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- - European weblog on food, health and environment
 

News - Week 49 - 2008


The Health Dangers of Fluoride


Bipolar disorder genes, pathways identified by Indiana University neuroscientists

Neuroscientists at the Indiana University School of Medicine have created the first comprehensive map of genes likely to be involved in bipolar disorder, according to research published online Nov. 21 in the American Journal of Medical Genetics. The researchers combined data from the latest large-scale international gene hunting studies for bipolar disorder with information from their own studies and have identified the best candidate genes for the illness. The methodology developed at the IU Institute of Psychiatric Research enabled Alexander B. Niculescu III, M.D., Ph.D., and his team to mine the data from the genome-wide association studies and other study results on the levels of gene activity in human blood samples and in animal models. Genes with the highest levels of prominence were determined to be the most active in contributing to the disorder. The researchers also were able to analyze how these genes work together and created a comprehensive biological model of bipolar disorder.

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Identifying blood biomarkers for mood disorders using convergent functional genomics

There are to date no clinical laboratory blood tests for mood disorders. We propose, and provide proof of principle for, a translational convergent approach to help identify and prioritize blood biomarkers of moodstate. Our preliminary studies suggest that blood biomarkers have the potential to offer an unexpectedly informative window into brain functioning and disease state. Panels of such biomarkers may serve as a basis for objective clinical laboratory tests, a longstanding Holy Grail for psychiatry. Biomarker-based tests may help with early intervention and prevention efforts, as well as monitoring response to various treatments.

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Med school discovery could lead to better cancer diagnosis, drugs

A Florida State University College of Medicine research team led by Yanchang Wang has discovered an important new layer of regulation in the cell division cycle, which could lead to a greater understanding of the way cancer begins. Wang, an assistant professor of biomedical sciences at the College of Medicine, said the findings will lead to an improved ability to diagnose cancer and could lead to the design of new drugs that kill cancer cells by inhibiting cell reproduction. His paper on the discovery has been published in the journal Proceedings of the National Academy of Sciences. "The correct timing of chromosome segregation during cell division is necessary to ensure normal, healthy growth," Wang said. "Now we have discovered a previously undetected layer of regulation in how the chromosomes separate, which helps to ensure the correct timing and decreases the potential for the formation of cancerous growth." The cell division cycle is a collection of tightly regulated events that lead to cell duplication. The most important events are the doubling of the hereditary information encoded within a set of chromosomes, and the division of that duplicated information into two daughter cells that are genetically identical to each other and the mother cell. The correct order of cell-cycle events is essential for successful cell division. Wang's article addresses the role of a particular protein enzyme, Cdc14, in ensuring that cell division events occur in exactly the right order. Defects in the regulation of the order of events can lead to cell death or the alteration of genetic information, which contributes to the formation of cancerous cells.

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Scripps research scientists identify blood component that turns bacteria virulent

Scientists from the Scripps Research Institute have discovered the key chemical that signals Bacillus anthracis, the bacterium that causes anthrax, to become lethal. This finding opens up new avenues of exploration for the development of treatments for bacterial infections. The study was published in the November 21 edition of the journal PLoS Pathogens. The Scripps Research scientists identified bicarbonate, a chemical found in all body fluids and organs that plays a major role in maintaining pH balance in cells, as providing the signal for Bacillus anthracis to unleash virulence factors. Without the presence of the bicarbonate transporter in the bloodstream, the scientists found, the bacteria do not become virulent. Scientists have known for some time that bicarbonate is implicated in many diseases, but controversy has existed about whether bicarbonate, carbon dioxide, or some combination of these two molecules are responsible for triggering bacterial pathogenesis. This study confirms, for the first time, that it is indeed bicarbonate, rather than carbon dioxide, that signals the gram-positive B. anthracis to become virulent. This finding also is significant because other pathogenic bacteria such as Streptococcus pyogenes, Escherichia coli, Borrelia burgdorferi, and Vibrio cholera have bicarbonate transport pathways similar to B. anthracis and thus are likely to have similar virulence triggering mechanisms. Gram-positive bacteria are the major culprits driving the increase of community and hospital acquired bacterial infections. The Centers for Disease Control and Prevention estimates that as many as 10 percent of all patients, or about 2 million people, contract hospital acquired infections each year. These bacteria are often resistant to multiple antibiotics, making the problem a growing public health concern and the need for new antibacterial treatment more urgent. Now, the bicarbonate transporter pathway may be investigated as a potential new target for drug intervention. "How a bacterium recognizes signals in the host that trigger pathogenesis mechanisms, and the nature of the mechanisms necessary to develop pathogenesis, remain poorly understood," said Scripps Research Associate Professor Marta Perego, Ph.D., who conducted the study with Scripps Research postdoctoral fellow Adam Wilson, Ph.D., and colleagues. "We have identified an essential component for the induction of virulence gene expression in response to host bicarbonate levels and have used this finding to learn more about the extracellular and intracellular signals controlling virulence."

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Ability to quit smoking may depend on ADHD symptoms, Columbia researchers find

Tobacco use is more prevalent and smoking cessation less likely among persons with Attention Deficit Hyperactivity Disorder (A.D.H.D.) In a study of smokers with attention deficit and hyperactivity symptoms, those who exhibited elevated hyperactivity and impulsivity, with or without inattention, showed lower quit rates after 8 weeks than those with inattention symptoms alone or those without the A.D.H.D. symptoms. The study, now available online in Nicotine and Tobacco Research, could help smokers and physicians to better tailor cessation treatment for individuals with A.D.H.D. "Greater understanding of the divergent associations that exist between the different kinds of A.D.H.D. have important public health consequences for smoking cessation and decreased tobacco-related mortality in this population," said the study's lead author Lirio Covey, Ph.D., professor of clinical psychology (in psychiatry) at Columbia University Medical Center and the New York State Psychiatric Institute. "The effect of A.D.H.D. by itself on smoking cessation has rarely been examined; the effects of the individual A.D.H.D. symptoms on smoking cessation, even less so. To our knowledge, the effects of inattention or hyperactivity at baseline as separate domains of A.D.H.D. on cessation treatment outcome have never been examined," Dr. Covey reported. During the initial, eight-week phase of a maintenance treatment study, 583 adult smokers, 43 of whom were identified with clinically significant A.D.H.D. symptom subtypes using the A.D.H.D. Current Symptom Scale, were treated with the medication buproprion (brand name Zyban®), the nicotine patch and regular cessation counseling. Compared to smokers without A.D.H.D., smokers of both A.D.H.D. subtypes combined showed lower abstinence rates throughout the study.

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Risk Factors and Event Rates in Patients With Atherothrombotic Disease in Germany

The traditional risk factors are common in patients with coronary heart disease, cerebrovascular disease (stroke and/or transient ischemic attack), or peripheral arterial occlusive disease. Many patients with these conditions or associated risk factors are not treated according to current guidelines. This may explain, at least in part, the high rates of cardiovascular events observed after one year.

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Hairspray is linked to common genital birth defect, says study

Women who are exposed to hairspray in the workplace during pregnancy have more than double the risk of having a son with the genital birth defect hypospadias, according to a new study published today in the journal Environmental Health Perspectives.The study is the first to show a significant link between hairspray and hypospadias, one of the most common birth defects of the male genitalia, where the urinary opening is displaced to the underside of the penis. The causes of the condition are poorly understood.

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Mechanisms of cardiovascular disease and cancer give clues to new therapies

Cardiovascular conditions leading to heart attacks and strokes are treated quite separately from common cancers of the prostate, breast or lung, but now turn out to involve some of the same critical mechanisms at the molecular level. This in turn provides clues to more effective therapies for both cancer and cardiovascular diseases, but requires researchers in these distinct fields to come together. The seeds were sown for closer cooperation between these two groups at a recent workshop organised by the European Science Foundation (ESF), which also highlighted the striking progress already made in understanding key common mechanisms underlying both disease categories.

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Household Exposure to Toxic Chemicals Lurks Unrecognized, Researchers Find

Although Americans are becoming increasingly aware of toxic chemical exposure from everyday household products like bisphenol A in some baby bottles and lead in some toys, women do not readily connect typical household products with personal chemical exposure and related adverse health effects, according to research from the December issue of the Journal of Health and Social Behavior. Brown University sociologist Phil Brown is a co-author of the study. “People more readily equate pollution with large-scale contamination and environmental disasters, yet the products and activities that form the backdrop to our everyday lives — electronics, cleaners, beauty products, food packaging — are a significant source of daily personal chemical exposure that accumulates over time,” said sociologist Rebecca Gasior Altman, lead author of the study, “Pollution Comes Home and Gets Personal - Women’s Experience of Household Chemical Exposure.” Altman received a Ph.D. from Brown in 2008.

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Red, red wine - How it fights Alzheimer's

Scientists call it the "French paradox" — a society that, despite consuming food high in cholesterol and saturated fats, has long had low death rates from heart disease. Research has suggested it is the red wine consumed with all that fatty food that may be beneficial — and not only for cardiovascular health but in warding off certain tumors and even Alzheimer's disease. Now, Alzheimer's researchers at UCLA, in collaboration with Mt. Sinai School of Medicine in New York, have discovered how red wine may reduce the incidence of the disease. Reporting in the Nov. 21 issue of the Journal of Biological Chemistry, David Teplow, a UCLA professor of neurology, and colleagues show how naturally occurring compounds in red wine called polyphenols block the formation of proteins that build the toxic plaques thought to destroy brain cells, and further, how they reduce the toxicity of existing plaques, thus reducing cognitive deterioration. Polyphenols comprise a chemical class with more than 8,000 members, many of which are found in high concentrations in wine, tea, nuts, berries, cocoa and various plants. Past research has suggested that such polyphenols may inhibit or prevent the buildup of toxic fibers composed primarily of two proteins — Aß40 and Aß42 — that deposit in the brain and form the plaques which have long been associated with Alzheimer's. Until now, however, no one understood the mechanics of how polyphenols worked.

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Scientists have invented a machine that sorts pomegranate seeds

A team of investigators from Valencia has developed a machine that separates automatically the seeds from the rind and pith of the pomegranate. The mechanism uses a computer vision system to distinguish and sort the different parts of this fruit, according to a study published on-line by the Journal of Food Engineering.The difficulty in peeling pomegranates and separating out the seeds disheartens many consumers when they eat the fruit of the pomegranate (Punica granatum). Now a Spanish invention enables this food to be de-seeded automatically. “This involves a machine that discards the non edible parts and sorts the seeds according to their quality”, José Blasco explains to SINC and who is from the Institute of Agrarian Research in Valencia (Instituto Valenciano de Investigaciones Agrarias [IVIA]), where they have carried out research. The results of the research have been published recently in the Journal of Food Engineering, and the patent has already been requested.

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Does hormone treatment predispose patients to breast cancer?

Breast cancer, the leading cause of death among women in France, is the most commonly occurring cancer in women. Sporadic breast cancer, which is non-hereditary, turns out to be the most widespread, representing 85 to 90% of all cases, but remains the least well-known. Researchers at CNRS and CEA (1), working with a team from Hôpital Saint-Louis (2), have just discovered the cause of 50% of sporadic breast cancers. The results should also explain epidemiological studies which suggest that hormone treatment predisposes patients to breast cancer. The work is published in 'Cancer Research'.More than four out of five breast cancers are not related to hereditary factors. These cancers, which are called sporadic, are due to causes which were until recently considered complex and poorly understood. On the other hand, hereditary forms of cancer, which represent only 10 to 15% of breast cancers, have for years been the subjects of studies, work which has resulted in the identification of ten genes whose mutation increases the risk of cancer in an individual. Among these genes, nine are involved in the DNA damage response system, which is the collection of cell mechanisms that optimize the repair of DNA. The tenth gene codes for a protein which inhibits the action of the AKT1 enzyme. And among these ten genes, two are responsible for 50% of hereditary breast cancers: BRCA1 and BRCA2. Researchers from the "Radiobiologie moléculaire et cellulaire" (CNRS / CEA) lab took these data on hereditary cancers as the starting point for their research into non-hereditary forms.

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Pregnancy study finds strong association between two antidepressants and heart anomalies

Women who took the antidepressant fluoxetine during the first three months of pregnancy gave birth to four times as many babies with heart problems as women who did not and the levels were three times higher in women taking paroxetine. Although some of the conditions were serious, others were not severe and resolved themselves without the need for medical intervention, according to a three-country study in the November issue of the British Journal of Clinical Pharmacology. Researchers have advised women taking the drugs to continue unless they are advised to stop by their doctor or consultant. But they are being urged to give up smoking, as the study also found that more than ten cigarettes a day was associated with a five-fold increase in babies with major heart problems. The team has also suggested that women on fluoxetine should be given a foetal echocardiogram in their second trimester to diagnose possible heart anomalies. International researchers from Israel, Italy and Germany followed the pregnancies of 2,191 women - 410 who had taken paroxetine during pregnancy, 314 who had taken fluoxetine and 1,467 controls who hadn't taken either of the drugs. "After we excluded genetic and cytogenic anomalies, we found a higher rate of major heart anomalies in the women who had been taking the antidepressants" says lead author Professor Asher Ornoy from the Israeli Teratology Information Service in Jerusalem, Israel. "Further analysis showed a strong association between major heart anomalies and taking fluoxetine in the first trimester. Women who smoked more than 10 cigarettes a day also had more babies with heart anomalies."

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Mineral oil contamination in humans - A health problem?

From a quantitative standpoint, mineral oil is probably the largest contaminant of our body. That this contaminant can be tolerated without health concerns in humans has not been proven convincingly. The current Editorial of the European Journal of Lipid Science and Technology reflects on this and concludes that this proof either has to be provided or we have to take measures to reduce our exposure – from all sources, including cosmetics, pharmaceuticals and the environmental contamination. In the Ukraine recently around 100,000 tonnes of sunflower oil were contaminated with mineral oil at concentrations often above 1000 mg/kg. Much of the contaminated oil was withdrawn, but there are products on the market which were produced before this contamination was detected; and this autumn there are still several 10,000 tonnes of contaminated oil in the Ukraine and other parts of the world. To protect consumers, a broad analytical campaign was initiated throughout Europe. The European Commission decided to apply a legal limit of 50 mg/kg to the mineral paraffins in Ukrainian sunflower oil and in September 2008 it organized a workshop together with the Official Food Control Authority of Zurich, Switzerland, to promote this campaign.

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Smoking, teens and their parents - New research

A new study found that adolescents were at the greatest risk of smoking when their parents began smoking at an early age and the parents' smoking quickly reached high levels and persisted over time. The study, published in the November issue of Health Psychology, draws from the long-running Indiana University Smoking Survey and builds on previous research that suggests smoking behavior is influenced by both genetics and the environment. "This particular study focuses more on the genetic influence in the specific case of a parent's smoking behavior impacting a teenage son or daughter's smoking," said Jon Macy, project director of the IU Smoking Survey in the Department of Psychological and Brain Sciences. "The study findings suggest that the characteristics of early onset and high levels of long-term smoking are great candidates for behavioral and molecular genetic studies of the causes of smoking and how smoking behavior is passed from one generation to the next. "Of course, environmental influences on adolescents such as parenting practices, availability of cigarettes in the home, and parents' attitudes about smoking are equally as important and can be addressed with effective public health interventions including family-based smoking prevention programs." Previous studies, many of which relied on parents' current smoking status only, offered mixed results about whether parental smoking is predictive of adolescent smoking. The current study, however, used longitudinal data to identify more detailed information about parental smoking behaviors such as amount of smoking, speed of escalation, peak of use and persistence over time.

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Stomach ulcer bug causes bad breath

Bacteria that cause stomach ulcers and cancer could also be giving us bad breath, according to research published in the December issue of the Journal of Medical Microbiology. For the first time, scientists have found Helicobacter pylori living in the mouths of people who are not showing signs of stomach disease. The mouth is home to over 600 different species of bacteria, some of which can cause disease. Helicobacter pylori has recently been shown to cause stomach ulcers and is also responsible for a large proportion of gastric cancers. Scientists estimate that between 20 and 80 % of people in the developed world and over 90 % of people in the developing world carry the bacterium. "Recently, scientists discovered that H. pylori can live in the mouth," said Dr Nao Suzuki from Fukuoka Dental College in Fukuoka, Japan. "We wanted to determine whether the bacteria can cause bad breath, so we tested patients complaining of halitosis for the presence of H. pylori." The researchers found the bacteria in the mouths of 21 out of 326 Japanese people with halitosis (6.4%). In these people, the concentration of a bad breath gas and the level of oral disease was significantly higher. In patients with periodontal (gum) disease, 16 of 102 people (15.7%) had H. pylori in their mouths.

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Scientists discover 21st century plague

Bacteria that can cause serious heart disease in humans are being spread by rat fleas, sparking concern that the infections could become a bigger problem in humans. Research published in the December issue of the Journal of Medical Microbiology suggests that brown rats, the biggest and most common rats in Europe, may now be carrying the bacteria. Since the early 1990s, more than 20 species of Bartonella bacteria have been discovered. They are considered to be emerging zoonotic pathogens, because they can cause serious illness in humans worldwide from heart disease to infection of the spleen and nervous system. "A new species called Bartonella rochalimae was recently discovered in a patient with an enlarged spleen who had travelled to South America," said Professor Chao-Chin Chang from the National Chung Hsing University in Taiwan. "This event raised concern that it could be a newly emerged zoonotic pathogen. Therefore, we decided to investigate further to understand if rodents living close to human environment could carry this bacteria." Scientists have found that rodents carry several pathogenic species of Bartonella, such as B. elizabethae, which can cause endocarditis and B. grahamii, which was found to cause neuroretinitis in humans. Although scientists are unsure about the main route of transmission, these infections are most likely to be spread by fleas. Ctenophthalmus nobilis, a flea that lives on bank voles, was shown to transmit different species of Bartonella bacteria. These pathogens have also been found in fleas that live on gerbils, cotton rats and brown rats.

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New research helps explain genetics of Parkinson's disease

A new study by Narendra et al. suggests that Parkin, the product of the Parkinson's disease-related gene Park2, prompts neuronal survival by clearing the cell of its damaged mitochondria. "[This is] an exciting new discovery that links the fields of mitochondrial quality control and the genetics of Parkinson's disease (PD)," writes Heidi McBride of the University of Ottawa Heart Institute. "…This work significantly increases our understanding of PD and provides a new framework for the development of therapeutic interventions." The study, as well as McBride's commentary, will appear in the December 1, 2008 print issue of the Journal of Cell Biology (JCB). Both articles will be published online Monday, November 24 (www.jcb.org). Loss-of-function mutations in the gene Park2, which encodes an E3 ubiquitin ligase (Parkin), are implicated in half the cases of recessive familial early-onset Parkinson's disease. Several lines of evidence suggest that Parkin loss is associated with mitochondrial dysfunction, but exactly how was unknown. To learn more about Parkin's role in cells, Narendra et al. examined the protein's subcellular location. They found that Parkin was present in the cytoplasm of most cells, but translocated to mitochondria in cells that had undergone mitochondrial damage such as membrane depolarization.

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Ultrasound waves aid in rapid treatment of DVT

The use of ultrasound waves for deep vein thrombosis may help dissolve blood clots in less time than using clot-busting drugs alone, according to researchers at Emory University. The study will be presented Sunday, Nov. 23, 2008 at the annual VEITHsymposium in New York City.

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Scripps research team defines new painkilling chemical pathway

Marijuana can be an effective painkiller, but social issues and unhealthy smoke inhalation complicate its use. As a result, researchers have focused great attention on understanding the biochemical system involved so they might manipulate it by other means. Toward that end, a Scripps Research Institute group has definitively identified a chemical pathway that, in mice, imitates marijuana's painkilling effect. The work could enable the development of new pain treatments.

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Scientists Discover New Cause of Fatal Brain Injury from Acute Viral Meningitis

What was once thought to be the culprit responsible for fatal brain damage in acute viral meningitis has now been found to be only an accomplice, say researchers at The Scripps Research Institute. In a November 16 advance, online publication of the journal Nature, the researchers say their discovery revamps common beliefs about how such potentially lethal infections may be ravaging the brain and suggests the possibility of new treatments."This is a paradigm shift in how we think about some forms of meningitis and possibly other infections," says the study's lead investigator, Dorian B. McGavern, an associate professor in the Department of Immunology at Scripps Research. "What we thought were the killers are actually immune cells that recruit other accessory cells that then drive the disease. If we can find ways to block recruitment of the cells that actually do the damage into the brain, we may be able to limit the impact of the virus."Meningitis occurs when the membrane (the meninges) that covers and protects the spinal cord and brain become inflamed, usually due to a bacterial or viral infection. The condition is considered a medical emergency because it can lead to an inflammatory response that results in brain swelling, seizures, blood clotting, epilepsy, or other complications, sometimes resulting in death. Many viruses can cause meningitis.

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'Wiring' in the Brain Influences Personality

Connections between the nerves is one factor determining whether a person welcomes a change or tends to avoid anything new Some people are constantly seeking a new kick; some prefer to stick to tried and tested things. Which group you belong to seems to be connected, inter alia, with the 'wiring' of specific centres of the brain. This was discovered by scientists at the University of Bonn using a new method. Even how much acceptance people seek is apparently also determined by nerve fibres in the brain. The study will appear in the next issue of the journal Nature Neuroscience (doi: 10.1038/nn.2228).

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Melatonin may save eyesight in inflammatory disease

Current research suggests that melatonin therapy may help treat uveitis, a common inflammatory eye disease. The related report by Sande et al., "Therapeutic Effect of Melatonin in Experimental Uveitis," appears in the December issue of The American Journal of Pathology. People with uveitis develop sudden redness and pain in their eyes, and their vision rapidly deteriorates. Untreated, uveitis can lead to permanent vision loss, accounting for an estimated 10-15% of cases of blindness in the US. Uveitis has a wide variety of causes, including eye injury, cancer, infection, and autoimmune diseases such as rheumatoid arthritis and multiple sclerosis. There is currently no optimal treatment for uveitis. Corticoid steroid eye drops are often used; however, long-term corticoid use has many negative side effects, including the possible development of glaucoma. Researchers lead by Dr. Ruth Rosenstein of The University of Buenos Aires and The National Research Council (CONICET) hypothesized that melatonin, which regulates sleep/wake cycles and reduces jet lag, may be able to prevent the ocular inflammation in uveitis. They found in an experimental model of uveitis that levels of two factors that contribute to inflammation, TNF? and NF?B, were reduced with melatonin treatment. Importantly, melatonin treatment also decreased the appearance of clinical symptoms of uveitis such as inflammation, blood vessel expansion and cataract, and protected the blood-ocular barrier integrity.

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Inherited genetic cause, possible treatment found for complex lung disorder

A tale of two sisters has helped researchers solve a medical mystery and discover a familial genetic mutation that causes an inherited form of the lung disease pulmonary alveolar proteinosis. Reporting their results in the Nov. 24 Journal of Experimental Medicine, a research team led by Cincinnati Children's Hospital Medical Center also points to the possibility of an inhaled therapy to overcome a chain of molecular events that lead to PAP.

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Pain is in the eyes of the beholder

By manipulating the appearance of a chronically achy hand, researchers have found they could increase or decrease the pain and swelling in patients moving their symptomatic limbs. The findings -- reported in the Nov. 25 issue of Current Biology, a Cell Press publication -- reveal a profound top-down effect of body image on body tissues, according to the researchers.

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Electronic health records may lower malpractice settlements

Use of electronic health records (EHRs) may help reduce paid malpractice settlements for physicians, according to a new study. The study, which appeared in the November 24 issue of Archives of Internal Medicine, showed a trend toward lower paid malpractice claims for physicians who are active users of EHR technology. This study was based at the Department of Ambulatory Care and Prevention of Harvard Medical School and Harvard Pilgrim Health Care. Health care policymakers have touted the benefits of EHRs, which include preserving and documenting patient health care data, reducing medication errors, improving efficiency of care, and allowing surveillance and monitoring of care for research and quality improvement."There is broad consensus that electronic health records are an essential foundation for the delivery of high quality care. As electronic health record adoption proceeds as a national health policy objective, some have wondered whether EHRs can help to prevent medical malpractice claims," says Assistant Professor Steven Simon, senior author on the paper. The study examined survey responses from 1140 practicing physicians in Massachusetts during 2005 concerning their demographic characteristics and the length and extent of their EHR use. The physicians' malpractice history was accessed using publicly available data from the Commonwealth of Massachusetts' Board of Registration in Medicine. The study team compared the presence or absence of malpractice claims among physicians with and without EHRs, including only claims that had been settled and paid.

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Tiny protein provokes healthy bonding between cells

In human relationships, a certain "spark" often governs whether we prefer one person to another. Critical first impressions can occur within seconds. Researchers have found that cell-to-cell "friendships" operate in much the same way and that dysfunctional bonding is linked to the spread of cancer.

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Transporting Broiler Chickens Could Spread Antibiotic-Resistant Organisms

Researchers at the Johns Hopkins Bloomberg School of Public Health have found evidence of a novel pathway for potential human exposure to antibiotic-resistant bacteria from intensively raised poultry—driving behind the trucks transporting broiler chickens from farm to slaughterhouse. A study by the Hopkins researchers found increased levels of pathogenic bacteria, both susceptible and drug-resistant, on surfaces and in the air inside cars traveling behind trucks that carry broiler chickens. The study is the first to look at exposure to antibiotic-resistant bacteria from the transportation of poultry. The findings are published in the first issue of the Journal of Infection and Public Health.

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Carnegie Mellon Scientists Offer Explanation for "Face Blindness;" New Research Provides Insight Into Intriguing Disorder

For the first time, scientists have been able to map the disruption in neural circuitry of people suffering from congenital prosopagnosia, sometimes known as face blindness, and have been able to offer a biological explanation for this intriguing disorder. Currently thought to affect roughly two percent of the population, congenital prosopagnosia manifests as the lifelong failure to recognize faces in the absence of obvious neurological damage, and in individuals with intact vision and intelligence. Studying subjects aged 33 to 72 using diffusion tensor imaging and tractography, the team of scientists from Carnegie Mellon University, Kings College in London and Ben-Gurion University in Israel were able to show that, unlike that of normal brains, there was a reduction in the integrity of the white matter tracts in the brains of individuals with congenital prosopagnosic. Moreover, the extent of the reduced white matter circuitry was related to the severity of the behavioral impairment.

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Understanding how oxidative stress impairs endothelial progenitor cell function

Researchers from the Herman B Wells Center for Pediatric Research at the Indiana University School of Medicine and Riley Hospital for Children report in the Nov. 2008 issue of the journal Antioxidants & Redox Signaling that a review of the scientific literature reveals that how endothelial progenitor cells respond to oxidantive stress appears to be a critical determinant in maintaining a healthy cardiovascular system.

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Proteins strangle cell during division

A Swedish research group, partly financed by NWO, has discovered a new mechanism for cell division in a microorganism found in extremely hot and acidic conditions. The results of the research offer insights into evolution, but also into the functioning of the human body. The research has been recently published in PNAS, the magazine of the American National Academy of Sciences. Thijs Ettema, member of the research group, received a Rubicon grant from NWO in 2006 to gain experience abroad.

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Children's Hospital scientists achieve repair of injured heart muscle in lab tests of stem cells

Researchers at Children's Hospital of Pittsburgh of UPMC have been able to effectively repair damaged heart muscle in an animal model using a novel population of stem cells they discovered that is derived from human skeletal muscle tissue.

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Feed a cold, feed a fever - Research shows calorie cut makes it harder to fight flu

Dieters or those who consume fewer calories during flu season could have a harder time fighting off the flu virus, according to research by Michigan State University nutritional immunology professor Elizabeth Gardner. In a study published in the Nov. issue of the Journal of Nutrition, Gardner showed that mice with a calorie-restricted diet were more likely to die during the first few days of infection than mice with a normal diet.

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Presence of gum disease may help dentists and physicians identify risk for cardiovascular disease

Individuals reporting a history of periodontal disease were more likely to have increased levels of inflammation, a risk factor for heart disease, compared to those who reported no history of periodontal disease, according to an American Journal of Cardiology report available online today. Led by investigators from Columbia University Medical Center and NewYork-Presbyterian Hospital, the findings suggest persons with increased levels of inflammatory markers associated with a higher risk of cardiovascular disease might be identified by asking about oral health history.

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Cancer cell 'bodyguard' turned into killer

If you're a cancer cell, you want a protein called Bcl-2 on your side because it decides if you live or die. It's usually a trusted bodyguard, protecting cancer cells from programmed death and allowing them to grow and form tumors. But sometimes it turns into their assassin. Scientists knew it happened, but they didn't know how to actually cause such a betrayal. Now they do and it may lead to the development of new cancer-fighting drugs.

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Scientists shed light on evolution of gene regulation

Scientists at Penn State have shed light on some of the processes that regulate genes and on the evolution of the DNA regions that regulate genes. The team focused on regulatory regions that, when bound to a certain protein, are thought to turn on genes that play an important role in the development of red blood cells. The research results could help in the development of drugs to treat sickle-cell anemia and other blood disorders.

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Potassium loss from blood pressure drugs may explain higher risk of adult diabetes

Johns Hopkins researchers have discovered that a drop in blood potassium levels caused by diuretics commonly prescribed for high blood pressure could be the reason why people on those drugs are at risk for developing type 2 diabetes. The drugs helpfully accelerate loss of fluids, but also deplete important chemicals, including potassium, so that those who take them are generally advised to eat bananas and other potassium-rich foods to counteract the effect.

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Mammals can be stimulated to regrow damaged inner retina nerve cells

For the first time the mammalian retina has now shown the capacity to regenerate new neurons after damage. This research in mice shows that at least some types of retinal damage can be repaired. The loss of neurons in the retina in people in conditions like glaucoma or macular degeneration leads to visual loss and blindness. This new research shows there might someday be a way to restore vision in people with these conditions.

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Adult brain neurons can remodel connections

Overturning a century of prevailing thought, scientists are finding that neurons in the adult brain can remodel their connections. In work reported in the Nov. 24 online edition of the Proceedings of the National Academy of Sciences (PNAS), Elly Nedivi, associate professor of neurobiology at the Picower Institute for Learning and Memory, and colleagues found that a type of neuron implicated in autism spectrum disorders remodels itself in a strip of brain tissue only as thick as four sheets of tissue paper at the upper border of cortical layer 2.

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A scientific breakthrough on the control of the bad cholesterol

A study performed by the team of Dr. Nabil G. Seidah, director of the Biochemical Neuroendocrinology Research Unit at the IRCM, shows for the very first time that the degradation by PCSK9 of the LDLR receptor, which is responsible for removing the bad cholesterol from the bloodstream, may be inhibited by a third protein, annexin A2. This major study was published on Nov. 14 in the Journal of Biological Chemistry.

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How safe is fructose for persons with or without diabetes?

Fructose causes metabolic syndrome because of its unique metabolism that results in intracellular ATP depletion, uric acid generation, endothelial dysfunction, oxidative stress, and lipogenesis. An understanding of the mechanisms clarifies the variability of responses reported in the literature. Rodent studies are often criticized, because they typically use large supraphysiological doses (60%). However, rodents are resistant to fructose because they synthesize vitamin C, have low uric acid concentrations, and have good endothelial function. If uric acid concentrations are raised or if low doses are prolonged , then insulin resistance is readily induced. The variability in human studies can also be explained by a clarification of fructose metabolism. For example, fructose uniquely up-regulates its own transporter (Glut5) and metabolism (fructokinase) and, thereby, the more fructose one eats, the more sensitive one becomes to its effects. This is a potential explanation for the fact that obese persons appear to be more sensitive to the lipogenic effects of acute fructose ingestion than are nonobese persons.

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Selenium may slow march of AIDS

Increasing the production of naturally occurring proteins that contain selenium in human blood cells slows down multiplication of the AIDS virus, according to biochemists. "We have found that increasing the expression of proteins that contain selenium negatively affects the replication of HIV," said K. Sandeep Prabhu, Penn State assistant professor of immunology and molecular toxicology. "Our results suggest a reduction in viral replication by at least 10-fold." Selenium is a micronutrient that the body needs to maintain normal metabolism. Unlike other nutrients, which bind to certain proteins and modulate the protein's activity, selenium gets incorporated into proteins in the form of an amino acid called selenocysteine. These proteins – selenoproteins – are especially important in reducing the stress caused by an infection, thereby slowing its spread.

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St. Jude identifies genomic causes of a certain type of leukemia relapse

Scientists at St. Jude Children's Research Hospital have identified distinctive genetic changes in the cancer cells of children with acute lymphoblastic leukemia (ALL) that cause relapse. The finding offers a pathway to designing treatments for ALL relapse in children and, ultimately, in adults. The most common childhood cancer, ALL affects thousands of children annually in the United States. Although more than 80 percent of ALL cases are cured, relapse is a significant problem, with only 30 percent of children with relapsed ALL surviving. Previous studies had found some evidence for genetic differences between the cancer cells of ALL patients at initial diagnosis and those who relapsed. That information was limited, and there had never been a broad comparison of the entire genomes of ALL at initial diagnosis and at subsequent relapse. In the study that appears in the Nov. 28, 2008, issue of the journal Science, St. Jude researchers compared the genomes of the cancer cells of 61 childhood ALL patients when they were initially diagnosed and after they had relapsed. The investigators used millions of genetic markers—characteristic genetic variations called single nucleotide polymorphisms—as guideposts to pinpoint genetic changes characteristic of relapsed cells. Using these genetic markers, the researchers analyzed all of the cells' chromosomes to look for genetic changes called copy number abnormalities specific to relapsed cells. These changes are considered a major type of damaging gene alterations in ALL. "In more than 90 percent of the cases, we found differences in the genetic alterations present at the time of diagnosis and at the time of relapse," said Charles Mullighan, M.D., Ph.D., assistant member in the St. Jude Department of Pathology and the paper's first author. "Examining the new changes that are arising at relapse tells us a lot about the individual genetic lesions that might confer resistance to treatment and be responsible for relapse." According to the researchers, the relapse-related genetic changes commonly disrupted the machinery by which white blood cells called B cells mature and proliferate. Importantly, the relapse-related genetic changes only infrequently involved genes directly regulating the responsiveness to anti-cancer drugs. The analysis also indicated that in most cases, the cancer cells responsible for relapse were related to those that originally gave rise to the cancer. Those relapse cells were present at low levels at diagnosis, the scientists' analysis indicated. However, in a few cases, the relapse cells evolved from genetically distinct cells, indicating that the relapsed leukemia was actually an entirely new cancer.

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A novel target for therapeutics against Staph infection

Researchers at the Texas A&M Health Science Center Institute of Biosciences and Technology, and the University of Edinburgh have uncovered how a bacterial pathogen interacts with the blood coagulation protein fibrinogen to cause methicillin-resistant Staphylococcus aureus (MRSA) infections, a finding that could aid in developing therapeutics against the potentially deadly disease. Their work appears November 28 in the open-access journal PLoS Pathogens. Once occurring more commonly in healthcare facilities, but now affecting segments of the general population, MRSA is a bacterial pathogen responsible for a range of diseases from mild skin infection to life-threatening sepsis. Even with antibiotics, these infections can still be fatal. Senior author Magnus Höök, Ph.D. and his colleagues carried out biochemical and structural studies to determine the binding mechanism of clumping factor A (ClfA), a surface protein that plays an important role in the pathogenesis of S. aureus. The group found that ClfA binds to the blood-clotting protein fibrinogen (Fg) at a site that is also responsible for inducing platelet activation and thrombosis (clot inside a blood vessel). The results show significant structural differences in how staphylococcal and platelet receptor proteins recognize fibrinogen. By exploiting this difference in recognition, the researchers show that agents could be designed that inhibit the ClfA–Fg interaction but do not interfere with the interaction of Fg with the platelet integrin, therefore avoiding unwanted side effects on the circulatory system.

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Experimental TB drug explodes bacteria from the inside out

An international team of biochemists has discovered how an experimental drug unleashes its destructive force inside the bacteria that cause tuberculosis. The finding could help scientists develop ways to treat dormant TB infections, and suggests a strategy for drug development against other bacteria as well.

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Master gene plays key role in blood sugar levels

When mice that lack steroid receptor-2, a master regulator gene called a coactivator, fast for a day, their blood sugar levels plummet. If they go another day without food, they will die. The severity of the hypoglycemia was unexpected, said Dr. Bert W. O'Malley, chair of molecular and cellular biology at Baylor College of Medicine and senior author of the report on the study that appears in the current issue of the journal Science.

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Molecular Partnership Controls Daily Rhythms, Body Metabolism, According to Penn Study

A research team led by Mitchell Lazar, MD, PhD, Director of the Institute for Diabetes, Obesity, and Metabolism at the University of Pennsylvania School of Medicine, has discovered a key molecular partnership that coordinates body rhythms and metabolism. Lazar and his colleagues, including the study’s first author, Penn Veterinary Medicine doctoral student Theresa Alenghat, studied a protein called NCoR that modulates the body’s responses to metabolic hormones. They engineered a mutation into mice that prevents NCoR from working with an enzyme that is normally its partner, HDAC3. These animals showed changes in the expression f clock and metabolic genes, and were leaner, more sensitive to insulin, and on different sleep-wake cycles than controls. The role of the NCoR-HDAC3 partnership in regulating the body’s internal clock was previously unknown. HDAC3 is an enzyme that affects gene expression by binding to receptors in the cell nucleus to affect genes' activity, but not by directly changing DNA. The findings suggest that HDAC via NCoR controls the body’s internal clock, and therefore metabolism, through this epigenetic change. Their findings are reported in this week’s issue of Nature. “In the fight against the obesity and diabetes epidemics, disruption of NCoR and its enzyme partner, might be a valuable new weapon,” says Lazar.

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Eye Divergence in Children Triples Risk of Mental Illness

Children whose eyes are misaligned and point outward are at significantly increased risk of developing mental illness by early adulthood, according to findings of a Mayo Clinic study published this month in a Pediatrics, the official journal of the American Academy of Pediatrics. The retrospective study examined the medical records of 407 patients with strabismus (misaligned eyes) and compared them with records of children matched for age and sex but with normal eye alignment. Children with eyes that diverged (exotropia) were three times more likely to develop a psychiatric disorder than were the control subjects, while those with inward deviating eyes (esotropia) showed no increase in the incidence of mental illnesses. Brian Mohney, M.D., the Mayo Clinic pediatric ophthalmologist who led the study, says the results can help alert physicians to potential problems in their pediatric patients. "Pediatricians and family practice physicians who see children with strabismus should be aware of the increased risk of mental illness," says Dr. Mohney. "They can hopefully be alert to the earliest signs of psychiatric problems in patients with exotropia, so they can consider having them seen by a psychologist or psychiatrist."

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Route to obesity passes through tongue

Obesity gradually numbs the taste sensation of rats to sweet foods and drives them to consume larger and ever-sweeter meals, according to neuroscientists. Findings from the Penn State study could uncover a critical link between taste and body weight, and reveal how flab hooks the brain on sugary food. "When you have a reduced sensitivity to palatable foods, you tend to consume it in higher amounts," said Andras Hajnal, associate professor of neural and behavioral sciences at Penn State College of Medicine. "It is a vicious circle." Previous studies have suggested that obese persons are less sensitive to sweet taste and crave sweet foods more than lean people. However, little is known about the specific differences between obese and lean individuals in their sense of taste and the pleasure they derive from sweet foods. Hajnal and his Penn State colleague Peter Kovacs, a post-doctoral fellow, investigated these differences by studying the taste responses of two strains -- OLETF and LETO rats. Compared to the lean and healthy LETO rats, the taste responses in OLETF rats mirror those in obese humans. These rats have normal body weight at first, but they tend to chronically overeat due to a missing satiety signal, become obese and develop diabetes. The obese rats also show an increased preference for sweet foods and also are willing to work harder to obtain sweet solutions as a reward for their learning. "When you have excess body weight, the brain is supposed to tell you not to eat more, or not choose high caloric meals" said Hajnal. "But this control apparently fails and thus the obesity epidemic is rising, and we want to find out how the sense of taste drives up food intake."The researchers implanted electrodes in the rodents' brains to record the firing of nerve cells when the rats' tongues were exposed to various tastes -- salt, citric acid, plain water and six different concentrations of sucrose.

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Vitamin K linked to insulin resistance in older men

A Tufts University study of 355 non-diabetic elderly men and women found men who took a vitamin K supplement had less progression of insulin resistance over a period of three years compared to men not receiving vitamin K. Vitamin K did not appear to protect supplemented women from age-related increases in insulin resistance.

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Nitric oxide can alter brain function

Research from the Medical Research Council (MRC) Toxicology Unit at the University of Leicester shows that nitric oxide (NO) can change the computational ability of the brain. This finding has implications for the treatment of neurodegenerative diseases such as Alzheimer’s Disease and our understanding of brain function more generally. The research is led by Professor Ian Forsythe and is reported in the journal Neuron on 26th November. Professor Forsythe, of the MRC Toxicology Unit, explains: “It is well known that nerve cells communicate via the synapse – the site at which chemical messengers (neurotransmitters such as acetylcholine or glutamate) are packaged and then released under tight control to influence their neighbours.“Nitric oxide is a chemical messenger which cannot be stored and can rapidly diffuse across cell membranes to act at remote sites (in contrast to conventional neurotransmitters which cannot pass across cell membranes). “It is broadly localized in the central nervous system, where it influences synaptic transmission and contributes to learning and memory mechanisms. However, because it is normally released in such minute quantities and is so labile, it is very difficult to study. “We have exploited an in vitro preparation of a giant synapse -called the calyx of Held, developed here at the University of Leicester in the 1990s- and its target in the auditory pathway to explore nitric oxide signalling in the brain.

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CSHL scientists show how a protein that determines cell polarity prevents breast cancer

A team of scientists at Cold Spring Harbor Laboratory has found that a protein called Scribble, originally discovered as a cell-shape regulator in fruit flies and worms, is an important regulator of breast cancer. They report that Scribble normally directs breast epithelial cells to form the structures that give breast tissue its shape and thereby resist cancer formation. When Scribble stops functioning, the tissue loses its shape and cancers ensue.

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Scientists at CSHL uncover new RNA processing mechanism and a class of previously unknown small RNAs

A very small fraction of our genetic material--about 2%-- performs the crucial task scientists once thought was the sole purpose of the genome: to serve as a blueprint for the production of proteins, the molecules that make cells work and sustain life. This 2% of human DNA is converted into intermediary molecules called RNAs, which in turn carry instructions within cells for protein manufacture.

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Baffling chronic pain linked to rewiring of brain

Scientists peered at the brains of people with a baffling chronic pain condition and discovered something surprising. Their brains looked like an inept cable guy had changed the hookups, rewiring the areas related to emotion, pain perception and the temperature of their skin. The new finding by scientists at Northwestern University's Feinberg School of Medicine, begins to explain a mysterious condition that the medical community had doubted was real. The people whose brains were examined have a chronic pain condition called complex region pain syndrome (CRPS.) It's a pernicious and nasty condition that usually begins with an injury causing significant damage to the hand or the foot. For the majority of people, the pain from the injury disappears once the limb is healed. But for 5 percent of the patients, the pain rages on long past the healing, sometimes for the rest of people's lives. About 200,00 people in the U.S. have this condition. In a hand injury, for example, the pain may radiate from the initial injury site and spread to the whole arm or even the entire body. People also experience changes in skin color to blue or red as well as skin temperature (hotter at first, then becoming colder as the condition turns chronic.) Their immune system also shifts into overdrive, indicated by a hike in blood immune markers.The changes in the brain take place in the network of tiny, white "cables" that dispatch messages between the neurons. This is called the brain's white matter. Several years ago, Northwestern researchers discovered chronic pain caused the regions in the brain that contain the neurons -- called gray matter because of it looks gray -- to atrophy.

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Molecule shuts down food intake and turns on 'siesta mode'

Researchers have identified a molecule that tells your brain your stomach is full – signaling that it's time to say no to a second piece of pumpkin pie and push back from the Thanksgiving table. In studies with mice and rats, researchers have found that a chemical messenger called NAPE is made in the small intestine after the animals ate a greasy meal. After eating, NAPE – N-acylphosphatidylethanolamine, a mouthful in itself -- enters the blood and travels to the brain, where it quashes hunger signals. Rats treated with extra NAPE for five days ate less and lost weight, hinting that studying NAPE could help researchers design better appetite suppressants or obesity drugs. Howard Hughes Medical Institute investigator Gerald Shulman at Yale School of Medicine led the research team, which reported its findings in the November 26, 2008, issue of the journal Cell. Shulman's research group is well known for its work on understanding how insulin resistance develops and leads to diabetes. In the course of that research, his team developed a sensitive system to identify and measure lipids in tissue samples. After seeing the power of that system in his diabetes research, Shulman was eager to see if it might also be applied to understanding obesity. Some 300 million adults worldwide are severely overweight and at risk for life-threatening illnesses such as type 2 diabetes and cardiovascular disease. But obesity is difficult to treat. "We do not have good medical therapies for obesity," Shulman says, noting that the small number of diet drugs on the market now come with intolerable side effects and have only modest impacts on weight. "It's very important to find other targets that might affect food intake." Despite many years studying the physiology of appetite and hunger, researchers still do not have a clear picture of how the brain keeps tabs on fat consumption. Fat is effective at satisfying hunger, so Shulman and his colleagues at Yale and the University of Cincinnati decided to see if they could find out whether the brain senses lipid intake directly. If they could learn how that happens, they suspected, their findings might point toward a new treatment for obesity. The team used Shulman's lipid analysis system to investigate what happens to fat that enters the blood after ingesting a high-fat meal. The scientists reasoned that the fat derivatives that enter the bloodstream might themselves serve as messengers to signal the brain that the body has been fed. They used this approach to compare the lipids present in blood plasma from rats that had fasted or eaten, and they zeroed in on NAPE.They found only low levels of NAPE in the blood of rats that had fasted for 12 hours. The level of NAPE shot up 40 to 50 percent in animals that had dined on high-fat chow. Furthermore, NAPE didn't increase in rodents that ate only protein or carbohydrate, suggesting that NAPE levels reflect the amount of fat eaten in a meal.

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Muscular Dystrophy - Misplaced Enzyme Is to Blame for Quick Fatigue After Mild Exercise

Howard Hughes Medical Institute scientists have uncovered a molecular explanation for the profound fatigue brought on by mild exercise in some people with muscular dystrophy. In studies with genetically engineered mice that showed this form of fatigue after mild exercise, the researchers found that an enzyme called neuronal nitric oxide synthase (nNOS) is not present at its normal location in the membrane surrounding muscle cells. This means the blood vessels that supply active muscles do not relax normally and the animals experience fatigue after very mild exercise. Howard Hughes Medical Institute researcher Kevin P. Campbell led a research team from the University of Iowa that reported its findings in the November 27, 2008, issue of the journal Nature. In identifying the mechanism for this specific form of fatigue, the researchers found that the fatigue can be alleviated pharmacologically. When the scientists administered Viagra-like drugs to the mice with muscular dystrophy, they noticed an increase in their ability to move, as well as a dramatic increase in their activity after mild exercise. The treated mice were two to four times more active than untreated mice with muscular dystrophy. Prior to treatment, the same mice would become virtually inert after a short burst of low-intensity activity. Nitric oxide signaling stimulates the generation of cGMP, a phosphodiester, which leads to a cascade of effects that culminates in the dilation of blood vessels.

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Stanford/Packard study shows no benefit from drug widely used to prevent premature births

When a pregnant woman goes into early labor, her obstetrician may give her drugs to quiet the woman's uterus and prevent premature birth. New research shows, however, that one popular drug works no better than a placebo at maintaining pregnancy after the initial bout of preterm labor is halted.

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Yale researchers enlist a new recruit in battle of the bulge

In the battle against obesity, Yale University researchers may have discovered a new weapon — a naturally occurring molecule secreted by the gut that makes rats and mice less hungry after fatty meals. The findings are published in the Nov. 26 issue of the journal Cell. The report suggests the molecule may help regulate how much animals and people eat, according to the team headed by Gerald I. Shulman, Yale professor of medicine and cellular & molecular physiology and a Howard Hughes Medical Institute investigator. Shulman's team studied a family of lipids called N-acylphosphatidylethanolamines, or NAPEs, which are synthesized and secreted into the blood by the small intestine after fatty foods are eaten. The team found that mice and rats injected regularly with NAPEs ate less food and lost weight. In addition, treatment with NAPEs appeared to reduce the activity of "hunger" neurons in the brain while stimulating activity in neurons that are believed to play a role in reducing appetite. In the last two decades, scientists have made great inroads toward understanding how the body communicates with the brain to control food intake. So far, hormones such as leptin that act as regulators of this complex system have proved disappointing when tested as potential weight-loss treatments in humans. The researchers are now planning to investigate how the findings in the Cell paper apply to humans. They will first study non-human primates to determine if NAPE concentrations increase in a similar fashion after fat ingestion. Then, says Shulman, "If chronic NAPE treatment is well tolerated and can cause weight loss by a reduction of food intake, we would have strong impetus to move forward with human NAPE trials."

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Study supports value of advanced CT scans to check for clogged arteries

In a development that researchers say is likely to quell concerns about the value of costly computed tomography scans to diagnose coronary artery blockages, an international team led by researchers at Johns Hopkins reports solid evidence that the newer, more powerful 64-CT scans can easily and correctly identify people with major blood vessel disease and is nearly as accurate as invasive coronary angiography.

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Inhaled Corticosteroids Raise Pneumonia Risk for Lung Disease Sufferers

Lung disease experts at Johns Hopkins are calling for physicians to show much greater caution in prescribing inhaled corticosteroid drugs for people with chronic obstructive pulmonary disease after finding evidence that the widely used anti-inflammatory medications increase the risk of pneumonia by a full third. More than 11 million Americans, the vast majority former or current smokers, are living with so-called COPD, marked by the potentially fatal, lung-diminishing conditions of emphysema and chronic bronchitis. The inhalers in question greatly relieve such symptoms as shortness of breath, wheezing, phlegm and physical exhaustion from light exercise. The call for caution is based on the Johns Hopkins team's review and analysis of adverse events recorded in 11 clinical studies that in total involved more than 14,000 men and women with COPD. The team's review, believed to be the largest and most comprehensive performed in the last decade among COPD sufferers, compared adverse events among those who took inhaled corticosteroids and others who did not.

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Research reveals mechanism linking serotonin with regulation of food intake

Genetic mouse models have provided surprising insight into mechanisms linking serotoninergic compounds with the regulation of feeding behavior and body weight. The research, published by Cell Press in the Nov. 26 issue of the journal Neuron, pinpoints a specific group of brain cells that mediate energy balance and may lead to the development of antiobesity drugs with fewer side effects.

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Where does the gene activity of youth go? New findings may hold the key

New evidence may explain why it is that we lose not only our youthful looks, but also our youthful pattern of gene activity with age. A report in the Nov. 26 issue of the journal Cell, a Cell Press publication, reveals that a protein perhaps best known for its role in the life-extending benefits of a low-calorie diet also maintains the stability of the mammalian genome -- the complete set of genetic instructions "written" in DNA.

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Bone formation goes with the gut, study finds

When it comes to remodeling our bones -- an ongoing process of break down and renewal that goes on throughout adulthood -- researchers have new evidence that our guts play a surprisingly important role. The findings point toward novel methods for increasing bone mass in patients with diseases characterized by impaired bone formation, including postmenopausal osteoporosis, according to the report in the Nov/ 26 issue of the journal Cell, a Cell Press publication.

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Kidney function discovery sheds light on genetic complexity of disease

To find a cure for cancer, haemophilia and other diseases, researchers need to be looking for complex, interacting genetic factors, according to the authors of a new study. A new study, published in the Journal of Clinical Investigation by researchers at the Centenary Institute, Royal Prince Alfred Hospital (RPA) and The Australian National University (ANU), has exposed a greater level of genetic complexity for diseases than was originally thought. The researchers looked at two disorders of kidney function - iminoglycinuria and hyperglycinuria. These disorders, first described 50 years ago, are conditions where large amounts of individual amino acids (the building blocks of proteins in our body) are wasted by the kidney. Professor John Rasko, Head, Gene and Stem Cell Therapy program at Centenary Institute and Cell and Molecular Therapies at RPA, says although up to one in every thousand babies has this disorder at birth, it usually resolves in the first year of life. For those individuals in whom it continues to occur, it is generally thought not to cause medical problems but previous cases have been linked to high blood pressure, kidney stones, deafness and problems in the brain. "Iminoglycinuria was observed to occur in families and the pattern of inheritance suggested that the cause might be due to an inherited abnormality of a specific pump on the surface of kidney cells," Professor Rasko explains.

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'Deranged calcium signaling' contributes to neurological disorder, UT Southwestern researchers find

Defective calcium metabolism in nerve cells may play a major role in a fatal genetic neurological disorder that resembles Huntington's disease, researchers at UT Southwestern Medical Center have found in a mouse study.

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Adiponectin is a metabolic link between obesity and bone mineral density

Researchers at the University of Toronto, faculty of medicine, Toronto, Canada, have discovered that adiponectin, a protein secreted from adipocytes, is a metabolic link that can explain, in part, the known positive relationship between obesity and both bone mineral density and reduced susceptibility to fractures.

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Estrogen therapy could be dangerous for women with existing heart risk

Hormone therapy could accentuate certain pre-existing heart disease risk factors and a heart health evaluation should become the norm when considering estrogen replacement, new research suggests. The research also showed that in women without existing atherosclerosis, hormone therapy use included some positive effects on lipids but also some negative effects related to heart health, said MaryFran Sowers, lead researcher and professor of epidemiology at the University of Michigan School of Public Health. The U-M study came about, Sowers said, in trying to explain what's behind the so-called timing hypothesis. The timing hypothesis suggests that if a woman implements a hormone therapy program within six years of her final menstrual period, this narrow window is enough to deter heart disease from developing with the onset of menopause. But the U-M findings suggest that explanation isn't quite so simple, Sowers said. Even within the six-year window, there were negative aspects related to heart disease. While the positive outcomes on HDL and LDL cholesterol levels were observed, Sowers said, researchers also saw negative outcomes in terms of the inflammation process—which can be related to heart disease.

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How Do Individuals React to Metabolic Stress? - Genetic Variation in Metabolism Identified

Metabolic diseases – in particular the increasingly prevalent type 2 diabetes – are caused by a complex interaction between genetic disposition and unfavorable lifestyle, above all unbalanced diet and too little physical exercise. Researchers at the Helmholtz Zentrum München have now for the first time been able to show a relationship between the genetic make-up of an individual and differences in his/her metabolism. The team of Professor Karsten Suhre of the Institute for Bioinformatics and Systems Biology at the Helmholtz Zentrum München and the Ludwig-Maximilians Universität München (LMU) and Dr. Christian Gieger and Thomas Illig of the Institute for Epidemiology in cooperation with the Innsbruck company Biocrates Life Sciences AG determined the blood test results of several hundred metabolites synchronously with more than 100 000 DNA variants (SNPs) of 284 adult test subjects. Their research was based on blood samples of participants of the population-based KORA study (Kooperative Gesundheitsforschung in der Region Augsburg [Cooperative Health Research in the Region of Augsburg] which is headed by Professor H.-Erich Wichmann).

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Exposure to organochlorate pollutants and lead weakens animals bones, according to a study

A new methodology developed by a researcher of the University of Granada will permit to determine the toxicological effects caused in animals which have been exposed to organochlorate pollutants and lead analysing their bones. This work has studied the effects of lead toxicity in the long term in wild birds populations, determining how this heavy metal causes bone weakening and fracture, provoking therefore a fall in the individual survival of the affected species. This work has been carried out by Pedro Álvarez Lloret, of the Department of Mineralogy and Petrology of the University of Granada, in collaboration with the University of Georgia (USA), the Karolinska Institute of Stockholm, the Research Institute for Hunting Resources (CSIC) and the Biological Station of Doñana (CSIC). The research work has been supervised by Professor Alejandro Rodríguez Navarro.

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Fast food a potential risk factor for Alzheimer’s

Mice that were fed a diet rich in fat, sugar and cholesterol for nine months developed a preliminary stage of the morbid irregularities that form in the brains of Alzheimer’s patients. The study results, published in a doctoral thesis from the Swedish medical university Karolinska Institutet (KI), give some indications of how this difficult to treat disease might one day be preventable.Alzheimer’s is the most common form of dementia, there being roughly 90,000 patients with the disease in Sweden today. The underlying causes of Alzheimer’s disease are still something of a mystery, but there are a number of known risk factors. The most common is a variant of a certain gene that governs the production of apolipoprotein E, one of the functions of which is to transport cholesterol. The gene variant is called apoE4 and is found in 15-20 per cent of the population.For her doctoral thesis, Susanne Akterin studied mice that had been genetically modified to mimic the effects of apoE4 in humans. The mice were then fed for nine months on a diet rich in fat, sugar and cholesterol, representing the nutritional content of most fast food.“On examining the brains of these mice, we found a chemical change not unlike that found in the Alzheimer brain,” says Ms Akterin, postgraduate at KI Alzheimer’s Disease Research Center.

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An emergency brake in the brain

Brain researchers at the University of Oslo in Norway have penetrated deeply into the innermost secrets of the brain to find out how brain cells can survive a stroke. Strokes are usually caused by occlusion of one of the blood vessels in the brain. When blood is prevented from supplying vital oxygen and energy to the brain cells, their electrochemical balance is upset, and they cause damage to themselves and to the surrounding brain cells before they collapse and die. Often this affects the memory centre, the hippocampus, where the cells are particularly vulnerable. There is hope, however. New research results indicate that the brain cells are equipped with an ingenious mechanism that can save them in extreme emergencies.

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Immune cells reveal fancy footwork

Our immune system plays an essential role in protecting us from diseases, but how does it do this exactly? Dutch biologist Suzanne van Helden discovered that before dendritic cells move to the lymph nodes they lose their sticky feet. This helps them to move much faster. Immature dendritic cells patrol the tissues in search of antigens. After exposure to such antigens they undergo a rigorous maturation process. During this maturation the dendritic cells migrate to the lymph nodes to activate T cells. Suzanne van Helden studied the adhesion and migration of both immature and mature dendritic cells. A dendritic cell can be compared with a pocket-sized general. As an immature cell he is on patrol in the bloodstream and in tissues in search of foreign bodies. The feet, or podosomes, help the cell to move around at a slow pace. As soon as immature dendritic cells detect a problem they must report back quickly to the T cells to warn them of impending danger. The dendritic cells are then hindered by their adhesive feet. This is the reason why at this point the cell undergoes modifications and loses its feet. In this way the mature dendritic cell can wing its way to the T cells at full speed. Once alerted, the T cells can intervene and tackle the problem in the body's infected tissues.

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