"OUT OF AFRICA"
New research uncovers genetic prints H. sapiens were infected with H.pylori when they set out on global trek
Blood test tells risk of heart attack, stroke
WASHINGTON
A simple blood test can foretell with strong probability a person's risk of heart attack or stroke and the likelihood cardiovascular-disease patients will die of their illness, according to a study published in the Journal of the American Medical Association. The research involving 987 men and women suffering from stable coronary disease found that a higher level of the protein NT-proBNP in blood meant a higher risk of heart attack, stroke, heart failure, or death.
"After adjusting for all other risk factors, it's clear that this marker is picking up something that we are otherwise unable to detect with standard tests such as echocardiography," said Mary Whooley, lead investigator and a physician at the San Francisco VA Medical Center in California.
The NT-proBNP protein is a marker in the blood for the hormone BNP, which "goes up during times of cardiac stretch or stress," Whooley explained. "When the heart wall is overexpanded by too much blood volume, or damaged by lack of blood flow to the heart itself, BNP goes up, and NT-proBNP along with it," she said.
The patients were divided into four groups with varying blood levels of NT-proBNP, and were each followed for an average of 3.7 years. Twenty-six percent of them died or suffered some level of heart failure during the study. Patients in the group with the highest levels of NT-proBNP were 3.4 times more likely to die or have a heart attack or stroke than patients with the lowest levels of the biological marker.
Whooley cautioned that the test should only be ordered for patients with known coronary heart disease. For others in seemingly good health, its usefulness is limited, she said. "It's much better at predicting risk in a population with a high incidence of heart disease."
The study was funded by the Robert Wood Johnson Foundation and the National Heart, Lung, and Blood Institute, a branch of the US National Institute of Health.
Breakthrough opens new path for Parkinson treatment
PARIS
Lab mice with Parkinson disease were able to move normally after researchers treated them with a classic anti-Parkinson drug and a compound to slow the breakdown of naturally-occurring marijuana-style chemicals in the brain.
Mice that had been genetically engineered to have the symptoms of Parkinson-a degenerative disease that causes trembling, jerkiness, and rigidity-went from being frozen in place to moving around freely in 15 minutes after the combination treatment.
The research, led by Robert Malenka and Anatol Kreitzer of Stanford University Medical Center in California, is published in Nature. "This study points to a potentially new kind of therapy for Parkinson's disease," Malenka said. "Of course, it is a long, long way to go before this will be tested in humans, but nonetheless, we have identified a new way of potentially manipulating the [brain] circuits that are malfunctioning in this disease."
Parkinson is linked to depletion of dopamine in the brain's substantia nigra, leading to dopamine shortage in the striatum, the part of the brain that helps coordinate motion. To compensate for this shortage, patients with Parkinson are given drugs that stimulate or mimic dopamine, although these treatments often have bad side effects and can start to wear off after a few years.
Working on mice, Malenka's team discovered that the striatum has two distinct types of cell, each forming a circuitry that initiates motion or restrains unwanted movement. One of the cell types turned out to have a sort of dopamine receptor-a docking point on the cell's surface-that the other cell did not have.
The team turned to previous work on dopamine and endocanna-binoids, a naturally occurring marijuana-like compound. Their hunch was that the two chemicals worked together to ensure smooth activation of the cell and its circuitry, which they believe inhibits unwanted movement. They combined a dopamine mimic called quinpirole with a new test compound, URB597, that slows the way enzymes break down endocannabinoids in the brain.
"The dopamine drug alone did a little bit but it wasn't great, and the drug that targeted the enzyme that degrades endocannabinoids basically did nothing alone," said Kreitzer. "But when we gave the two together, the animals really improved dramatically."
Kreitzer and Malenka caution Parkinson patients against the idea of smoking marijuana to try to achieve the same result. They point out that their technique aims at stimulating the activity of endocan-nabinoids in a selected part of the brain where it occurs naturally. This process is the opposite and more fine-tuned compared to boosting levels of endocannabinoids by smoking marijuana.
Bioengineering helps toothless mice smile
PARIS
In a world first, Japanese researchers reported they had successfully replaced natural teeth in mice with teeth that were created in a lab dish from single cells. Writing in the journal Nature Methods, a team led by Takashi Tsuji of the Tokyo University of Science described how they took two kinds of cell-mesenchymal and epithelial cells-that develop into a tooth.
They first grew each cell type separately to make larger numbers of them and then injected them into collagen. The tooth germ grew into a tiny tooth about 1.3 millimeters long. The researchers then extracted the incisor from an eight-week-old adult mouse and inserted the bioengineered tooth. After two weeks, the transplant was found to be growing perfectly, with root, enamel, dental pulp, bone, blood vessel-the same composition and structure as a normal tooth.
The study "provides the first evidence of successful reconstitution of an entire organ via the transplantion of bioengineered material," the authors said.
The tooth could be grown in 14 days either in organ culture or in a subrenal capsule, which means it was attached to the kidney of another mouse in order to grow.
MRI can predict schizophrenia
LONDON
British researchers say magnetic resonance imaging (MRI) could be used in combination with other clinical assessments to predict schizophrenia in people at high risk of developing the brain disorder before they actually started showing the symptoms. "Changes in grey matter could be used as part of a predictive test for schizophrenia in people at enhanced risk for (family) reasons," the team of scientists at Edinburgh University said in an abstract published on the BMC Medicine web site.
"Current methods are good for predicting who won't develop schizophrenia but not who will," lead researcher Dominic Job told the BBC. "By combining brain imaging with traditional clinical assessments it might be possible to detect people who are at highest risk of the illness early."
The researchers pointed out, however, that their study had only covered a small group of people and a larger-scale independent test was required to confirm the results.
The Edinburgh team spent 10 years following 200 young people at high risk of developing schizophrenia because two or more members of their family had already been diagnosed with the disorder, the BBC reported on its web site. They analyzed results of MRI taken about every 18 months of 65 of these people, and looked for changes in grey matter-the brain tissue that transmits messages and helps store memories.
Eight of the 65 developed schizophrenia about two years after their first scan. Interestingly, the scans of each of these eight people revealed that changes had started happening in their grey matter before they started displaying symptoms of the disorder, the BBC explained. These changes appeared in a part of the brain involved in processing anxiety. "People who develop schizophrenia are known often to exhibit signs of raised anxiety levels up to two years before the onset of full psychosis," the BBC pointed out.
Individuals in high-risk groups have, on average, a 13-percent risk of developing schizophrenia. But if they exhibit brain changes of the type pinpointed by the researchers, their risk of developing full-blown psychosis rises to a massive 60 percent, the BBC said.
"Although there are no preventative treatments for the illness, an accurate predictive test could help researchers to assess possibilities for prevention in the future," Job told the BBC.
Jo Loughran, of the schizophrenia charity Rethink, welcomed the research. "Schizophrenia is notoriously difficult to diagnose. Therefore Rethink welcomes any new research or progress into understanding the causes of schizophrenia," she told the BBC.
H. pylori hitched ride "out of Africa"
PARIS
The bacterium that causes most kinds of stomach ulcers has been present in the human digestive tract ever since Homo sapiens ventured out of Africa some 60,000 years ago. Scientists led by Mark Achtman of the Max Planck Institute for Biology Infections in Germany compared variations in the genome of the Helicobacter pylori with those in the human genetic code.
Previous research has found that, among humans, genetic variety becomes narrower the farther the population is from East Africa. The theory for this is that, tens of thousands of years ago, as H. sapiens cautiously spread out, pioneers became progressively more isolated from the rest of the human gene pool. On a chart, the diversity thins out in waves.
Achtman's team found almost identical patterns when they analyzed the genetic variety among 769 samples of H. pylori, taken from volunteers around the world from 51 ethnic backgrounds. Crunched through a computer model, the data showed the bacteria migrated from East Africa around 58,000 years, mirroring when humans set out on their global trek. "Anatomically modern humans were already infected by H. pylori before their migrations from Africa," they report in a study published by Nature. "H. pylori has remained intimately associated with their human host populations ever since."
Under the "out of Africa" scenario, H. sapiens emerged in East Africa roughly 200,000 years ago. The breakout from Africa is variously put at between 50,000 and 70,000 years ago. However, the routes and the timeline of the great trek are poorly understood, and the breakout itself may have occurred in several waves. If H. pylori is a reliable indicator of human migration, the germ may help us to fill these knowledge gaps, the study argues.
Protein on flu virus key to preventing pandemic
WASHINGTON
A protein on the surface of the flu virus appears crucial to its ability to transmit efficiently among humans and could provide clues to preventing a pandemic. "Understanding flu transmission could assist researchers in their challenge to stop the spread of influenza, especially as concerns mount with the current avian-flu epidemic in chickens and the possibility that it will spread to humans," researchers said in Science magazine.
Experts believe the avian-flu virus H5N1 that has killed 164 people since 2003 underwent a mutation facilitating its transmission among humans. Researchers from the National Center for Infectious Diseases and the Centers for Disease Control and Prevention analyzed the hemagglutinin protein covering the surface of the 1918 influenza virus that they recreated in 2005. With "genetic-sequence similarities" to avian-influenza viruses, the 1918 virus killed at least 50 million people worldwide between 1918 and 1920.
The researchers altered two amino acids in the 1918 virus hemagglutinin giving it the configuration of the H5N1 virus, and injected it into ferrets, considered good predictors of influenza-virus transmissibility among humans. The inoculated ferrets fell severely ill, but healthy ferrets placed close enough to the sick ferrets to catch the virus remained healthy. The findings suggest that the avian-flu virus is not easily transmissible among humans unless its hemagglutinin is capable of naturally attaching itself to cells of the human respiratory system, which is not the case at present. M
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