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Scientists Are Trying to Figure Out If Humans Can Hibernate

Studies of hibernators and experiments inducing short-term torpor in humans may answer whether human hibernation is possible

By Marissa Fessenden

Dive into a science fiction story that sends humans exploring the reaches of space, and you'll likely find the crew waking from some kind of suspended animation. But the idea is also bandied about in science fact: human hibernation would be a boon to astronauts traveling for months or years. So far, research in this area remains fairly speculative, though, in experiments, surgeons have cooled people down to extend surgeries.

The problem is, hibernation isn’t just a deep, months-long sleep. And even if it was, humans aren't built to survive such inactivity.

What we do know about hibernation comes from studying bears, squirrels, lemurs and dormice. All hibernators wake up occasionally - to stretch and perhaps urinate or defecate. Some snack on stored food; others fast and live off of internal fat reserves. The information scientists are gleaning from these habits is now helping to inform study of potential human hibernation, reports Eric Niiler for the Washington Post.

“We see the science has advanced enough to put some of the science fiction into the realm of science reality,” Leopold Summerer, head of advanced concepts team of the European Space Agency, told Niiler. “It doesn’t mean we will have hibernating astronauts anytime soon, but we are learning from nature how to understand some of the things that happen to animals during hibernation, such as preventing bone loss or preventing muscle loss. This is already something that would be a great benefit for long-distance spaceflight.”

The ESA, NASA and other space agencies are interested not only because humans in space would skip months of boredom if they could hibernate, but because they would need less food, produce less waste and require less space. But they would need a hibernaculum, or suitable space in which to hibernate, reports Tariq Malik for He writes:

As envisioned by ESA researchers, such a shelter would provide the proper environment for hibernation - such as the proper temperature - and also serve as a bed in the waking part of the mission. It would also have to protect crewmembers from solar flares, monitor life functions and serve the physiological needs of the hibernator, [Mark Ayre, with ESA] said.

Some clues as to what humans will need to survive long-term in space will likely come from astronaut Scott Kelly’s year in space. (However, privacy concerns may keep the data from that twin study from becoming public.) So for now, our best clues are coming from animals.

Kelly Drew, of the University of Alaska at Fairbanks, is one researcher looking at hibernation in animals, Niiler reports.

Kelly and her colleagues at the university’s Institute of Arctic Biology are looking at how the Arctic ground squirrel can get so cold without dying. She believes she has found the molecule that does the job, the A1 adenosine receptor. While she has learned that stimulating this receptor makes the animal get cold, she hasn’t found what triggers it.

We don’t know what the natural signal is for torpor,” she said. “We don’t know where the signal occurs in the brain - it could be in the brain stem or the hypothalamus.”

Still, humans will face challenges that hibernating animals don’t have. Hibernating bears are able to recycle the urea waste generated by metabolizing their fat reserves. Instead of excreting urea, they can actually break it down and use it to build up muscle and organ tissues while they sleep, reports Forrest Wickman for Slate. Humans can’t do that. This fact gives some researchers doubts that human hibernation will ever be a thing.

“I think it’s probably not doable,” H. Craig Heller, of Stanford University told Niiler. “The hibernator [animal] has evolved so that all the enzymes and biochemical systems are adapted to run at low temperature. That is not true of animals that don’t experience it. We can lower body temperature and survive that for a short period of time; it’s unlikely we can allow all of our systems to go to a much lower temperature and continue to function.”

More research will offer a definitive answer, either way. However, we don’t need studies to predict that no hibernating human will be as cute as this snoring dormouse: Snoring dormouse with sound - Listen

Is the Gaze from Those Big Puppy Eyes the Look of Your Doggie's Love?

Research finds that sustained eye contact between a dog and its owner causes oxytocin to spike in both - but not so in wolves. What it means remains to be seen

April 16, 2015 |By Julie Hecht

Unlike porcupines, dogs are a relatively hands-on (actually, paws-on) species, both with one another and with us. YouTube has numerous videos of dogs essentially saying, “Just keep petting me, please. Yes, that’s it…more.”

But this relationship is not one-sided. Many studies find that positive interactions between people and dogs can be beneficial for both species. Increases in β-endorphin (beta-endorphin), oxytocin and dopamine - neurochemicals associated with positive feelings and bonding - have been observed in both dogs and people after enjoyable interactions like petting, play and talking. Essentially, interacting with a dog, particularly a known dog, can have some of the same psychophysiological markers as when two emotionally attached people spend time together.

But do certain types of interactions have an outsized impact? Dogs are incredibly attentive to human faces and, in some cases, even specific facial expressions. This seemingly routine, benign behavior - your dog turning to gaze on your beautiful face as you do his or hers - could actually hold a very important piece of the puzzle in our relationship with dogs, suggests a study published this week in Science.

The new study, by Miho Nagasawa of Azabu University in Japan and colleagues, builds on Nagasawa’s previous work, published in Hormones and Behavior in 2009, that found owners and dogs sharing a long mutual gaze had higher levels of oxytocin in their urine than owners of dogs giving a shorter gaze. (Oxytocin, a humble peptide of nine amino acids that is sometimes called the “cuddle hormone,” has been implicated in social bonding and is instrumental to the cascade of hormonal changes leading up to and following birth.) Nagasawa and her colleagues concluded that their finding was “a manifestation of attachment behavior.” By describing it in this context, the researchers postulated that gaze between a dog and human (particularly a known human), will share similar properties to mother–infant relationships.

Nagasawa’s new study investigates whether a dog’s gazing behavior affected not just the owner’s oxytocin concentrations but the dog’s as well. In the first experiment the researchers collected urine from 30 dog-and-owner pairs before and after a 30-minute interaction. As in the earlier study, owners whose dogs showed the most gazing behavior had a notable increase in oxytocin concentration. But this time the researchers also found a similar increase in the neurochemical in the dogs.

A second experiment aimed to disentangle whether a causal relationship could be observed between mutual gaze and the release of oxytocin. Another set of 30 dogs was given an intranasal spray of either oxytocin or saline prior to interacting with people. They found that female dogs that sniffed oxytocin gazed longer at their owners than when given saline. As expected, this gazing also stimulated oxytocin secretion in the owner recipients of the gaze. The mutual effects were not seen between dogs and unfamiliar humans - and for reasons that require further investigation, they were not seen in male dogs and their owners. These sex differences were not observed in the first part of the experiment.

A story emerges - and probably one that will make dog lovers cheer: Mutual gaze between dogs and the people who care for them produces a very similar physiological profile to what’s observed between mothers and infants. This overlap could both contribute to and facilitate our intense and deep-seated relationship with dogs.

Reflecting on her findings in an interview conducted via Skype, Nagasawa recommends that “dog owners not just say commands at their dogs, but to build up the relationship [and] consider the potentially beneficial role that mutual gaze can hold.”

The paper feeds into an ongoing discussion among researchers about whether the biological synchronization observed between dogs and humans indicates “coevolution of human–dog bonds,” as the title of the Science study suggests. Nagasawa and colleagues also investigated whether the increased oxytocin observed in dogs appears in hand-raised wolves that have interacted with a known human. The wolves, however, rarely held a gaze with the humans for more than a few moments. This divergence led the researchers to postulate that “dog-to-owner gaze as a form of social communications probably evolved during domestication” with humans.

Testing evolutionary theories (particularly coevolution) is notoriously tricky. Whereas it is exciting to include socialized wolves in these studies, differences between dogs and wolves should not necessarily be immediately followed by the tooting of a coevolutionary horn. Zsófia Virányi, a senior research scientist at the University of Veterinary Medicine, Vienna's Messerli Research Institute and a co-founder of the Wolf Science Center asks, “how much the differences we see are explained by evolutionary factors or differences in raising conditions.”

Researchers are finding more examples of areas where wolves perform successfully in sociocognitive tasks with humans, including attending to our social cues. For example, in a recent study Virányi found that both dogs and wolves learned from human demonstrators. In a chapter in the edited volume, The Social Dog: Behavior and Cognition, by Juliane Kaminski and Sarah Marshall-Pescini, Virányi and her colleague Friederike Range reflect on the numerous hypotheses attempting to understand dog domestication. They suggest “dog–wolf differences do not mean, however, that domestication is either necessary or sufficient to explain humanlike behavior in dogs.”

And then there’s also the numbers game. Although 60 dogs contributed to the current investigation, the coevolution question was ultimately tackled with just five human-reared wolves. The study began with 11 wolves - but guess what?: It’s hard to collect urine from a wolf. In one case a wolf’s urine was collected two hours after the desired time because the subject fell asleep - which is another way of saying the researchers maybe did not want to wake a sleeping wolf.

It would be useful to know more about the in-study behaviors of these five wolves. For example, were they exploring the novel environment where the testing took place or trying to get out, and could those factors contribute to why they did not orient toward their handlers? Virányi even wonders whether gaze would be the crucial factor in oxytocin effects between wolves and handlers. If other social exchanges besides gaze were tested, would a positive hormonal loop between wolves and humans appear? “It may not be fair to suggest the complete absence of an oxytocin-mediated positive loop in wolves as a species from these results,” says Monique Udell, an assistant professor at Oregon State University who has investigated human–wolf interactions at the research and conservation organization, Wolf Park. “We know that maternal–offspring attachment is important to this species and many other nondomesticated animals and that humans and wolves can show attachment bonds.” Additionally, wolf oxytocin levels, even before interacting with their handlers, are notably higher than that of all dogs tested. Maybe we simply haven’t discovered all the details of wolf oxytocin mechanisms yet.

In other words, don’t count wolves, or other species, out just yet. “I’m not convinced that this is something dog-specific,” Virányi adds. “The oxytocin system is so ancient that if socialization is there, then you can easily put a member of another species into these contexts.”

Generic Version of Copaxone, Multiple Sclerosis Drug, Is Approved

The Food and Drug Administration on Thursday approved the first generic substitute for Copaxone, a widely used drug for multiple sclerosis and the biggest-selling product for Teva Pharmaceutical Industries.


The approval of the generic, which was developed by the team of Sandoz and Momenta Pharmaceuticals - could bring some price competition to the market for multiple sclerosis drugs. Prices for those drugs have tripled in the last several years, to over $60,000 a year, even as more products have come to market.

“It’s the inverse of what you normally expect when there is competition,” said Dr. Dennis N. Bourdette, chairman of neurology at Oregon Health and Science University. “There’s no apparent reason for the skyrocketing prices of those drugs, aside from that we have no cost controls in this country.”

Dr. Bourdette welcomed the generic, but said its impact would depend on its price. Citing competitive reasons, Momenta and Sandoz declined to say when the generic version would go on sale and how much it would cost.

When there are many generic competitors, prices can drop as much as 90 percent. But when there is only one generic, as is the case so far with Copaxone, the discount to the brand-name product is typically much smaller.

Even though about 10 drugs are now approved to treat multiple sclerosis, none of them has had a generic equivalent with the exception of mitoxantrone, which is not widely used. It is possible that the introduction of generic Copaxone could help keep prices of all the drugs in check.

Multiple sclerosis is a nerve disease that can cause problems like blurred vision and difficulty walking.

Teva is the largest manufacturer of generic drugs in the world and has often challenged the tactics used by brand-name drug companies to stave off generic competition.

But with Copaxone, which is a brand-name product, Teva has resorted to many of those same tactics. That is because Copaxone had sales of $4.2 billion last year, accounting for 21 percent of Teva’s revenue and nearly half its profit.

About $3.1 billion of those sales were in the United States, where Copaxone is the most widely used multiple sclerosis drug, accounting for about 30 percent of prescriptions.

Teva began selling a more concentrated formulation of Copaxone that requires an injection only three times a week instead of once a day and has a longer patent life. It began an aggressive campaign to get patients to switch, calling them and treating them to dinners. It also priced the new version lower than the old one.

About two-thirds of patients using Copaxone have already switched to the new version and might be reluctant to switch to the generic, which is a copy of the original Copaxone and would require them to inject themselves every day again.

Teva has also filed eight petitions with the F.D.A. arguing that Copaxone, known generically as glatiramer acetate, has such a complex composition that it is impossible to copy exactly, and that subtle differences might harm patients. Copaxone is made of four different amino acids linked in chains of various size and sequence. It is not exactly clear how the drug works.

The F.D.A. on Thursday posted a detailed response to Teva’s arguments and sought to assuage any such concerns.

“Before approving this generic product, given its complexity, we reviewed additional information to make sure that the generic product is as safe and effective as the brand-name product,” Dr. Janet Woodcock, the director of the agency’s drug division, said in a statement.

Copaxone was first approved in 1996 and sold for about $9,000 a year. Momenta and Sandoz, which is the generic division of Novartis, first applied for approval at the end of 2007 and had hoped to have it before now.

Craig A. Wheeler, the chief executive of Momenta, said the delay, which gave Teva more time to switch patients to the newer version of drug, “certainly gives us a higher hill to climb to bring this product up to what we had hoped for originally.”

He said he did not expect many patients taking Teva’s three-times-a-week version to switch back to the once-a-day version, though some insurers might try to bring that about. However, he said, insurers might insist new patients try the generic first instead of any other drug.

“We think there is really substantial demand across the board for getting a lower-cost generic product into the marketplace here,” he said.

Teva has a patent on Copaxone that lasts until Sept. 1. It was invalidated last year by a federal appeals court. But in January the Supreme Court sent the case back to the appellate court to reconsider.

It seems likely that Sandoz and Momenta will wait until that decision before starting to sell their drug, or wait until September if the appeals court upholds the patent.

In an unusual move, Sandoz and Momenta gave their generic drug a brand name, Glatopa, suggesting they might actively market the drug, in addition to relying on substitution at the pharmacy, which is how most generic drugs are sold.

Mylan, a leading generic manufacturer, and Synthon, a Dutch company, are also trying to win approval for generic versions of Copaxone.

Correction: April 18, 2015

An article on Friday about approval of a generic version of a drug to treat multiple sclerosis misstated the availability of generic versions of drugs to treat that disease. Generic versions are available for mitoxantrone, which is approved for treatment of multiple sclerosis but is not widely used; it is not the case that there are no generic versions of multiple sclerosis drugs.

Effectiveness of new stroke treatment confirmed

Endovascular therapy (ET) for ischemic stroke is the best treatment option for many patients

A research paper published in the New England Journal of Medicine (NEJM) today confirms earlier findings that a procedure called endovascular therapy (ET) for ischemic stroke is the best treatment option for many patients by reducing the incidents of disability. This is the fourth research paper published this year that confirms the efficacy of the treatment.

"Endovascular treatment using stent retrievers will become the standard of care for patients with acute ischemic stroke" says Dr. Mayank Goyal, University of Calgary, Cumming School of Medicine, Hotchkiss Brain Institute (HBI) and Department of Radiology.

The paper was co-authored by Goyal and Dr. Jeffrey Saver, Professor of Neurology, Geffen School of Medicine at UCLA and Director, UCLA Comprehensive Stroke Center.

Overall, positive outcomes for patients increased from 35 per cent to 60 per cent.

The clinical trial is known by the acronym SWIFT-PRIME. (Solitaire with the Intention for Thrombectomy as Primary Endovascular Treatment) randomized 196 patients to receive either t-PA, a clot busting drug or tPA plus ET.

The study had 39 participating sites in the United States and Western Europe.

ET is performed by inserting a thin tube into the artery in the groin, through the body, and into the brain vessels to the clot.

This is done under image-guided care using an X-ray.

The clot is then removed by a retrievable stent and pulled out, restoring blood flow to the brain.

This is the second NEJM publication for Goyal this year.

In February Goyal, along with HBI and Department of Clinical Neuroscience members Drs. Michael Hill and Andrew Demchuk, led an international stroke trial showing that ET for ischemic stroke victims dramatically improved outcome.

The trial known as ESCAPE (Endovascular treatment for Small Core and Anterior circulation Proximal occlusion with Emphasis on minimizing CT to recanalization times), showed positive outcomes for patients increased from 30 per cent to 55 per cent.

In many cases, instead of suffering major neurological disability, patients went home to resume their lives. The overall mortality rate was reduced from two in 10 patients for standard treatment of care to one in 10 patients - a 50 per cent reduction with ET.

ESCAPE was led by the HBI along with the departments of clinical neurosciences and radiology at the Cumming School of Medicine. ESCAPE had 316 patients, at 22 sites in five countries.

Eleven of these sites were in Canada.

As a result of all four publications, policy makers are now in the process of rewriting international clinical care guidelines for stroke care.

The study was sponsored by Medtronic - who produce the Solitaire clot retrieving device.

Evidence grows that melanoma drugs benefit some lung cancer patients

Many patients with BRAF-mutant cancers benefit from treatment with BRAF inhibitors, European researchers report at ELCC

Geneva, Switzerland, 17 April 2015 - A subset of lung cancer patients can derive important clinical benefits from drugs that are more commonly used to treat melanoma, the authors of a new academic clinical trial in Europe have reported at the European Lung Cancer Conference (ELCC) in Geneva, Switzerland.

Dr. Oliver Gautschi, a medical oncologist from Lucern Cantonal Hospital in Switzerland, presented the results of the retrospective EURAF cohort study, which included lung cancer patients whose tumours carried specific mutations in the BRAF gene. The study was conducted by a network of European oncologists, without company involvement.

BRAF mutations are commonly seen in melanoma patients, and are found in about 2% of lung adenocarcinomas, Gautschi explains. Several inhibitors of the B-Raf protein, including vemurafenib and dabrafenib, have been developed for use in melanoma patients, however there is currently no approved drug for BRAF-mutant lung cancer.

As a result, experience with B-Raf inhibitors in lung cancer remains limited. "In the current study, we wanted to find out how many patients in Europe received B-Raf inhibitors outside of a clinical trial, and what their outcomes were," Gautschi says.

The EURAF study gathered information on 35 lung cancer patients who had been identified as carrying BRAF mutations, who were treated with B-Raf inhibitors between 2012 and 2014. Most of those patients received vemurafenib,, some dabrafenib, and one sorafenib. Overall response rate was 53% as measured by the widely used Response Evaluation Criteria In Solid Tumors (RECIST) guidelines. Overall, progression-free survival time in this group was 5 months.

Most patients were pretreated, and not eligible for enrolment in a clinical trial, which means these results are encouraging, the researchers say, although the study's small size and retrospective nature mean the analysis of the magnitude of benefit should be treated cautiously.

"The bottom line is that clinicians should be sure to test patients for so-called 'rare' driver mutations in lung cancer, because individual patients may derive substantial benefit from targeted therapy," says Gautschi.

Commenting on the findings, Dr David Planchard, pulmonary oncologist at Gustave Roussy in Villejuif, France, said that the results of the trial confirm the benefit of B-Raf inhibitors in BRAF-mutant non-small cell lung cancer. The current trial also confirmed the good tolerance of the drugs with no new side-effects, he said. Planchard and colleagues have presented a separate phase II study in this area with dabrafenib.

"This trial is important because due to the low frequency of this mutation in non-small cell lung cancer we will have few trials on this population," Planchard commented. "The more data we have, the better we understand how important it is to test for the mutation, especially in adenocarcinomas, and to expose mutation-positive patients to a specific B-Raf inhibitor."

The results also add to growing support for the approval of B-Raf inhibitors for use in lung cancer, Planchard added. This is important because the rarity of this mutation means that performing the kind of randomized phase III trials usually required for licensing approval will be extremely difficult, he noted.

Looking ahead, it will also be important to see results of combination therapy with inhibitors of B-Raf and a related protein, Mek, in non-small cell lung cancer carrying BRAF-V600E mutations, the researchers note, as this combination has shown a higher clinical benefit in BRAF-mutant melanoma.
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