ZNAK SAGITE — više od fantastike — edicija, časopis, knjižara...

Hm...

Ebola vaccine trial proves 100% successful in Guinea

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


The results of the trials involving 4,000 people are remarkable because of the unprecedented speed with which the development of the vaccine and the testing were carried out.

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

"Having seen the devastating effects of Ebola on communities and even whole countries with my own eyes, I am very encouraged by today's news," said Børge Brende, the foreign minister of Norway, which helped fund the trial.

"This new vaccine, if the results hold up, may be the silver bullet against Ebola, helping to bring the current outbreak to zero and to control future outbreaks of this kind. I would like to thank all partners who have contributed to achieve this sensational result, due to an extraordinary and rapid collaborative effort," he said on Friday.

There have been a total of 27,748 cases of Ebola in Guinea, Liberia and Sierra Leone up to 26 July, with 11,279 reported deaths, although the outcome of many cases is unknown and the toll will be significantly higher. In the week ending 26 July, there were just four new cases in Guinea and three in Sierra Leone.


Because of the diminishing number of Ebola cases in west Africa and the shifting nature of the epidemic, with many sudden small outbreaks occurring across the region, researchers hit on a novel design for the trial.

The "gold standard" approach would be to take a population at risk of Ebola and vaccinate half of them while giving the other half a placebo. Instead, the researchers used a "ring" design, similar to that which helped prove the smallpox vaccine worked in the 1970s.

When Ebola flared up in a village, researchers vaccinated all the contacts of the sick person who were willing – the family, friends and neighbours – and their immediate contacts. Children, adolescents and pregnant women were excluded because of an absence of safety data for them. In practice about 50% of people in these clusters were vaccinated.

To test how well the vaccine protected people, the cluster outbreaks were randomly assigned either to receive the vaccine immediately or three weeks after Ebola was confirmed. Among the 2,014 people vaccinated immediately, there were no cases of Ebola from 10 days after vaccination – allowing time for immunity to develop – according to the results published online in the Lancet medical journal (pdf). In the clusters with delayed vaccination, there were 16 cases out of 2,380.

In another precedent-breaker, the trial was sponsored by the World Health Organisation because "nobody wanted to step into this role so we took the risk", said assistant director-general, Dr Marie-Paule Kieny.

Funding came from the Wellcome Trust and other partners, including the governments of Norway and Canada. Others involved included Médecins sans Frontières, whose volunteer doctors were on the front line, and the London School of Hygiene and Tropical Medicine. About 90% of the trial staff were from Guinea, a country where no clinical research had been carried out before. The vaccine is made by Merck.

Kieny said: "We believe that the world is on the verge of an efficacious Ebola vaccine."

The trial will continue, but without randomisation, which means that in Guinea, where there have been 3,786 cases and 2,520 confirmed deaths, every contact of a person who develops Ebola – and their contacts – will be offered it. Work in Gabon has now established that the vaccine is safe for children and adolescents, so they will be offered it, too.

In terms of vaccines, which are usually trialled in hundreds of thousands of people, Kierny said the numbers were small but highly promising. It is likely when larger numbers are collected that efficacy will be between 75% and 100%.

The future of two other potential Ebola vaccines, one from GlaxoSmithKline and the other from Johnson & Johnson, is now in question, because there are too few cases of Ebola for their trials to be completed.

The authors of the research said the ring design made it "logistically feasible" to conduct trials even in poor countries in the middle of a fading epidemic and it was a promising strategy for the future.

"This trial dared to use a highly innovative and pragmatic design, which allowed the team in Guinea to assess this vaccine in the middle of an epidemic," said Jeremy Farrar, director of the Wellcome Trust and one of the world's leading experts on infectious disease. "It is a remarkable result which shows the power of equitable international partnerships and flexibility.


"Our hope is that this vaccine will now help bring this epidemic to an end and be available for the inevitable future Ebola epidemics. This partnership also shows that such critical work is possible in the midst of a terrible epidemic. It should change how the world responds to such emerging infectious disease threats."

John-Arne Røttingen, the head of infectious disease control at the Norwegian Institute of Public Health and chair of the trial's steering group, said it had been a race against time in the most challenging circumstances.

"We are really pleased with the interim results," he said. "It is really important to add the vaccine to the traditional hygiene measures we have used in the response so far. I believe this will be an important contribution to getting down to zero cases."

Médecins sans Frontières said it was keen for the vaccine to be used in Sierra Leone and Liberia, where there were still cases.

Bertrand Draguez, MSF's medical director, said: "In parallel with the ring vaccination we are also conducting a trial of the same vaccine on front-line workers. These people have worked tirelessly and put their lives at risk every day to take care of sick people. If the vaccine is effective, then we are already protecting them from the virus.


"With such high efficacy, all affected countries should immediately start and multiply ring vaccinations to break chains of transmission and vaccinate all front-line workers to protect them."

Margaret Chan, the director general of of the WHO, said the vaccine trial's success was a promising development. "The credit goes to the Guinean government, the people living in the communities and our partners in this project."

The British government contributed £1m of the trial funding and has said it will increase that amount to help allow the testing to continue.

"Ebola has claimed thousands of lives and devastated communities across west Africa," the international development secretary, Justine Greening, said. "The results of these UK-backed vaccine trials are hugely promising and represent a significant breakthrough in our battle against this deadly disease. The vaccine offers hope for a future where we never have to face an Ebola epidemic like this again."

Trial data will now go to regulatory agencies in the hope of getting a licence for the vaccine that will allow it to be stockpiled for future Ebola epidemics. It is likely to be used only for people at risk in outbreaks and not given to whole populations.

The rVSV-ZEBOV vaccine is sometimes known as the Canadian vaccine as it was originally developed by the Public Health Agency of Canada before being sold to Merck to conclude the testing.

Quote from: Meho Krljic on 02-08-2015, 07:31:34
Hm...

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

hm...

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

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

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

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

http://youtu.be/lf5OMQbcJ90

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


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

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

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

My father and my baby sisters did not die because the vaccines for measles or the antiretroviral drugs for HIV were not available. They died, in large part, because life-saving vaccines and medicines were priced beyond our reach. I hope to become more involved in furthering the cause of OSP, and as I do, I'll continue to write about it, beginning with more detail regarding the underlying concepts. If you'd like to learn more, visit the Open Source Pharma site here.

 Antibiotic 'last line of defence' breached in China

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


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


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

O istoj stvari:


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

A Harvard professor says he can cure aging, but is that a good idea?

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At the gene-editing summit, you can't miss George Church. He's the big guy with the bushy beard and wavy hair, someone who looks like he stepped out of an 18th century painting of "natural philosophers." Church, who is 61, is among several hundred scientists, policymakers and thinkers on hand to discuss the powerful technology known as CRISPR, a new method for editing genes. The technique was invented in the past four years, and Church is among those who can claim at least partial credit for the innovation (there's an intense legal battle over patents — a story for another day).

I mentioned to Church that this is the kind of work for which Nobels are awarded. He quickly responded that there are more important things in the balance than prizes. There are cures for human diseases, he said.

[How George Church used gene editing to improve the likelihood of pig-to-human organ transplants]

Church thinks that one of the ailments he can cure is aging. When I met him early this year, in his laboratory at Harvard Medical School, where he is professor of genetics, he expressed confidence that in just five or six years he will be able to reverse the aging process in human beings.

"A scenario is, everyone takes gene therapy — not just curing rare diseases like cystic fibrosis, but diseases that everyone has, like aging," he said.

He noted that mice die after 2.5 years but bowhead whales can live to be 180 or 200.

"One of our biggest economic disasters right now is our aging population. If we eliminate retirement, then it buys us a couple of decades to straighten out the economies of the world," he said.

Eliminate retirement? (I briefly envisioned being on deadline in my 90s.)

"If all those gray hairs could go back to work and feel healthy and young," he said, "then we've averted one of the greatest economic disasters in history."

He went on: "Someone younger at heart should replace you, and that should be you. I'm willing to. I'm willing to become younger. I try to reinvent myself every few years anyway."

So on Tuesday, I asked him if he was still on track to reversing the aging process in the next five years or so. He said yes — and that it's already happening in mice in the laboratory. The best way to predict the future, he said, is to predict things that have already happened.

Even without CRISPR, genetic engineering was becoming part of the fabric of modern life (your grocery store is full of products from soybeans and corn that have been genetically modified in laboratories). The big difference with CRISPR is how cheap it is, how handy, how flexible. This will put an amazing tool in the hands of a lot more researchers. (Another co-inventor of CRISPR, Feng Zhang, told the summit attendees that soon there will be an entire "toolbox" of CRISPR-like techniques that can be used to edit genes.)

For most of us lay people, what's striking here is not the way that scientists fiddle with the code of life but the mere fact that they do it at all. Awed though we may be by the skills of the experimenters, we naturally question whether this is a good idea.

That's the whole point of the gene-editing summit: To find a path forward that fosters innovation but avoids crossing into ethically dubious territory. Gene-editing could be a tool for eliminating heritable diseases. But it just as easily could be used for purely cosmetic enhancements, or for something smacking of eugenics. The gravest concern is that CRISPR enables germline edits that get passed on to future generations. You're permanently changing the human species when you do that.

Who calls the shots here?

Intellectual humility requires scientists to go slowly. Editing genes isn't like renovating your kitchen. As  Klaus Rajewsky, of the Max Delbruck Center for Molecular Medicine, pointed out Tuesday, "We have become masters in the art of manipulating genes, but our understanding of their function and interaction is far more limited."

Eric Lander, who heads the Broad Institute in Cambridge and was a leader of the effort to sequence the human genome, offered a valediction to Tuesday's session that addressed both the enormous possibilities of the new technologies and the reasons for being extremely cautious. He said there are 4,000 to 5,000 genetic variants associated with human diseases. But these variants don't necessarily cause those diseases; they just make them slightly more prevalent. Moreover, genes can have multiple purposes — day jobs and night jobs, as Lander put it. These are complex systems, not modules that you can pop out and replace with a better version with zero unintended consequences.

Lander said he could think of only a handful of human diseases that CRISPR could plausibly address at this time, and even then, he said, we should ask whether such genetic manipulation is a good idea. That's because Nature has had millions of years to do the same experiment and has not done so.

"If it is such a good idea, I want to scratch my head and say why didn't evolution try to do that, and increase that in the population?" Lander said.

"We largely exist in a state of limited knowledge," he said. "Before we make permanent changes to the human gene pool, we should exercise considerable caution."

Which brings us back to aging. Is it a bug, or a feature?

—

In reporting this item I came across a story I wrote on biotech [please forgive bad formatting] and Craig Venter, published on Nov. 29, 1998, in the Post magazine. The most surprising line came from Venter:

"Intelligent application of this technology is one to two centuries away."

A surprising comment from one of the big boosters of synthetic biology.

The story ends with my quasi-neo-crypto-Luddite peroration:

Perfection may be a dangerous goal. Nature has feedback systems. There are microbes that adapt to our every move. We think of ourselves as the rulers of the planet; the microbes think of us as a useful host. At some level, we're still just a bunch of meat.
Perfection may not even be a goal worth pursuing. There is something more interesting about a mortal, imperfect life. Here's a thought: The revolutionaries of the future will be the people who keep their lives natural. They will choose to grow old. They will allow themselves to experience pain and suffering, so that their joys and triumphs will be all the more intense. They will walk in the woods and sing songs and appreciate the bounty of the planet. Two lovers might put down a blanket and have a picnic. They will fall asleep, because they still get sleepy. They will do this instead of going to the lab to be genetically reengineered.

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

This guy lost 25 pounds by eating mostly fat

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For a whole year, geneticist Jim McCarter went on a super-low-carb, high-fat diet to see what would happen.

He gave up sugar and high-carb foods and got 80% of his calories from fat. McCarter presented what he learned at the 2015 Quantified Self Conference.

Low-carb diets (think Atkins) have been one of the most common ways to treat obesity since the 1960s.

McCarter's method, called a ketogenic diet, or keto for short, is a diet extremely low in carbohydrates (often less than 20 grams a day) that is most commonly recommended by doctors to treat epilepsy in children. It's also typically high in fat in and low in protein.

According to the Mayo Clinic, side effects can include "nausea, headache, mental and physical fatigue, and bad breath." In children on the diet long term, more serious side effects, like kidney stones and brittle bones, have been observed.

For dieters, the idea is that reducing carbohydrate intake so dramatically will force the body to burn stored fat, a state called ketosis. This kind of eating plan has been shown in some scientific studies to control hunger and lead to weight loss.

In his Quantified Self talk, which we first saw on BoingBoing, McCarter said he saw similar results: He got hungry less easily, lost 25 pounds, and shed half his body fat.

He also reported better concentration, better stamina, and better cholesterol. (Bear in mind that these are the self-reported effects from a single person; large studies would be needed to test whether some of the effects McCarter saw are the norm.)

For a while though, McCarter said it took him longer to warm up for a workout. He also frequently had muscle cramps, and he got cold more easily. But he said getting about 5 grams of sodium a day had prevented these issues.

That level of salt is above the recommended upper limit of 2.3 grams, and he referred to a 2014 study finding that 4 to 6 grams of sodium a day could increase cardiovascular risk. But that's not putting McCarter off his ketogenic diet.

"I've learned that the benefits of ketosis, for me, are substantial, and they make me want to continue," McCarter said at the conclusion of the talk. "Getting rid of sugar was the easy part — more challenging has been moderating protein and getting enough fat and salt. And that requires contradicting conventional wisdom about nutrition."

A scientific review published this November concluded that ketogenic diets were more effective for weight loss than low-fat diets were, supporting previous studies suggesting this was the case.

But the Mayo Clinic advises caution: "It's not clear what kind of possible long-term health risks a low-carb diet may pose because most research studies have lasted less than a year."

How long people stay on a diet can matter much more than the type, since keeping weight off can be harder than losing it. That's one reason extreme diets, like some version of the ketogenic diet, don't work for many people.

Most important, your overall health should take priority over simply your weight. The ketogenic diet may well be a good bet for some people, but consult your doctor or a licensed dietician before dramatically changing your eating habits.

Watch McCarter's full talk here:

The Effects of a Year in Ketosis by James McCarter on Vimeo

Quote from: Meho Krljic on 19-12-2015, 07:09:41
Ako nije bilo jasno koliko nam je potebno da izbacimo šećer iz ishrane:

..trebalo bi da nam bude jasno posle ovoga? oh wait...

Nakon mračnih tvrdnji da dve trećine svog kancera nema veze ni sa čim do sa lošom srećom, nova studija veli da su stvari ipak malo manje nasumične. Nemam ja para da to platim, pa evo samo abstrakt:

Substantial contribution of extrinsic risk factors to cancer development

Quote
Recent research has highlighted a strong correlation between tissue-specific cancer risk and the lifetime number of tissue-specific stem-cell divisions. Whether such correlation implies a high unavoidable intrinsic cancer risk has become a key public health debate with the dissemination of the 'bad luck' hypothesis. Here we provide evidence that intrinsic risk factors contribute only modestly (less than ~10–30% of lifetime risk) to cancer development. First, we demonstrate that the correlation between stem-cell division and cancer risk does not distinguish between the effects of intrinsic and extrinsic factors. We then show that intrinsic risk is better estimated by the lower bound risk controlling for total stem-cell divisions. Finally, we show that the rates of endogenous mutation accumulation by intrinsic processes are not sufficient to account for the observed cancer risks. Collectively, we conclude that cancer risk is heavily influenced by extrinsic factors. These results are important for strategizing cancer prevention, research and public health.

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

nevermind, zaključak je:

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

ako neko hoće ceo rad (da se bavi ), javljajte.

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

QuoteI've been seeing an uptick in my social media feeds over the past couple of weeks about anti-vaxxers and their dangerous nonsense. As usual, they're upset because the real world has once again contradicted their view of it.
   First, a new study has shown that, once again, the Gardasil vaccine is not causing widespread health problems.
   Gardasil is a vaccine that protects us from the human papillomavirus, or HPV, a nasty bug that causes all sorts of horrid problems like genital warts and cancer of the throat, penis, vulva, vagina, and cervix. In the United States alone, 4,000 women die every year from cervical cancer, roughly one-third of those who get it. By fighting against HPV, Gardasil can seriously cut back on the occurrence of these deaths, and all those other cancers as well. The Centers for Disease Control and Prevention recommends it for preteen girls and boys, and it is given in three separate doses spread out over time.

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

Quote from: Meho Krljic on 14-01-2016, 09:59:36
Gardasil: More Anti-Vax Nonsense Collapses Under the Gaze of Reality

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

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

mali problem je što na ovoj divnoj planeti imamo (dosad detektovanih) oko 140 tipova HPV od kojih smo za 10-ak sigurni (dugogodišnje studije humane populacije potvrdile rezultate in vitro eksperimenata) da su high-risk (što ne znači da još bar 20 out of 140 takođe nije), a samo za 2 (gorepomenuti tipovi 16 i 18) od tih 10-ak poznatih imamo vakcinu. sreća pa su 16 i 18 najrasprostranjeniji i odgovorni za oko 75% slučajeva obe vrste raka, te je vakcinacija pametan potez.

sigurno ima i neke kros-reaktivnosti sa nekim drugim tipovima (kao što je i kod influence slučaj), što je utehica za one koji upadnu u onih 25% pa se i u tim slučajevima preporučuje vakcinisanje u terapeutske svrhe.

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

austrija krenula da vakciniše i dečake i devojčice.

Quote from: Meho Krljic on 07-09-2015, 13:53:26
Joj, mene ovakve stvari intenzivno brinu. Namera je dobra, to je jasno, ali ove ideje mi deluju vrlo nerazborito. Mislim, wikipedija je sjajna stvar ali nije zamena za prave izbore znanja....

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

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

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

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

Quote from: Meho Krljic on 14-01-2016, 23:30:53
Apropo HPV vakcinisanja, samo da podsetim, od raka cerviksa, najizlečivijeg kancera na svetu, koga izazivaju pomenuti tipovi HPV, u Srbiji godišnje umre 500 žena. Zato što ne mogu da makar jednom u pet godina vide ginekologa i urade papa test. Dakle kod nas je vakcinisanje zapravo način da se spasu stotine života. Ali ženskih, priznajem.

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

btw, ne budimo diskriminatorski orjentisani prema muškarcima i setimo se  majkija daglasa

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

o bre mehane, matematiko moja!     

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

a da idu retko na preglede, idu.

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

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

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

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

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

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

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



Crno al tako mu je to.

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

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

rat se nastavlja

Does the 'monogamy hormone' make us better soldiers?

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

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

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

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

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

http://authors.library.caltech.edu/64303/

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

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

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

http://ajcp.oxfordjournals.org/content/144/6/885.full
(science)

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

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



Scientists mull prospect of contagious cancer

QuoteFor all its peculiar horror, cancer comes with a saving grace. If nothing else can stop a tumor's mad evolution, the cancer ultimately dies along with its host. Everything the malignant cells have learned about outwitting the patient's defenses — and those of the oncologists — is erased. The next case of cancer, in another victim, must start anew.
Imagine if instead, cancer cells had the ability to press on to another body. A cancer like that would have the power to metastasize not just from organ to organ, but from person to person, continuing to evolve deadly new skills along the way. While there is no sign of an imminent threat, several recent papers suggest that the eventual emergence of a contagious human cancer is within the realm of medical possibility. This would not be a disease, like cervical cancer, that is triggered by the spread of viruses, but rather one in which cancer cells actually travel from one person to another and thrive in their new location.

  So far this is known to have happened only under the most unusual circumstances. A 19-year-old laboratory worker who pricked herself with a syringe of colon cancer cells developed a tumor in her hand. A surgeon acquired a cancer from his patient after accidentally cutting himself during an operation. There are also cases of malignant cells being transferred from one person to another through an organ transplant or from a woman to her fetus.



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

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

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

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


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

Zaista veoma zanimljivo!


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

Quote from: Mica Milovanovic on 06-04-2016, 20:06:41
Zaista veoma zanimljivo!


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

To znaci da ako niste vakcinisani ili prelezali male boginje bilo bi dobro da se vakciniste.
Ja sam prosle godine primila dve doze MMRa.

Evo kakva je preporuka za vakcinaciju odraslih ovde u Kanadi

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

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

Quote from: Mica Milovanovic on 06-04-2016, 21:46:20
Ma, prelezao sam, na vreme... Mama mi je bila medicinska sestra, pa sam prelezao sve zivo sto se moglo prelezati... Pitam cisto iz radoznalosti...

Quote from: Mica Milovanovic on 06-04-2016, 20:06:41
Zaista veoma zanimljivo!

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

obe opcije su validne al druga zvuči lepše!

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

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

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

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

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

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

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

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


    Addi and Cassi Fund 

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

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


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

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

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


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

Quote from: Meho Krljic on 25-04-2016, 08:54:26
BioViva's Liz Parrish makes progress in controversial gene quest to reverse aging

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

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

evo shemica kakva je biohemija kontrole apetita:


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

To objašnjava zašto se moja žena i ja gojimo paralelno 

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

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

Па шта ће ми то у 22. вијеку

Уосталом, ја одувијек тврдим да се мрша од свињетине, и то је неки протеин

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

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


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

australija odobrila truvadu posle 4 godine birokratije

http://www.starobserver.com.au/news/national-news/hiv-prevention-pill-approved-in-australia/149049

john oliver razbio i naučne studije i nauku i istraživače

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

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