Archive for March 2012
US doctors have carried out what they say is the most extensive face transplant ever performed.
The operation at the University of Maryland gave Richard Norris a new face, including jaw, teeth and tongue.
The 37-year-old has lived as a recluse for 15 years after being severely injured in a gun accident, and wore a mask whenever he went outside.
The surgery was funded by the US Navy, which hopes the techniques will help casualties from Iraq and Afghanistan.
Surgeons who carried out the 36-hour operation say it was part of a series of transplant operations lasting 72 hours, using organs from one donor in five patients including Mr Norris.
A Penn- and MIT-led team explained how rapamycin, a drug that extends mouse lifespan, also causes insulin resistance. The researchers showed in an animal model that they could, in principle, separate the effects, which depend on inhibiting two protein complexes, mTORC1 and mTORC2, respectively.
The study suggests that molecules that specifically inhibit mTORC1 may combat age-related diseases without the insulin-resistance side effect, which can predispose people to diabetes.
Senior author Joseph A. Baur, PhD, assistant professor of Physiology, Perelman School of Medicine, University of Pennsylvania, and colleagues at the Whitehead Institute for Biomedical Research and Broad Institute, Massachusetts Institute of Technology, in Cambridge, MA, describe their work in this week’s issue of Science. Baur is also a member of Penn’s Institute for Diabetes, Obesity, and Metabolism.
The first volume of a “book of cancer knowledge” has been published, which scientists say will speed up the search for new cancer drugs.
The “encyclopaedia” details how hundreds of different cancer cells respond to anti-cancer agents.
UK, US and European researchers say the data, published in Nature, is a step towards tailoring cancer medicine to a patient’s genetic profile.
A cancer charity said the work would help in testing new cancer drugs.
Cancer cells grown in the laboratory are an essential tool in cancer research.
Ebola and its relatives, like Marburg virus, above, are considered among the most fearsome in nature. People infected with these long, wire-shaped filoviruses often bleed to death from every orifice, so the bugs make ideal villains for apocalyptic films like “Outbreak” and “28 Days Later.”
The infections are considered incurable, but several advances have been made in laboratories suggesting that cures may be possible. None have been tested in the field yet.
Late last month, scientists from the National Institute of Allergy and Infectious Diseases reported that two well-known cancer drugs used against leukemia, Gleevec and Tasigna, prevented Ebola virus from replicating in a lab colony of human kidney cells.
Eye of Science/Photo Researchers
Sleep has many functions—including facilitating learning.Now a study finds that when we acquire new information, and how soon we sleep after that may affect our retention of the info. That’s according to research in the journal Public Library of Science One.Scientists had more than 200 subjects memorize related words like “fire and smoke,” or unrelated word pairs like “insect and truth.” Some studied the words at 9 am, others at 9pm.The researchers tested the subjects’ ability to remember the pairs after 30 minutes, 12 hours or 24 hours.Sleep had little effect on the ability to recall related words. But subjects who slept between tests were significantly better at remembering the unrelated words than those who got no shuteye.
“That’s not FAIR!”
This is the line that rings through most houses with at least one kid. We all know when something’s not fair. That car that drove up the shoulder while you waited in traffic (rrrrr)? That’s a cheater, and that’s not fair. The person who cut in line at the grocery store instead of waiting? That’s not fair either.
We get a sense of what is fair or unfair at a pretty young age, and we also understand that we are allowed, and indeed encouraged in some cases, to punish unfair behavior. But we don’t all punish unfair behavior the same way, especially when punishment may be detrimental to us. What is responsible for this difference? What mediates our reactions to what is unfair?
The authors of this study think it might be serotonin, and that it may have as much to do with honesty as it does with a sense of what is fair.
Mouse ‘avatars’ could in future allow physicians to find the most effective cocktail of cancer drugs to combat a particular tumour before giving them to a patient, according to researchers at the annual meeting of the Human Genome Organisation (HUGO) in Australia last week.
“Using a personalized cancer avatar makes it possible to try out different combinations and make some mistakes before going into the clinic,” says Edison Liu, president of HUGO and head of the Jackson Laboratory at Bar Harbor in Maine. “It’s the direction in which a lot of research groups are going.”
An ‘avatar’ is a term informally used by cancer researchers to describe a mouse or other animal onto which tissue from a human tumour is grafted to create a personalized model of one patient’s cancer. In one example of this approach, cancer researcher Sean Grimmond of the University of Queensland in Brisbane, with his colleagues from the Australian Pancreatic Cancer Genome Initiative, analysed a patient’s pancreatic tumour to identify mutations that make the cancer susceptible to particular drugs. The researchers then created a personalized mouse model of that specific pancreatic cancer by xenografting a piece of the patient’s tumour onto immunodeficient mice. This allowed them to test the tumour’s response to the drug mitomycin C, which their initial analysis had shown might be an effective treatment for the patient’s cancer. Reporting their preliminary results at the meeting in Sydney, the researchers found that the tumours shrank after the mouse was administered the drug; however, the patient died before he could be treated with it.
apses in oversight that prevented a US university from identifying the flawed research behind a series of clinical trials are symptomatic of a larger problem says a report by the US Institute of Medicine (IOM), released today. The case in question, which revolves around papers relating to cancer treatment published by researcher Anil Potti, indicates a need for higher standards in the development of tests based on genomics, proteomics and similar large-scale studies, the report says.
Loosely dubbed ‘omics’, such large-scale studies of genes, proteins and other molecular characteristics of whole organisms have been lauded as a way potentially to detect disease and evaluate how people respond to drugs. In theory, the approach could pave the way to personalized treatments. But the development of reliable clinical tests based on omics findings has taken longer than expected.
revious human studies have suggested that early life exposure to microbes (i.e., germs) is an important determinant of adulthood sensitivity to allergic and autoimmune diseases such as hay fever, asthma and inflammatory bowel disease.
This concept of exposing people to germs at an early age (i.e., childhood) to build immunity is known as the hygiene hypothesis.
Medical professionals have suggested that the hygiene hypothesis explains the global increase of allergic and autoimmune diseases in urban settings. It has also been suggested that the hypothesis explains the changes that have occurred in society and environmental exposures, such as giving antibiotics early in life.
However, neither biologic support nor a mechanistic basis for the hypothesis has been directly demonstrated. Until now. Read the rest of this entry »
On a small table in his office at the Scripps Research Institute in La Jolla, California, Ray Stevens spreads out a sheet of paper covered with colourful branched lines, each sprouting and thinning before terminating in an esoteric code. “This is the dream,” he declares.
The intricate diagram represents the largest family of receptor proteins encoded in the genome — the G-protein-coupled receptors (GPCRs), ubiquitous cell-surface molecules that are activated by light, odours, hormones and neurotransmitters. Stevens wants to determine the atomic structures of receptors on all branches of the tree. This week, that goal moved two receptors closer: Stevens’s group has solved the atomic structure of the κ-opioid receptor (κ-OR)1, and a team led by Brian Kobilka at Stanford University in California has solved the medically crucial μ-opioid receptor (μ-OR)2. The structures, published in Nature, bring the tally of GPCR structures solved this year alone up to five.
Our fond or fearful memories — that first kiss or a bump in the night — leave memory traces that we may conjure up in the remembrance of things past, complete with time, place and all the sensations of the experience. Neuroscientists call these traces memory engrams.
But are engrams conceptual, or are they a physical network of neurons in the brain? In a new MIT study, researchers used optogenetics to show that memories really do reside in very specific brain cells, and that simply activating a tiny fraction of brain cells can recall an entire memory — explaining, for example, how Marcel Proust could recapitulate his childhood from the aroma of a once-beloved madeleine cookie.
“We demonstrate that behavior based on high-level cognition, such as the expression of a specific memory, can be generated in a mammal by highly specific physical activation of a specific small subpopulation of brain cells, in this case by light,” says Susumu Tonegawa, the Picower Professor of Biology and Neuroscience at MIT and lead author of the study reported online today in the journal Nature. “This is the rigorously designed 21st-century test of Canadian neurosurgeon Wilder Penfield’s early-1900s accidental observation suggesting that mind is based on matter
Researchers have identified a biological pathway previously unknown to have a role in male pattern hair loss.
Published today in Science Translational Medicine1, the study finds that a lipid compound called prostaglandin D2 (PGD2) has a role in inhibiting hair growth.
The study “is likely to lead to new hair growth products based on prostaglandin biology,” says Anthony Oro, an epithelial biologist at Stanford University in California, who was not involved in the study.
Male pattern baldness, or androgenetic alopecia (AGA), affects around 80% of men at some point in their lives. Only one predisposing factor — a mutation in a testosterone receptor — has been identified, and it is found in only a minority of men with AGA. Other causes are largely unknown, and present treatments were discovered serendipitously — finasteride (Propecia) was originally prescribed for prostate enlargement, and minoxidil (Rogaine) for hypertension. Their molecular mechanisms are unclear.
To look for other factors involved in AGA, researchers led by George Cotsarelis, a dermatologist at the University of Pennsylvania in Philadelphia, examined gene expression in balding and non-balding scalp tissue from five men with AGA. They found that PGD2 was more abundant in the balding scalp tissue, as was prostaglandin D2 synthase, which catalyses PGD2.
The authors also found that, in mice, PGD2 expression peaks during the hair-growth cycle stage in which the follicle begins regressing. Cultured human follicles and mice treated with PGD2 also had hair growth inhibited
Scientists in Seattle are reporting a potential breakthrough in the treatment of pancreas cancer, a disease which stubbornly resists most therapies.
Pancreas cancer tumors are resistent to chemotherapy partly because they form a biological barrier around themselves.
Researchers at the Fred Hutchinson Cancer Research Center believe they’ve found a way to break that barrier down.
“Pancreas cancer actually has the highest one-year and five-year mortalities of any cancer,” says Sunil Hingorani, senior author of the study published in Cancer Cell.
There’s a moment in the history of medicine that’s so cinematic it’s a wonder no one has put it in a Hollywood film. The scene is a London laboratory. The year is 1928. Alexander Fleming, a Scottish microbiologist, is back from a vacation and is cleaning up his work space. He notices that a speck of mold has invaded one of his cultures of Staphylococcus bacteria. It isn’t just spreading through the culture, though. It’s killing the bacteria surrounding it.
Fleming rescued the culture and carefully isolated the mold. He ran a series of experiments confirming that it was producing a Staphylococcus-killing molecule. And Fleming then discovered that the mold could kill many other species of infectious bacteria as well. “I had a clue that here was something good, but I could not possibly know how good it was,” he later said.
We do currently have “antiviral” drugs, but they’re a pale shadow of their bacteria-fighting counterparts. People infected with HIV, for example, can avoid developing AIDS by taking a cocktail of antiviral drugs. But if they stop taking them, the virus will rebound to its former level in a matter of weeks. Patients have to keep taking the drugs for the rest of their lives to prevent the virus from wiping out their immune system.
The case for using aspirin to prevent cancer continues to build, particularly if people are at increased risk of the disease.
Three new studies led by researchers at Oxford University also raise the possibility that a daily low dose of the drug could be effective, not just as a preventative measure, but as an additional treatment for those with cancer.
It follows the finding that aspirin can reduce the chances of tumours spreading to other parts of the body.
The three papers by Professor Peter Rothwell of the Nuffield Department of Clinical Neurosciences and colleagues are published today, two in the medical journal The Lancet and the other in The Lancet Oncology.
Professor Rothwell says: ‘We are not at the stage of recommending aspirin use in everybody, but the guidelines on use of aspirin in the healthy middle-aged population certainly need to be updated in order to take into account the effects on the risk and outcome of cancer as well as on the risk of heart attacks and strokes.’
Researchers from Chalmers and the University of Gothenburg have shown that nanocellulose stimulates the formation of neural networks. This is the first step toward creating a three-dimensional model of the brain. Such a model could elevate brain research to totally new levels, with regard to Alzheimer’s disease and Parkinson’s disease, for example.
Over a period of two years the research group has been trying to get human nerve cells to grow on nanocellulose.
When the nerve cells finally attached to the scaffold they began to develop and generate contacts with one another, so-called synapses. A neural network of hundreds of cells was produced. The researchers can now use electrical impulses and chemical signal substances to generate nerve impulses, that spread through the network in much the same way as they do in the brain. They can also study how nerve cells react with other molecules, such as pharmaceuticals.
In studies on mice which had been genetically modified to have the mutation, the mice consumed up to 80% more food than normal.
After a meal, hormones such as insulin and leptin should tell the brain that the body is full and should stop eating. The researchers showed that in the mutated mice the message was not being passed on from the hormones in the blood to the correct part of the brain.
One of the researchers Prof Baoji Xu said: “If there is a problem with the BDNF gene, neurons can’t talk to each other, and the leptin and insulin signals are ineffective, and appetite is not modified.”
He said the discovery “may open up novel strategies to help the brain control body weight” such as finding a “drug that can stimulate BDNF expression”.
Michael Snyder knows his body better than anyone in history.
For two-and-a-half years, he’s had regular blood samples drawn, and tracked the ebb and flow of 40,000 different molecules within his cells, from hormones to blood sugar, to the proteins of the immune system and mutated genes. Snyder also watched as his genetic vulnerability to diabetes turned into actual disease.
In a paper published today in the journal Cell, Snyder, a genetics professor at Stanford University, and his collaborators recount 14 months of living a Truman Show kind of life, but with a microscope instead of a television camera. His story marks the first time anyone’s physiology has ever been followed this closely, and portends the future of personalized medicine, according to Snyder and others.
“This article reminds us that the future is now,” says Charis Eng, a professor of genomic medicine at the Cleveland Clinic. “I think we’re heading in this direction, and I think we must prepare in every way, not just scientifically, not just medically, but as a society—[considering] all the ethical, moral, and regulatory issues.”
The aging brain loses its ability to recognize when it is time to move on to a new task, explaining why the elderly have difficulty multi-tasking, Yale University researchers report.
“The aged brain seems to get lost in transition,” said Mark Laubach, associate professor at the John B. Pierce Laboratory and the Yale School of Medicine, and senior author of a study that appears in the March 14 issue of The Journal of Neuroscience.
Laubach’s team was studying the impact of aging on working memory, the type of memory that allows you to recall that dinner is in the oven when you are talking on the phone. The researchers examined brain activity in the medial prefrontal cortex of young and older rats that is related to spatial working memory — the type of memory that allows you to recall, for example, that mashed potatoes are on the stove and the turkey is in the oven
Based on previous studies, they expected that it would be spatial memory most affected by aging. Instead, the Yale team found that the aged brain seems to lose its ability to respond to cues that indicate when it is time to move on to a new task. Read the rest of this entry »
Movies and television shows are full of scenes where a man tries unsuccessfully to interact with a pretty woman. In many cases, the potential suitor ends up acting foolishly despite his best attempts to impress. It seems like his brain isn’t working quite properly and according to new findings, it may not be.
Researchers have begun to explore the cognitive impairment that men experience before and after interacting with women. A 2009 study demonstrated that after a short interaction with an attractive woman, men experienced a decline in mental performance. A more recent study suggests that this cognitive impairment takes hold even w hen men simply anticipate interacting with a woman who they know very little about.
An algorithm designed by US scientists to trawl through a plethora of drug interactions has yielded thousands of previously unknown side effects caused by taking drugs in combination.
The work, published today in Science Translational Medicine1, provides a way to sort through the hundreds of thousands of ‘adverse events’ reported to the US Food and Drug Administration (FDA) each year. “It’s a step in the direction of a complete catalogue of drug–drug interactions,” says the study’s lead author, Russ Altman, a bioengineer at Stanford University in California.
Although clinical trials are often designed to assess the safety of a drug in addition to how well it works, the size of the trials needed to detect the full range of drug interactions would surpass even the large, late-stage clinical trials sometimes required for drug approval. Furthermore, clinical trials are often done in controlled settings, using carefully defined criteria to determine which patients are eligible for enrolment — including other conditions they might have and which medicines they can take alongside the trial drug.
In the first months after her surgery, shopping for groceries was infuriating. Standing in the supermarket aisle, Vicki would look at an item on the shelf and know that she wanted to place it in her trolley — but she couldn’t. “I’d reach with my right for the thing I wanted, but the left would come in and they’d kind of fight,” she says. “Almost like repelling magnets.” Picking out food for the week was a two-, sometimes three-hour ordeal. Getting dressed posed a similar challenge: Vicki couldn’t reconcile what she wanted to put on with what her hands were doing. Sometimes she ended up wearing three outfits at once. “I’d have to dump all the clothes on the bed, catch my breath and start again.”
In one crucial way, however, Vicki was better than her pre-surgery self. She was no longer racked by epileptic seizures that were so severe they had made her life close to unbearable. She once collapsed onto the bar of an old-fashioned oven, burning and scarring her back. “I really just couldn’t function,” she says. When, in 1978, her neurologist told her about a radical but dangerous surgery that might help, she barely hesitated. If the worst were to happen, she knew that her parents would take care of her young daughter. “But of course I worried,” she says. “When you get your brain split, it doesn’t grow back together.”
The big push in cancer treatment these days is to sample a person’s tumor, test it for mutations, and give the patient a drug tailored to a genetic weak spot in the tumor. A new study suggests one reason why this targeted drug strategy doesn’t always work. A solid tumor, it turns out, is not a mass of identical cancerous cells but a mosaic of genetically different cells that aren’t captured with a single biopsy. Some of these distinct cells may be resistant to the targeted drugs, allowing a tumor to persist or grow.
The classic view of how cancer develops is that a single, normal cell accumulates mutations that eventually allow or force it to divide uncontrollably. This “clone” then grows into a tumor of identical cells, which can also sow seed cells into the bloodstream that then take root somewhere else in the body, or metastasize. The assumption that tumors grow out from a single clone has spurred a rush to find drugs that block one of the clone’s genetic weak spots. But although the strategy has resulted in some very effective drugs—Iressa for lung cancer and a new melanoma drug called Zelboraf, for example—these drugs often stop working within a year or two. One reason could be that solid tumors already harbor a few cells, or clones, with “resistance” mutations that take over when the cells targeted by the drug are wiped out.
As the United States seeks to reinvigorate its job market and move past economic recession, MIT News examines manufacturing’s role in the country’s economic future through this series on work at the Institute around manufacturing.
Traditional drug manufacturing is a time-consuming process. Active pharmaceutical ingredients are synthesized in a chemical manufacturing plant and then shipped to another site, where they are converted into giant batches of pills. Including transport time between manufacturing plants, each batch can take weeks or months to produce.
Five years ago, MIT and pharmaceutical company Novartis launched a research effort to transform those procedures. Instead of manufacturing drugs using this conventional batch-based system, they envision a continuous manufacturing process, all done in one location, which would cut down on time and cost.
Posted March 12, 2012on:
A single injection of cocaine or methamphetamine in mice caused their brains to put the brakes on neurons that generate sensations of pleasure, and these cellular changes lasted for at least a week, according to research by scientists at the Salk Institute for Biological Studies.
Their findings, reported March 7 in Neuron, suggest this powerful reaction to the drug assault may be a protective, anti-addiction response. The scientists theorize that it might be possible to mimic this response to treat addiction to these drugs and perhaps others, although more experiments are required to explore this possibility.
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Posted March 12, 2012on:
A study by Columbia researchers suggests that cells in the patient’s intestine could be coaxed into making insulin, circumventing the need for a stem cell transplant. Until now, stem cell transplants have been seen by many researchers as the ideal way to replace cells lost in type I diabetes and to free patients from insulin injections.
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A retinoid called all-trans retinoic acid (ATRA), which is a vitamin A-derivative, is already used successfully to treat a rare sub-type of acute myeloid leukemia (AML), however this drug has not been effective for the more common types of AMLs.
Team leader Arthur Zelent, Ph.D., and colleagues at the ICR have been working to unlock the potential of retinoids to treat other patients with AML. In a paper published in Nature Medicine today, they show that the key could be an antidepressant called tranylcypromine (TCP).
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Making berries a part of your daily diet may help keep your memory sharp, a new review shows.
The review shows there’s strong evidence that eating berries boosts brain function and may prevent age-related memory loss.
“In addition to their now well-known antioxidant effects, dietary supplementation with berry fruits has direct effects on the brain,” writes researcher Marshall Miller, of the USDA-ARS Human Nutrition Research Center on Aging, and colleagues in the Journal of Agricultural and Food Chemistry.
Researchers say laboratory and animal studies suggest that eating berries has beneficial effects on brain signaling pathways involved in inflammation and cell death. The net effect of these improvements in brain function may stall age-related brain disorders like Alzheimer’s disease and dementia.
UK scientists have found that the drug donepezil, which is approved for use only in the mild to moderate stages of Alzheimer’s disease, could benefit patients in the later stages of the disease. The study is published in the New England Journal of Medicine.
The study, led by researchers at King’s College London, set out to assess the effects of two Alzheimer’s drugs – donepezil (often known as Aricept) and memantine (known as Ebixa or Axura). Donepezil is currently licensed in the UK for use in people with mild to moderate Alzheimer’s, while memantine is used in people in the moderate and severe stages of the disease. Both drugs can help with some of the symptoms of Alzheimer’s.
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How do we recognize a face? To date, most research has answered “holistically”: We look at all the features — eyes, nose, mouth — simultaneously and, perceiving the relationships among them, gain an advantage over taking in each feature individually. Now a new study overturns this theory. The researchers — Jason M. Gold and Patrick J. Mundy of the Indiana University and Bosco S. Tjan of the University of California Los Angeles — found that people’s performance in recognizing a whole face is no better than their performance with each individual feature shown alone. “Surprisingly, the whole was not greater than the sum of its parts,” says Gold. The findings appear in the journal Psychological Science, which is published by the
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Larry Smarr stops a visitor and says, “Before you go, let me show you my stool sample.”
The UC San Diego physicist-futurist reaches into his kitchen refrigerator, past the milk, and pulls out a small white box. He marvels over its contents.
“The bacteria in here contains more info than you’d find on a computer chip,” Smarr says. “It’s a window into your health. Within 10 years, people won’t dream of going to a doctor without first getting a sample like this.”
Feeling squeamish? Smarr can have that effect on people. Virtually nothing is out-of-bounds these days when he promotes the “Quantified Self,” an emerging movement in which people use biosensors and other gadgets to closely monitor their bodies in the name of wellness.
At 63, Smarr thinks he’s found the future of personal health care. Time will tell. But colleagues note that he’s one of the most original thinkers in the country, with an almost eerie gift for sensing and shaping where society and technology are going.
In Silicon Valley, the line between computing and biology has begun to blur in a way that could have enormous consequences for human longevity.
Bill Banyai, an optical physicist at Complete Genomics, has helped make that happen. When he began developing a gene sequencing machine, he relied heavily on his background at two computer networking start-up companies. His digital expertise was essential in designing a factory that automated and greatly lowered the cost of mapping the three billion base pairs that form the human genome.
The promise is that low-cost gene sequencing will lead to a new era of personalized medicine, yielding new approaches for treating cancers and other serious diseases. The arrival of such cures has been glacial, however, although the human genome was originally sequenced more than a decade ago.
Last month, the FDA issued an unusual warning. It wasn’t about counterfeit prescription drugs, an unsafe medicine, or a recalled product. Rather, the warning was for something that grows naturally in the groves of Florida: the sour, juicy grapefruit.
The FDA consumer update confirmed what users of drugs like statins have known for a long time—you shouldn’t eat grapefruit or drink grapefruit juice if you’re taking any of a number of medications. In the report, Shiew Mei Huang, the acting director of the FDA’s Office of Clinical Pharmacology, noted that for many drugs, “the juice increases the absorption of the drug into the bloodstream. When there is a higher concentration of a drug, you tend to have more adverse events.”
The strange “grapefruit effect” was first discovered entirely by accident. As part of a 1989 study, scientists at London’s Victoria Hospital were attempting to discover whether ethanol—the molecule responsible for the intoxicating effects of alcoholic drinks—could negatively interact with a drug called felodipine, developed to treat high blood pressure. They happened to use grapefruit juice to mask the taste of the alcohol, and discovered unexpectedly high levels of the drug in the blood. After further investigation, they realized it wasn’t the alcohol causing the surge—it was grapefruit.
A newly identified form of DNA—small circles of non-repetitive sequences—may be widespread in somatic cells of mice and humans, according to a study in this week’s issue of Science. These extrachromosomal bits of DNA, dubbed microDNA, may be the byproducts of microdeletions in chromosomes, meaning that cells all over the body may have their own constellation of missing pieces of DNA.
“It’s an intriguing finding,” said James Lupski, a geneticist at Baylor College of Medicine in Houston who did not participate in the research. Most DNA studies use cells drawn from blood, but that snapshot of a person’s genome may not be giving a complete picture, Lupski explained, if cells in other organs have their own set of chromosomal snippets missing.
But the findings do not surprise Sabine Mai, who studies genomic instability at the University of Manitoba. Extrachromosomal DNA is a well-studied phenomenon in cells ranging from plants to humans, she says. This research is just renaming an old phenomenon, previously referred to small polydispersed DNA. Small circles of DNA have been identified before, Mai says, though new deep sequencing techniques will allow for a “deeper characterization” of these extrachromosomal snippets.
Eating foods laced with too much salt may be as risky as smoking cigarettes, at least in terms of a risk factor for heart attacks called coronary flow reserve, a new study of middle-aged American men finds.
Coronary flow reserve, or CFR, offers a gauge of how well tiny blood vessels in the heart dilate or contract in response to hormonal commands. The lower the CFR, the stiffer the vessels — and the less responsive they become to the heart’s constantly changing workloads.
The new study examined CFR and salt intake among 143 pairs of male twins in their 50s or older. CFR declined by about 10 percent for each additional 1,000 milligrams of sodium that a man consumed per day compared with his brother.
“That’s huge,” says Viola Vaccarino of Emory University in Atlanta and coauthor of the study, which appears in the March American Journal of Clinical Nutrition. The difference in CFR for men with the highest sodium intake versus those with the lowest, she notes, was equivalent to changes other studies had linked to smoking.
Graft-versus-host disease (GvHD) is a common and often deadly complication of bone-marrow transplantation that occurs when immune cells from an unrelated donor attack the transplant recipient’s tissue. Now, researchers have for the first time managed to completely replace people’s bone-marrow-derived stem cells with those from unrelated donors without causing GvHD1. And because of this, the recipients could also accept kidneys from the same donors without the need for drugs that suppress the immune system.
“The outcome has been amazing,” says Lindsay Porter, a 47-year-old Chicago resident with polycystic kidney disease who was one of the study subjects. She has been off immunosuppressive drugs for seven months. “I feel so normal, it feels like it’s not a big deal.”
Researchers in Cambridge have deciphered the genetic code of the gorilla – the last of the Great Ape genuses to be sequenced.
Writing in the journal Nature, the scientists say that researchers can now begin to examine the similarities and differences between the apes.
Genome sequences of humans, chimpanzees and orangutans are already published.
The team hopes their work will help to uncover genetic mutations that led to language, culture and science.
“I’d like to think that in the next 20 or 30 years we will get a deeper understanding of what happened genetically in our evolutionary history, and of how those genes affect the brain and other properties that make us modern humans,” said Richard Durbin of the Wellcome Trust Sanger Institute, who led the study.
A new study turns the well established theory that antibodies are required for antiviral immunity upside down and reveals that an unexpected partnership between the specific and non-specific divisions of the immune system is critical for fighting some types of viral infections. The research, published online on March 1st in the journal Immunity by Cell Press, may lead to a new understanding of the best way to help protect those exposed to potentially lethal viruses, such as the rabies virus.
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Image: Ivan Konstantinov, Yury Stefanov, Aleksander Kovalevsky, Yegor Voronin/Visual Science Company
Posted March 2, 2012on:
The American Cancer Society estimates that 44,000 new cases of pancreatic cancer will be diagnosed this year and that 37,000 people will die from the disease. These are not strong odds. A new drug, rigosertib, allows pancreatic cancer cells to rush through replication – and then stops them cold, killing them in in the middle of a step called M phase. Healthy cells that don’t rush are unharmed.
Data from a phase I clinical trial of patients with advanced pancreatic cancer and additional solid tumors recently published in the journal Clinical Cancer Research shows the strategy has promise. While the goal of any phase I trial is to establish the dosage that best balances effectiveness against side effects, 11 of the 19 patients treated achieved stable disease, which lasted for a median of 113 days.
“Really, the drug takes one of cancer’s greatest strengths and turns it into a weakness,” says Wells Messersmith, MD, co-leader of the Developmental Therapeutics Program at the University of Colorado Cancer Center and the clinical trial’s national principal investigator.
Instead of going with the flow of the natural cell cycle, cancer cells amplify two signals – PLK1 and PI3K – which allows them to blast through the cell cycle and divide much more quickly. In the process, they break this step of the natural cell cycle, known as the G1 regulatory mechanism, and thus depend on the kick of PLK1 and P13K to push at a frenzied pace through replication.
It’s specifically these two signals, PLK1 and PI3K, that rigosertib targets. With these signals turned off, cancer cells get stuck and die in the stage of the cell cycle called M phase – while healthy cells that stuck to the slower, natural method of division chug past unharmed.
Wells Messersmith, MD, co-leader of the Developmental Therapeutics Program at the University of Colorado Cancer Center
“This one-two punch, targeting these two distinct signaling pathways, allows us to interfere twice with cancer cells’ ability to replicate,” Messersmith says. And it also allows doctors to target cancers that may have evolved resistance to one or the other target.
A 16-year-old boy who was born with a life-threatening immune disorder has become the first patient to benefit from a new form of gene therapy.
Doctors at Great Ormond Street Hospital in London said the treatment had only a temporary effect but was sufficient to help the boy overcome a lung infection. Remy Halbawi, who is at school in Wimbledon, south London, had been ill for two years with the fungal infection and would not have survived without radical treatment, doctors said.
Remy was born with a genetic condition called x-CGD (Chronic Granulomatous Disorder) that affects boys. Patients with the disorder have a faulty gene that disrupts a subset of immune cells called neutrophils, which act as the body’s first line of defence against infection.
Children born with x-CGD struggle to fight infections caused by fungi or bacteria, and are often hospitalised with severe infections in the first few years of life. A bone marrow transplant from a suitable donor is the only cure for the condition.
he smallpox vaccine was the first, and arguably most successful, vaccine ever put into practice, and it was scratched into the skin of individuals. With the invention of syringes and hypodermic needles, vaccination shifted toward administration directly into the muscle, under the assumption that it is better to get a vaccine straight into the body. But it turns out scientists may have had it right the first time.
A paper published this week in Nature suggests that the most important part of the human immune system actually resides in peripheral tissues, and that vaccination through those tissues may be more effective than traditional vaccination into the muscle.
The finding is “quite remarkable,” said Onur Boyman, an immunologist at the University of Zurich, who was not involved in the current study. The researchers showed that a population of immune cells called resident memory T cells, which are present in parts of the body that are in contact with the environment, such as the skin, gut, and lungs, mediate an immune response far stronger than circulating, or central, memory T cells in the blood stream.
Researchers from the University of Nottingham have demonstrated how a species of flatworm overcomes the ageing process to be potentially immortal. The discovery, published in the Proceedings of the National Academy of Sciences, is part of a project funded by the Biotechnology and Biological Sciences Research Council (BBSRC) and Medical Research Council (MRC) and may shed light on the possibilities of alleviating ageing and age-related characteristics in human cells.
Hoping to learn more about how inactivity affects disease risk, researchers at the University of Missouri recently persuaded a group of healthy, active young adults to stop moving around so much. Scientists have known for some time that sedentary people are at increased risk of developing heart disease and Type 2 diabetes. But they haven’t fully understood why, in part because studying the effects of sedentary behavior isn’t easy. People who are inactive may also be obese, eat poorly or face other lifestyle or metabolic issues that make it impossible to tease out the specific role that inactivity, on its own, plays in ill health.
So, to combat the problem, researchers lately have embraced a novel approach to studying the effects of inactivity. They’ve imposed the condition on people who otherwise would be out happily exercising and moving about, in some cases by sentencing them to bed rest.
A diet lacking in omega-3 fatty acids, nutrients commonly found in fish, may cause your brain to age faster and lose some of its memory and thinking abilities, according to a study published in the February 28, 2012, print issue of Neurology®, the medical journal of the American Academy of Neurology. Omega-3 fatty acids include the nutrients called docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA).
“People with lower blood levels of omega-3 fatty acids had lower brain volumes that were equivalent to about two years of structural brain aging,” said study author Zaldy S. Tan, MD, MPH, of the Easton Center for Alzheimer’s Disease Research and the Division of Geriatrics, University of California at Los Angeles.
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Louise Levy attends regular Tai-chi classes, retired three years ago from her secretarial job and says she would still be driving today if her car had not “conked out before I did.” None of which would be particularly unusual, except Mrs. Levy is 101 years old.
“My mind is still clear and I don’t have a memory problem,” says the resident of Rye, N.Y., about the latest chapter in a life that began when movies were silent and the Model-T Ford cutting edge. “It’s been absolutely marvelous.”
Mrs. Levy’s long and generally healthy life is the focus of a fascinating scientific study, itself at the forefront of a little-noticed but radical approach to medical research. Turning upside down the traditional quest to understand and cure specific diseases, some researchers are examining instead healthy and long-lived humans and animals for their biological secrets.
By reverse engineering the source of that vigour, scientists hope to develop drugs or supplements that could give less genetically fortunate people more protection against the ravages of aging and chronic illness.