Akira Suzuki, Ei-ichi Negishi, and Richard Heck.
These three scientists won the Nobel Prize for Chemistry this morning for their discoveries that made it easier and cheaper to build long carbon chains in the lab, and use those chains to develop new drugs, build electronics, and more.
Despite the ubiquity of carbon chains in nature, they’re hard to make in the lab at room temperature. The three chemists independently created essentially the same way to skirt this problem, using palladium to link carbon atoms through a process called palladium-catalyzed cross coupling. The palladium is a go-between, bonding to carbon to bring its atoms closer to one another than they could go on their own. The carbons then break their attachment to palladium and bond together in chains.
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When we last covered little brown bats it was with big bad news: A study in Science suggested that white nose syndrome could kill enough of the bats to make them regionally extinct in many parts of the United States by 2020. This week, though, brought a glimmer of hope. Scientists at the New York State Department of Health led by Vishnu Chaturvedi say some anti-fungal drugs work against the mysterious fungus causing the bat die-off.
They tested six strains of the novel fungus against drugs already used to treat people and animals such as cats and dogs for ailments ranging from athlete’s foot to life-threatening infections. “We found that two major classes of antifungal drugs have very good activity” against the bat germ, Chaturvedi reported Sunday in Boston at a meeting of the American Society for Microbiology. The drugs include fluconazole, the most widely used antifungal drug, which is sold as Diflucan by Pfizer Inc. and in generic form. Four other drugs also seem highly effective, Chaturvedi said. [AP]
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Chronic fatigue syndrome’s headaches, muscle aches, tiredness, and concentration problems have no known cause, so a paper published online yesterday, in which researchers report finding a type of virus in 87 percent of 37 chronic fatigue syndrome (CFS) patients tested, seems a promising step. But in statements to the media the researchers stress caution in interpreting results. The group also noted that it had delayed publishing the paper, originally meant to appear in the Proceedings of the National Academy of Sciences in May, due to conflicting reports from other scientists.
The National Institutes of Health’s Dr. Harvey Alter, senior author of the paper, said in a conference call with reporters, “It’s an association, but that’s all it is.” He was careful to say the findings don’t prove that a virus causes CFS. [NPR]
Alter’s caution is understandable, especially given recent CFS research history:
October 2009: A virus, XMRV (xenotropic murine leukemia virus–related virus), is found in 68 of 101 CFS patients.
January 2010: XMRV is not found in a British study that tested CFS patients.
July 2010: XMRV is not found in a Center for Disease Control study testing CFS patients.
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The antibiotics-resistant superbug that emerged in South Asia appears to have claimed its first life. According to doctors who treated a man in Belgium, he went to a hospital in Pakistan after a car accident, and there he picked up the bacterial infection. While the man died back in June, his doctors announced today that he carried the superbug.
This new health scare intensified this week after researchers published a study in The Lancet Infectious Diseases characterizing “a new antibiotic resistance mechanism” in the U.K., India, and Pakistan. How bad is this “mechanism?”
It’s bad:
The problem isn’t a particular kind of bacteria. It’s a gene that encodes an enyzme called New Delhi metallo-lactamase-1 (NDM-1). Bacteria that carry it aren’t bothered by traditional antibiotics, or even the drugs known as carbapenems deployed against antibiotic-resistant microbes.
The NDM-1 gene is a special worry because it is found in plasmids — DNA structures that can easily be copied and then transferred promiscuously among different types of bacteria. These include Escherichia coli, the commonest cause of urinary tract infections, and Klebsiella pneumoniae, which causes lung and wound infections and is generated mainly in hospitals [AFP].
It’s no worse than what we had before:
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Recreational drug users call it “Special K.” Large, frequent doses of the anesthetic ketamine can give users vivid hallucinations, but a recently published study hints that the drug may have a medicinal use: temporarily treating depression brought on by bipolar disorder.
The small, proof-of-concept study appears in the journal Archives of General Psychiatry. National Institutes of Health researchers randomly gave 18 depressed patients ketamine or a placebo on two different days, two weeks apart. They used a much smaller dose of the drug than the amount used for recreation or anesthesia, but within 40 minutes 71 percent of the patients who received ketamine showed a significant improvement in mood, which lasted for three days, as measured using a psychiatric depression rating scale.
The quick response time is unusual for the drugs typically used to treat bipolar disorder’s depression, such as lithium or antidepressants like Prozac, and many of the study’s patients had failed to respond to other treatments. On average, the study participants had tried seven antidepressants and 55 percent of participants had failed to respond positively to the extreme measures of electroconvulsive therapy (ECT)–seizures brought on by electrical current. Ketamine’s apparent success may have to do with the neurotransmitter, glutamate:
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Around the United States, state governments are rushing to enact bans on K2, the hot new (and still mostly legal) drug made with synthetic cannabinoids: lab-created compounds designed to mimic the effects of THC, the active ingredient in marijuana.
Often marketed as incense, K2 — which is also known as Spice, Demon or Genie — is sold openly in gas stations, head shops and, of course, online. It can sell for as much as $40 per gram. The substance is banned in many European countries, but by marketing it as incense and clearly stating that it is not for human consumption, domestic sellers have managed to evade federal regulation [The New York Times].
Missouri is the most recent state to move against K2, the origin of which dates back to the work of Clemson University scientist John Huffman, who was developing these synthetic compounds in the 1990s. Scientifically, the chemicals are interesting for their potential to mimic some of the pain-relieving aspects of marijuana, which advocates of medical marijuana legality point to, without the negative health effects that come with setting a plant on fire and inhaling the smoke. The chemical used in most varieties of K2 is called JWH-018.
Huffman was interviewed by The Guardian last year when K2 was spreading around Europe. Now in his late 70s, he seems to understand something that many politicians can’t seem to get through their heads: Risk-taking teenagers will go to about any length, legal or illegal, to get high. Huffman says he wouldn’t oblige the numerous enterprising types who asked him how to make his substances, and that the substances are always labeled not for human consumption. But he figured someone was going to figure it out sooner or later, especially considering the chemical doesn’t show up on drug tests.
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Twelve years have passed since Pfizer’s little blue pill for erectile dysfunction, Viagra, hit the market. The pill became so popular and ubiquitous that subsequent attempts by drug companies to make a libido-booster for women invariably drew the moniker “female Viagra.” Those attempts have failed, but today the Food and Drug Administration is considering approval for a new contender—a drug that has stirred up plenty of controversy.
The drug is called flibanserin, and the company is a German one, Boehringer Ingelheim. The first problem with evaluating the daily oral pill is figuring out whether it really has an effect that appears in trials.
The flibanserin data involved about 2,400 women treated with either flibanserin or a placebo for about six months. The agency said the two groups showed an increase in their number of sexually “satisfying” events but didn’t show a boost in a sexual-desire score. The “overall response rate… is not particularly compelling,” the FDA said, even though many of the differences in response rates between the two groups were statistically significant [Wall Street Journal].
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July: a time of sweltering heat, fireworks-related injuries, and newbie doctors roaming the halls of teaching hospitals, ready to learn medicine by practicing on you. The “July Effect”—the idea that medical mistakes spike in that month because new, inexperienced residents are on the scene— has become the subject of repeated studies trying to sort out whether it’s real or just conventional “wisdom.” Those studies have reached differing results. So, should we believe the newest one, which attributes a 10 percent July spike in fatal medical errors to those freshmen docs?
The study by David Phillips and Gwendolyn Barker, to be published in the Journal of General Internal Medicine, has a large sample size going for it. Phillips says that many prior “July effect” studies have examined just a single hospital’s population. But:
He and Barker, by contrast, probed a national database of more than 62 million death certificates that spanned from 1979 (when hospital status was first recorded in those records) through 2006 (the most recent year for which data were available). They turned up almost a quarter-million deaths that were coded as having not only occurred in a hospital setting, but also been due to medication errors. Both in-patient and out-patient cases were included [U.S. News & Report].
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Yesterday the Food and Drug Administration gave its OK to Provenge, a new treatment for prostate cancer. It’s not a “vaccine” in the old-fashioned sense, but it could be a way to make the immune system wake up and take notice to the presence of cancer.
In a standard vaccination, a person receives an attenuated or dead version of a microorganism to spur them to produce antibodies (against, for example, the virus that causes smallpox). Provenge is not that—it doesn’t prevent prostate cancer—but it is a variation on the theme. To oversimplify quite a bit: with Provenge vaccination begins with a blood draw. Blood is then sent to the lab, where technicians extract immune cells known as antigen presenting cells (APCs) from the sample. From here, Dendreon combines the immune cells with proteins that are prevalent on the surface of prostate cancer cells. An immune boosting substance is also added into the mix [TIME]. That awakens the APCs, which doctors then inject back into the bloodstream. And once there, the APCs put white blood cells on high alert against cancer.
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Who needs poppy plants to produce morphine? Last month scientists said they’d isolated the genes those plants use to synthesize the narcotic chemical and made it themselves in a lab. Now, in a study in the Proceedings of the National Academy of Sciences, another team has suggested that we mammals might possess the pathway to create our own morphine.
Because we have receptors for the opiate in our brains (which makes it such an effective and addictive painkiller), and because morphine traces show up in our urine, scientists had long wondered if animals could produce the drug themselves. But studies using living animals yielded inconclusive results because of possible contamination from external sources of morphine in their food or in the environment [Nature]. In addition, the body breaks down and changes morphine, which complicates the task.
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College students holed up in the library or cramming for an exam have always relied on stimulants like coffee, but recently they’ve been increasingly turning to the off-label use of drugs like Ritalin and Modafinil to help them stay focused. Now scientists have found how Ritalin, a drug normally prescribed for children with attention deficit hyperactivity disorder (ADHD), helps boost learning.
In a new study of rats published online in Nature Neuroscience, scientists found that Ritalin appears to boost both attention and enhance the speed of learning by increasing the activity of the chemical messenger dopamine [Technology Review]. The study also found that one type of dopamine receptor aids the ability to focus, and another type improves the learning itself [DNA].
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Researchers have found a pharmaceutical way to clear some of the cognitive fog that results from a sleepless night. In a new study using lab mice, researchers corrected the memory problems in sleep-deprived mice through a drug that suppressed levels of a certain enzyme in a brain region called the hippocampus, which plays an important role in memory and learning.
The study, published in Nature, helps tease out the specific effects of sleep deprivation on the brain. Says lead researcher Christopher Vecsey: “One of the main problems is that sleep deprivation does a lot of things to the brain, and it’s easy to get caught in a mish-mash of different effects” [Nature News].
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A team of researchers recently discovered that Tamiflu, the leading flu-fighting drug, is accumulating in rivers downstream from sewage-treatment plants in Kyoto. How is this possible? Tamiflu’s active ingredient, oseltamivir phosphate, is excreted in the urine of people taking the medication. Concerns are now building that birds, which are natural influenza carriers, are being exposed to waterborne residues of Tamiflu’s active form and might develop and spread drug-resistant strains of seasonal and avian flu [Science News]. The resistant virus strains would be of the conventional seasonal or avian flu variety, not the H1N1 swine flu strain that is currently pandemic in humans. Seasonal flu, however, kills thousands of people each year.
Study coauthor Gopal Ghosh explains that the team took measurements during normal flu season, and found concentrations that seem “high enough to lead to antiviral resistance in waterfowl” [Science News]. Computer models show that oseltamivir phosphate will survive sewage treatment, but it should break down when exposed to sunlight and its concentrations should decrease by half every three weeks. The high concentrations were found during a period where 1,738 flu cases were reported in Kyoto, according to the study, published in the journal Environmental Health Perspectives. In the United States, Tamiflu is only recommended for the very sick or those with compromised immune system, while Japan has a more liberal policy.
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Image: flickr / law_keven
Although researchers searching for an HIV vaccine have been down the path of optimism and disappointment many times before, a new finding has nevertheless brought fresh hope to the flagging effort. Researchers have discovered two antibodies that can effectively fight back most strains of the HIV virus, and say they’ll now try to make a vaccine that can teach the human body to produce these antibodies.
The weapons in question are called broadly neutralising antibodies…. These are antibodies that deactivate a wide range of HIV strains—which is particularly important for an effective vaccine, because HIV is so variable [The Economist]. Researchers found the two new antibodies after screening blood samples from 1,800 people around the world who were infected with HIV but hadn’t yet developed AIDS; the two antibodies both came from an African donor. Of these two potent antibodies, one neutralized 127 of 162 HIV strains and the other neutralized 119.
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Residents of the U.K. who go overseas for surgery have imported a new “superbug.” The bacteria, which is resistant to antibiotics and is even more difficult to treat than infamous infections such as MRSA, has killed two people and seriously sickened 18 others in the past year.
Britain’s Health Protection Agency has declared the infection “a notable public health risk” as the bacteria continues to pop up all over the U.K. In fact, 17 hospitals in Scotland and England have seen the infection, which is in the enterobacteriaceae family. Many of those contracting the superbug, which produces an enzyme that destroys even the most powerful antibiotics, have had cosmetic surgery, liver and kidney transplants in India and Pakistan [Daily Mail].
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