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News - Week 16 - 2009

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Urgent: Support the Proposed New Law in California Requiring Doctors to Provide Patients with Information on Diabetes and
Heart Disease

Patients often receive inadequate and/or incorrect information from their doctors on diabetes and heart disease. Last month’s newsletter was on the heart disease side of this bill. Concerning type-2 diabetes, health professionals and pharmaceutical companies disseminate incorrect and inadequate information on these four important issues:

1) Patients are told diabetic medications for type-2 diabetes will prolong life and prevent complications of diabetes, while extensive scientific research says otherwise for the most commonly prescribed oral medications.

2) Patients are told that their blood sugars (and hemoglobin A1c levels) must be lowered as close to normal levels as possible. However, all six major studies show intensive therapy increases the risk of heart disease, death, and serious side effects.

3) The public receives almost no education about the role of the rich Western diet in the cause of type-2 diabetes and about the right way to eat to prevent this disease.

4) Patients are rarely told that changing to a healthy, low-fat, plant-food based diet, exercise, and associated weight loss will improve their health and often cure their type-2 diabetes.

Assembly Bill 1478 has been introduced by California state assembly member Tom Ammiano, representing the 13th District, to require that a physician obtain a patient's written acknowledgment confirming the receipt of information, as specified, regarding treatment through medical nutrition therapy prior to delivering nonemergency treatment for type-2 diabetes. My supporting letter on this matter is provided below. Last month’s newsletter (March 2009) has a similar letter from me about heart disease treatments and a request for your support.

Read more

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Researchers find promotion is bad for mental health and stops you visiting the doctor

New research by economics and psychology researchers at the University of Warwick has found that promotion on average produces 10% more mental strain and gives up to 20% less time to visit the Doctors. In a research paper entitled “Do People Become Healthier after Being Promoted” Chris Boyce and Professor Andrew Oswald of the University of Warwick questioned why people with higher job status seem to have better health. A long-held assumption by researchers is that an imprvement to a person’s job status, through a promotion, will directly result in better health due to an increased sense of life control and self-worth.
The researchers tested this. They drew upon the British Household Panel Survey data set, collected annually between 1991 and 2005, with information on approximately 1000 individual promotions. They found no evidence of improved physical health after promotion – nor that self-assessed feelings of health declined.

Genes from tiny marine algae suggest unsuspected avenues for new research

By sequencing the DNA of two tiny marine algae, a team of scientists has opened up a myriad of possibilities for new research in algal physiology, plant biology, and marine ecology. The project was led by Alexandra Worden at the Monterey Bay Aquarium Research Institute (MBARI) and the Joint Genome Institute (JGI). The genome analyses involved a collaborative effort between MBARI, JGI, and an international consortium of scientists from multiple institutions, including University of Washington, Ghent University (Belgium), and Washington University in St. Louis. Initial discoveries from the research appear in the April 10, 2009 edition of Science magazine. Biologists generally agree that all land plants, from tiny mosses to giant redwoods, evolved from an ancestral green alga. Some of the closest representatives of these ancestral green algae living today are thought to be the Prasinophytes, a group of microscopic green algae found across the world's oceans. Microbial oceanographer Alexandra Worden led a team of scientists that sequenced the genomes of two Prasinophytes in the genus Micromonas. Each Micromonas cell is only about one fiftieth the width of a human hair. However, they are widespread and may serve as important links in marine food webs. They may also influence the amount of carbon dioxide the oceans take up from the atmosphere. Worden's team spent four years compiling a complete list of the approximately 21 million chemical building blocks (called bases) that make up Micromonas' DNA. The recent Science paper highlights key aspects of this genetic "Morse code." The paper also compares Micromonas' genes with genes found in other organisms.

Study finds multidrug-resistant gram-negative bacteria high in long-term care

The prevalence of a certain form of drug-resistant bacteria, called multidrug-resistant gram-negative (MDRGN) organisms, far surpassed that of two other common antimicrobial-resistant infections in long-term care facilities, according to a study conducted by researchers at Hebrew SeniorLife's Institute for Aging Research. Residents at long-term care facilities are one of the main reservoirs of antimicrobial-resistant bacteria. Epidemiological studies have focused primarily on two common antimicrobial-resistant organisms—methicillin-resistant Staphylococcus aureas (MRSA) and vancomycin-resistant enterococci (VRE).
"Recently, it has become apparent that multidrug resistance among gram-negative bacteria is becoming an even greater problem in these facilities, with nearly half of long-term care facility residents harboring multidrug-resistant gram-negative bacteria," write the researchers, led by IFAR's Erin'O'Fallon, M.D., M.P.H., in the January issue of the Journal of Gerontology: Medical Sciences. MDRGN infection can lead to toxins in the bloodstream that cause inflammation and destroy healthy tissue. Left untreated, these infections can be fatal. More than 80 percent of the MDRGN cases in the study were resistant to commonly prescribed antimicrobial medications, including ciprofloxacin, trimethoprim-sulfamethoxazole, and amipicillin/sulbactam. By definition all of the identified MDRGN bacteria were resistant to at least three different classes of antimicrobial drugs, with one-third of them resistant to four.

Test quickly assesses whether Alzheimer's drugs are hitting their target

A test developed by physician-scientists at Washington University School of Medicine in St. Louis may help assess more quickly the ability of Alzheimer's drugs to affect one of the possible underlying causes of Alzheimer's disease in humans, accelerating the development of new treatments. Scientists used the test to show that an Alzheimer's drug given to healthy volunteers reduced production of a substance known as amyloid beta (A-beta), a normal byproduct of human metabolism that builds to unhealthy levels forming brain plaques in Alzheimer's patients. The drug candidate, LY450139, which is also known as semagacestat, is being studied in clinical trials by Eli Lilly and Company.Ongoing clinical trials are studying the effect that semagacestat may have on cognitive function and biochemical and brain imaging biomarkers in patients with Alzheimer's disease. Washington University researchers wanted to see whether the new measurement technique, stable isotope-linked kinetics (SILK), could detect the study drug's impact on A-beta synthesis in healthy volunteers. "Bringing an Alzheimer's disease drug into clinical trials from tests in animal models has always been challenging," says study director Randall Bateman, M.D., a Washington University neurologist who treats patients at Barnes-Jewish Hospital. "We haven't had a way to quickly and accurately assess a drug's effects, and that meant there always had to be some degree of educated guesswork when it came to setting the optimal dosage for humans. SILK may help to eliminate much of that guesswork."

Scientists show how a neuron gets its shape

Ask a simple question, get a simple answer: When Abraham Lincoln was asked how long a man’s legs should be, he absurdly replied, “Long enough to reach the ground.” Now, by using a new microscopy technique to watch the growth of individual neurons in the microscopic roundworm Caenorhabditis elegans, Rockefeller University researchers are turning another deceptively simple question on its head. They asked, “How long should a worm’s neurons be?” And the worms fired back, “Long enough to reach their targets.” The researchers’ surprising result: Rather than growing like the branches of a tree — extending outward - certain neurons work backward from their destination, dropping anchor and stretching their dendrites behind them as they crawl away. The work, led by Shai Shaham, head of the Laboratory of Developmental Genetics, and Maxwell Heiman, a research associate in the lab, not only addresses an age-old question of how neurons get their shape, but is also changing the way scientists think about the genetic program that wires the brain and allows it to grow throughout development.

Vitamin D Deficiency Related to Increased Inflammation in Healthy Women, MU Study Finds

According to a recent study in the Archives of Internal Medicine, 75 percent of Americans do not get enough Vitamin D. Researchers have found that the deficiency may negatively impact immune function and cardiovascular health and increase cancer risk. Now, a University of Missouri nutritional sciences researcher has found that vitamin D deficiency is associated with inflammation, a negative response of the immune system, in healthy women.  Increased concentrations of serum TNF-?, an inflammatory marker, were found in women who had insufficient vitamin D levels. This study is the first to find an inverse relationship between vitamin D levels and concentrations of TNF-? in a healthy, non-diseased population. This may explain the vitamin's role in the prevention and treatment of inflammatory diseases, including heart disease, multiple sclerosis and rheumatoid arthritis. "The findings reveal that low vitamin D levels negatively impact inflammation and immune response, even in healthy women," said Catherine Peterson, assistant professor in the MU College of Human Environmental Sciences. "Increased inflammation normally is found in people with obesity or chronic diseases; a small decrease in vitamin D levels may aggravate symptoms in people who are sick."

How tumor cells move

Researchers in Heidelberg discover new protein that is suppressed in particularly aggressive cancer cells / Article in Nature Cell Biology. If cancer cells lack a certain protein, it could be much easier for them to penetrate healthy body tissue, the first step towards forming metastases. Scientists at the Pharmacology Institute of the University of Heidelberg have discovered the previously unknown cell signal factor SCAI (suppressor of cancer cell invasion), which inhibits the movement and spread of tumor cells in laboratory tests. When the factor’s functioning was disrupted, the cancer cells moved much more effectively in what are known as three-dimensional matrix systems, which imitate some of the tissue properties of the human body. “The protein is apparently suppressed in many types of tumors, e.g. breast, lung, or thyroid,” explains Dr. Robert Grosse, head of the Emmy Noether Junior Research Group funded by the German Research Association (DFG) at the Pharmacology Institute. The new factor could be an interesting starting point for research into new mechanisms for fighting cancer. The research team’s results have now been published online in the prestigious international journal Nature Cell Biology.

Scientists identify key gene that protects against leukemia

Researchers have identified a gene that controls the rapid production and differentiation of the stem cells that produce all blood cell types—a discovery that could eventually open the door to more streamlined treatments for leukemia and other blood cancers, in which blood cells proliferate out of control. Additionally, in investigating the mechanisms of this gene, the scientists uncovered evidence that could lead to a protocol for bone marrow transplants that could boost the chance of a cure in some patients. The research, led by Emmanuelle Passegué, PhD, of the University of California, San Francisco, demonstrates that the JunB gene is at the center of a complex network of molecular and environmental signals that regulate the proliferation and differentiation of hematopoietic stem cells, the multipotent, self-renewing cells that give rise to all blood cell types.

Human ES cells progress slowly in myelin's direction

Scientists from the University of Wisconsin, USA, report in the journal Development (dev.biologists.org) the successful generation from human embryonic stem cells of a type of cell that can make myelin, a finding that opens up new possibilities for both basic and clinical research.  The cells the researchers made are called oligodendrocytes, which are responsible for making myelin in the central nervous system. Myelin forms an insulating sheath that surrounds nerve fibres, both protecting them and speeding up the transmission of nerve impulses. Its loss or damage has serious consequences, as is seen in the condition of multiple sclerosis, because without it nerves lose the ability to transmit impulses to each other and to function properly. Unlike human embryonic stem (ES) cells, it's relatively easy to persuade mouse ES cells to turn into oligodendrocytes; it's often done by exposing these cells to a protein called Sonic Hedgehog, which produces oligodendrocytes in the spinal cord of developing embryos. Now Su-Chun Zhang and his co-workers show in the May issue of Development (dev.biologists.org) that treating human ES cells with this same protein also turns them into oligodendrocytes – they just take longer to do it, 14 weeks as opposed to the 2 weeks taken by mouse ES cells. They also report another difference between mouse and human ES cells: a growth factor called Fgf2 that promotes oligodendrocyte development in mouse ES cells actually stalls it in human ES cells. As Dr Zhang reveals, these findings were quite unexpected. 'This was quite a surprise given that this is exactly how we direct mouse ES cells to become oligodendrocytes. But we have discovered an unexpected twist in the cell's response to the same external factor', explained Dr Zhang. 'It nevertheless explains why so many research groups have failed to persuade human neural stem cells to become oligodendrocytes for the past decade.' As Dr Zhang went on to discuss, these findings are also of clinical importance. 'We are now able to generate a relatively enriched population of oligodendrocyte precursor cells that may be used to repair lost myelin sheaths. These findings also raise awareness of the direct translatability of animal studies to human biology. In this regard, the human oligodendrocytes generated from human ES cells or the generation of disease-induced pluripotent stem cells can provide a useful tool in the future for screening pharmaceuticals directly on human cells.'

Researcher uses GPS to find asthma causes

David Van Sickle is looking for a few pioneering asthmatics. He wants to attach a GPS device to their inhalers before they boldly go out into a spring world filled with allergens.His goal is to map where and when environmental exposures trigger asthma symptoms, prompting them to puff on their “rescue” inhalers, which deliver the medicine that keeps them breathing.

Vitamin D may exacerbate autoimmune disease

Deficiency in vitamin D has been widely regarded as contributing to autoimmune disease, but a review appearing in Autoimmunity Reviews explains that low levels of vitamin D in patients with autoimmune disease may be a result rather than a cause of disease and that supplementing with vitamin D may actually exacerbate autoimmune disease. Authored by a team of researchers at the California-based non-profit Autoimmunity Research Foundation, the paper goes on to point out that molecular biologists have long known that the form of vitamin D derived from food and supplements, 25-hydroxyvitamin D (25-D), is a secosteroid rather than a vitamin. Like corticosteroid medications, vitamin D may provide short-term relief by lowering inflammation but may exacerbate disease symptoms over the long-term. The insights are based on molecular research showing that 25-D inactivates rather than activates its native receptor - the Vitamin D nuclear receptor or VDR. Once associated solely with calcium metabolism, the VDR is now known to transcribe at least 913 genes and largely control the innate immune response by expressing the bulk of the body's antimicrobial peptides, natural antimicrobials that target bacteria. Written under the guidance of professor Trevor Marshall of Murdoch University, Western Australia, the paper contends that 25-D's actions must be considered in light of recent research on the Human Microbiome. Such research shows that bacteria are far more pervasive than previously thought – 90% of cells in the body are estimated to be non-human – increasing the likelihood that autoimmune diseases are caused by persistent pathogens, many of which have yet to be named or have their DNA characterized. Marshall and team explain that by deactivating the VDR and subsequently the immune response, 25-D lowers the inflammation caused by many of these bacteria but allows them to spread more easily in the long-run. They outline how long-term harm caused by high levels of 25-D has been missed because the bacteria implicated in autoimmune disease grow very slowly. For example, a higher incidence in brain lesions, allergies, and atopy in response to vitamin D supplementation have been noted only after decades of supplementation with the secosteroid. Furthermore, low levels of 25-D are frequently noted in patients with autoimmune disease, leading to a current consensus that a deficiency of the secosteroid may contribute to the autoimmune disease process. However, Marshall and team explain that these low levels of 25-D are a result, rather than a cause, of the disease process. Indeed, Marshall's research shows that in autoimmune disease, 25-D levels are naturally down-regulated in response to VDR dysregulation by chronic pathogens. Under such circumstances, supplementation with extra vitamin D is not only counterproductive but harmful, as it slows the ability of the immune system to deal with such bacteria. The team points out the importance of examining alternate models of vitamin D metabolism. "Vitamin D is currently being recommended at historically unprecedented doses," states Amy Proal, one of the paper's co-authors. "Yet at the same time, the rate of nearly every autoimmune disease continues to escalate."

Acupuncture wristbands Ease Nausea with Cancer Treatment

Cancer patients who wore acupressure wristbands had much less nausea while receiving radiation treatment, making the bands a safe, low-cost addition to anti-nausea medication, according to a study in the Journal of Pain and Symptom Management by University of Rochester Medical Center researchers. Previous research has suggested that the placebo effect – essentially, an outcome related to your body that you expect to happen – might be why elastic wristbands reduce nausea. However, the findings of the latest study do not support that notion, even though researchers continue to believe in the mind’s powerful influence over symptoms. “We know the placebo effect exists, the problem is that we don’t know how to measure it very well,” said Joseph A. Roscoe, Ph.D., corresponding author and research associate professor at the James P. Wilmot Cancer Center at URMC. “In this study we attempted to manipulate the information we gave to patients, to see if their expectations about nausea could be changed. As it turned out, our information to change people’s expectations had no effect – but we still found that the wristbands reduce nausea symptoms.” The clinical trial enrolled 88 people divided into three groups. All had reported some degree of nausea after receiving at least two radiation treatments for any type of cancer. Although chemotherapy is more closely linked with producing nausea and vomiting, radiation to the intestinal tract can also cause nausea, Roscoe said.

Gene therapy appears safe to regenerate gum tissue

Scientists at the University of Michigan have developed a method of gene delivery that appears safe for regenerating tooth-supporting gum tissue—a discovery that assuages one of the biggest safety concerns surrounding gene therapy research and tissue engineering.Gene therapy is an accepted, viable therapeutic concept, but safety is a major hurdle, said William Giannobile, professor at the U-M School of Dentistry. The most notable incident highlighting the safety concerns of gene therapy research and treatment occurred several years ago when a teenager died when given the adenovirus during a gene therapy clinical trial at the University of Pennsylvania. The U-M therapy also uses the adenovirus, Giannobile said, but the big difference in the U-M approach lies in the local application and much lower dose. Instead of injecting the genes into the blood vessels, where they can then travel through the bloodstream and result in unexpected and sometimes fatal reactions, U-M scientists put the genes on a localized area, directly on the tissue during surgery much like a paste.

Phasic firing of dopamine neurons is key to brain's prediction of rewards

Researchers are one step closer to understanding the neurobiology that allows people to successfully learn motivated behaviors by associating environmental cues with rewarding outcomes, according to a study published yesterday in the Proceedings of the National Academy of Sciences' online Early Edition. Carlos Paladini, assistant professor of neuroscience at The University of Texas at San Antonio (UTSA) and UTSA graduate student Collin Lobb collaborated with researchers at The University of Washington at Seattle to study the firing patterns of midbrain dopamine neurons in mice during reward-based learning. "Our research findings provide a direct functional link between the bursting activity of midbrain dopamine neurons and behavior. The research has significant applications for the improvement of health, because the dopamine neurons we are studying are the same neurons that become inactivated during Parkinson's Disease and with the consumption of psychostimulants such as cocaine and amphetamine," said Paladini, who is also a member of UTSA's Neurosciences Institute. Midbrain dopamine neurons fire in two characteristic modes, tonic and phasic, which are thought to modulate distinct aspects of behavior. When an unexpected reward is presented to an individual, midbrain dopamine neurons fire high frequency bursts of electrical activity. Those bursts of activity allow us to learn to associate the reward with cues in our environment, which may predict similar rewards in the future. The burst of electrical spikes observed in dopamine neurons is facilitated by a protein called the NMDA receptor, which is expressed on the surface of the dopamine cells. In this study, researchers removed the NMDA receptor from the dopamine cells only, leaving the dopamine neurons unable to fire bursts. The cells would otherwise fire normally.

Is there a prospective association between obesity and periodontal disease?

This is the question asked by a team of investigators from the Harvard School of Public Health and the University of Puerto Rico, reporting their findings today during the 87th General Session of the International Association for Dental Research, convening at the Miami Beach Convention Center. The investigators evaluated the association between different measures of obesity and risk of periodontal disease. They analyzed data from 36,903 men from the Health Professionals Follow-Up Study who were free of reported periodontal disease at the start of follow-up, and we followed them for up to 16 years (1986-2002). Height was assessed at the start of follow-up, and weight and self-reported periodontal disease data were collected at baseline and on follow-up questionnaires mailed every two years. Measures of central obesity were made by waist and hip circumference through self-assessed measurements and reported in 1987 with the aid of printed instructions and a tape measure. Self-reported periodontal disease and adiposity measures had been previously validated. They evaluated the effect of body mass index (BMI kg/m2), waist circumference (WC), and waist-to-hip ratio (WHR), on first report of periodontal disease diagnosis. The team observed significant associations between all measures of obesity and periodontal disease when accounting for age, smoking, race, dental profession, physical activity, fruit and vegetable intake, and diabetes status at baseline. Obesity (BMI > 30 kg/m¬2) at the beginning of follow-up and over follow-up was significantly associated with a 25% and 29% increased risk compared with normal weight (BMI 18.5-24.9 kg/m2), respectively. Men with WC > = 40 inches compared with < 40 inches was significantly associated with a 19% increased risk of periodontal disease, compared with men with a WC < 40 inches. WHR > = 0.95 compared with < 0.95 exhibited a significant 16% increased risk of periodontal disease. When BMI was accounted for (i.e., overall obesity), the effects of WC and WHR (i.e., central obesity) were weakened. The associations of BMI and WC were significant even among non-diabetics and among those who had never smoked. These results provide the first evidence following a large group of people over time with clear evidence of obesity occurring prior to periodontal disease, and support an association between obesity and risk of periodontal disease. Given the high prevalence of obesity and periodontal disease, this association may be of substantial public health importance.

Resolvins have the potential to resolve periodontal inflammation and restore tissue health

Periodontal (gum) disease is a chronic inflammation initiated by bacteria that affect the gums and bone supporting the teeth, and may eventually result in tissue and tooth loss. It is similar to other chronic inflammatory diseases such as arthritis, where inflammation causes tissue damage and is responsible for the disease. To date, the prevention of gum disease has been limited to successful oral hygiene and regular professional care. However, despite these preventive actions, in susceptible individuals with a high inflammatory response, plaque control is not enough to prevent disease. Today, during the 87th General Session of the International Association for Dental Research, scientists from Boston University are reporting on the discovery of Resolvins, a new family of biologically active products of omega-3 fatty acids with the therapeutic potential to resolve periodontal inflammation and restore the gums to health. Oil from fish contains eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA); both are omega-3 fatty acids. These omega-3 fatty acids keep blood triglycerides in control and may inhibit the progression of atherosclerosis. EPA and DHA also have anti-inflammatory activity and are often used to help people with various inflammatory conditions, such as Crohn's disease and rheumatoid arthritis. The Resolvins are natural endogenous regulators of the immune system against inflammation. Compounds derived from EPA are designated Resolvins of the E series (RvE1), and those biosynthesized from DHA are denoted Resolvins of the D series (RvD). The investigators have previously shown that topical application of RvE1 in experimental gum disease provided protection against soft tissue and bone loss associated with gum disease and, remarkably, restored the lost soft tissue and bone to healthy levels. Since, in recent studies, DHA-derived Resolvin D1 (RvD1) was shown to provide protection against tissue damage in several systemic inflammation models, the Boston team conducted experiments to test the actions of RvD1 in regulating tissue destruction and resolution of inflammation in gum disease. Experimental gum disease characterized by tissue inflammation and bone loss was stimulated in rabbits by the application of specific bacteria that cause human gum disease. The results demonstrate that RVD1 is similar to the EPA-derived lipid mediator, RvE1, in resolving periodontal inflammation and tissue regeneration. These results support the hypothesis that both EPA- and DHA-derived Resolvins have therapeutic potential in resolving periodontal inflammation and restoring the tissues' health.

Study finds new evidence of periodontal disease leading to gestational diabetes

A new study by NYU dental researchers has uncovered evidence that pregnant women with periodontal (gum) disease face an increased risk of developing gestational diabetes even if they don't smoke or drink, a finding that underscores how important it is for all expectant mothers – even those without other risk factors – to maintain good oral health.The study, led by Dr. Ananda P. Dasanayake, Professor of Epidemiology & Health Promotion at New York University College of Dentistry in collaboration with the Faculty of Dental Sciences at the University of Peradeniya, Sri Lanka, eliminated smoking and alcohol use among a group of 190 pregnant women in the South Asian island nation of Sri Lanka, where a combination of cultural taboos and poverty deter the majority of women from smoking and drinking. The findings support an earlier study led by Dr. Dasanayake that found evidence that pregnant women with periodontal disease are more likely to develop gestational diabetes than pregnant women with healthy gums. That study, which followed 256 women at New York's Bellevue Hospital Center through their first six months of pregnancy, showed that 22 of the women developed gestational diabetes. Those women had significantly higher levels of periodontal bacteria and inflammation than the other women in the study. The findings were published in the April 2008 issue of the Journal of Dental Research. More than one-third of the women in the new study, which was conducted over the course of one year, reported having bleeding gums when they brushed their teeth. The women were given a dental examination and a glucose challenge test, which is used specifically to screen for gestational diabetes. According to Dr. Dasanayake, those women found to have the greatest amount of bleeding in their gums also had the highest levels of glucose in their blood. Dr. Dasanayake, who presented the findings today at the annual meeting of the International Association for Dental Research in Miami, said that he expected the final data to show that between 20 and 30 of the women had developed gestational diabetes.

Big belly and obesity linked to increased risk of restless legs syndrome

A new study shows both obesity and a large belly appear to increase the risk of developing restless legs syndrome (RLS), a common sleep disorder characterized by an irresistible urge to move your legs. The research is published in the April 7, 2009, print issue of Neurology®, the medical journal of the American Academy of Neurology. It is estimated that 5-10 percent of adults in the United States have RLS and the disorder often has a substantial impact on sleep, daily activities and quality of life. For the study, researchers questioned 65,554 women and 23,119 men, all of whom were health professionals who took part in the Health Professionals Follow-Up Study or the Nurses' Health Study II. None of the participants had diabetes, arthritis or were pregnant. Of the groups, 6.4 percent of the women and 4.1 percent of the men were identified as having RLS. The research found men and women with a body mass index (BMI) score over 30 were nearly one-and-a-half times more likely to have RLS than people who were not obese. In addition, people who were in the top 20 percent of the group for highest waist circumference were more than one-and-a-half times more likely to have RLS than the bottom 20 percent of the group with the lowest belly size. The results were the same regardless of age, smoking, use of antidepressants or anxiety. "These results may be important since obesity is a modifiable risk factor that is becoming increasingly common in the U.S.," said study author Xiang Gao, MD, PhD, with the Harvard School of Public Health in Boston. "More research is needed to confirm whether obesity causes RLS and whether keeping a low BMI score and small waist size could help prevent RLS." Gao says some studies suggest that obese people have lower dopamine receptor levels in the brain. "Since decreased dopamine function is believed to play a critical role in RLS as well, this could be the link between the two." Dopamine is a chemical naturally produced by the body that transmits signals between nerve cells.

Gene helps protect tumor suppressor in breast cancer

Scientists at The University of Texas M. D. Anderson Cancer Center have discovered a gene that protects PTEN, a major tumor-suppressor that is reduced but rarely mutated in about half of all breast cancers. The gene Rak helps protect and regulate PTEN, which also is important in several other types of cancer, the team reports in the April edition of Cancer Cell. Causes for diminished PTEN protein levels in breast cancer absent a mutation of the PTEN gene have eluded researchers, who knew for several years that a piece of the puzzle was missing. "We've clearly discovered the missing link that explains how Rak can stabilize PTEN protein to prevent breast cancer development," said lead author Shiaw-Yih Lin, Ph.D., an assistant professor in the Department of Systems Biology at M. D. Anderson. "Our research explains why PTEN is defective in breast cancer and provides important clues for the development of effective therapy in Rak- or PTEN-defective breast cancers." In addition to breast cancer, PTEN frequently is mutated or inactivated in glioblastoma, melanoma, and cancers of the prostate and endometrium. The severity of PTEN irregularities strongly correlates with the tumor stage and grade. For example, complete loss of PTEN expression is found more frequently in metastatic cancer than in primary tumors. In the laboratory, researchers found Rak can stabilize PTEN protein and function as a tumor suppressor gene to prevent breast cancer development.

M. D. Anderson Study Finds Pre-Surgical Stress Management Improves Mood, Quality of Life for Prostate Cancer Patients

Brief stress management sessions prior to and immediately after surgery may have both short- and long-term benefit for men undergoing a radical prostatectomy for early-stage prostate cancer, according to research from The University of Texas M. D. Anderson Cancer Center. The study, in the current issue of the Journal of Clinical Oncology, is the first to examine the benefits of psychosocial intervention for prostate cancer patients prior to surgery. It found that men who participated in the sessions experienced less short-term mood disturbance and better long-term quality of life, compared to patients who had the procedure but did not have any behavioral intervention. Most psychosocial interventions in cancer of any type have been studied after patients have completed surgery, explained Lorenzo Cohen, Ph.D., the study's senior author and professor in M. D. Anderson's Departments of Behavioral Science and General Oncology, and director of the Integrative Medicine Program. "We know that for men with early-stage prostate cancer, the time when they are making treatment decisions is very stressful," said Cohen. "A radical prostatectomy is not without possible, very personal, consequences, including urinary incontinence and erectile dysfunction. Patients may also be worried about the uncertainty that the surgery will cure their cancer. "From other areas of research, we know that going into a surgical setting overly stressed may increase a patient's recovery time. With this study, we wanted to intervene in the pre- and post-surgical setting and try to help relieve stress and minimize mood disturbance, such as depression, anxiety and distress, both in the short- and long-term."
For the randomized study, 159 early stage prostate cancer, radical prostatectomy patients were assigned to receive either: two 60-90 minute sessions of pre-surgical stress management intervention and brief booster sessions the morning of, and 48 hours following surgery; two 60-90 minute individual supportive attention sessions and boosters similar to the stress management group; or standard care. Assessments occurred before the sessions, one month before, one week before, and the morning of surgery, as well as six weeks, six and 12 months following surgery.

Is There a Seat of Wisdom in the Brain?

Researchers at the University of California, San Diego School of Medicine have compiled the first-ever review of the neurobiology of wisdom – once the sole province of religion and philosophy. The study by Dilip V. Jeste, MD, and Thomas W. Meeks, MD, of UC San Diego’s Department of Psychiatry and the Stein Institute for Research on Aging, will be published in the Archives of General Psychiatry on April 6. “Defining wisdom is rather subjective, though there are many similarities in definition across time and cultures,” said Jeste, who is the Estelle and Edgar Levi Chair in Aging, professor of psychiatry and neuroscience and chief of geriatric psychiatry at UC San Diego. “However, our research suggests that there may be a basis in neurobiology for wisdom’s most universal traits.” Wisdom has been defined over centuries and civilizations to encompass numerous psychological traits. Components of wisdom are commonly agreed to include such attributes as empathy, compassion or altruism, emotional stability, self-understanding, and pro-social attitudes, including a tolerance for others’ values. “But questions remain: is wisdom universal, or culturally based?” said Jeste. “Is it uniquely human, related to age? Is it dependent on experience or can wisdom be taught?”

Substituting water for sugar-sweetened beverages can reduce excess calorie consumption

eplacing consumption of sugar-sweetened beverages (SSBs) with water could eliminate an average of 235 excess calories per day among children and adolescents, according to a study published in the April 2009 Archives of Pediatrics & Adolescent Medicine. The study's authors conclude that such a replacement would be a simple and effective way to reduce excess intake of calories causing childhood overweight and obesity, as well as address dental cavities and other health problems associated with added sugar. And they predict no detrimental effects on nutrition. "The evidence is now clear that replacing these 'liquid calories' with calorie-free beverage alternatives both at home and in schools represents a key strategy to eliminate excess calories and prevent childhood obesity," said Y. Claire Wang, MD, ScD, assistant professor of Health Policy and Management at Columbia University Mailman School of Public Health and the study's lead author. Dr. Wang and colleagues analyzed what children and teens reported they ate and drank on two different days, using nationally representative data from the 2003-2004 National Health and Nutrition Examination Survey. They then estimated the impact of substituting water for SSBs on the total energy intake of youths ages two to 19. No data suggest that youths increase their consumption of other foods and beverages to compensate for drinking fewer SSBs, and so every can of soda or fruit drink that is replaced by water means a net reduction of calories. Almost 90 percent of U.S. children and adolescents currently consume SSBs on any given day, including soda, fruit drinks, punches, sports drinks and sweetened tea, and the calories contained in these drinks can represent more than 10 percent of their total daily intake. There is growing evidence that sugar-sweetened beverage consumption is an important contributor to rising youth obesity rates in the United States.

New technique invented to reveal pancreatic stem cells

Just like those absconders chased by police all over the world, everybody can tell about their good deeds but none really knows how to recognize them. Yet, as of today, thanks to a study just published in the Proceedings of the National Accademy of Sciences (PNAS) and authored by Nobel Laureate for Medicine in 2007 Mario Capecchi and by the researcher from the Catholic University of Rome Eugenio Sangiorgi, we now know how to reveal the stem cells camouflaged in the pancreas.A stem cell is a cell capable of generating all the other cells constituting the same tissue (sometimes also called "adult stem cell"). "Reading the newspapers sometimes one would doubt it – says Sangiorgi – but we don't know many things about stem cells. It might look odd, but for instance we don't have a method to distinguish a priori between a stem cell and any other cell in the same tissue. We can only infer that a cell really is a stem cell by observing its behaviour". In other words, when a researcher encounters a tissue, it's not immediately possible to identify with certainty and thus isolate a stem cell. In some case, like in the meadows, we now know where they are located and how to single them out – and hence we have been capable of successful life saving transplants for many years. But in the case of the pancreas, as in that of many other tissues, until some years ago we doubted that these special cells were even present there. "Together with Professor Capecchi, we had already designed in the past a novel way to mark the stem cells in a tissue: a sort of little flag, capable of helping us to effectively label the cells we were looking for", explains Sangiorgi. In order to achieve this, Capecchi and Sangiorgi used a molecular switch, that is a piece of DNA, which activates itself once the mouse under scrutiny takes a special drug. When the switch is "on", a special fluorescent protein is produced (and, as a matter of fact, the study about this type of proteins won the Nobel Prize in Chemistry last October). The luminous cells are indeed the long-sought stem cells. "In order to understand that these are really stem cells, we need only to wait", comments Sangiorgi. "A normal cell is sooner or later destined to die. A stem cell, instead, retains its capacity to renew itself and replicate. Thus, if we can still observe, many months later, that a cell is still alive, that means it is indeed a stem cell – or a cell derived directly from the division of a stem cell". In the newly published article, Sangiorgi and Capecchi have shown with their technique that a particular subset of the pancreatic cells, the so-called acinar cells, are indeed stem cells. The truly interesting aspect of their results is that these cells also produce important digestive enzymes.

Premature ejaculation spray enables men to last 6 times longer after penetration

Men with premature ejaculation who used a topical spray five minutes before intercourse were able to delay their orgasm six times longer than normal, according to a study in the April issue of BJU International. Three hundred men with clinically diagnosed lifelong premature ejaculation (PE) from 31 centres in the UK, Czech Republic, Hungary and Poland, were randomised into two groups. Two hundred used the PSD502 spray, which contains 7.5mg of lidocaine and 2.5mg of prilocaine, and 100 used a placebo spray with no active ingredients. Every time they had intercourse during the three-month study period, each couple measured the time from vaginal penetration to ejaculation with a stopwatch. The men were asked to abstain from sexual activity or masturbation for 24 hours before each recorded encounter. The time from penetration to ejaculation increased from an average of 0.6 minutes to 3.8 minutes in the medicated group and to just 1.1 minutes in the placebo group. When these figures were adjusted to take account of any variations between the two groups, these showed that the treatment group were able to last 6.3 times longer after penetration when they used the spray. The placebo group lasted 1.7 times longer.

New risk variant for atopic dermatitis identified

Scientists of the Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch and Charité – University Medical School, Berlin, Germany, in collaboration with researchers from the Klinikum rechts der Isar of Technical University Munich and Christian Albrecht University, Kiel, have identified a gene variant on chromosome 11 that is associated with an increased risk of atopic dermatitis. In a large genome-wide association study the researchers scanned the genomes of more than 9600 participants from Germany, Poland and the Czech Republic. "Our findings cast new light on the pathogenesis of the disease," said Professor Young-Ae Lee (Charité / MDC). The pediatrician-researcher and her collaborators hope the study will lead to a new approach to targeted therapy for this chronic skin disorder. (Nature Genetics doi: 10.1038/ng.347)*. More and more people suffer from atopic dermatitis, which is also known as atopic or infantile eczema. Atopic dermatitis is a chronic (long-lasting) inflammatory skin disease that typically affects the large flexures such as the bend of the elbows or the back of the knees. Patients suffer from recurrent flares of intense itching, dryness and redness of the skin, with weeping of clear fluid in the acute stage, and skin thickening (lichenification) in the chronic stage. Along with hay fever and asthma, atopic dermatitis is one of the most common allergic disorders. In the industrialized countries about 15 percent of young children are affected. Atopic dermatitis is typically the first clinical manifestation of allergic disease. In most cases atopic dermatitis appears within the first few years of life. For the majority of affected children this marks the beginning of an "allergic career", which in later years evolves into hay fever or asthma. Just what triggers the outbreak of atopic dermatitis is not yet fully understood. However, epidemiological studies indicate that the genetic contribution is substantial. For that reason, of the total of 9600 study participants, the scientists decided to scrutinize the genomes of 3011 individuals more closely. These included children and adults with atopic dermatitis, healthy controls, as well as entire families in which at least two children have atopic dermatitis. The researchers scanned the entire genome, searching for genetic variants that are especially common in atopic dermatitis patients. The study demonstrates that several genes are involved in the pathogenesis of atopic dermatitis. Most importantly, the researchers identified a variant on chromosome 11 that is particularly common in the patients with atopic dermatitis. This variant is located in a region containing the gene C11orf30 which encodes the protein EMSY. The scientists suspect that a mutation in this gene is associated with atopic dermatitis. However, the exact role of EMSY in atopic dermatitis still needs to be investigated.

Young adults at future risk of Alzheimer's have different brain activity, says study

Young adults with a genetic variant that raises their risk of developing Alzheimer's Disease show changes in their brain activity decades before any symptoms might arise, according to a new brain imaging study by scientists from the University of Oxford and Imperial College London. The results may support the idea that the brain's memory function may gradually wear itself out in those who go on to develop Alzheimer's.
The research, published today in the journal Proceedings of the National Academy of Sciences, provides clues as to why certain people develop Alzheimer's Disease (AD) and it may be a step towards a diagnostic test that identifies individuals at risk. The degenerative condition is the most common cause of dementia and it affects around 417,000 people in the UK. The APOE4 genetic variant is found in about a quarter of the population. Not everyone who carries the variant will go on to develop AD, but people who inherit one copy of APOE4 have up to four times the normal risk of developing the late-onset variety of the disease. People who have two copies have around ten times the normal risk. The researchers behind today's study stress that most carriers of APOE4 will not go on to develop Alzheimer's and carriers should not be alarmed by the study's findings.

Stem cell therapy grows new blood vessels

Research led by David Hess of the Robarts Research Institute at The University of Western Ontario has identified how to use selected stem cells from bone marrow to grow new blood vessels to treat diseases such as peripheral artery disease. It's one of the severe complications often faced by people who've had diabetes for a long time. Reduced blood flow (ischemia) in their limbs can lead to resting pain, trouble with wound healing and in severe cases, amputation. The research is published in Blood. Hess drew human bone marrow and simultaneously isolated three different types of stem cells that co-ordinate together to form new blood vessels. These are called pro-angiogenic stem cells. They were purified to remove any inflammatory or contaminated cells, and then injected into the circulation of mice which had one of their leg arteries ligated and removed. The researchers showed how these stem cells have a natural ability to hone in on the area of ischemia to induce blood vessel repair and improve blood flow. Hess says this research is clinically-applicable because they studied the function of human stem cells in immune-deficient mice. The preclinical data from Hess’ research was used by a biopharmaceutical company, Aldagen (www.aldagen.com) to receive FDA clearance for a multi-center clinical trial involving 21 patients with end-stage peripheral artery disease. The clinical study has been successfully completed, and the group of treated patients experienced improvements in overall clinical status as well as increased blood flow in the affected limb. Aldagen has also successfully completed a 20 patient study using these pro-angiogenic stem cells in patients with end-stage ischemic heart failure. "We can select the right stem cells from the patient's own bone marrow and put them back in the area of ischemia to allow these cells to coordinate the formation of new blood vessels." says Hess, a professor in physiology and pharmacology at Western's Schulich School of Medicine & Dentistry. "These principles could be applied not only to ischemic limbs, but to aid in the formation of new blood vessels in ischemic tissue anywhere in the body, for example after a stroke or heart attack."

Link between widely used osteoporosis drugs and heart problems probed

New research at Wake Forest University School of Medicine evaluated the link between a common class of drugs used to prevent bone fractures in osteoporosis patients and the development of irregular heartbeat. The study's findings appear in the current issue of Drug Safety, a publication of the International Society of Pharmacovigilance covering the safe and proper use of medicines. "Some trials show there could be a potential link between the use of bisphosphonates and the development of serious heart rhythm problems, but in our study the link wasn't conclusive," said Sonal Singh, M.D., M.P.H., an assistant professor of internal medicine and lead investigator for the study. "So we urge that additional investigations be conducted." Bisphosphonates, found in prescription drugs including BonivaTM, FosomaxTM, ReclastTM and ActonelTM, inhibit the breakdown of bones, which reduces the risk of fractures, especially those of the spine and hips in older patients. The first such drugs were approved for use in the mid-1990s.
Early studies indicated that the use of bisphosphonates might cause problems with heart rhythm, or atrial fibrillation, which increases the risk for stroke or heart attack. For the study published this month, researchers analyzed the data from previous observational studies and clinical trials to determine the link between bisphosphonate therapy and irregular heart beat. Researchers found that bisphosphonate use was associated with a significant increase in the incidence of "serious" heart rhythm disturbances, classified by hospitalization, disability or death resulting from the condition. However, when they included "non-serious" cases in their analysis, they found no overall increased risk of atrial fibrillation, the study shows."Our findings were discordant, with conflicting results," Singh said. "The challenge now is to figure out what it all means."

Fat-derived inflammatory factor may explain diseases that come with obesity

An inflammatory factor already linked to several diseases, including pulmonary disease, lung cancer, and arthritis, may also be responsible for the insulin resistance that comes with obesity, according to a new study published in the April issue of Cell Metabolism, a Cell Press publication. Researchers have found that the inflammatory chemokine known as CXCL5 rises and falls with obesity and subsequent weight loss in humans. (Chemokines are structurally related signaling proteins that are secreted by cells.) They found further evidence tying the inflammatory factor, which is produced and secreted at high levels by fat tissue, to insulin resistance in mice. What's more, they show that treatments designed to block its action improves the animals' sensitivity to insulin. "Clearly, this finding could be a big development for understanding the side effects of obesity," said Lluis Fajas of INSERM in France. "It offers a new target for therapy and new hope for subjects to improve their pathology." Fat tissue known as white adipose tissue (WAT) is primarily involved in energy storage in the form of triglycerides and energy release in the form of free fatty acids, Fajas' team explained. However, WAT is more than a fat storage organ; it also secretes numerous other factors with roles in both health and disease. In the new study, the researchers show that CXCL5 is one of those factors. The chemokine is expressed at high levels in WAT, particularly in immune cells known as macrophages. Moreover, they report that CXCL5 is dramatically increased in the blood of people who are obese compared to those who are lean. Those CXCL5 levels drop when obese people lose weight and are also lower in obese individuals that continue to respond to insulin than in those who are insulin resistant. They further found that treatment with recombinant CXCL5 blocks insulin-stimulated glucose uptake in the muscles of mice. What's more, treatment of obese, insulin-resistant mice with either anti-CXCL5 neutralizing antibodies or drugs that block the receptor it triggers (known as CXCR2) reverses those symptoms. Mice lacking the CXCL5 receptor are also protected against obesity-induced insulin resistance. Overall, the findings show that CXCL5 produced by fat tissue "represents a link between obesity, inflammation, and insulin resistance." Interestingly, they added, the CXCR2 receptor is active outside of muscle, in cells that line blood vessel walls and in the lung and intestine, for example. Therefore, increased CXCL5 circulating levels as observed in obesity could lead to other problems, including atherosclerosis and other inflammatory diseases."Studies aiming to elucidate the role of WAT-secreted CXCL5 in all these obesity-related pathologies are likely to be forthcoming in the near future," they wrote. "Inhibiting CXCL5 secretion or function in obese individuals may not only ameliorate their insulin sensitivity, but could also decrease the risk of developing other major obesity-related pathologies."

Too much protein, eaten along with fat, may lead to insulin resistance

A clue about the blood chemistry of obese people who develop insulin resistance, a precursor to diabetes, has been confirmed in animal studies at the Duke University Medical Center. Obese people have been found to harbor proteins called branched-chain amino acids (BCAAs) at far higher levels than non-obese people. The suspicion has been that these amino acids, in combination with a high-fat diet, contribute to inulin resistance. The team found that the BCAA signature in obese humans consisted of the branched-chain amino acids themselves, plus a cluster of several products related to the body's breakdown processes for BCAA. "In the case of the amino acids, we also are finding increased levels of their metabolic breakdown products, which suggests the whole system for handling the amino acid metabolic process has been overloaded," said senior author Christopher Newgard, Ph.D., director of the Sarah W. Stedman Nutrition and Metabolism Center and W. David and Sarah W. Stedman Distinguished Professor at Duke. "Our rat studies show that this overload causes changes at the cellular level that can lead to insulin resistance." To determine whether the BCAA signature in obese humans might signal that their intake is harmful, the scientists performed a feeding study in rats that showed an independent contribution of BCAAs to insulin resistance. "These findings, however, would need to be confirmed in studies with people before any dietary recommendations could be issued," said Laura Svetkey, M.D., director of the Duke Hypertension Center, director of clinical research at the Sarah W. Stedman Nutrition and Metabolism Center, and co-senior author of the study, published in Cell Metabolism. "Insulin resistance occurred in animals with a diet high in the branched-chain amino acids, but only if they were ingested along with a high level of fat in the diet," Newgard said. Because obese humans tend to ingest high-fat diets, the combination of high-BCAA and high-fat intake might contribute to insulin resistance in obese humans, but additional studies are needed. BCAAs comprise as much as 25 percent of amino acids in dietary protein, and are particularly enriched in diets high in animal (meat) proteins. "I want to be clear that our animal data suggest that there is nothing wrong with obtaining protein from sources that are high in branched-chain amino acids, as long as you are not eating beyond what your energy needs are," said Newgard, who is a professor of pharmacology and cancer biology and professor of medicine at Duke. "If you add a lot of unneeded protein to a fatty diet, perhaps that's where you get into problems. The ancient Greeks were right: everything in moderation." Insulin resistance happens when insulin, released by the beta cells in the pancreas, doesn't work normally to stimulate glucose uptake into tissues. Rats on a high-fat diet gained substantially more weight than rats that ate BCAAs with high-fat chow or those that ate standard chow. However, the rats eating the high-fat diet with BCAA became as insulin resistant as rats fed a high-fat only diet, even though they weren't eating as much.

Joslin study pinpoints role of insulin on glucagon levels

Researchers at the Joslin Diabetes Center have shown for the first time that insulin plays a key role in suppressing levels of glucagon, a hormone involved in carbohydrate metabolism and regulating blood glucose levels. The study helps in the understanding of why those with diabetes have high blood glucose levels and could lead to development of a drug aimed at targeting glucagon levels. "This is a very important finding because until now scientists have only speculated that insulin may be involved in keeping glucagon levels in check," said Rohit N. Kulkarni, M.D., Ph.D., Principal Investigator in the Joslin Section on Cellular and Molecular Physiology and senior author of the study published today in the April issue of Cell Metabolism. Produced by the alpha cells in the pancreas, glucagon acts on the liver to help raise blood glucose when it becomes low. It has the opposite effect on the liver as insulin, which is released from pancreatic beta cells to lower blood glucose when it is high. In a healthy individual, the two counter each other to keep blood glucose levels balanced. In individuals with long-standing type 1 or type 2 diabetes, inappropriate glucagon secretion can increase the chances of hypoglycemia (low blood glucose levels) and can interfere with insulin therapy. The finding suggests that for people with either type 1 or type 2 diabetes, a therapeutic approach could be developed to target insulin receptors or proteins in alpha cells in order to suppress glucagon secretion. In addition, the research may also help in the understanding of why patients with type 1 diabetes in particular, who are required to inject insulin on a regular basis, are at risk for hypoglycemia. It was thought that this increased risk was linked in some way to insulin receptors in the alpha cells, an idea that today's study suggests is in fact the case, Dr. Kulkarni explained. "This gives us some insight into the cause of hypoglycemia, the most common complication in patients with type 1 diabetes," he said. "Injecting insulin leads to a decrease in blood glucose. If it starts to go too low, glucagon normally kicks in to prevent hypoglycemia. But, what happens in diabetes is the alpha cells become desensitized by repeated insulin injections over many years and they start to behave abnormally. We believe this is linked to insulin receptor function."

Joslin Study Identifies ‘Good’ Energy Burning Fat in Lean Adults

Researchers at the Joslin Diabetes Center have demonstrated that adult humans still have a type of “good” fat previously believed to be present only in babies and children. Unlike white fat, which stores energy and comprises most body fat, this good fat, called brown fat, is active in burning calories and using energy. The finding, reported in the April 9th issue of The New England Journal of Medicine, could pave the way for new treatments both for obesity and type 2 diabetes.Scientists had thought that brown fat only existed in humans during childhood and was mostly gone by adulthood. The paper shows that brown fat not only exists in adult humans, but also for the first time, that the fat is metabolically active. “The fact that there is active brown fat in adult humans means this is now a new and important target for the treatment of obesity and type 2 diabetes,” said C. Ronald Kahn, M.D., senior author and Head of the Joslin Section on Obesity and Hormone Action and the Mary K. Iacocca Professor of Medicine at Harvard Medical School. Obesity is a major risk factor for type 2 diabetes. According to the researchers, the idea behind a new therapy would be to find a way to stimulate brown fat growth to both control weight and improve glucose metabolism. “Not only did we find active brown fat in adult humans, we found important differences in the amount of brown fat based on a variety of factors such as age, glucose levels and, most importantly, level of obesity,” said lead author Aaron Cypess, M.D., Ph.D., a Research Associate and Staff Physician at Joslin. Not surprisingly, the study found that younger patients were more likely to have larger amounts of brown fat, and the brown fat was more active during colder weather, keeping with its role of burning energy to generate heat. Brown fat was also more common in adults who were thin and had normal blood glucose levels.

Cigarette smoke may alter immune response in COPD exacerbations

Smoking cigarettes is not only the principle cause of chronic obstructive pulmonary disease (COPD), but it may change the body's immune responses to bacteria that commonly cause exacerbations of the disease, according to new research in a mouse model. "It is well established that smoking is the main risk factor for COPD. But our research also suggests that cigarette smoke substantially changes the immune response to bacteria, which means that patients with COPD who smoke are weakening their body's ability to deal effectively with bacterial invaders. This may cause even further progression of the disease," said Martin Stämpfli, Ph.D., an associate professor at McMaster University, the principle investigator of the study. "We wanted to see whether and how cigarette smoke would change the inflammatory response to the bacteria that is the culprit behind many COPD exacerbations, nontypeable Haemophilus influenzae or NTHI." Their results were published in the second issue of April of the American Journal of Respiratory and Critical Care Medicine. Dr. Stämpfli and colleagues tested the effects of cigarette smoke exposure on inflammation and immune response in mice that were exposed to cigarette smoke twice daily five days a week for either eight weeks or four days then challenged with an intranasal inoculation of NTHI. The cigarette smoke exposure roughly approximated that of an "average" human smoker (within the limitations of a model with differing metabolic processes.) Control mice were not exposed to cigarette smoke, but were inoculated with NTHI as were the cigarette smoke-exposed mice. The researchers found that mice that were exposed to cigarette smoke, whether for four days or for eight weeks, showed distinct shifts in their immune-response profile, namely an increase in inflammation of the lungs after the NTHI challenge, increased weight-loss in response to the bacterial infection and, notably, a shift in the expression of inflammatory markers.

New, simple method identifies preterm infants at risk of eye disease

A simple way of establishing which preterm infants are at risk of developing the eye disease ROP is to follow their weight gain. A new study from the Sahlgrenska Academy, University of Gothenburg, Sweden, suggests that following weekly weight development might replace the need for considerably more expensive ophthalmological examinations. Every year around 1000 Swedish infants are born more than two months prematurely. Preterm infants are at increased risk of damage to several important organs, including the brain, lungs, guts and eyes. Around 350 of these infants develop the eye disease retinopathy of prematurity (ROP) which, if left untreated, can threaten their sight. Ten per cent, or around one hundred, of the preterm infants need the same treatment to prevent blindness. "In the past 50 years it has been routine for all infants born very prematurely to be examined several times by ophthalmologists to identify children who need treatment for ROP, but this expensive method of screening can now perhaps be replaced by a considerably simpler and cheaper method, so that ophthalmological examination can be avoided in most cases," says Professor Ann Hellström of Sahlgrenska Academy. The research team has previously identified another important link between preterm birth and vascular disease in the eye, the protein IGF-1, which is strongly linked to the infant's weight gain. Assisted by statisticians at the University of Gothenburg, the researchers have developed an assessment model known as WINROP (Weight IGF-1 Neonatal ROP), which is based on weekly measurements of the infant's weight and analyses of the serum levels of IGF-1. "However, one would prefer not to take any blood samples from the preterm infants, and therefore we wanted to investigate whether our surveillance model worked if we only used the infant's weight. We found that it works extremely well," says Professor Hellström. In a review of medical records, information on the weekly weights of 350 infants was entered into the model, and the outcome was compared with the ophthalmological examinations performed on them. "All infants at risk were on average identified a few months before the ophthalmologist had seen signs of ROP requiring treatment. The method could therefore not just save money but also make it possible for infants with eye problems to be identified earlier," says Professor Hellström.

Altered gene can increase risk of schizophrenia

Rutgers geneticist Linda Brzustowicz and her colleagues have identified a specific DNA change that is likely to increase risk for developing schizophrenia in some people. It provides a potential mechanism that may be a point of entry for drug therapy, consistent with the growing trend of personalized medicine. The research findings are reported in the April issue of the American Journal of Psychiatry (AJP). An accompanying editorial highlights the significance of this work. Brzustowicz, a professor of genetics at Rutgers, The State University of New Jersey, and board-certified psychiatrist, said that the research has demonstrated a functional DNA change that increases gene expression. This conclusion is based on its presence in the genes of a Canadian study population of 24 families where multiple individuals had been diagnosed with schizophrenia. The gene in question, NOS1AP, previously known as CAPON, is one which Brzustowicz has been studying for six years. The paper also presents an innovative statistical method, Posterior Probability of Linkage Disequilibrium (PPLD). This is the work of co-author Veronica Vieland of The Research Institute at Nationwide Children's Hospital, Columbus, Ohio. The new analytical technique quantifies the statistical evidence for association, in this case between the altered gene and schizophrenia. The researchers evaluated 60 variants of the gene or single nucleotide polymorphisms (SNPs). "Our use of the PPLD was really helpful in sorting the evidence. It showed that of the 60 SNPs we were evaluating, three had a much higher probability of association with the illness," Brzustowicz said. "This paved the way for our next step – doing a functional analysis using cells grown in culture – which is much more labor intensive. We had reduced our 60 candidates down to a short list of three, which greatly simplified this next step." Each of the three candidate SNPs was introduced into separate cultures of identical cloned cells derived from human brain tissue. The cultures differed only in which of the SNP variants was introduced. The challenge was to measure the quantity of overexpression, that is, how much excess protein was being produced by each of the three variants.

Oral contraceptives associated with increased risk of lupus

The ratio of women to men with the autoimmune disease systemic lupus erythematosus (SLE) is nine to one and the incidence increases after puberty. Hormones secreted by the body are therefore believed to play an important role in the origins of the disease. A new large, population-based observational study found that the use of oral contraceptives was associated with an increased risk of SLE, particularly among women who had recently started taking them. The study was published in the April issue of Arthritis Care & Research (http://www3.interscience.wiley.com/journal/77005015/home). Led by Dr. Samy Suissa of the Centre for Clinical Epidemiology at Jewish General Hospital of McGill University in Montreal, researchers obtained data on more than 1.7 million women ages 18-45 from the U.K. General Practice Research Database, which contains more than 6 million people. The women all had prescriptions for combined oral contraceptives (COCs) containing estrogen and progestogen. During an average of eight years of follow-up, 786 women had a first-time diagnosis of SLE. Each case was matched with up to 10 controls among women without SLE at the time of the case's diagnosis. The results showed that the use of COCs was associated with a significant increased risk of newly diagnosed SLE. This was mostly limited to the first three months of use with first- and second-generation contraceptives containing higher doses of estrogen, suggesting "an acute effect in susceptible women and possibly a dose-response effect of estrogen on SLE onset," according to the authors. They note that estrogen can directly modulate the immune response, which could complete the action of some sex-linked genes and contribute to the genetic predisposition of the disease, and it has also been shown to have an effect on the breakdown of immune tolerance seen in SLE. Previous studies on the risk of SLE following use of oral contraceptives have had conflicting results, but the results of the current study are consistent and complement those of the NIH-sponsored Nurses' Health Study. "Our findings that longer-term use of contraceptives is associated with an increased risk of incident SLE (albeit of lower magnitude) and that current use of contraceptives with higher doses of ethinyl estradiol is associated with an increased risk of incident SLE, suggest a possible dose-response effect of estrogen on SLE onset, which could be an alternative or additional mechanism to favor occurrence of the disease," the authors state. They note that the absence of significant increased risk in third-generation contraceptives may be related to the lower doses of estrogen compared to earlier generations.

Growth factor TGF-B helps maintain health of retinal blood vessels

Scientists at Schepens Eye Research Institute have found that the growth factor known as TGF-? is essential to the health of blood vessels in the retina and that blocking it can cause retinal dysfunction. These findings, published in the April 2 issue of PLoS ONE, may have an important impact on the prevention and treatment of diseases such as diabetic retinopathy and macular degeneration. "These results are significant because they add to our understanding of the molecules that help to maintain blood vessels in a healthy state," says Patricia D'Amore, PhD, senior scientist at Schepens and principal investigator of the study, who adds that this information may be useful in understanding the changes that occur in the retinal microvasculature prior to the development of proliferative diabetic retinopathy. "Insight into the role of this growth factor may also help clinicians monitor the use of systemic drugs targeting TGF-?, which is elevated in a number of conditions (such as cancer and fibrotic diseases) to limit any vision problems that might occur as a side effects." adds Tony Walshe, PhD, the first author of the study and a Postdoctoral Fellow in the D'Amore's laboratory team. Capillaries are the smallest blood vessels in the body and the site at which oxygen and nutrients are transferred from the blood to the tissues. A capillary is composed of an endothelial cell, which forms the lining of the small tube, and a pericyte, which wraps around the outside of the tube. Scientists have long believed that communication between these two cell types is necessary to maintain blood vessel structure and function. According to Walshe, the goal of the PLoS ONE study was to determine if TGF-? plays a role in keeping blood vessels functioning normally. In previous experiments using tissue cultures, the D'Amore laboratory had identified TGF-? as a protein that results from the communication between the two cell types and which they use to maintain the health of the small blood vessels. In the current study, the team wanted to confirm that finding in animals.

Test predicts who will develop end-stage renal disease

Measuring kidney function by assessing two different factors—glomerular filtration rate (GFR) and urinary albumin levels—helps determine which patients with chronic kidney disease (CKD) will develop end-stage renal disease (ESRD), according to a study appearing in the May 2009 issue of the Journal of the American Society Nephrology (JASN). This combination test could help physicians identify patients at high risk of serious kidney trouble and allow them to intervene at an early stage. While there is a high prevalence of CKD worldwide, relatively few individuals with the disease develop ESRD, expected to affect 785,000 people in the U.S. by 2020 (current annual cost: $32 billion). Physicians and researchers have looked for ways to identify which patients will progress to ESRD in order to target patients most in need of extensive treatment, and help establish clinical guidelines and public health plans for treating patients with CKD. Stein Hallan, MD, PhD (St. Olav University Hospital, Norway), and his colleagues recently conducted a study to see if combining two tests commonly used to measure kidney function might help predict ESRD. One test measures an individual's estimated glomerular filtration rate (eGFR—a measure of the volume of fluid filtered by the kidneys), while the other measures the amount of albumin (the predominant protein in the blood) that is excreted in urine. A high urinary albumin level indicates a rapid rate of kidney disease progression, and a low eGFR indicates an advanced stage of disease. The researchers analyzed data from 65,589 adults who participated in the population-based Nord-Trøndelag Health (HUNT 2) Study and found 124 individuals who developed ESRD after more than 10 years of follow-up. Combining urinary albumin and eGFRs results identified more than 65% of patients who would develop this condition. Other factors such as hypertension, diabetes, smoking, obesity, and cardiovascular disease did not provide any additional information that could be used to predict who would develop ESRD. "We provide clear evidence… that reduced eGFR should always be complemented by information on urine-albumin to yield optimal prediction of the risk of progression to ESRD," said Dr. Hallan. He added that combining these measurements might also help reduce the number of patients referred to specialists without losing the ability to detect future ESRD cases.

Enzyme therapy slows kidney function decline

For men with Fabry disease, enzyme replacement therapy (ERT) with agalsidase alfa slows deterioration of kidney function, reports a study in the online edition of the Journal of the American Society of Nephrology (JASN). "The results provide further evidence that ERT with agalsidase alfa may slow the progression of kidney disease, provided that ERT is initiated early in the disease process," comments Michael L. West, MD (Dalhousie University, Canada). The researchers pooled the results of three previous clinical trials of ERT with agalsidase alfa in 108 men with Fabry disease—a rare genetic disorder. Without treatment, Fabry disease causes progressive loss of kidney function, eventually leading to end-stage renal disease. During treatment with an inactive placebo, kidney function declined rapidly. By comparison, during treatment with agalsidase alfa (1 to 4.5 years), the rate of decline slowed considerably. The response to treatment was not as good for patients with lower initial kidney function. "This underlines the importance of prompt diagnosis and intervention in patients with Fabry disease," adds Dr. West. The study was one of the largest ever of men with Fabry disease and included the most accurate techniques of measuring kidney function. The study also had important limitations: it used data from different studies performed at different times; it represented a relatively narrow range of patient characteristics, specifically excluding children and women; and it lacked adequate data for full statistical analysis. While not approved for use in the US, Agalsidase alfa is approved for use in over 40 countries including Canada, European countries, Argentina, Australia, and Japan. A related drug called agalsidase beta is approved in the US.

Prune juice not necessary - New research should make bowel movements easier

If you hate prune juice and chalky fiber supplements, just sit down and relax. Help is on the way. In a research report published online in The FASEB Journal (http://www.fasebj.org), a team of researchers has discovered a new way to make it a lot easier to go to the bathroom, especially when all other methods fail. Specifically, they have found a group of nerve ending receptors which, when stimulated, causes the bowels to pass waste, and the specific receptor needed to activate bowel clearance. Furthermore, they tested chemicals that work with those receptors, providing a blueprint for the development of new laxatives. "We hope that the receptor identified by our study would be exploited more in the design of drugs to treat constipation," said Bindu Chandrasekharan, a researcher from Emory University who was involved in the study.
The research involved two groups of mice, focusing on a type of receptor also present on human nerves in the gut (a type of adenosine receptor). The first group of mice had normal adenosine receptors on these nerves and normal bowel movements. The second group of mice completely lacked these adenosine receptors and showed familiar signs of constipation. The researchers started with simple experiments such as comparing the wet weight, dry weight, and water content in the stools of both groups. The mice were also made to drink a dye not absorbed by the body to see how it passed or did not pass. In addition, the researchers used microscopic lasers to separate the nerve cells from the bowel to determine exactly where the receptors are located. Then they tested various chemicals that can activate or inhibit the nerve receptors.

Blood tests reveal tobacco smoke residues in non-smoking New Yorkers

More than half of non-smoking New Yorkers have elevated levels of cotinine in their blood – meaning that they were recently exposed to toxic second-hand smoke in concentrations high enough to leave residues in the body. Cotinine, a by-product of nicotine breakdown, is not harmful itself but signals exposure to environmental tobacco smoke. A Health Department study, published online this week in the journal Nicotine and Tobacco Research, shows that 57% of adult New Yorkers (2.5 million) have elevated cotinine levels, compared to 45% of adults nationwide – a finding that may reflect the city's dense, urban character. Second-hand smoke contains many harmful chemicals. It is known to cause cancer and heart disease in adults, as well as serious health problems for children. The data come from the New York City Health and Nutrition Examination Survey, which was conducted in 2004, one year after New York City's smoke-free air law took effect. Although the law protects non-smokers from the dangers of second-hand smoke at work and in some public places, this study shows that many non-smokers are not fully protected. Creating a smoke-free home is the most important step that New Yorkers can take to protect their families. "Tobacco smoke is a toxic pollutant," said Dr. Thomas R. Frieden, New York City Health Commissioner. "Most New York City non-smokers are breathing in dangerous chemicals in second-hand smoke, potentially increasing the risk of cancer and heart disease. Households with a smoker should set a 'no smoking' policy at home to protect the family. We encourage all New Yorkers who smoke to quit – this is the best way to protect yourself and others."
"The study provides more evidence of the pervasiveness of second-hand smoke," said Jennifer Ellis, PhD, a former Health Department epidemiologist and the study's lead author. "It's not clear why New Yorkers experience more exposure, despite the city's relatively low smoking rate. It may be that living and working in close quarters with one another puts us at higher risk."

Parkinson's disease medication triggers destructive behaviors

A new study conducted at Mayo Clinic reports that one in six patients receiving therapeutic doses of certain drugs for Parkinson's disease develops new-onset, potentially destructive behaviors, notably compulsive gambling or hypersexuality. The study extends findings from two Mayo case series published in 2005 that reported a connection between dopamine agonist medications and compulsive gambling or hypersexuality. Dopamine agonists are a class of drugs that include pramipexole and ropinirole. They are commonly used to treat Parkinson's disease, but low doses also are used for restless legs syndrome. They uniquely stimulate brain limbic circuits, which are thought to be fundamental substrates for emotional, reward and hedonistic behaviors. "The 2005 case series alerted us that something bad was happening to some unfortunate people. This study was done to assess the likelihood that this effect would happen to the average Parkinson's patient treated with these agents," says J. Michael Bostwick, M.D., Mayo Clinic psychiatrist who spearheaded the new study. It is published in the April issue of Mayo Clinic Proceedings. The researchers analyzed the medical records of patients with Parkinson's disease residing in counties surrounding Rochester, Minn., who received their primary neurological care at Mayo Clinic in Rochester between 2004 and 2006. This group included 267 patients. Of those, 66 were taking dopamine agonists for their Parkinson's disease. Of those 66, 38 were taking the drugs in therapeutic doses (doses expected to be at least minimally beneficial). The findings were definitive. Seven patients experiencing new-onset compulsive gambling or hypersexuality were taking dopamine agonists in therapeutic doses. None of the other Parkinson's disease patients developed compulsive gambling habits or hypersexuality, including the 28 patients on subtherapeutic dopamine agonist doses or the other 201 patients not taking dopamine agonists. None of the 178 patients treated only with the standard drug for Parkinson's disease, carbidopa/levodopa, developed these behaviors.

Music Reduces Stress in Heart Disease Patients

Listening to music may benefit patients who suffer severe stress and anxiety associated with having and undergoing treatment for coronary heart disease. A Cochrane Systematic Review found that listening to music could decrease blood pressure, heart rate, and levels of anxiety in heart patients. Living with heart disease is extremely stressful. The uncertainties and anxieties surrounding diagnosis and the various medical procedures involved in treatment can significantly worsen the condition. For example, stress can increase blood pressure, leading to increased risk of complications. Music listening may help to alleviate stress and therefore reduce this risk. "Our findings suggest music listening may be beneficial for heart disease patients," says Joke Bradt, who works at the Arts and Quality of Life Research Center at Temple University in Philadelphia. "But the trials we looked at were generally small and varied in terms of styles of music used and length of music sessions. More research on the specifics of music listening is certainly warranted." The researchers reviewed data from 23 studies, which together included 1,461 patients. Two studies focused on patients treated by trained music therapists, but most did not, using instead interventions where patients listened to pre-recorded music on CDs offered by healthcare professionals.

Weak social ties at workplace increase risk of burn-out

Long-term leaves of absence tied to stress-related diagnoses are often preceded by a long period without any secure and comforting social relations. This is shown in a recently published study in public health science at Karlstad University in Sweden. “Sickness leaves are a multifaceted problem with consequences for the individual, the person’s closest friends and relations, the employer, and society,” says Ulla-Britt Eriksson, who authored the doctoral dissertation in public health science. “Enhanced knowledge of what conditions affect the process leading to long-term sickness leave provides a valuable platform for both preventive and rehabilitative measures.” The dissertation described how long-term sickness leave due to burn-out and other mental diagnoses can be understood. What preceded the sickness leave is depicted as a process in which the individual is gradually emptied of feelings that sustain the life-giving force that provides joy and involvement and serves as a basis for mental well-being. This force is nourished by secure and comforting social relations with other people. Individuals on long-term sickness leave made it clear that these preconditions were lacking in their surroundings. “The overall aim of the dissertation has been to describe and understand the processes that lead to long-term sickness leave from the point of view of the individual taking the leave,” says Ulla-Britt Eriksson. “The focus has been on sickness leaves tied to mental, stress-related diagnoses, with a special emphasis on so-called burn-out diagnoses.”

CSHL researchers explain process by which cells 'hide' potentially dangerous DNA segments

The DNA in the 23 pairs of chromosomes in each of the billions of cells of the human body is so tightly packed that it would measure six feet in length if stretched end to end. A genome of this size can squeeze into a cell's tiny nucleus because it is compressed into highly condensed chromatin fibers by proteins called histones.All chromatin in the cell nucleus represents a massive condensation of the genetic material. But a portion of it might well be called super-condensed; it forms a kind of chromatin called heterochromatin. The genes contained within these portions of the genome are effectively "silenced" because they cannot be accessed by the cell's DNA-activating machinery. These "hidden" parts of the genome also include highly repetitive, gene-poor, regions. Some of these, if unpacked, would set loose DNA sequences that act like parasites – able to jump around to other areas, sometimes randomly, unleashing genetic chaos.To assemble heterochromatin, numerous molecules participate in an elaborate series of maneuvers that have gradually come to light. "But scientists have been a little hazy on the initial steps and requirements that get this process going," says Professor Leemor Joshua-Tor, Ph.D., of Cold Spring Harbor Laboratory (CSHL). She and her research team have now brought this process into sharper focus by identifying a critical requirement for heterochromatin to be established in the nucleus.In a report that appears online on April 9th in the journal Molecular Cell, they show that the assembly of heterochromatin depends on the strength with which a protein called Chp1 binds to a specific target site located on a histone protein that has attached to the double helix.

Small RNAs can play critical roles in male infertility/contraception

University of Nevada School of Medicine scientists in the Department of Physiology and Cell Biology have discovered insight into the reproductive workings of the male sex chromosome that may have significant implications for male infertility and contraception. This important discovery has been published in Nature Genetics, one of the highest-ranking journals in the field of biomedical research based upon the impact factor.
The study findings indicate that the X chromosome in developing sperm cells encodes numerous tiny ribonucleic acids called microRNAs despite the fact that that most of genes on the X chromosomes are suppressed. This unprecedented observation implies that these small RNAs have critical roles in chromosome inactivation and also in sperm formation. "The sex chromosome silencing in meiotic male germ cells is a well-known phenomenon, which has been termed meiotic sex chromosome inactivation. I was surprised when we first observed that numerous microRNAs were highly expressed in these cells," said Wei Yan, M.D., Ph.D., principal investigator for the study and associate professor of physiology and cell biology at the School of Medicine. Working in collaboration with Dr. John McCarrey, professor of molecular biology and reproductive biology at the University of Texas, San Antonio, Yan's research group further investigated all the known X-linked microRNAs. Their data confirm that these X chromosome-derived microRNAs indeed escape the silencing effects and mange to be expressed. "This finding opens a new avenue towards understanding the role of these small RNA species in the control of sperm production. Worldwide, one in nine couples in their reproductive age experience infertility. On the other hand, the number of unintended pregnancy is increasing yearly. Since these small RNAs are involved in the control of sperm formation, they can be causative factors in male infertility and also can be used as non-hormonal male contraceptive targets," added Yan.

Scientists identify chemical compound that may stop deadly brain tumors

Researchers at the University of North Carolina at Chapel Hill School of Medicine have identified a compound that could be modified to treat one of the most deadly types of cancer, and discovered how a particular gene mutation contributes to tumor growth. The findings and potential treatment apply to a type of brain tumor called secondary glioblastoma multiforme (GBM). GBMs are part of a larger group of brain tumors called malignant gliomas, which is the type of cancer Senator Edward Kennedy suffers from. A report of the research will appear in the April 10, 2009 issue of the journal Science. In experiments with tumor cells, the researchers reversed the effects of a mutation in a gene called isocitrate dehydrogenase-1 (IDH1) by replenishing a compound called ?-ketoglutarate (?-KG). "When the IDH1 gene is mutated, the level of ?-KG is reduced, which in turn contributes to tumor growth by helping to increase the supply of nutrients and oxygen to tumor cells. When we added the ?-KG to tumor cells, the effects caused by the IDH1 mutation were reversed," said Yue Xiong, Ph.D., William R. Kenan Jr., Distinguished Professor of Biochemistry and Biophysics and a member of the UNC Lineberger Comprehensive Cancer Center. "If scientists can develop ?-KG into a clinical drug, it could potentially be used for treating brain tumor patients who have this specific gene mutation. The ?-KG compound is already there; it only needs to be modified to be used clinically, so that may save a lot of time," Xiong said.

New therapeutic strategy could target toxic protein in most patients with Huntington's disease

Howard Hughes Medical Institute researchers have designed tiny RNA molecules that shut off the gene that causes Huntington's disease without damaging that gene's healthy counterpart, which maintains the health and vitality of neurons. Laboratory studies suggest that a single small interfering RNA could reduce production of the damaging Huntingtin protein in nearly half of people with the disease. Another 25 percent of patients might benefit from one of a set of four additional small interfering RNAs. Phillip D. Zamore, an HHMI investigator at the University of Massachusetts Medical School in Worcester, and his colleagues reported their findings in an article published April 9, 2009, in the journal Current Biology. There is no treatment for Huntington's disease, which is caused by a mutant form of the Huntingtin gene. Huntingtin is required for healthy nerve cells, but the mutant gene makes a toxic protein that contains excess amounts of the amino acid glutamine. The key to whether the Huntingtin gene is normal or defective lies in a kind of genetic stutter: a repetitive sequence of the DNA triplet CAG, which codes for the amino acid glutamine. Stretches of CAG "repeats" appear in every human being's Huntingtin gene, but the length varies. Whereas the normal gene has a sequence of between six and 34 CAG repeats, the abnormal gene contains many more. In fact, any stretch of DNA containing more than 40 of these repeats ensures that its bearer will develop Huntington's—the greater the number of repeats, the earlier the disease strikes and the greater its ferocity. The abnormal Huntingtin protein causes movement disorders, cognitive failure, and ultimately, death. Children who have a parent with Huntington's disease have a 50 percent chance of inheriting the disease themselves. Zamore studies how RNA interference can be used to silence genes selectively. In the 1990s, he and other scientists learned they could shut down the production of specific proteins by introducing double-stranded RNA into the cell that is identical to the RNA they wanted to turn off. These strands of RNA, known as short interfering RNA (siRNA), slice apart the original RNA, which the cell then destroys. But nine years ago, when researcher Neil Aronin, who is also at UMass Medical School, proposed using the technique to attack Huntington's, Zamore couldn't see a way. "I explained to him that you can't," Zamore said. The problem was that the disease gene and its healthy allele are almost identical, and Zamore told Aronin that he wouldn't be able to distinguish between the two forms of Huntingtin. "Then, as he was leaving my office, it occurred to me that you could," he recalled. The key was something called a single nucleotide polymorphism or SNP.

Biological FM signal maintains inflammation in cancer, asthma and other diseases

A study published tomorrow (10 April) in Science examines a key player in conditions such as cancer, inflammatory bowel disease, rheumatoid arthritis and asthma and has shown that cells use a sophisticated communication system to coordinate responses to infection and maintain inflammation in the body. This system is now a target for designing drugs to treat these conditions. Scientists funded by the Biotechnology and Biological Sciences Research Council (BBSRC), the Medical Research Council (MRC) and the Engineering and Physical Sciences Research Council (EPSRC) have combined biological experiments and mathematics to discover the secrets of NF-kappaB – a biological machine that coordinates the setting up and maintenance of inflammation in the body by broadcasting a signal to surrounding cells. The team from the Universities of Liverpool, Manchester and Warwick, along with scientists from pharmaceutical company AstraZeneca (AstraZeneca R & D, Charnwood) have used Systems biology – a multidisciplinary approach that uses a combination of experimental and theoretical techniques to tackle biological problems – to investigate the role of NF-kappaB. Professor Michael White of the University of Liverpool, who led the research said: "We know that successive peaks and troughs in the amount of NF-kappaB – forming a wave-like pattern over time – can exert exquisite control over many biological processes that underlie the symptoms of inflammation. Furthermore, what we now see is that different cell processes are determined once they pick up the frequency of peaks and troughs in the NF-kappaB signal, just like tuning in to an FM radio signal."

ISU researcher identifies protein that concentrates carbon dioxide in algae

Increasing levels of carbon dioxide in the atmosphere are a concern to many environmentalists who research global warming. The lack of atmospheric carbon dioxide (CO2) concentration, however, actually limits the growth of plants and their aquatic relatives, microalgae. For plants and microalgae, CO2 is vital to growth. It fuels their photosynthesis process that, along with sunlight, manufactures sugars required for growth.
CO2 is present in such a limiting concentration that microalgae and some plants have evolved mechanisms to capture and concentrate CO2 in their cells to improve photosynthetic efficiency and increase growth.
An Iowa State University researcher has now identified one of the key proteins in the microalgae responsible for concentrating and moving that CO2 into cells.

Aerosols may drive a significant portion of arctic warming

Though greenhouse gases are invariably at the center of discussions about global climate change, new NASA research suggests that much of the atmospheric warming observed in the Arctic since 1976 may be due to changes in tiny airborne particles called aerosols. Emitted by natural and human sources, aerosols can directly influence climate by reflecting or absorbing the sun's radiation. The small particles also affect climate indirectly by seeding clouds and changing cloud properties, such as reflectivity. A new study, led by climate scientist Drew Shindell of the NASA Goddard Institute for Space Studies, New York, used a coupled ocean-atmosphere model to investigate how sensitive different regional climates are to changes in levels of carbon dioxide, ozone, and aerosols. The researchers found that the mid and high latitudes are especially responsive to changes in the level of aerosols. Indeed, the model suggests aerosols likely account for 45 percent or more of the warming that has occurred in the Arctic during the last three decades. The results were published in the April issue of Nature Geoscience. Though there are several varieties of aerosols, previous research has shown that two types -- sulfates and black carbon -- play an especially critical role in regulating climate change. Both are products of human activity. Sulfates, which come primarily from the burning of coal and oil, scatter incoming solar radiation and have a net cooling effect on climate. Over the past three decades, the United States and European countries have passed a series of laws that have reduced sulfate emissions by 50 percent. While improving air quality and aiding public health, the result has been less atmospheric cooling from sulfates. At the same time, black carbon emissions have steadily risen, largely because of increasing emissions from Asia. Black carbon -- small, soot-like particles produced by industrial processes and the combustion of diesel and biofuels -- absorb incoming solar radiation and have a strong warming influence on the atmosphere.

Ancient diatoms lead to new technology for solar energy

Engineers at Oregon State University have discovered a way to use an ancient life form to create one of the newest technologies for solar energy, in systems that may be surprisingly simple to build compared to existing silicon-based solar cells.The secret; diatoms. These tiny, single-celled marine life forms have existed for at least 100 million years and are the basis for much of the life in the oceans, but they also have rigid shells that can be used to create order in a natural way at the extraordinarily small level of nanotechnology. By using biology instead of conventional semiconductor manufacturing approaches, researchers at OSU and Portland State University have created a new way to make "dye-sensitized" solar cells, in which photons bounce around like they were in a pinball machine, striking these dyes and producing electricity. This technology may be slightly more expensive than some existing approaches to make dye-sensitized solar cells, but can potentially triple the electrical output. "Most existing solar cell technology is based on silicon and is nearing the limits of what we may be able to accomplish with that," said Greg Rorrer, an OSU professor of chemical engineering. "There's an enormous opportunity to develop different types of solar energy technology, and it's likely that several forms will ultimately all find uses, depending on the situation." Dye-sensitized technology, for instance, uses environmentally benign materials and works well in lower light conditions. And the new findings offer advances in manufacturing simplicity and efficiency. "Dye-sensitized solar cells already exist," Rorrer said. "What's different in our approach are the steps we take to make these devices, and the potential improvements they offer." The new system is based on living diatoms, which are extremely small, single-celled algae, which already have shells with the nanostructure that is needed. They are allowed to settle on a transparent conductive glass surface, and then the living organic material is removed, leaving behind the tiny skeletons of the diatoms to form a template.

Babraham researchers reveal how immune cells can be harnessed to target melanoma

Researchers at the Babraham Institute and the University of Catanzaro "Magna Graecia", Italy, co-ordinating an international network of scientists and clinicians from Europe, the USA and Japan, have identified new mechanisms through which the immune system recognises and responds to tumours like melanomas. This discovery may offer therapeutic approaches for tackling metastatic melanoma, an aggressive form of skin cancer responsible for around 2,000 deaths in the UK each year. These exciting new findings, published in the online edition of the Journal of Clinical Investigation, reveal how a type of white blood cell - Natural Killer (NK) cells - tackles tumours, characterising for the first time the molecular interactions that lead to melanoma destruction. This has advanced understanding of melanoma recognition by the immune system and has the potential to open up new avenues of research into the prevention of metastasis by harnessing NK cells’ natural immunity. Natural Killer cells are found in the blood, the lymph glands and in tissues such as the liver, the lungs and the uterus, where they participate in immune defences against infection, cancer, in reproductive success and in transplantation. They play a key role in the immune response that targets tumour cells, while sparing healthy cells; mouse models revealed that NK cells prevent and control tumour growth although, in the case of melanomas, the molecular interactions behind this and how NK cells control metastatic progression had until now remained elusive. The team of researchers, led by Francesco Colucci, Group Leader at the Babraham Institute and Ennio Carbone, of the University of Catanzaro "Magna Graecia", Italy, studied both human metastatic melanomas - aggressive forms of skin cancer that have spread to other sites - and spontaneous mouse melanomas.

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