Лекови, дроге и терапије будућности

[дејан]

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:

[дејан]

A Drug That Could Destroy Political Movements

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

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

[дејан]

Scientists Say They Need Philosophers to Continue Their Research

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

[Meho Krljic]

Scientists find Achilles' heel of antibiotic resistant bacteria

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]

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

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]

Malo širenja panike za Subotnje jutro
 Making viruses in the lab deadlier and more able to spread: an accident waiting to happen
 

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]

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...

[Meho Krljic]

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


Ebola Drug Saves Infected Monkeys

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]

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

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]

To je, valjda, i očekivano. Pored lekovitih dejstava marihuane. O njima sam čitao još u HERBS, Eyewitness handbooks, 1994.

[Meho Krljic]

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

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]

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

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

[дејан]

виа ио9

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

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.

[дејан]

а ово је спекулација на могуће ефекте ноцеба

The Anthropocebo Effect Explains How Our Minds Can Destroy the World

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

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.

[Meho Krljic]

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

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.”

[Meho Krljic]

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

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]

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

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.

[Meho Krljic]

Ovo su strahote:


Dumped drugs lead to resistant microbes

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'

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.

[дејан]

ноцебо аген!
виа ио9

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

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.

[Meho Krljic]

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'

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.

[Meho Krljic]

   We’re Closer Than Ever to a Birth Control Pill for Men

[zakk]

http://www.businessinsider.com/the-biggest-biotech-discovery-of-the-century-is-about-to-change-medicine-forever-2015-2

[Meho Krljic]

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

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 well^3,8. Similar studies were conducted by questioning drug users, resulting in a high correlation to the previous expert judgements^10,11,12. 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 beverages^20,21 or tobacco products^22,23. 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 1Toxicological thresholds selected for calculating the margin of exposureTo determine the typical range of individual daily dosage, various textbook and internet sources^{21,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41} 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 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. 5^th 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 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 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 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 2^{27,37,42,43,44,45,46,47,48,49,50,51,52,53,54}. 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 THC^21,55,56,57) 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 0–100^3,9, 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 ethanol^20,21. 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 itself^22,23. 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 conducted^65,66,67. The MOE approach was used for risk assessment^18,19. 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]

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


New Alzheimer’s treatment fully restores memory function

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]

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.

[Albedo 0]

što je onda zovu ''neinvazivnom'' metodom?

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

[mac]

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

[Albedo 0]

sorry, ja to stvarno laički shvatam

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

kao neće biti ožiljaka a unutra pire krompir

a neka antibiotska terapija iz predostrožnosti ne bi riješila stvar?

[Meho Krljic]

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
 

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]

Everything you need to know about the new street drug 'flakka' — its insane side effects aren't even the worst part

[Meho Krljic]

Kako preduprediti demenciju pod stare dane? Lako, budite gojazni!!!!!! 
 
 Being overweight 'reduces dementia risk'
 

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]

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

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]

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]

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

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? 

[Meho Krljic]

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

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 month^{2, 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]

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



Are We Seeing the End of Homeopathy?

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]

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.

[mac]

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]

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.

[zakk]

To baš i zeza: ZNAMO da je to samo šećerna kuglica, ali uprkos tome neki ljudi reše da im bude bolje. Ili kako već

[mac]

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]

New Letters Added to the Genetic Alphabet

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

[mac]

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]

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]

Sad ću da lupim.
Palijativna farmacija je daleko isplativija od kurativne, koja često završi u ćorsokaku.

[Meho Krljic]

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]

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

[scallop]

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.

[Father Jape]

Divni Ben Goldejker:

http://www.buzzfeed.com/bengoldacre/deworming-trials

[Meho Krljic]

Pa, da.
 

That’s the point. Science thrives on public debate