hopkins University with 51 patients, that a single dose of the medication can lead to immediate reduction in the depression and anxiety caused by cancer and that the effect can last up to eight months, “is unprecedented,” said Ross. “We don’t have anything like it.”

The results of the studies were very similar, with around 80% of the patients attributing moderately or greatly improved wellbeing or life satisfaction to a single high dose of the drug, given with psychotherapy support.

Professor Roland Griffiths, of the departments of psychiatry and neuroscience who led the study at Johns Hopkins University school of medicine, said he did not expect the findings, which he described as remarkable. “I am bred as a sceptic. I was sceptical at the outset that this drug could produce long-lasting changes,” he said. These were people “facing the deepest existential questions that humans can encounter - what is the nature of life and death, the meaning of life.”

But the results were similar to those they had found in earlier studies in healthy volunteers. “In spite of their unique vulnerability and the mood disruption that the illness and contemplation of their death has prompted, these participants have the same kind of experiences, that are deeply meaningful, spiritually significant and producing enduring positive changes in life and mood and behaviour,” he said.
Patients describe the experiences as “re-organisational”, said Griffiths. Some in the field had used the term “mystical”, which he thought was unfortunate. “It sounds unscientific. It sounds like we’re postulating mechanisms other than neuroscience and I’m certainly not making that claim.”

Ross said psilocybin activates a sub-type of serotonin receptor in the brain. “Our brains are hard-wired to have these kinds of experiences - these alterations of consciousness. We have endogenous chemicals in our brain. We have a little system that, when you tickle it, it produces these altered states that have been described as spiritual states, mystical states in different religious branches.
“They are defined by a sense of oneness – people feel that their separation between the personal ego and the outside world is sort of dissolved and they feel that they are part of some continuous energy or consciousness in the universe. Patients can feel sort of transported to a different dimension of reality, sort of like a waking dream.”

Some patients describe seeing images from their childhood and very commonly, scenes or images from a confrontation with cancer, he said. The doctors warn patients that it may happen and not to be scared, but to embrace it and pass through it, he said.
The commentators writing in the journal include two past presidents of the American Psychiatric Association, the past president of the European College of Neuropsychopharmacology, a previous deputy director of the Office of USA National Drug Control Policy and a previous head of the UK Medicines and Healthcare Regulatory Authority.

The journal editor, Professor David Nutt, was himself involved in a small trial of psilocybin in a dozen people with severe depression in the UK in May. The ten commentators in the journal, he writes in an editorial, “all essentially say the same thing: it’s time to take psychedelic treatments in psychiatry and oncology seriously, as we did in the 1950s and 1960s.”
Much more research needs to be done, he writes. “But the key point is that all agree we are now in an exciting new phase of psychedelic psychopharmacology that needs to be encouraged not impeded.”

The studies were funded by the Heffter Research Institute in the USA. “These findings, the most profound to date in the medical use of psilocybin, indicate it could be more effective at treating serious psychiatric diseases than traditional pharmaceutical approaches, and without having to take a medication every day,” said its medical director George Greer.

Meho Krljic

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1 Patient, 7 Tumors and 100 Billion Cells Equal 1 Striking Recovery



Quote
The remarkable recovery of a woman with advanced colon cancer, after treatment with cells from her own immune system, may lead to new options for thousands of other patients with colon or pancreatic cancer, researchers are reporting.

lilit

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1 Patient, 7 Tumors and 100 Billion Cells Equal 1 Striking Recovery
Quote
The remarkable recovery of a woman with advanced colon cancer, after treatment with cells from her own immune system, may lead to new options for thousands of other patients with colon or pancreatic cancer, researchers are reporting.

e pa mehane, ovo je to zbog čega se imunologija voli. :lol:

ljudi su uspeli da lociraju autologe CD8+ limfocite (in general ih imunski sistem koristi kao asasine) koji specifično prepoznaju neopeptide koji su se eksprimirali na malignim ćelijama kancera (i nema ih na zdravim ćelijama! :) ) kao posledica tzv. KRAS (Kirsten rat sarcoma viral oncogene) point mutacije (samo JEDNA (!) aminokiselina u proteinu je izmenjena a dobili smo "mašinu od proteina" koju ne možemo više da isključimo):


http://www.youtube.com/watch?v=GU-QZp5FwM8


evo i CD8+ asasina:

http://www.youtube.com/watch?v=oqI4skjr6lQ



Some things you have to do yourself.

Meho Krljic

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Pa, to i ja kažem! EKSPRIMIRALI  :-| :-| :-| :-|

lilit

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aj dobro, sledeći put ću biti preciznija i reći da su ti tumorski neopeptidi delovi endogeno sintetisane citoplazmatske mutirane GTPaze koji su prikazani u sklopu MHC molekula I klase i koje prepoznaju autologi tumor-infiltrirajući CD8+ T limfociti.  xrofl
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Meho Krljic

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CD8+. Sej nou mor.  :lol:

lilit

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samo da podelim sa sagiticom :lol: kojom vakcinom bockam drage roditelje protiv gripa, odlično se pokazala za ljude preko 65 godina koji su generalno slabi responderi kad je ta vakcina u pitanju:
http://www.fluzone.com/fluzone-high-dose-vaccine.cfm
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Meho Krljic

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Evo, turisti nek se strpe a domoroci nek se snalaze do 2017. godine:
 Successful Ebola vaccine will be fast-tracked for use
Quote

A highly effective vaccine that guards against the deadly Ebola virus could be available by 2018, says the World Health Organization.
Trials conducted in Guinea, one of the West African countries most affected by an outbreak of Ebola that ended this year, show it offers 100% protection.
The vaccine is now being fast-tracked for regulatory approval.
Manufacturer Merck has made 300,000 doses of the rVSV-ZEBOV vaccine available for use should Ebola strike.
GAVI, the global vaccine alliance, provided $5m for the stockpile.
Results, published in The Lancet medical journal, show of nearly 6,000 people receiving the vaccine, all were free of the virus 10 days later.
In a group of the same size not vaccinated, 23 later developed Ebola.
Only one person who was vaccinated had a serious side effect that the researchers think was caused by the jab. This was a very high temperature and the patient recovered fully.
It is not known how well the vaccine might work in children since this was not tested in the trial.
 Analysis - Tulip Mazumdar, Global Health CorrespondentEbola has been around for 40 years now. But it wasn't until the height of the 2014 outbreak in West Africa that the world decided to invest some serious money into finding treatments and cures.
I watched as families of those who had become infected were isolated in their homes. Often entire neighbourhoods were quarantined behind orange fencing. That was their best chance of not becoming infected and infecting others.
 
But as hundreds of people continued to die, and cases started being exported to Europe and the US - the world decided to act.
Now, two years later, we have a vaccine. It usually takes around 10 years.
There were some mild side effects reported in this trial, and the vaccine is only known to protect against one of the strains of Ebola, but it is the most deadly Zaire strain.
Today's news is a very welcome and much needed breakthrough. However, as the WHO points out, more lives would be saved if countries invested in vaccines before outbreaks, rather during them.

The director of British-based medical research institute the Wellcome Trust described the findings as "remarkable".
"Had a vaccine been available earlier in the Ebola epidemic, thousands of lives might have been saved," Jeremy Farrar said.
"We have to get ahead of the curve and make promising diagnostics, drugs and vaccines for diseases we know could be a threat in the future."
Ebola - mapping the outbreak
The trial was led by the World Health Organization (WHO), working with Guinea's health ministry and international groups.
The WHO's Marie-Paule Kieny said the results could help combat future outbreaks.
"While these compelling results come too late for those who lost their lives during West Africa's Ebola epidemic, they show that when the next Ebola outbreak hits, we will not be defenceless," said Dr Kieny, the lead author of the study.
Other drug companies are developing different Ebola vaccines that could be used in the future too.
The Ebola virus was first identified in 1976 but the recent outbreak in West Africa, which killed more than 11,000 people, highlighted the need for a vaccine.
The outbreak began in Guinea in 2013 and spread to Liberia and Sierra Leone.
 

lilit

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well, trebalo je ranije uvesti ebolu u krajeve velikog belog čoveka...

Some things you have to do yourself.

džin tonik

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trebao je sad veliki bijeli covjek loviti zirafe, plesati oko totema, zuriti u nebo, stancati djecu i vikati kuku, pa bi mali crni mozda razvio cjepivo...

lilit

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putuješ negde?  :mrgreen: :lol:
Some things you have to do yourself.

lilit

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Prvo marihuana...

btw, ovih dana čitam studije vezane za upotrebu kanabinoid ulja (CBD) u tretmanu psihoze al nekako mi sve to nije ubedljivo. javlja mi se da je psihoterapija jedina stvar koja eventualno može pomoći, a i to samo ukoliko je osoba svesna da joj je pomoć potrebna.
Some things you have to do yourself.

Meho Krljic

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U Americi:
 
 Fewer people are dying of cancer than ever before
 
Quote

The number of Americans dying of cancer has dropped to a 25-year low, equaling an estimated 2,143,200 fewer deaths in that period, says the new annual report from the American Cancer Society. In that time, the racial and gender disparities that exist in cancer rates have also narrowed somewhat, but they remain wide in many places.
Though the incidence of cancer remained stable for women and dropped slightly — by 2 percent — in men, rates remain overall 20 percent higher in men while rate of death for men is 40 percent higher than in women. The rates of both incidence and death vary wildly based on the type of cancer. The data that the ACS is using run through the end of 2014 for incidents of cancer and through 2013 for deaths.
Lung cancer remains the leading cause of cancer death in the United States for both men and women. Overall, lung cancer rates are continuing to decline faster in men than in women, as historically women took up smoking in larger numbers than men and were, according to their data, slower to quit. The ACS predicts that the largest number of new cancer diagnoses — nearly 300,000 of them — for men will be prostate cancer, while the largest number of new cancer diagnoses for women will be in the form of breast cancer.
The ACS reports that though the cancer death rate remains 15 percent higher for blacks than whites for 2014, the passing of the "Patient Protection and Affordable Care Act may expedite the narrowing racial gap." The data shows that from 2010 to 2015 the number of uninsured blacks was cut in half, from 21 percent to 11 percent, while the number of uninsured Hispanics fell from 31 percent to 16 percent.
The decline in deaths from cancer is attributed largely to the fact that fewer people smoke — from about 42 percent in 1965 to 17 percent in 2013 — as well as earlier detection for certain types of cancer.
 

 
Doduše, možda je to zato jer umiru od drugih bolesti više nego što bi trebalo:
 
 Life Expectancy In U.S. Drops For First Time In Decades, Report Finds
 
Quote

One of the fundamental ways scientists measure the well-being of a nation is tracking the rate at which its citizens die and how long they can be expected to live.
So the news out of the federal government Thursday is disturbing: The overall U.S. death rate has increased for the first time in a decade, according to an analysis of the latest data. And that led to a drop in overall life expectancy for the first time since 1993, particularly among people younger than 65.
"This is a big deal," says Philip Morgan, a demographer at the University of North Carolina, Chapel Hill who was not involved in the new analysis.
"There's not a better indicator of well-being than life expectancy," he says. "The fact that it's leveling off in the U.S. is a striking finding."
Now, there's a chance that the latest data, from 2015, could be just a one-time blip. In fact, a preliminary analysis from the first two quarters of 2016 suggests that may be the case, says Robert Anderson, chief of the mortality statistics branch at the National Center for Health Statistics, which released the new report.  Anderson says government analysts are awaiting more data before reaching any definitive conclusions.
"We'll have to see what happens in the second half of 2016," he says.
Still, he believes the data from 2015 are worth paying attention to. Over that year, the overall death rate increased from 724.6 per 100,000 people to 733.1 per 100,000.
While that's not a lot, it was enough to cause the overall life expectancy to fall slightly. That's only happened a few times in the past 50 years. The dip in 1993, for example, was due to high death rates from AIDS, flu, homicide and accidental deaths that year.
On average, the overall life expectancy, for someone born in 2015, fell from 78.9 years to 78.8 years. The life expectancy for the average American man fell two-tenths of a year — from 76.5 to 76.3. For women, it dropped one-tenth — from 81.3 to 81.2 years.
"It's remarkable," Morgan says. "There are lots of things about this that are unexpected."
Most notably, the overall death rate for Americans increased because mortality from heart disease and stroke increased after declining for years. Deaths were also up from Alzheimer's disease, respiratory disease, kidney disease and diabetes. More Americans also died from unintentional injuries and suicide. In all, the decline was driven by increases in deaths from eight of the top 10 leading causes of death in the U.S.
"When you see increases in so many of the leading causes of death, it's difficult to pinpoint one particular cause as the culprit," Anderson says.
The obesity epidemic could be playing a role in the increase in deaths from heart disease, strokes, diabetes and possibly Alzheimer's. It could also be that doctors have reached the limit of what they can do to fight heart disease with current treatments.
The epidemic of prescription opioid painkillers and heroin abuse is probably fueling the increase in unintentional injuries, Arun Hendi, a demographer at Duke University, wrote in an email. The rise in drug abuse and suicide could be due to economic factors causing despair.
"Clearly, that could be related to the economic circumstances that many Americans have experienced in the last eight years, or so, since the recession," says Irma Elo, a sociologist at the University of Pennsylvania.
Whatever the cause, the trend is concerning, especially when the death rate is continuing to drop and life expectancy is still on the rise in most other industrialized countries.
"It's pretty grim," says Anne Case, an economist at Princeton University studying the relationship between economics and health.
 

Meho Krljic

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The Tiny Robots Revolutionizing Eye Surgery



Quote
Machines that are capable of making precise operations inside the human eye will make it possible to perform entirely new procedures.


Last September, Robert MacLaren, an ophthalmologist and professor at Oxford University, plunged a tiny robotic arm into William Beaver’s eye. A membrane had recently contracted on the 70-year-old priest’s retina, pinching it into an uneven shape and causing him to see the world as if reflected in a hall of mirrors.
Using a joystick and a camera feed, MacLaren guided the arm of the Robotic Retinal Dissection Device, or R2D2 for short, through a tiny incision in the eye, before lifting the wrinkled membrane, no more than a hundredth of a millimeter thick, from the retina, and reversing Beaver’s vision problems.
It was the first operation performed inside the human eye using a robot. Since September, five more patients have undergone robot-assisted operations at Oxford’s John Radcliffe Hospital in England, including one in which a virus, used in gene therapy to halt the effects of retinal degeneration, was planted on the retina itself, a procedure only made possible by R2D2’s unprecedented precision.
“My movements were improved and finessed by the robot,” MacLaren says. “I could even let go and the robot would hold everything securely in place.”
In the past decade the use of robots in surgery has become commonplace. Da Vinci, an American-made surgical robot that is used to repair heart valves, among other things, has operated on more than three million patients around the world. Robotic surgery provides numerous benefits, offering surgeons a greater degree of control while simultaneously reducing a patient’s trauma and risk of infection. The market for medical robotic systems will exceed $17 billion by 2020, according to some estimates. But until now surgical robots have been too bulky to be used in certain procedures at small scale (da Vinci, for example, is around the size of an elephant, its bulk necessary to push against the forces of the body wall).
R2D2, which was developed by Preceyes BV, a Dutch medical robotics firm established by the University of Eindhoven, is not the only robot targeting the human eye. Chris Wagner, head of advanced surgical systems at Cambridge Consultants, has led a team in the development of Axsis—one of the smallest known robots for surgical use, its external body is the size of a can of soda.
“Building a surgical robot that can work on the size scale of the lens of an eye, which is less than 10 millimeters across, is difficult,” says Wagner, whose team began work on Axsis last April. For example, the cables that enable the robot to navigate are each 110 microns across, a little over the diameter of a human hair.
Both R2D2, which, according to MacLaren’s estimates, will cost around $1 million, and Axsis are prototype robots currently unavailable on the market. Cambridge Consultants hopes that future versions of its Axsis robot will prove affordable for smaller hospitals, thereby lowering the barrier to entry for less experienced robotic surgeons.
“With this system, we're trying to expand the range of procedures that should be considered candidates for robotic technology, in terms of the size of the manipulations and the size of the access,” says Wagner. He hopes that Axsis could, for example, be used to operate on cataracts, the most commonly performed surgery in developed countries. Oxford’s MacLaren, however, is skeptical of the need for robotic support in this kind of routine eye operation. To meet the demand, “thousands of machines” would have to be manufactured, he says. “It’s clearly not necessary. But these robots do open up a new chapter of operations that are currently impossible.”
MacLaren believes that R2D2 and other robots like it will enable surgeons to, for the first time, operate underneath the retina and interact with blood vessels in the eye. “Undoubtedly this will lead to improvements in quality of eye surgery that require highly technical procedures,” he says. “But most significantly they will open the door to new operations for which the human hand does not have the necessary control and precision.”

zakk

  • Očigledan slučaj RASTROJSTVA!
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Jako lepo za nas bogate i matore!
Why shouldn't things be largely absurd, futile, and transitory? They are so, and we are so, and they and we go very well together.

ЖивОзбиљан

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First human-pig chimeras spark hopes for transplantable organs — and debate

http://www.pbs.org/newshour/rundown/first-human-pig-chimeras-spark-hopes-transplantable-organs-debate/

Spiderpig, spiderpig!
šta će mi bogatstvo i svecka slava sva kada mora umreti lepa Nirdala


Meho Krljic

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A s druge strane i srodno ovom splajsovanju čoveka i svinje iz Batinog posta, kod miševa izlečen dijabetes pomoću ćelija koje su uzgojene u pacovima:
 
 Scientists have discovered a process that could transform human organ transplants
 
Quote

Hundreds of people die every day while waiting for an organ transplant. A solution to this horrible reality is to make human organs readily available—by growing them on-demand in labs or even other animals.
Scientists in Japan and the US have taken a huge step in that direction. In a study published in Nature, they report to have cured mice of diabetes by transplanting mouse cells grown in rats.
To achieve this feat, researchers injected mouse pluripotent stem cells into a rat embryo. As the name suggests, these pluripotent stem cells are able to transform themselves into all types of cells. The mouse cells intermingled with rat cells, and created a chimera whose organs and tissues were almost all created from a mix of mouse and rat cells.
Crucially, however, they had modified the rat to not produce pancreatic cells. They achieved this by knocking out a gene called Pdx1. The upshot was that the pancreas in the chimera was almost completely made of mouse cells.
When the rat-mouse chimeras became adults, the researchers removed the animals’ pancreases and from them, isolated endocrine islets, which contain β-cells that produce insulin. The β-cells were then transplanted to diabetic mice that had lost all their native β-cells.
Every human-to-human organ transplant requires the use of drugs that suppress the immune system. Though these drugs have severe side effects, without them, the body would consider the transplanted object foreign and unleash the immune system on it. Often a transplant patient has to take these drugs for life.
Anticipating a similar reaction, the mice that received the transplant were put on mild immunosuppressant drugs. However, the scientists found they only needed to administer the drugs for five days after transplantation. Surprisingly, the few rat cells that came along during the transplant (mostly in the blood vessels in the islets) had been destroyed and replaced by the mouse’s own cells.
Scientists don’t know yet how this happened. Qiao Zhou of Harvard University, who was not involved in the research, thinks that one way this could have occurred is that, despite the mild immunosuppressant drugs, the mouse’s immune system recognized the few rat cells present in the transplantation, and destroyed them. At the same time, native mouse cells started building blood vessels to replace them.
The β-cells in mice that got the transplants functioned just as they would in a healthy mouse for more than a year, which was the complete observation period. These lab mice only live for two to three years, which makes a one-year observation fairly long. The research opens up the door for growing human organs inside, say, a pig, using the patient’s own stem cells and then transplanting the organ when it’s mature and ready.
There are, of course, many obstacles before we achieve that feat. For instance, the pancreas is a relatively uncomplicated organ, genetically speaking. Scientists only had to knock out one gene to ensure that rat cells didn’t participate in creating the organ and mouse cells could monopolize the construction. Creation of more complex organs like the heart or kidney are controlled by many more genes, which often have multiple purposes in the body, and thus will require a more complicated genetic modification technique—or some other workaround to ensure that the changes made won’t destroy some other part of the body.
In addition, mice and rats, though separate species, are close cousins. Transplanting from a pig to a human would be a bigger leap, and it will come with its own challenges. (Pigs have some organs that are roughly the same size as humans, which is why they are good candidates for future organ transplant techniques).
And maybe we won’t even have to do all that. Researchers are also trying a different tack: xenotransplantations, where organs from a different species are used without the need to create a chimera. In 2013, researchers at Northwestern University showed that endocrine islets from rats could survive and thrive in mice without the use of immunosuppressant drugs.
 

Naravno da bi miš ozdravio, pacov mora da strada... tako da...

lilit

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Krejzi:
 
 Nicotine shown to reduce symptoms of schizophrenia

nije krejzi nimalo, vrlo je logično. :)
vrlo sličan mehanizam kao kod parkinsona, a za sve je naravno kriv dopamin!!!
(naravno, pojednostavljeno do bola jer svaka šiza ima svoje različitosti, a i parkinsoni nisu svi isti)

https://www.ncbi.nlm.nih.gov/pubmed/25925389

u stvari, ljudi se "self medicate" cigaretama  :idea: :lol:
Some things you have to do yourself.

lilit

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A s druge strane i srodno ovom splajsovanju čoveka i svinje iz Batinog posta, kod miševa izlečen dijabetes pomoću ćelija koje su uzgojene u pacovima:

imunski sistem svinja je toliko sličan čovekovom i jedina njihova sreća da su relativno komplikovane za hendlovanje (milion aspekata) pa miševe ipak nećemo menjati.  :mrgreen: :lol:
trenutno radimo neki tretman okularne hlamidijalne infekcije baš na svinjama, neverovatno je koliko nam je konjunktiva ista.
Some things you have to do yourself.

Meho Krljic

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Predviđam budućnost u kojoj vegani i vegetarijanci poput mene odbijaju transplantaciju organa jer su uzgojeni na svinji.

ЖивОзбиљан

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Ma dobro, neće tebi ništa da otkaže, praktično bez mesa i alkohola jedva i da si živ!

Prava dilema je dal ti prasići s hlamidijom mogu poslije da se jedu, misim da spojimo lijepo i korisno!
šta će mi bogatstvo i svecka slava sva kada mora umreti lepa Nirdala

Meho Krljic

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LSD je svakako droga budućnosti pošto se još uvek proučava kako i šta on to tačno radi. U najnovijim vestima:

Why an LSD high lasts for so long



Quote
One drop of LSD can erase your entire sense of being until—interminable hours later—you recapitulate your identity, one puzzle piece at a time. Beyond that and the iconic kaleidoscope visual effects, lysergic acid diethylamide has supposedly inspired revolutionary ideas, too. It has been famously (and controversially) credited, in part, for the creation of the iPhone and the polymerase chain reaction, the tool used to clone DNA.
And all it takes is 100 micrograms of the drug, roughly the weight of two and a half eyelashes. By contrast, a common dose of dimethyltryptamine (DMT)—the main psychedelic ingredient in the increasingly popular and purportedly therapeutic plant brew ayahuasca—is 20,000 to 40,000 micrograms. The mechanism that makes a tiny, diaphanous strip of acid-flecked paper exert such power over the brain and behavior, and for such a long time, is only just coming to light.
A new study published this week in Cell examines LSD’s peculiar way of binding to brain receptor proteins—and may be a key step toward unraveling the inner workings of the drug.



“There’s always been confusion about why it lasts the duration it does, and why it seems to be extraordinarily potent,” says Adam Halberstadt, a pharmacologist at the University of California, San Diego, who was not involved in the new study. “So this is pretty impressive.”
LSD and other psychoactive drugs work by binding to specialized proteins called receptors on the surfaces of neural cells. On the receptor protein is a sculpted “pocket,” into which molecules with the right shape can fit and thus stick to the cell, where they initiate changes in the brain. But different substances can often fit into the same receptor. Many receptors that bind LSD and DMT, for example, also fit the natural chemical messenger serotonin—which is produced in the body and helps regulate mood. Figuring out how each drug interacts with the same receptor in a different way is key to understanding why an LSD trip lasts all day whereas an experience with extracted DMT is often over in 15 minutes or less.
By freezing an LSD molecule bound to a single brain cell receptor as a crystal in a lab, researchers were able to get a 3-D x-ray image of the drug and the protein locked together.
“My lab has been trying to do this since the early 1990s,” says Bryan Roth, a pharmacologist at the University of North Carolina at Chapel Hill and senior author on the paper. “I remember Dan Wacker [a co-author, also at U.N.C.] showing the image. It was basically a moment of silence. I started to fight back tears of gratitude that we had finally gotten it.”
It is the first 3-D image of a psychedelic bound to a brain receptor, Roth says.


The image showed Roth and his co-authors something strange about the way LSD fit inside this receptor. Drugs typically come and go from receptor proteins like ships pulling in and out of a port. But when an LSD molecule lands on the receptor, the molecule snags onto a portion of the protein and folds it over itself as the molecule binds to the receptor.
“There was this lid that came over the molecule. It looked like it trapped LSD in the receptor,” Roth says. “That immediately suggested to us why LSD lasts so long.”


LSD seems to stimulate the receptor for the entire time it is trapped underneath the protein “lid,” Roth says. Proteins are in constant motion, so he thinks the lid eventually flops open, allowing the drug to fly out and the effects to wear off. But the team ran computer models that suggest it could take hours for that to happen. Until then, the trip goes on.
Roth’s experiments also suggest that the longer LSD stimulates the receptor, the more powerful the effects become. “What we show in the paper is that LSD becomes a hundred times to a thousand times more potent [after a few hours],” Roth says. “It begins to explain not only why standard recreational doses have this profound effect, but also why microdoses (about 10 micrograms of LSD) might have an effect.”
So-called microdoses are minute amounts of LSD—usually about 10 times smaller than a typical recreational dose. LSD is outlawed around the world and is a Schedule I drug in the U.S. (putting it in a category with heroin and ecstasy). But microdosing has gained some traction among Silicon Valley technology workers as a creativity-boosting “smart drug.” The practice has become more popular since psychologist James Fadiman wrote about it in his book The Psychedelic Explorer’s Guide in 2011.
Scientists have suggested LSD might have some broad clinical use for conditions such as anxiety or addiction, and there is early evidence that it could treat cluster headaches. Roth says more research needs to be done on all of these applications, however.



“In terms of microdosing, what we really need are controlled clinical trials, and we don’t have any,” he explains. Some microdosers claim the practice can enhance productivity, focus and mood. Ayelet Waldman, who recently published A Really Good Day: How Microdosing Made a Mega Difference in My Mood, My Marriage and My Life, asserts that microdosing on LSD helped her overcome depression and bipolar disorder. “I was suicidal, and now I’m not dead,” Waldman says.
Roth says he had initially believed the effects of microdosing, which users say are nearly imperceptible, could be attributed to a placebo phenomenon. “Previously, I thought these are just ‘homeopathic’ doses—not doing anything,” he says. But “these low doses, it’s clear now, really can have significant effects at these receptors.”
Halberstadt thinks that idea is interesting. “This could be a reason why LSD is so potent,” he says. “If it has a really long dissociation rate that would magnify the effect of even very small concentrations.”
But it is still unclear exactly how, once bound to LSD, these receptor proteins go on to create the specific, often bizarre effects of LSD—like the frequently reported destruction of one’s sense of self, or careening uncontrollably into one’s deepest, most personal memories and emotions. The work only studied two of 40 known receptors that LSD touches in the brain, says Nicholas Cozzi, a pharmacologist at the University of Wisconsin–Madison who was not involved with the study.
Any combination of those receptors working in concert, and the different ways LSD might interact with each one, may be contributing to the feeling of oneness with the universe, shifting reality or generally elevated mood often attributed to the drug.
“It’s like a musical chord formed by notes,” Cozzi says.
This article is reproduced with permission from Scientific American. It was first published on Jan. 27, 2017. Find the original story here.

lilit

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mehane, prijaviću nas za clinical trial. :lol:

a ovo je zašto se research toliko voli  xlove5

Quote

“My lab has been trying to do this since the early 1990s,” says Bryan Roth, a pharmacologist at the University of North Carolina at Chapel Hill and senior author on the paper. “I remember Dan Wacker [a co-author, also at U.N.C.] showing the image. It was basically a moment of silence. I started to fight back tears of gratitude that we had finally gotten it.”
Some things you have to do yourself.

Meho Krljic

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Ja sam poznati strejter, ali mogu da shvatim zašto ljude toliko fascinira esid. A vidimo da su i istraživači emotivna bića  :lol:

lilit

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možda je u esidu budućnost, al ima nešto i u starenju. leonard hayflick je uvek tu kad nam je najviše potreban. :lol:

Quote
The future of ageing

Leonard Hayflick

Advances in our knowledge of age-associated diseases have far outpaced advances in our understanding of the fundamental ageing processes that underlie the vulnerability to these pathologies. If we are to increase human life expectancy beyond the fifteen-year limit that would result if today's leading causes of death were resolved, more attention must be paid to basic research on ageing. Determination of longevity must be distinguished from ageing to take us from the common question of why we age to a more revealing question that is rarely posed: why do we live as long as we do? But if the ability to intervene in ageing ever becomes a reality, it will be rife with unintended and undesirable consequences.

savršeno i jednostavno napisano, vredi pročitati: http://www.nature.com/nature/journal/v408/n6809/full/408267a0.html
Some things you have to do yourself.

Meho Krljic

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Može li negde integralna verzija tog teksta za nas koji ne plaćamo pretplatu a čita nam se?



U drugim vestima, ako se ignoriše klikbejtaški naslov, ovo je vrlo zanimljivo:

Reached Via a Mind-Reading Device, Deeply Paralyzed Patients Say They Want to Live



Quote
A brain-computer interface records “yes” and “no” answers in patients who lack any voluntary muscle movement.


In 1995, Jean-Dominique Bauby suffered a massive stroke that left him paralyzed and speechless, with only the ability to blink his left eyelid. Using just that eye, he silently dictated his memoir, The Diving Bell and the Butterfly, later adapted into a film.
  Recommended for You   Bauby suffered from “locked-in syndrome,” in which patients are completely paralyzed except for some eye movement. Some patients eventually lose even the ability to blink, cutting off all contact with the world and raising questions of whether they are still fully conscious and, if so, whether they still wish to live.
Now researchers in Europe say they’ve found out the answer after using a brain-computer interface to communicate with four people completely locked in after losing all voluntary movement due to Lou Gehrig’s disease, or amyotrophic lateral sclerosis.
In response to the statement “I love to live” three of the four replied yes. They also said yes when asked "Are you happy?" The fourth patient, a 23-year-old woman, wasn’t asked open-ended questions because her parents feared she was in a fragile emotional state.
Designed by neuroscientist Niels Birbaumer, now at the Wyss Center for Bio and Neuroengineering in Geneva, the brain-computer interface fits on a person’s head like a swimming cap and measures changes in electrical waves emanating from the brain and also blood flow using a technique known as near-infrared spectroscopy.
To verify the four could communicate, Birbaumer’s team asked patients, over the course of about 10 days of testing, to respond yes or no to statements such as “You were born in Berlin” or “Paris is the capital of Germany” by modulating their thoughts and altering the blood-flow pattern. The answers relayed through the system were consistent about 70 percent of the time, substantially better than chance.
Birbaumer says “the relief was enormous” for family members who were able to communicate with their loved ones after as many as four years of total silence, and to learn they wished to remain alive on ventilators. They detail their experiments in a study appearing today in the journal PLOS Biology.
In 2010, British neuroscientist Adrian Owen first reported that changes in blood flow in certain parts of the brain showed that a patient previously written off as being in a vegetative state was actually conscious.
No one has a clear idea of how many locked-in patients there are, says Jane Huggins, who runs the Direct Brain Interface Laboratory at the University of Michigan, although an estimate by Dutch researchers puts it at less than one in 150,000 in that country.
Some may be misdiagnosed as being comatose because they lack eye movement or it’s so subtle. Birbaumer and his team say their system could be used as a diagnostic to determine who actually remains conscious and aware, and he hopes to develop a technology to allow people with complete locked-in syndrome to select letters so they can communicate beyond answering yes-or-no questions.

lilit

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Izvinjavam se, meni ga otvara, a uvek zaboravim na privilegije.  :lol:
Evo ga: https://www.dropbox.com/s/ztxqyys8u7t4lnz/the%20future%20of%20ageing.pdf?dl=0
Javi ako ima problema s linkom. I kako ti deluje Leonard. Mnogo volim da ga čitam, ima tu neku crtu u pisanju koju volim.

A ovo drugo videh juče. Fascinira koliko toga može biti omogućeno, a opet verovatno nikad neće biti dostupno širokim narodnim masama.
Quote
...their system could be used as a diagnostic to determine who actually remains conscious and aware, and he hopes to develop a technology to allow people with complete locked-in syndrome to select letters so they can communicate beyond answering yes-or-no questions.
Some things you have to do yourself.

Meho Krljic

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Hvala puno, ovo je za celu našu kancelariju zanimljiv tekst.

Meho Krljic

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 GM Salmonella destroys cancer
 
Quote
A genetically modified bacterium destroys tumors by provoking an immune response, according to a study published Wednesday.
 
Using mice and cultures of human cancer cells, a South Korean-led scientific team demonstrated that Salmonella typhimurium engineered to make a foreign protein caused immune cells called macrophages and neutrophils to mobilize against the cancer.
The bacterium came from an attenuated strain that has little infectious potential. Such strains have been tested as vaccines. The protein, called FlaB, is made by a gene in the estuarine bacterium Vibrio vulnificus, a close relative of the cholera bacterium, Vibrio cholerae.
  Tumors shrank below detectable levels in 11 out of 20 mice injected with the modified Salmonella, said the study, published in Science Translational Medicine.
Go to j.mp/salcancer for the study. The first author was Jin Hai Zheng of Chonnam National University Hwasun Hospital, in Jeonnam, South Korea.
The engineered Salmonella provoke a sustained immune response, in addition to preventing the spread of a human colon cancer implanted in a mouse. The bacterium also were found to be nontoxic, multiplying almost exclusively inside tumors.
Sandip Patel, MD, of UC San Diego Moores Cancer Center, praised the study’s “very novel strategy.”
“The importance of the host bacteria (the microbiome) on immune responses against tumor is increasingly appreciated and a very active area of research,” Patel said by email. “To utilize bacteria as a delivery system builds on this concept.”
“The immune effects induced by Salmonella here are an important first step in stimulating an immune environment that is primed to kill tumors. Further research looking into this therapeutic strategy, as well alternative means of modulating the tumor microenvironment (toll-like receptor agonists), will be needed to help our patients have the most effective options to fight their cancer.”
Researchers have explored the use of Salmonella against cancer for years, because it grows in the low-oxygen environment inside solid tumors. This environment is hard for the immune system to reach.
UC San Diego researcher Jeff Hasty has developed engineered Salmonella that deliver cancer-killing toxins inside the tumor. This bacterium periodically self-destructs when it reaches a certain population density, releasing the toxins. Some of the engineered Salmonella survive, rebuilding the population until it reaches the self-destruct density. So the tumor receives periodic doses of targeted chemotherapy.
Bacterial immunotherapy itself began more than 100 years ago, with experiments by bone surgeon and cancer researcher William Coley. But the results were inconsistent, and the method was abandoned in favor of advances in radiation, chemotherapy and surgery.

Meho Krljic

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Fasting diet 'regenerates diabetic pancreas'



Quote
The pancreas can be triggered to regenerate itself through a type of fasting diet, say US researchers.
Restoring the function of the organ - which helps control blood sugar levels - reversed symptoms of diabetes in animal experiments.
The study, published in the journal Cell, says the diet reboots the body.
Experts said the findings were "potentially very exciting" as they could become a new treatment for the disease.
People are advised not to try this without medical advice.
In the experiments, mice were put on a modified form of the "fasting-mimicking diet".
It is like the human form of the diet when people spend five days on a low-calorie, low-protein, low-carbohydrate but high unsaturated-fat diet.
It resembles a vegan diet with nuts and soups, but with around 800 to 1,100 calories a day.
Then they have 25 days eating what they want - so overall it mimics periods of feast and famine.
Previous research has suggested it can slow the pace of ageing.Diabetes therapy?But animal experiments showed the diet regenerated a special type of cell in the pancreas called a beta cell.
These are the cells that detect sugar in the blood and release the hormone insulin if it gets too high.
Dr Valter Longo, from the University of Southern California, said: "Our conclusion is that by pushing the mice into an extreme state and then bringing them back - by starving them and then feeding them again - the cells in the pancreas are triggered to use some kind of developmental reprogramming that rebuilds the part of the organ that's no longer functioning."
There were benefits in both type 1 and type 2 diabetes in the mouse experiments.
Type 1 is caused by the immune system destroying beta cells and type 2 is largely caused by lifestyle and the body no longer responding to insulin.
Further tests on tissue samples from people with type 1 diabetes produced similar effects.
Dr Longo said: "Medically, these findings have the potential to be very important because we've shown - at least in mouse models - that you can use diet to reverse the symptoms of diabetes.
"Scientifically, the findings are perhaps even more important because we've shown that you can use diet to reprogramme cells without having to make any genetic alterations."

What's it like?

BBC reporter Peter Bowes took part in a separate trial with Dr Valter Longo.
He said: "During each five-day fasting cycle, when I ate about a quarter of the average person's diet, I lost between 2kg and 4kg (4.4-8.8lbs).
"But before the next cycle came round, 25 days of eating normally had returned me almost to my original weight.
"But not all consequences of the diet faded so quickly."
His blood pressure was lower as was a hormone called IGF-1, which is linked to some cancers.
He said: "The very small meals I was given during the five-day fast were far from gourmet cooking, but I was glad to have something to eat."
Peter Bowes: Fasting for science
Peter Bowes: Intermittent fasting and the good things it did to my body

Separate trials of the diet in people have been shown to improve blood sugar levels. The latest findings help to explain why.
However, Dr Longo said people should not rush off and crash diet.
He told the BBC: "It boils down to do not try this at home, this is so much more sophisticated than people realise."
He said people could "get into trouble" with their health if it was done without medical guidance.
Dr Emily Burns, research communications manager at Diabetes UK, said: "This is potentially very exciting news, but we need to see if the results hold true in humans before we'll know more about what it means for people with diabetes.
"People with type 1 and type 2 diabetes would benefit immensely from treatments that can repair or regenerate insulin-producing cells in the pancreas."



Palmer Eldrič

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Malo o bioinformatici i upotrebi data mininga u medicini:



https://startit.rs/bioinformatika-saveti-programiranje/

lilit

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našli ljudi marker da se u ranim fazama bolesti vidi da li je šizofrenija il depresija, a samim tim tretman prilagodi pre nego se situacija pogorša i lekari krenu s predlozima da je klozapin iz raja izašao.

Quote
First physiological test for schizophrenia and depression
March 13, 2017

Researchers have found a new way of using proteins in nerve cells to identify people with depression and schizophrenia. The method, reported in Experimental Physiology, will help identify people whose depression or schizophrenia involves signalling via a receptor called NMDAR, and differentiate between the two diseases. At present, there are no diagnostic tests to help distinguish them.

NMDA receptor signalling may be decreased in schizophrenia patients and increased in those with depression. The authors hope that this research is the first step towards producing a test to identify certain forms of depression and schizophrenia. Distinguishing this specific form of these diseases could allow for earlier and more accurate diagnoses as well as more targeted treatment.

Depression is thought to affect over 300 million people worldwide1 and schizophrenia affects as many as 51 million people2. Both diseases have severe impacts on sufferers' lives3.

The researchers infused patients with a high concentration salt solution to induce the release of the hormone arginine-vasopressin (AVP), and then measured the level of the hormone in their blood. Previously, animal studies had shown that the release of AVP in response to the salt solution depends on NMDA receptor signalling. In this study, they found that AVP release can distinguish schizophrenia from depression.

Depressed patients showed an increased release of the hormone, while patients with schizophrenia showed a decreased response. Clinically, it is difficult to distinguish between these two diseases in their early phases, because symptoms are non-specific and relatively mild. This hormone test may be a simple way to distinguish and identify patients with NMDA receptor malfunction in each disorder. The study was a collaboration among Yale University, The John B. Pierce Laboratory, New Haven and the VA Medical Center, West Haven, Connecticut.

Handan Gunduz-Bruce, co-author of the paper, said, "This is the first objective, physiological marker for two major psychiatric disorders that, once fully developed into a clinical test, can allow for earlier and more accurate diagnosis, and selection of more appropriate medications for patients."

https://medicalxpress.com/news/2017-03-physiological-schizophrenia-depression.html

http://onlinelibrary.wiley.com/doi/10.1113/EP086212/epdf
Some things you have to do yourself.

Meho Krljic

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Molecule kills elderly cells, reduces signs of aging in mice
 
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Even if you aren’t elderly, your body is home to agents of senility—frail and damaged cells that age us and promote disease. Now, researchers have developed a molecule that selectively destroys these so-called senescent cells. The compound makes old mice act and appear more youthful, providing hope that it may do the same for us.
 
“It’s definitely a landmark advance in the field,” says cell and molecular biologist Francis Rodier of the University of Montreal in Canada who wasn’t connected to the study. “This is the first time that somebody has shown that you can get rid of senescent cells without having any obvious side effects.”
 
As we get older, senescent cells build up in our tissues, where researchers think they contribute to illnesses such as heart disease, arthritis, and diabetes. In the past, scientists have genetically modified mice to dispatch their senescent cells, allowing the rodents to live longer and reducing plaque buildup in their arteries. Such genetic alterations aren’t practical for people, but researchers have reported at least seven compounds, known as senolytics, that kill senescent cells. A clinical trial is testing two of the drugs in patients with kidney disease, and other trials are in the works.
 
However, current senolytic compounds, many of which are cancer drugs, come with downsides. They can kill healthy cells or trigger side effects such as a drop in the number of platelets, the cellular chunks that help our blood clot.
 
Cell biologist Peter de Keizer of Erasmus University Medical Center in Rotterdam, the Netherlands, and colleagues were investigating how senescent cells stay alive when they uncovered a different strategy for attacking them. Senescent cells carry the type of DNA damage that should spur a protective protein, called p53, to put them down. Instead, the researchers found that a different protein, FOXO4, latches onto p53 and prevents it from doing its duty.
 
To counteract this effect, De Keizer and colleagues designed a molecule, known as a peptide, that carries a shortened version of the segment of FOXO4 that attaches to p53. In a petri dish, this peptide prevented FOXO4 and p53 from hooking up, prompting senescent cells to commit suicide. But it spared healthy cells. 
 
The researchers then injected the molecule into mutant mice that age rapidly. These rodents live about half as long as normal mice, and when they are only a few months old, their fur starts to fall out, their kidneys begin to falter, and they become sluggish. However, the peptide boosted the density of their fur, reversed the kidney damage, and increased the amount of time they could scurry in a running wheel, the scientists report online today in Cell. When the researchers tested the molecule in normal, elderly mice, they saw a similar picture: In addition to helping their kidneys and fur, the molecule also increased their willingness to explore their surroundings.
 
“The paper adds a potentially new way to target senescent cells,” says diabetes researcher James Kirkland of the Mayo Clinic in Rochester, Minnesota. He cautions, however, that peptides like the one De Keizer and colleagues developed have their own limitations. The digestive system destroys them, so they can only be delivered through inhalation or an injection–you can’t just swallow a pill, he notes.
 
Although the molecule did not reduce the number of platelets in either mouse group, killing off large numbers of senescent cells could still trigger a potentially fatal complication sometimes suffered by cancer patients. Moreover, senescent cells foster wound healing, and destroying the cells could impair this ability.
 
That’s why De Keizer says he and his colleagues plan to move cautiously with their molecule. “I don’t think you should start treating frail people in their 90s.” Instead, he says, they want to determine whether the molecule kills cancer cells, which share some similarities with senescent cells, starting with the brain tumor glioblastoma. If the compound continues to prove safe, they can think about testing the peptide against age-related diseases or even aging itself.
 


Meho Krljic

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'Exercise-in-a-pill' boosts athletic endurance by 70 percent
 
Quote

 
Every week, there seems to be another story about the health benefits of running. That's great -- but what if you can't run? For the elderly, obese or otherwise mobility-limited, the rewards of aerobic exercise have long been out of reach.
  Salk Institute scientists, building on earlier work that identified a gene pathway triggered by running, have discovered how to fully activate that pathway in sedentary mice with a chemical compound, mimicking the beneficial effects of exercise, including increased fat burning and stamina. The study, which appears in Cell Metabolism on May 2, 2017, not only deepens our understanding of aerobic endurance, but also offers people with heart conditions, pulmonary disease, type 2 diabetes or other health limitations the hope of achieving those benefits pharmacologically.
"It's well known that people can improve their aerobic endurance through training," says senior author Ronald Evans, Howard Hughes Medical Institute investigator and holder of Salk's March of Dimes Chair in Molecular and Developmental Biology. "The question for us was: how does endurance work? And if we really understand the science, can we replace training with a drug?"
Developing endurance means being able to sustain an aerobic activity for longer periods of time. As people become more fit, their muscles shift from burning carbohydrates (glucose) to burning fat. So researchers assumed that endurance is a function of the body's increasing ability to burn fat, though details of the process have been murky. Previous work by the Evans lab into a gene called PPAR delta (PPARD) offered intriguing clues: mice genetically engineered to have permanently activated PPARD became long-distance runners who were resistant to weight gain and highly responsive to insulin -- all qualities associated with physical fitness. The team found that a chemical compound called GW1516 (GW) similarly activated PPARD, replicating the weight control and insulin responsiveness in normal mice that had been seen in the engineered ones. However, GW did not affect endurance (how long the mice could run) unless coupled with daily exercise, which defeated the purpose of using it to replace exercise.
In the current study, the Salk team gave normal mice a higher dose of GW, for a longer period of time (8 weeks instead of 4). Both the mice that received the compound and mice that did not were typically sedentary, but all were subjected to treadmill tests to see how long they could run until exhausted.
Mice in the control group could run about 160 minutes before exhaustion. Mice on the drug, however, could run about 270 minutes -- about 70 percent longer. For both groups, exhaustion set in when blood sugar (glucose) dropped to around 70 mg/dl, suggesting that low glucose levels (hypoglycemia) are responsible for fatigue.
To understand what was happening at the molecular level, the team compared gene expression in a major muscle of mice. They found 975 genes whose expression changed in response to the drug, either becoming suppressed or increased. Genes whose expression increased were ones that regulate breaking down and burning fat. Surprisingly, genes that were suppressed were related to breaking down carbohydrates for energy. This means that the PPARD pathway prevents sugar from being an energy source in muscle during exercise, possibly to preserve sugar for the brain. Activating fat-burning takes longer than burning sugar, which is why the body generally uses glucose unless it has a compelling reason not to -- like maintaining brain function during periods of high energy expenditure. Although muscles can burn either sugar or fat, the brain prefers sugar, which explains why runners who "hit the wall" experience both physical and mental fatigue when they use up their supply of glucose.
"This study suggests that burning fat is less a driver of endurance than a compensatory mechanism to conserve glucose," says Michael Downes, a Salk senior scientist and co-senior author of the paper. "PPARD is suppressing all the points that are involved in sugar metabolism in the muscle so glucose can be redirected to the brain, thereby preserving brain function."
Interestingly, the muscles of mice that took the exercise drug did not exhibit the kinds of physiological changes that typically accompany aerobic fitness: additional mitochondria, more blood vessels and a shift toward the type of muscle fibers that burn fat rather than sugar. This shows that these changes are not exclusively driving aerobic endurance; it can also be accomplished by chemically activating a genetic pathway. In addition to having increased endurance, mice who were given the drug were also resistant to weight gain and more responsive to insulin than the mice who were not on the drug.
"Exercise activates PPARD, but we're showing that you can do the same thing without mechanical training. It means you can improve endurance to the equivalent level as someone in training, without all of the physical effort," says Weiwei Fan, a Salk research associate and the paper's first author.
Although the lab's studies have been in mice, pharmaceutical companies are interested in using the research to develop clinical trials for humans. The team can envision a number of therapeutic applications for a prescription drug based on GW, from increasing fat burning in people suffering from obesity or type 2 diabetes to improving patients' fitness before and after surgery.
 

   Story Source:
Materials provided by Salk Institute. Note: Content may be edited for style and length.
 

Journal Reference:
 
  • Weiwei Fan, Wanda Waizenegger, Chun Shi Lin, Vincenzo Sorrentino, Ming-Xiao He, Christopher E. Wall, Hao Li, Christopher Liddle, Ruth T. Yu, Annette R. Atkins, Johan Auwerx, Michael Downes, Ronald M. Evans. PPARδ Promotes Running Endurance by Preserving Glucose. Cell Metabolism, 2017; 25 (5): 1186 DOI: 10.1016/j.cmet.2017.04.006



Meho Krljic

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Ne znamo kako će biti u budućnosti ali u sadašnjost, američki zdravstveni sistem ispašta zbog nestašice - sode bikarbone:

Baking soda shortage has hospitals frantic, delaying treatments and surgeries

lilit

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ovo je američki zdravstveni sistem (bez preterivanja)

https://www.youtube.com/watch?v=yw_nqzVfxFQ
Some things you have to do yourself.

Meho Krljic

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Ancient Chinese Medicine Outright Blocks Sperm From Egg



Quote
What if there was a birth control that was hormone-free, 100 percent natural, resulted in no side effects, didn’t harm either eggs nor sperm, could be used in the long-term or short-term, and — perhaps the best part of all — could be used either before or after conception?
Thanks to ancient Chinese folk medicine, that’s not a far-out dream.
Research published Monday in the journal Proceedings of the National Academy of Sciences by scientists at the University of California, Berkeley, identified two plant compounds that could hold the secret to preventing conception.
Here’s how it works: In order to actually penetrate the egg, sperm need to whip their tails faster to pick up momentum. But there are two plant compounds that can prevent sperm from doing this, no matter how valiantly they may try — lupeol, found in mango and dandelion root, and pristimerin, from a plant called the “thunder god vine,” the leaves of which had been used as birth control in traditional Chinese medicine. The sperm and egg are never actually harmed; they’re just never able to meet.


“Because these two plant compounds block fertilization at very, very low concentrations — about 10 times lower than levels of levonorgestrel in Plan B — they could be a new generation of emergency contraceptive we nicknamed ‘molecular condoms,’” team leader Polina Lishko, an assistant professor of molecular and cell biology, said in a press release. “If one can use a plant-derived, non-toxic, non-hormonal compound in lesser concentration to prevent fertilization in the first place, it could potentially be a better option.”


In previous research, the team had identified progesterone as a key hormone in triggering the sperm tail-whipping, which it facilitates by binding to a protein called ABHD2. While reading up on folk medicines and indigenous methods of natural contraception, they found the lupeol and pristimerin and eventually determined that both work by keeping progesterone and ABHD2 apart. The concentrations of the two substances that exist naturally in plants aren’t high enough for cost-effective commercial birth control, so the researchers are now looking for alternative sources.
Hormone-based birth control methods are generally well-tolerated by most people who take them, but they can also bring accompanying side effects that a lupeol- or pristimerin-based method would not. And even though they could also be used as emergency contraception taken after conception, like Plan B, it’s possible this would be a more palatable option to some who disapprove of Plan B because it can stop fertilized eggs from being implanted and prevent the egg from being fertilized in the first place.

>Abstract


The calcium channel of sperm (CatSper) is essential for sperm hyperactivated motility and fertility. The steroid hormone progesterone activates CatSper of human sperm via binding to the serine hydrolase ABHD2. However, steroid specificity of ABHD2 has not been evaluated. Here, we explored whether steroid hormones to which human spermatozoa are exposed in the male and female genital tract influence CatSper activation via modulation of ABHD2. The results show that testosterone, estrogen, and hydrocortisone did not alter basal CatSper currents, whereas the neurosteroid pregnenolone sulfate exerted similar effects as progesterone, likely binding to the same site. However, physiological concentrations of testosterone and hydrocortisone inhibited CatSper activation by progesterone. Additionally, testosterone antagonized the effect of pregnenolone sulfate. We have also explored whether steroid-like molecules, such as the plant triterpenoids pristimerin and lupeol, affect sperm fertility. Interestingly, both compounds competed with progesterone and pregnenolone sulfate and significantly reduced CatSper activation by either steroid. Furthermore, pristimerin and lupeol considerably diminished hyperactivation of capacitated spermatozoa. These results indicate that (i) pregnenolone sulfate together with progesterone are the main steroids that activate CatSper and (ii) pristimerin and lupeol can act as contraceptive compounds by averting sperm hyperactivation, thus preventing fertilization.
 

Meho Krljic

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Često kažu da je malo crnog vina dobro za kardiovaskularni sistem, antioksidansi, ovoono, ali evo sad ovo:

Even moderate drinking can damage the brain, claim researchers



Meho Krljic

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New frontier in cancer care: Turning blood into living drugs



Quote
SEATTLE (AP) -- Ken Shefveland's body was swollen with cancer, treatment after treatment failing until doctors gambled on a radical approach: They removed some of his immune cells, engineered them into cancer assassins and unleashed them into his bloodstream.
Immune therapy is the hottest trend in cancer care and this is its next frontier — creating "living drugs" that grow inside the body into an army that seeks and destroys tumors.
Looking in the mirror, Shefveland saw "the cancer was just melting away." A month later doctors at the Fred Hutchinson Cancer Research Center couldn't find any signs of lymphoma in the Vancouver, Washington, man's body.
"Today I find out I'm in full remission — how wonderful is that?" said Shefveland with a wide grin, giving his physician a quick embrace.
This experimental therapy marks an entirely new way to treat cancer — if scientists can make it work, safely. Early-stage studies are stirring hope as one-time infusions of supercharged immune cells help a remarkable number of patients with intractable leukemia or lymphoma.
"It shows the unbelievable power of your immune system," said Dr. David Maloney, Fred Hutch's medical director for cellular immunotherapy who treated Shefveland with a type called CAR-T cells.
"We're talking, really, patients who have no other options, and we're seeing tumors and leukemias disappear over weeks," added immunotherapy scientific director Dr. Stanley Riddell. But, "there's still lots to learn."
T cells are key immune system soldiers. But cancer can be hard for them to spot, and can put the brakes on an immune attack. Today's popular immunotherapy drugs called "checkpoint inhibitors" release one brake so nearby T cells can strike. The new cellular immunotherapy approach aims to be more potent: Give patients stronger T cells to begin with.
Currently available only in studies at major cancer centers, the first CAR-T cell therapies for a few blood cancers could hit the market later this year. The Food and Drug Administration is evaluating one version developed by the University of Pennsylvania and licensed to Novartis, and another created by the National Cancer Institute and licensed to Kite Pharma.
CAR-T therapy "feels very much like it's ready for prime time" for advanced blood cancers, said Dr. Nick Haining of the Dana-Farber Cancer Institute and Broad Institute of MIT and Harvard, who isn't involved in the development.
Now scientists are tackling a tougher next step, what Haining calls "the acid test": Making T cells target far more common cancers — solid tumors like lung, breast or brain cancer. Cancer kills about 600,000 Americans a year, including nearly 45,000 from leukemia and lymphoma.
"There's a desperate need," said NCI immunotherapy pioneer Dr. Steven Rosenberg, pointing to queries from hundreds of patients for studies that accept only a few.
For all the excitement, there are formidable challenges.
Scientists still are unraveling why these living cancer drugs work for some people and not others.
Doctors must learn to manage potentially life-threatening side effects from an overstimulated immune system. Also concerning is a small number of deaths from brain swelling, an unexplained complication that forced another company, Juno Therapeutics, to halt development of one CAR-T in its pipeline; Kite recently reported a death, too.
And, made from scratch for every patient using their own blood, this is one of the most customized therapies ever and could cost hundreds of thousands of dollars.
"It's a Model A Ford and we need a Lamborghini," said CAR-T researcher Dr. Renier Brentjens of New York's Memorial Sloan Kettering Cancer Center, which, like Hutch, has a partnership with Juno.
In Seattle, Fred Hutch offered a behind-the-scenes peek at research underway to tackle those challenges. At a recently opened immunotherapy clinic, scientists are taking newly designed T cells from the lab to the patient and back again to tease out what works best.
"We can essentially make a cell do things it wasn't programmed to do naturally," explained immunology chief Dr. Philip Greenberg. "Your imagination can run wild with how you can engineer cells to function better."
TWO LONG WEEKS TO BREW A DOSE
The first step is much like donating blood. When leukemia patient Claude Bannick entered a Hutch CAR-T study in 2014, nurses hooked him to a machine that filtered out his white blood cells, including the T cells.
Technicians raced his bag of cells to a factory-like facility that's kept so sterile they must pull on germ-deflecting suits, booties and masks just to enter. Then came 14 days of wait and worry, as his cells were reprogrammed.
Bannick, 67, says he "was almost dead." Chemotherapy, experimental drugs, even a bone marrow transplant had failed, and "I was willing to try anything."
GENETICALLY ENGINEERING CELLS
The goal: Arm T cells with an artificial receptor, a tracking system that can zero in on identifying markers of cancer cells, known as antigens. For many leukemias and lymphomas, that's an antigen named CD19.
Every research group has its own recipe but generally, scientists infect T cells with an inactive virus carrying genetic instructions to grow the desired "chimeric antigen receptor." That CAR will bind to its target cancer cells and rev up for attack.
Millions of copies of engineered cells are grown in incubators, Hutch technicians pulling out precious batches to monitor if they're ready for waiting patients.
If they work, those cells will keep multiplying in the body. If they don't, the doctors send blood and other samples back to researchers like Riddell to figure out why.
WHAT'S THE DATA?
Small, early studies in the U.S. made headlines as 60 percent to 90 percent of patients trying CAR-Ts as a last resort for leukemia or lymphoma saw their cancer rapidly decrease or even become undetectable. Last week, Chinese researchers reported similar early findings as 33 of 35 patients with another blood cancer, multiple myeloma, reached some degree of remission within two months.
Too few people have been studied so far to know how long such responses will last. A recent review reported up to half of leukemia and lymphoma patients may relapse.
There are long-term survivors. Doug Olson in 2010 received the University of Pennsylvania's CAR-T version for leukemia. The researchers were frank — it had worked in mice but they didn't know what would happen to him.
"Sitting here almost seven years later, I can tell you it works," Olson, now 70, told a recent meeting of the Leukemia and Lymphoma Society.
Bannick, the Hutch patient treated in 2014, recalls Maloney calling him "the miracle man." He had some lingering side effects that required blood-boosting infusions but says CAR-T is "giving me a second life."
SCARY SIDE EFFECTS
"The more side effects you have, that sort of tells everybody it's working," said Shefveland, who was hospitalized soon after his treatment at Hutch when his blood pressure collapsed. His last clear memory for days: "I was having a conversation with a nurse and all of a sudden it was gibberish."
As CAR-T cells swarm the cancer, an immune overreaction called "cytokine release syndrome" can trigger high fevers and plummeting blood pressure and in severe cases organ damage. Some patients also experience confusion, hallucinations or other neurologic symptoms.
Treatment is a balancing act to control those symptoms without shutting down the cancer attack.
Experienced cancer centers have learned to expect and watch for these problems. "And, most importantly, we've learned how to treat them," said Dr. Len Lichtenfeld of the American Cancer Society, who is watching CAR-T's development.
FIGHTING SOLID TUMORS WILL BE HARDER
CAR-Ts cause collateral damage, killing some healthy white blood cells, called B cells, along with cancerous ones because both harbor the same marker. Finding the right target to kill solid tumors but not healthy organ tissue will be even more complicated.
"You can live without some normal B cells. You can't live without your lungs," Riddell explained.
Early studies against solid tumors are beginning, targeting different antigens. Time-lapse photos taken through a microscope in Riddell's lab show those new CAR-T cells crawling over aggressive breast cancer, releasing toxic chemicals until tumor cells shrivel and die.
CARs aren't the only approach. Researchers also are trying to target markers inside tumor cells rather than on the surface, or even gene mutations that don't form in healthy tissue.
"It's ironic that the very mutations that cause the cancer are very likely to be the Achilles heel," NCI's Rosenberg said.
And studies are beginning to test CAR-Ts in combination with older immunotherapy drugs, in hopes of overcoming tumor defenses.
HOW WILL PATIENTS GET THE FIRST CAR-T THERAPIES?
If the FDA approves Novartis' or Kite's versions, eligible leukemia and lymphoma patients would be treated at cancer centers experienced with this tricky therapy. Their T cells would be shipped to company factories, engineered, and shipped back. Gradually, more hospitals could offer it.
Because only certain patients would qualify for the first drugs, others would have to search for CAR-T studies to try the treatment. A drug industry report lists 21 CAR-T therapies in development by a dozen companies.
"This is the hope of any cancer patient, that if you stay in the game long enough, the next treatment's going to be just around the corner," said Shefveland, the Hutch patient.
___
This Associated Press series was produced in partnership with the Howard Hughes Medical Institute's Department of Science Education. The AP is solely responsible for all content

lilit

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quite big paper izašao juče, ljudi izneli dokaze da parkinson ima autoimunsku etiologiju (naš imunski sistem nas vidi kao neprijatelja i kreće da nas napada kao što napada bakterije i viruse). ako se potvrdi, ugasili smo. :lol:

https://www.nature.com/nature/journal/vaop/ncurrent/full/nature22815.html?sf90794231=1
Some things you have to do yourself.

Meho Krljic

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Ugasili smo u smislu "do sada neizlečiva bolest nastavlja da bude neizlečiva ali na nov način"?

lilit

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verovatno sam biased al (meni) sve što ne uključuje imunski sistem kao neprijatelja zvuči kao, u nekoj relativno bližoj budućnosti, rešiva varijanta.
Some things you have to do yourself.

Meho Krljic

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Jasno. I ima smisla.

lilit

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premda, ako lociramo gene odgovorne za autoimunost i krenemo da koristimo CRISPR gene editing, mogućnosti su beskrajne. u teoriji. :lol:

ovo je pravi SF današnjice:

http://www.youtube.com/watch?v=YYrP_wSf7G8

i naravno, kao i sva deca mankinda, pati od poznatih boljki:

http://www.youtube.com/watch?v=lhif85AjejI

propade nam komunizam načisto. :lol:
Some things you have to do yourself.


lilit

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The Myth of Drug Expiration Dates

naravno da je mit, i naravno da je horor i naravno da smo svesni toga odavno.
problem je što farma ovo vidi kao communism in practice i sumnjam da će zaživeti.
Some things you have to do yourself.


Аксентије Новаковић

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  • Homo Superior
Прошле године сам на форуму помињао пројекат "Дрогирање Америке", у коме су учествовали нпр. Хаксли и Тимоти Лири, а ево сада нам стиже и пројекат "Дрогирање Европе".

Кад видим чему служи пројекат "Дрогирање Европе", тада постаје много јасније чему је служио пројекат "Дрогирање Америке".

Quote

Njemački znanstvenici savjetuju drogiranje Europljana kako bi prihvatili imigraciju

Netko bi pomislio da je u pitanju „fake news“, dok ne shvatite da je rad objavljen na službenim znanstvenim portalima.

Njemački znanstvenici sa Sveučilišta u Bonnu predlažu korištenje kombinacije raznih supstanci i „utjecaja okoline“ kako bi Europljane podčinili i prisilili na prihvaćanje velikog broja imigranata u njihovoj sredini.

Istraživanje je u izvornom obliku objavljeno na web stranici Proceedings of the National Academy of Sciences (PNAS), a prenio ga je i poznati znanstveno-orijentirani portal Science Daily.

Oxytocin-enforced norm compliance reduces xenophobic outgroup rejection
http://www.pnas.org/content/early/2017/08/08/1705853114.short?rss=1

Oxytocin and social norms reduce xenophobia
https://www.sciencedaily.com/releases/2017/08/170814162334.htm


U istraživanju su sudjelovale 183 osobe, pri čemu je svakoj od njih dano 50 eura koje su potom mogli donirati imigrantima ili lokalnim siromašnim stanovnicima.

Istraživači sa Sveučilišta u Bonnu, uz suradnju sa Sveučilištem u Lübecku te američkim Laureate Institute for Brain Research, bili su „iznenađeni“ otkrićem da su isprva ispitanici donirali 20 posto više novca imigrantima nego lokalnim stanovnicima. Međutim, nakon što im je dana supstanca poznata kao oksitocin – takozvani „hormon ljubavi“ – sudionici su imigrantima dali još više novaca.

Ljudi koji su imali „negativne stavove prema imigrantima“ nisu podlegli utjecaju. Međutim, nakon što su vidjeli kako su drugi bili velikodušni, u kombinaciji s drogom, „donirali su 74 posto više novaca.“

Rene Hurlemann, profesor na psihijatrijskom odjelu Sveučilišta, zaključio je da je „kombinirano djelovanje oksitocina i utjecaja okoline“ učinkovito riješilo problem opisan kao „sebični motivi.“

„Uz pogodne okolnosti, oksitocin može pomoći u prihvaćanju integracije imigranata u zapadnjačke zemlje,“ dodao je.

Unatoč činjenici da su veliki dijelovi Afganistana, Iraka i Sirije očigledno sigurni za povratak, čemu svjedoči niz akcija UNHCR-a u proteklo vrijeme, europski pro-imigracijski sustav izgleda ne želi priznati takvo stanje. Pored već niza izmišljenih problema oko deportacija onih kojima je zahtjev za azil odbijen, sada se očigledno pokušava stvoriti nova ideja po kojoj bi Europljani trebali biti pokusni kunići u već odavno propalom eksperimentu masovne imigracije.

http://tribun.hr/njemacki-znanstvenici-savjetuju-drogiranje-europljana-prihvatili-imigrante

Meho Krljic

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Fentanil nije droga budućnosti, pošto ovaj tekst objašnjava da je u nekim delovima SAD premašio heroin u smislu opioidne incidence, ali opet, možda bude droga budućnosti kod nas? (Popsugar inače nije sajt koji bih linkovao za išta ozbiljno ali ovaj tekst deluje relativno profi napisan...)


The Opioid Epidemic's Biggest Culprit Isn't Heroin Anymore — It's Something Deadlier

Meho Krljic

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A cancer treatment that one expert called the 'most exciting thing I've seen in my lifetime' just got approved 
 
Quote

The US Food and Drug Administration just approved a cutting-edge cancer therapy.
On Wednesday, the FDA approved Novartis' Kymriah, also known as tisagenlecleucel, a treatment for pediatric acute lymphoblastic leukemia.
"I think this is the most exciting thing I've seen in my lifetime," said Dr. Tim Cripe, an oncologist who was part of the FDA advisory committee panel that voted in July to recommend the drug's approval.
The highly personalized treatment is called CAR T-cell therapy (CAR is short for chimeric antigen receptor). It's a type of cancer immunotherapy, which harnesses the body's immune system to take on cancer cells. It removes a person's cells, reengineers them, then puts them back in their body to attack cancer cells.
"We're entering a new frontier in medical innovation with the ability to reprogram a patient's own cells to attack a deadly cancer," the FDA commissioner, Scott Gottlieb, said in a statement. "New technologies such as gene and cell therapies hold out the potential to transform medicine and create an inflection point in our ability to treat and even cure many intractable illnesses. At the FDA, we're committed to helping expedite the development and review of groundbreaking treatments that have the potential to be life-saving."
The one-time treatments won't come cheap — Novartis said it would cost $475,000, though it also said in a news release Wednesday that it was working with the Centers for Medicare and Medicaid Services to come up with a payment system that reflects how well the drug works in a person. As part of the collaboration, CMS will have to pay "only when pediatric and young adult [acute lymphoblastic leukemia] patients respond to Kymriah by the end of the first month," Novartis said.
Novartis' therapy is one of two cutting-edge treatments for blood cancers that are poised to get approved by the end of the year.
The FDA is also expected to make a decision about another CAR-T therapy, from Kite Pharma, which just got acquired by Gilead Sciences, for aggressive B-cell non-Hodgkin lymphoma. Kite said in February that of the 101 patients in its trial, 36% had a complete response to the treatment (meaning the cancer had disappeared) after six months.
It's a type of cancer that Novartis also wants to get approval to treat. In June, Novartis released data from its Phase 2 trial of tisagenlecleucel in adult patients with diffuse large B-cell lymphoma, an aggressive form of lymphoma. Of the 51 patients in the trial, 23 had either a complete response or a partial response (meaning their tumor displayed signs of shrinking).
New treatments like Kymriah face some other challenges:
 
  • Manufacturing the drugs is no small feat, considering the personalized treatment requires taking out a person's cells, reprogramming them, then reinserting them. The company that can do that quickly and safely could have the advantage in the competitive CAR-T therapy space.
  • Trials of these kinds of treatments have been deadly in the past. In May, Kite disclosed that one person had died in a clinical trial for its late-stage CAR-T therapy from cerebral edema, a condition in which excessive fluid causes the brain to swell. And last year, another company, Juno Therapeutics, said five people in its clinical trials had died, all from cerebral edema.
 


Meho Krljic

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Nanomachines that drill into cancer cells killing them in just 60 seconds developed by scientists   
 
Quote

      Nanomachines which can drill into cancer cells, killing them in just 60 seconds, have been developed by scientists.
The tiny spinning molecules are driven by light, and spin so quickly that they can burrow their way through cell linings when activated.
In one test conducted at Durham University the nanomachines took between one and three minutes to break through the outer membrane of prostate cancer cell, killing it instantly.       The 'motor' is a rotor-like chain of atoms that can be prompted to move in one direction, causing the molecule to rotate at high speed.
Dr Robert Pal of Durham University said: "We are moving towards realising our ambition to be able to use light-activated nanomachines to target cancer cells such as those in breast tumours and skin melanomas, including those that are resistant to existing chemotherapy.
“Once developed, this approach could provide a potential step change in non-invasive cancer treatment and greatly improve survival rates and patient welfare globally."    The scientists, whose work is reported in the journal Nature, created several different light-activated motorised molecules designed to home in on specific cells.
They found that the nanomachines needed to spin at two to three million times per second to overcome nearby obstacles and outpace natural Brownian motion, the erratic movement of microscopic particles suspended in fluid.    The molecules could be used either to tunnel into cells carrying therapeutic agents, or to act as killer weapons that blast open tumour membranes.
Videos showed the cancer cell membranes bubbling under the assault.
Without an ultraviolet trigger, the motor molecules located target cells but then remained harmlessly on their surfaces.    When triggered, the molecules rapidly drilled through the cell membranes.
Dr James Tour, a member of the international team from Rice University in Houston, US, said: "These nanomachines are so small that we could park 50,000 of them across the diameter of a human hair, yet they have the targeting and actuating components combined in that diminutive package to make molecular machines a reality for treating disease.
"In this study we have shown that we can drill into cells, animal cells, human cells using these nanomachines, they will attach to the surface and then a light will be shone upon them and they will drill right into the cell.
"For many years I never had envisioned the nanomachines being used medically, I though they were way too small, because they are much much smaller than a cell, but now this work has really changed my thoughts on this and I think therapeutically this will be a whole new way to treat patients, it's going to be an excellent application for cancer treatment, not just for killing of cells but for the treatment of cells, interacting with the human body using molecular machines." 


lilit

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well, well, well, kad čovek vidi ovaj senzacionalistički naslov, dođe mu da ne izađe iz kuće. :lol:
jeste, lišmanijaza je teška bolest, klasifikovana kao neglected tropical disease, što bi trebalo da znači da opasnosti, ako sedimo u svojim belim prćijama, nema. plus, svi smo lepo podgojeni, bez kompromitovanog imunskog sistema, šanse za razvoj bolesti i da nas ujede komarac su minimalne.
upravo zato i research na vakcini kasni koliko kasni, e.g. nema neposredne opasnosti po one koji mogu da plate vakcinu.
Some things you have to do yourself.

Meho Krljic

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To i jeste poenta teksta, da rad na vakcini ozbiljnije počinje tek kad se bela, zapadna populacija oseti ugroženom. Ali, da, naslov jeste malo fearmongerski.

lilit

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ma dobro, takve naslove većina ljudi izgleda najbolje razume. pa još kad ga blic/informer/kurir prevede, doći ćemo verovatno i do neposredne opasnosti po državu. ekspertska preporuka bi mogla da bude da je najbolje da se razvije domaća vakcina, što da se uvozi strana, tako ćemo dobiti autizam.
glava me boli.
Some things you have to do yourself.

Meho Krljic

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Videćemo šta Vučić kaže. Sa svojim autoritetom on bi u stvari mogao da bude osoba koja u vaskolikoj srpskoj javnoj svesti možda malo razbije tu stigmu koju autizam sa sobom nosi. Da ne bude zabune, ne mislim da je autizam nešto poželjno & dobrodošlo ali, da ga jebem, nije ni instant presuda na život u zaključanoj sobi. Ogroman broj osoba na spektru autizma živi sasvim uobičajene živote, ima poslove, porodice itd.

lilit

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naravno. crno je što sam do nedavno mislila da se to sve podrazumeva.
u vučiću je spas. :lol:
Some things you have to do yourself.

džin tonik

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...
upravo zato i research na vakcini kasni koliko kasni, e.g. nema neposredne opasnosti po one koji mogu da plate vakcinu.


lilit

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vakcina protiv velikog kašlja (heavy bolest koju uzrokuje bakterija bordetella pertussis) je napravljena tridesetih godina dvadesetog veka. full efikasna, al sa određenim nus-efektima (koje imaju sve vakcine napravljene od cele bakterije - u detalje ne idem!  xrofl ). sedamdesetih godina se krenulo u razvoj acelularne vakcine (samo proteini bakterije) al je farma zanemarila šta nauka priča, pa smo dobili prilično neefikasnu (a skuplju  :mrgreen: ) vakcinu.
kako će se sve to rešiti, videćemo za koju deceniju, al lepo je videti da se pokrenula priča o nečemu što se zna bar trideset godina.

evo tekst iz štampe:
https://www.news-medical.net/news/20170921/Global-resurgence-of-whooping-cough-can-be-attributed-to-immunological-failures-of-vaccines.aspx

a evo i abstract rada na koji se pozivaju:


welcome u 2017.
Some things you have to do yourself.

Meho Krljic

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Na engleskom se veliki kašalj kaže "whooping cough"  xrofl xrofl xrofl xrofl

Mislim, znam da vama iz branše ovo nije ni novo ni smešno, al meni, laiku i nepoznavaocu... jeste.  :lol: