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News - Week 13 - 2009

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Garrett is a 15-year old boy living in the Alaskan wilderness with a menagerie of orphaned animals. Growing up close with nature has given him a deep understanding of nutritional needs required by diet sensitive animals on the reserve. Unfortunately, the untimely and tragic death of his mother propelled him into a downward spiral and he risked flunking out of school. This led to his fathers decision to home-school Garrett. His first assignment was to study a controversial book written by Dr. Max Gerson. Written over 50 years ago, Dr. Gerson found that diet could, and did, cure cancer. Controversial at the time (and even today), Garrett took on the challenge of researching this amazing therapy, which drew the interest of his neighbors in the small Alaskan community. With the help of Dr. Gersons daughter, Charlotte Gerson, and grandson, Howard Strauss, they gave him the ammunition needed to go in search for the truth a truth that would affect not only him, but his entire Alaskan village all of whom wanted to know if these claims were true. After a number of cancer patients, who were diagnosed as terminal, shared their stories and their medical records with Garrett, it became abundantly clear that, contrary to the disinformation campaign spear-headed by the multi-billion dollar medical and pharmaceutical industry, a cure for virtually all cancers and chronic diseases does exist and has existed for over 80 years!

Scientists closer to understanding how to control high blood sugar

Scientists are closer to understanding which proteins help control blood sugar, or glucose, during and after exercise. This understanding could lead to new drug therapies or more effective exercise to prevent Type 2 diabetes and other health problems associated with having high blood sugar. Insulin resistance happens when insulin produced by the body doesn't properly stimulate the transport of glucose into the cells for energy. Too much glucose in the bloodstream can cause a host of medical problems, including Type 2 diabetes, said Gregory Cartee, professor at the University of Michigan School of Kinesiology. Insulin and muscle contractions are the two most important stimuli to increase glucose transport into muscle cells. Cells then use the glucose for energy. However, scientists aren't entirely sure how this works. Cartee and colleague Katsuhiko Funai, a graduate student researcher in kinesiology, looked at how two different proteins believed to be important in stimulating glucose transport react to two different enzymes also related to glucose transport. The goal of the study was to understand the contribution of the two proteins, AS160 and TBC1D1, in skeletal muscle stimulated by insulin. "We're trying to rule out or rule in which proteins are important with exercise," Cartee said.

U.S. trial shows no early mortality benefit from annual prostate cancer screening

The prostate cancer screening tests that have become an annual ritual for many men don't appear to reduce deaths from the disease among those with a limited life-expectancy, according to early results of a major U.S. study involving 75,000 men. Results released today from the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial show that six years of aggressive, annual screening for prostate cancer led to more diagnoses of prostate tumors but not to fewer deaths from the disease. The study, led by researchers at Washington University School of Medicine in St. Louis and conducted at 10 sites, will appear online March 18 in the New England Journal of Medicine (and in the journal's print edition on March 26). "The important message is that for men with a life expectancy of seven to 10 years or less, it is probably not necessary to be screened for prostate cancer," says the study's lead author and principal investigator Gerald Andriole, M.D., chief urologic surgeon at the Siteman Cancer Center at Washington University School of Medicine and Barnes-Jewish Hospital.

Scientists trial device to treat chemotherapy-related nausea

Trials to test acupressure wrist bands as a drug-free alternative for chemotherapy-related nausea are to take place at the University of Liverpool. More than 75% of patients undergoing chemotherapy experience nausea, which can impact negatively on their quality of life. Acupressure wrist bands can reduce the symptoms of travel sickness by applying force to the Nei Kuan pressure point on each wrist. The national study of more than 700 patients, at nine NHS cancer centres, will now measure the cost and clinical effectiveness of acupressure wrist bands in reducing and controlling chemotherapy-related nausea. Led by Professor Mari Lloyd-Williams, from the University’s Academic Palliative and Supportive Care Studies Group, the team will analyse a wide range of patients, diagnosed with different types of cancer and undergoing chemotherapy, in order to discover which patient groups would most benefit from the intervention. Professor Lloyd-Williams said: “Developments in anti-emetic drugs – used to combat nausea and vomiting – have decreased the symptoms suffered by chemotherapy patients but nausea remains a debilitating and poorly controlled symptom. “Patients rank nausea and vomiting amongst the most distressing side effects of chemotherapy. In some cases, poorly controlled symptoms can lead to patients choosing to stop potentially curative treatment. These symptoms can contribute towards a loss of social life, prevent people from working, and lead to anxiety and depression.

3-D snapshots of eyes reveal details of age-related blindness

To get a better look at the abnormalities that cause age-related macular degeneration (AMD), the leading cause of vision loss in Americans and Europeans over 50, the research groups of James Fujimoto at the Massachusetts Institute of Technology and collaborators Jay Duker of the Tufts University School of Medicine, and Joel Schuman of the University of Pittsburgh School of Medicine have created ultra-detailed 3-D images of the eyes of more than 2,000 people from different ethnic groups, 400 of whom have AMD. Selected electronic data, published in the special Interactive Science Publishing (ISP) issue of Optics Express, the Optical Society’s (OSA) open-access journal, may pave the way for new diagnostic software useful for developing new treatments. AMD is a condition in which the macula -- the region of highest visual acuity in the retina -- stops functioning properly. AMD causes blurred vision and, in advanced cases, a large blind spot in the center of one’s vision. Optical coherence tomography (OCT) has become a standard tool for assessing AMD and other eye diseases. An OCT instrument shoots beams of infrared light into the retina, where they are reflected to greater or lesser extent by different structures within the eye. By measuring the echoe time delays of reflected light, an ophthalmologist can have a cross-sectional or three dimensional view of the retina’s layers. This high resolution, three dimensional image reveals abnormalities that can be used to track disease progression and response to treatment.

Lab-Grown Nerves Promote Nerve Regeneration After Injury, Penn Study Finds

Researchers at the University of Pennsylvania School of Medicine have engineered transplantable living nerve tissue that encourages and guides regeneration in an animal model. Results were published this month in Tissue Engineering. About 300,000 Americans suffer peripheral nerve injuries every year, in many cases resulting in permanent loss of motor function, sensory function, or both. These injuries are a common consequence of trauma or surgery, but there are insufficient means for repair, according to neurosurgeons. In particular, surgeons need improved methods to coax nerve fibers known as axons to regrow across major nerve injuries to reconnect healthy targets, for instance muscle or skin.

Queen’s expands testing for fetal alcohol syndrome

Improved technology, partnerships and collaboration across two provinces have allowed Queen's University scientists to dramatically expand the use of eye-movement tests that help identify and assess children with Fetal Alcohol Spectrum Disorder (FASD). "Our initial study was carried out with a relatively small group of children who had to travel to Queen's to participate in the experiment," notes Pharmacology and Toxicology professor James Reynolds, who leads the project. "Establishing a mobile laboratory allowed us to go where the kids are, and carry out these experiments in community settings." Thanks to the cooperation of local health professionals and community members, the researchers tested more than 200 children in nine different Ontario and Alberta locations. "Now we know that the results of eye movement testing are consistent across different geographical locations - something that is absolutely critical if this type of testing is to be widely applicable," says Dr. Reynolds. Until now, there have been few objective tools that will accurately measure brain function in young children. This breakthrough will add eye movement testing to the standard clinical assessment protocols currently in use, to determine the potential for identifying at-risk children.

New study reveals genetic link to blood cancers

The study, published in the journal Nature Genetics, has shown that susceptibility to a series of blood cancers, known as myeloproliferative disorders (MPDs), is linked to a particular area of the patient's DNA, which is prone to developing mutations. Myeloproliferative disorders are characterised by the overproduction of red and white blood cells, which increases the risk of strokes and heart attacks. Many cases of MPDs are caused by a mutation in a gene called JAK2. When the JAK2 gene has mutated, it sends abnormal messages to the blood stem cells to produce more and more blood cells. Scientists, funded by Leukaemia Research, have found that a particular region of chromosome 9 that carries the JAK2 gene is predisposed to acquiring mutations, but only in individuals with a particular genetic makeup. It is likely that this finding will lead to a much better understanding of how the JAK2 gene mutations happen and why they lead to an increased risk of someone developing an MPD. The study, carried out at the Wessex Regional Genetics Laboratory in Salisbury and the University of Southampton, has proved that people carrying this mutation-prone region of DNA on chromosome 9 that includes the JAK2 gene have triple the risk of developing an MPD.

Cardiac Arrythmias Are Often Accompanied by Sleep-Disordered Breathing

Breathing during sleep is often impaired in patients with atrial fibrillation. In the current edition of Deutsches Ärzteblatt International (Dtsch Arztebl Int 2009; 106(10): 164–70), Thomas Bitter and his coauthors from the Ruhr University in Bochum investigate how often sleep-disordered breathing occurs in this form of cardiac arrythmia and what the different types are. The authors used cardiorespiratory polygraphy to investigate whether 150 patients (110 men and 40 women) with atrial fibrillation suffered from sleep-disordered breathing. To avoid statistical bias, they only included patients with normal systolic left ventricular function. The mean age of the patients was around 65 years. Breathing during sleep was impaired in 74% of the patients. 43% of the group suffered from obstructive sleep apnea (OSA). This means that the upper respiratory tract is constricted during the night, leading to oxygen deficiency. The authors found that 31% of patients suffered from central sleep apnea (CSA). This type of disorder is characterized by periodic decreases and increases in the respiratory depth and rate. Breathing becomes flatter and flatter, until it is interrupted for an interval.

University researchers to develop coatings that kill superbugs

Researchers at the University of Bath are to be part of a €3 million Europe-wide research collaboration to pioneer research into safer, more effective anti-bacterial plastics and coatings that can be used in items such as food packaging, medical devices to wound dressings, and nappies. The Bath team has developed a range of new compounds which have been shown to be highly effective against common hospital bacterial infections such as MRSA and are safer than existing anti-bacterials based on silver nanoparticles. They will develop these compounds so they can be cheaply and efficiently incorporated into a wide range of materials from medical devices, wound dressings, food packaging and even nappies. Led by Dr Toby Jenkins at the University of Bath, the research team comprises chemists Dr Andrew Johnson and Dr Gareth Price, and biologist Dr Nick Waterfield as well as colleagues in Barcelona, Exeter, St. Gallen (Switzerland), Mainz and Cologne (both Germany). From the total grant, Bath will receive just less than three quarters of a million Euros, which will fund equipment and a team of three PhD students and a Research Fellow. So-called “superbug” bacteria such as MRSA are dangerous because they are resistant to most conventional antibiotics, a problem that is getting worse each year. To try and understand this problem, the researchers will also be studying which genes allow bacteria to become resistant.

Exposure to insecticide may play role in obesity epidemic among some women

Prenatal exposure to an insecticide commonly used up until the 1970s may play a role in the obesity epidemic in women, according to a new study involving several Michigan State University researchers. More than 250 mothers who live along and eat fish from Lake Michigan were studied for their exposure to DDE – a breakdown of DDT. The study, published as an editor’s choice in this month’s edition of Occupational and Environmental Medicine, analyzed DDE levels of the women’s offspring. Compared to the group with the lowest levels, those with intermediate levels gained an average of 13 pounds excess weight, and those with higher levels gained more than 20 pounds of excess weight. “Prenatal exposure to toxins is increasingly being looked at as a potential cause for the rise in obesity seen worldwide,” said Janet Osuch, a professor of surgery and epidemiology at MSU’s College of Human Medicine, who was one of the lead authors of the study. “What we have found for the first time is exposure to certain toxins by eating fish from polluted waters may contribute to the obesity epidemic in women.” Though DDT was banned in 1973 after three decades of widespread use, the chemical and its byproducts remain toxic in marine life and fatty fish. The study was funded by a $300,000 grant from the federal Agency for Toxic Substances and Disease Registry. Osuch said the study’s findings can have a huge impact on how researchers treat – and seek to prevent – obesity. The research team has been awarded a $1 million grant from the same federal agency, the ATSDR, to assess the impact of pollutants and toxins on a wide variety of disorders by determining the importance of second- and third-generation health effects.

Monoclonal antibodies primed to become potent immune weapons against cancer

New research suggests that monoclonal antibody therapy of cancer can be improved to be much more powerful than it is today, says a researcher at Georgetown University Medical Center's Lombardi Comprehensive Cancer Center in the March 21 issue of the Lancet. "We believe that antibody therapy has the capacity to immunize people against cancer," says Louis Weiner, MD, director of the cancer center at GUMC and an internationally recognized expert in development and use of monoclonal antibodies. "Treatment modifications might be able to prolong, amplify, and shape a continuous immune response to cancer cells." Weiner was asked by Lancet editors to write a review article discussing the newest research in this field. His co-authors are Madhav Dhodapkar, MD, of Yale University and Soldano Ferrone, MD, of the University of Pittsburgh. Their analysis, based on reviewing the last eight years of research on monoclonal antibody treatment, suggests that a new era in use of these therapies is just around the corner. "Scientists have been able to use new tools to measure effectiveness of these therapies, and have found that antibodies are capable of stimulating the immune system in ways that had not been appreciated to date, and which we can now take advantage of," Weiner says. Antibodies are immune system proteins that seek out and neutralize molecules they recognize as foreign to a body, such as viruses and bacteria. Monoclonal antibodies are proteins crafted in a laboratory to recognize specific receptors, or antigens, on cancer cells; some antigens promote uncontrolled growth. These antibodies are designed to both attach to cancer receptors to inhibit their function and to alert and activate the immune system to the presence of these receptor proteins.

Environmental cleaning intervention reduces transmission of multidrug-resistant organisms in ICUs

A rigorous environmental cleaning intervention can reduce the transmission of methicillin-resistant Staphylococcus aureus (MRSA) and other multidrug-resistant organisms in hospital intensive care units (ICUs), according to a new study released today at the annual meeting of the Society for Healthcare Epidemiology of America (SHEA). Researchers found that following an enhanced cleaning protocol reduced the spread of MRSA to patients exposed to rooms in which the prior occupant had been colonized or infected. The multi-modal cleaning intervention consists of three parts: a change from use of a pour bottle to bucket immersion for applying disinfectant to cleaning cloths; an educational campaign involving the environmental services staff at the hospital; and feedback method using removal of intentionally-applied marks visible only under UV light. "We know that environmental contamination with highly antibiotic-resistant bacteria can still occur in hospitals where cleaning policies exceed national standards established by the CDC," said Rupak Datta, MPH, an MD/PhD candidate at the University of California at Irvine. "Although the risk of acquiring MRSA and VRE is already low, this study suggests that there are additional preventative measures that hospitals can take to reduce the risk of transmission from one patient to another." The retrospective study of more than 13,000 hospital stays in10 ICUs at a large, tertiary care academic medical center in Boston, measured the risk of MRSA and vancomycin-resistant Enterococci (VRE) acquisition before (Sept. 2003-April 2005) and during the cleaning intervention (Sept. 2006-April 2008). Routine admission and weekly screenings for MRSA and VRE were conducted during both periods providing a systematic method to identify new cases of MRSA and VRE. During the pre-intervention period, 3.9% of the 1,454 patients exposed to a prior occupant with MRSA acquired the pathogen compared to just 1.5% of the 1,443 patients exposed during the intervention. Of the 1,291 patients exposed to VRE prior to the intervention, 4.5% acquired VRE compared to 3.5% of 1,446 patients during intervention. The study builds upon a body of research conducted by Datta and his co-authors. In a 2006 study, they found that patients admitted to an ICU room whose prior occupant had been infected with MRSA or VRE had as much as a 40 percent increased risk of acquiring either pathogen, suggesting environmental contamination could play a significant role in their transmission. In a subsequent study, the authors showed that a multi-modal cleaning intervention could reduce environmental cultures for MRSA and VRE. The current study now suggests that this same intervention reduces acquisition of these pathogens, particularly MRSA, in subsequent room occupants.

Genetic irregularities linked to higher risk of COPD among smokers

Scientists at Duke University Medical Center have discovered two genetic markers that appear to put some smokers at significantly higher risk of developing chronic obstructive pulmonary disease (COPD). The findings come from the first-ever genome-wide association study of COPD and suggest that those who carry the markers may be able to reduce their risk if they quit smoking before the first symptoms of COPD occur. "The public health message would probably be 'quit before it's too late,'" says David Goldstein, Ph.D., director of the Institute for Genome Sciences Center for Human Genome Variation at Duke and the senior author of the study appearing in PLoS Genetics. Chronic obstructive pulmonary disease is one of the leading causes of death worldwide. While smoking is the biggest risk factor, there is considerable variation among those who develop the disease. Genetics plays a role, but until now, there has only been one biological marker proven to be associated with COPD – a deficit of the protein A1AT, which has also been linked to the development of lung cancer. "But we know that A1AT deficiency appears in only 1-2 percent of people with COPD, so we were pretty sure that there had to be other genetic variants at work, as well," says Goldstein. To discover if that hunch might prove true, Goldstein led an international team of investigators in examining the genomes of 823 people with COPD and 810 smokers without COPD in Norway. They were looking for the presence of the 100 top genetic variations already documented in individuals with COPD enrolled in the family-based International COPD Genetics Network. They then took the most frequently occurring alterations from that study and evaluated them in three additional, independent groups: patients in the U.S. National Emphysema Treatment Trial, individuals enrolled in the Boston Early-Onset COPD study and a control group from the Normative Aging Study.

New study finds hospital practices strongly impact breastfeeding rates

Hospital practices, such as supplementing newborns with formula or water or giving them pacifiers, significantly reduce the chances that mothers who intend to exclusively breastfeed will achieve that intention, according to a new study led by a Boston University School of Public Health researcher. In a study which appears online March 19 in the American Journal of Public Health, a research team led by Eugene Declercq, PhD, professor of Maternal and Child Health, found a significant drop-off between the numbers of mothers who intend to exclusively breastfeed, and those who fulfill that intention one week after giving birth. Among first-time mothers, 70 percent reported an intention to exclusively breastfeed, but only 50 percent achieved that goal at one week. The study found that hospital practices were strongly related to those outcomes. Specifically, the practice of hospital staff providing formula or water to supplement breastfeeding was significantly related to the failure to achieve exclusive breastfeeding. Mothers whose infants were not offered supplementation were far more likely to achieve their intention to breastfeed – 4.4 times more likely among primiparas (first-time mothers), and 8.8 times more likely among multiparas. Other hospital practices also influenced outcomes. First-time mothers who delivered in hospitals that practiced at least six out of seven recommended steps to encourage breastfeeding -- such as helping mothers get started and not giving babies pacifiers – were six times more likely to fulfill their intention to exclusively breastfeed than mothers who reported experiencing one or none of these practices. "Very often, research studies yield conclusions that don't translate easily into changes in practice or policy," Declercq said. "In this case, the message is loud and clear – hospital practices can make a difference in early breastfeeding success and in particular, every effort should be made to avoid supplementation of healthy babies of mothers who intended to exclusively breastfeed."

Heightened level of amygdala activity may cause social deficits in autism

Something strange is going on in the amygdala – an almond-shaped structure deep in the human brain – among people with autism.
Researchers at the University of Washington have discovered an increased pattern of brain activity in the amygdalas of adults with autism that may be linked to the social deficits that typically are associated with the disorder. Previous research at the UW and elsewhere has shown that abnormal growth patterns in the amygdala are commonly found among young children diagnosed with autism.The amygdala is popularly associated with the "fight-or-flight response" in dangerous situations. But it has other functions, including identifying faces and situations and evaluating social information such as emotions. The new research shows that brain activation in adults with autism remains elevated long after similar brain regions of typically developed adults have stopped being activated when exposed to a series of pictures of human faces. A decrease in activation over time to the same type of information is called neural habituation and is connected with learning, according to Natalia Kleinhans, lead author of the new study and a UW research assistant professor of radiology. "What we are seeing is hyperexcitability or overarousal of the amygdala, which suggests that neurons in the amygdala are firing more than expected," said Kleinhans, who is associated with the UW Autism Center. "If you consider that habituation reflects learning in as simple a task as looking at a face, slowness to habituate in people with autism may contribute even more markedly to difficulty with more complex social interactions and social cognition. If the brain is not reacting typically to a static face with a neutral expression, you can imagine how difficult it may be for someone with autism to pick up more subtle social cues." The National Institute of Child Health and Human Development and the National Institute of Mental Health funded the research, which appears in the online edition of The American Journal of Psychiatry.

A paradigm shift in immune response regulation

Over the past decade various pieces of the puzzle how signal transmission controls immunity have been coming together. Now, in Cell an international team reports a paradigm shift in the regulation of immune response. Their results show that interaction with a linear ubiquitin chain is crucial for nuclear factor kappa B activation. Their findings may also contribute towards structure-based drug design to target the defective NF-?B pathway in diseases such as cancer, inflammation and immunodeficiency. The body's first line of defence against bacteria and viruses is the innate immune system where phagocytes identify the foreign organism and initiate an alarm reaction, often accompanied by inflammation. As a consequence, molecular cues are produced in the blood, such as Tumor Receptor Factors (TNF) or interleukin-1, and these stimulate further reactions in the immune system. But what exactly happens after the molecular cues have docked onto the cell receptors that specialize in immune response? What is the basis of signal transmission from the cellular receptors into the cellular interior? Over the past decade, the overall picture of this large puzzle has been gradually pieced together to show that modifications in the cell protein - including the addition of phosphate groups (phosphorylation) or the conjugation of small modifier ubiquitin (ubiquitination) - play a central role in controlling the immune system. Scientists at Frankfurt's Goethe University led by Prof. Ivan Dikic have established an international collaboration to investigate the role of ubiquitin modification in these pathways. The international team includes the laboratories of Soichi Wakatsuki (Photon factory, Tsukuba, Japan), Fumiyo Ikeda (MedILS, Split, Croatia), Felix Randow (LMB, Cambridge, UK) and David Komander (LMB, Cambridge, UK). They have been investigating how a transcription factor known as the nuclear factor kappa-B (NF-?B) coordinates the gene expression necessary for the cell's immune response. NF-?B is activated by an enzyme (IkappaB-Kinase, IKK) with a regulatory subunit that brings to mind the mysterious captain in Jules Verne's science fiction novels: NEMO.

Pitt vaccine to prevent colon cancer being tested in patients

Researchers at the University of Pittsburgh School of Medicine have begun testing a vaccine that might be able to prevent colon cancer in people at high risk for developing the disease. If shown to be effective, it might spare patients the risk and inconvenience of repeated invasive surveillance tests, such as colonoscopy, that are now necessary to spot and remove precancerous polyps. Colon cancer takes years to develop and typically starts with a polyp, which is a benign but abnormal growth in the intestinal lining, explained principal investigator Robert E. Schoen, M.D., M.P.H., professor of medicine and epidemiology at the University of Pittsburgh. Polyps that could become cancerous are called adenomas. In a novel approach for cancer prevention, the Pitt vaccine is directed against an abnormal variant of a self-made cell protein called MUC1, which is altered and produced in excess in advanced adenomas and cancer. Vaccines currently in use to prevent cancer work via a different mechanism, specifically by blocking infection with viruses that are linked with cancer. For example, Gardasil protects against human papilloma virus associated with cervical cancer and hepatitis B vaccine protects against liver cancer. "By stimulating an immune response against the MUC1 protein in these precancerous growths, we may be able to draw the immune system's fire to attack and destroy the abnormal cells," Dr. Schoen said. "That might not only prevent progression to cancer, but even polyp recurrence." According to co-investigator Olivera Finn, Ph.D., professor and chair of the Department of Immunology at Pitt's School of Medicine, MUC1 vaccines have been tested for safety and immunogenicity in patients with late-stage colon cancer and pancreatic cancer.

Acetaldehyde in alcohol -- no longer just the chemical that causes a hangover

New evidence by researchers at the Centre for Addiction and Mental Health (CAMH) and researchers in Germany shows that drinking alcohol is the greatest risk factor for acetaldehyde-related cancer. Heavy drinkers may be at increased risk due to exposure from multiple sources. Acetaldehyde is ubiquitous in daily life in Ontario. Widely present in the environment, it is inhaled from the air and tobacco smoke, ingested from alcohol and foods, and produced in the human body during the metabolism of alcoholic beverages. Research indicates that this organic chemical plays a significant role in the development of certain types of cancers (especially of the upper digestive tract), and it is currently classified as possibly carcinogenic by the International Agency for Research on Cancer of the World Health Organization. New research from CAMH in Toronto and the Chemical and Veterinary Investigation Laboratory Karlsruhe (CVUA) in Germany recently provided the necessary methodology for calculating the risk for the ingestion of alcoholic beverages.
The team found that risk from ingesting acetaldehyde via alcoholic beverages alone may exceed usual safety limits for heavy drinkers. Their risk assessment study found that the average exposure to acetaldehyde from alcoholic beverages resulted in a life-time cancer risk of 7.6/10,000, with higher risk scenarios (e.g. contaminations in unrecorded alcohol) in the range of 1 in 1,000. As such, the life-time cancer risks for acetaldehyde from ingestion of alcoholic beverages greatly exceed the usual limits for cancer risks from the environment.

Genetic clues hold key to schizophrenia treatment

Researchers have taken a step forward in understanding the genetics of mental illnesses such as schizophrenia and bipolar disorder. The study, conducted by the University of Edinburgh, found that a gene called DISC1 – known to play a role in the development of mental illness – may control the way some patients respond to psychiatric medication. They also identified seven proteins that are important to the development of mental illness and hope the research could help to create new medicines that target these proteins. The research was based on existing data from the Human Genome Project, a pioneering study, which mapped all the genes in human DNA. The team analysed variations of the DISC1 gene and found that it affects a number of other genes that current medications are designed to target. They believe that by identifying those patients in whom DISC1 may be a root cause of illness, they could find the patients for whom these drugs would be most effective.

Leaky blood vessels may cause fifth of strokes, study suggests

One in five strokes may be caused by a weakening of the tiny arteries in the brain, a study has found. New research shows that the brain damage caused by lacunar strokes - which occur in tiny rather than large arteries - may be caused by a gradual weakening of the artery wall. It was previously thought that this type of stroke was caused only by reduced blood flow to the brain. Scientists at the University of Edinburgh believe that this weakening occurs in the protective lining of the small arteries - known as the blood-brain barrier - which stops potentially harmful substances getting into the brain. The research involved two groups of stroke patients - one with lacunar stroke and one with the large artery type. Both groups were injected with magnetic dye before having brain scans that showed how the dye travelled through their blood vessels.
In the lacunar patients, more dye leaked out of the blood vessels into the brain than was the case in the other group. This could only have happened if the dye were able to leak through the protective barrier.

Compound is key coordinator of clock and metabolism

Our circadian clock, or biological timing system, governs our daily cycles of feeding, activity and sleep. Research using cells has produced a solid portrait of the clock at the genetic and molecular levels, but understanding how those mechanisms contribute to the health and disease of living animals, including humans, has been elusive. Now researchers at Northwestern University and Washington University School of Medicine, in a new study to be published online March 19 by the journal Science, have uncovered a surprising new connection between the circadian clock and metabolism in mammals. The findings could help researchers better understand the circadian disruptions that often afflict the elderly. The results also offer a new target for the development of therapies for the treatment of metabolic disorders related to circadian disruption, such as those experienced by shift workers or even those whose circadian system is disrupted due to obesity or diabetes. In a study of laboratory mice, the researchers discovered the circadian clock genes strongly regulate the production of nicotinamide adenine dinucleotide (NAD), a critical cofactor involved in numerous cellular reactions and essential to energy utilization. In turn, NAD regulates the activity of an enzyme called SIRT1, which is a known key regulator of aging, metabolism and longevity. This discovery -- that NAD and SIRT1 together function as a molecular "switch" to coordinate the internal clock with metabolic systems -- will help researchers better understand how aging, metabolism and the circadian clock are interconnected in living animals through this intricate molecular pathway. "This is one of the sought-after links that couples changes with the cellular environment and nutrient state with changes in the internal clock," said Joe Bass, M.D., Ph.D., a co-senior author on the paper and assistant professor of medicine and of neurobiology and physiology at Northwestern. The researchers also found that levels of NAD oscillate, or move up and down according to the animal's internal clock. This is the first evidence of a "metabolic oscillator," an oscillating factor that is not part of the core clock machinery. Research out of Bass' lab a few years ago showed a clear link between disruption of the circadian clock with the development of obesity and the metabolic syndrome in mammals. The new findings help explain, in part, the molecular activity underlying those pathologies, says Bass.

Ticking of body's 24-hour clock turns gears of metabolism and aging

All animals, including humans, have an internal 24-hour clock or circadian rhythm that creates a daily oscillation of body temperature, brain activity, hormone production and metabolism. Studying mice, researchers at Washington University School of Medicine in St. Louis and Northwestern University found how the biological circadian clock mechanism communicates with processes that govern aging and metabolism. Reported March 19, 2009 through advance online publication in Science, their findings can potentially explain why the waning of the circadian rhythm with age could contribute to age-related disorders such as insulin resistance and type 2 diabetes. "Our study establishes a detailed scheme linking metabolism and aging to the circadian rhythm," says one of the lead authors, Shin-ichiro Imai, M.D., Ph.D., who researches aging at Washington University School of Medicine. "This opens the door to new avenues for treating age-related disorders and ways to restore a healthy daily circadian rhythm. It could also yield new interventions to alleviate metabolic disorders such as obesity and diabetes." Imai, associate professor of medicine and of developmental biology, focuses on the molecular mechanisms of aging and longevity. Earlier, he demonstrated that a gene called SIRT1 was at the center of a network that regulates aging. A form of the gene is found in every organism on earth, and seven forms of the gene exist in humans. SIRT1 has a broad reach, influencing glucose breakdown and production, cholesterol metabolism, fat burning and insulin sensitivity. Basically, the gene coordinates metabolic reactions throughout the body and manages the body's response to nutrition. Interestingly, increasing the activity of proteins related to SIRT1 extends the life span of organisms such as yeast, worms and flies. SIRT1 is activated when calories are restricted below normal, which has been shown to extend the life spans of some laboratory animals. "Under nutritional scarcity, SIRT1 may delay aging and extend life span to assure survival until food becomes more readily available," Imai explains.
Imai's collaborator in the current study, Joseph Bass, M.D., Ph.D., assistant professor of medicine and neurobiology at Northwestern University, earlier demonstrated that interfering with the circadian clock of mice led to metabolic complications including obesity and type 2 diabetes.

Report warns of jury service 'trauma'

A new report by psychologists at the University of Leicester warns of the dangers of jurors facing trauma because of their exposure to harrowing and gruesome evidence. In the first study of its kind, the research highlights how women jurors are more vulnerable, particularly if the trial covers material that resonates with their personal histories. The research confirms that jury service, particularly for crimes against people, can cause significant anxiety, and for a vulnerable minority it can lead to severe clinical levels of stress or the symptoms of post traumatic stress disorder. The study led by clinical psychologist Dr Noelle Robertson has been published in The Howard Journal. It warns of the perils of undergoing jury service- and the fact that people cannot talk about their experiences for fear of being held in contempt of court. Dr Robertson, with University of Leicester colleagues Professor Emeritus Graham Davies and graduate student Alice Nettleingham, is the first UK exploratory study to look at the possible traumatisation of jurors.

When intestinal bacteria go surfing

The EHECs adhere to the surface of the mucosal cells and alter them internally: a part of the cellular supportive skeleton - the actin skeleton - is rearranged in such a manner that the cell surface beneath the bacteria forms plinth-like growths, so-called pedestals. The bacteria are securely anchored to this pedestal; the pedestals, in contrast, are mobile. This enables the bacteria, seated upon them, to surf over the cell surface and reproduce upon it, without being flushed from the intestine. But how do the bacteria bring the host cells to convert the actin skeleton? Researchers at the Helmholtz Centre for Infection Research (HZI) have now identified the signal pathway that leads to the formation of this pedestal. "Prerequisite for this signal pathway is a special secretion system - a sort of molecular syringe, through which the bacteria insert entire proteins in the host cell," explains Theresia Stradal, head of the Signal Transduction and Motility research group at HZI. Two factors, Tir and EspFU, are brought into the host cell from the bacterium for pedestal formation. Following this, the host cell presents Tir on its surface; the bacterium recognises "its" molecule Tir and adheres to the host cell. EspFU then triggers the signal for local actin conversion. "It has been unclear thus far how the two bacterial effectors Tir and EspFU enter into contact with one another in the host cell," says Theresia Stradal. Her research group has now found the missing link: "The molecule comes from the host cell, is called IRSp53 and gathers on the cell surface, directly beneath the bacteria sitting on it," explains cell biologist Markus Ladwein, who is also involved in the project. IRSp53, then, establishes the connection between Tir and EspFU. It ensures that actin conversion is concentrated locally. Together with the biochemist Dr. Stefanie Weiß, a former post-graduate student with the research group, Markus Ladwein also provided the counter evidence: "Cells in which IRSp53 is lacking are no longer able to form pedestals for the bacteria."

Dioxin alters ability to fight infection, mouse study finds

Researchers find for the first time that mice exposed to the contaminant dioxin during development or while nursing have a diminished capacity to fight a flu infection later in life. Mouse pups born to pregnant mice that were exposed to a small amount of the ubiquitous and persistent pollutants had fewer white blood cells that normally kill the flu virus and more of a different kind that increases lung inflammation. The increased inflammation can make the disease more severe and recovery more difficult.

Computer learning, electrical stimulation offer hope for paralyzed

Trainers have used it for decades to help athletes build muscle. Late-night TV commercials hawk it as an effortless flab buster. But a University of Florida engineering researcher says electrical stimulation — a simple, decades-old technique to prompt muscles to contract — can be combined with sophisticated computer learning technology to help people regain more precise, more life-like control of paralyzed limbs.
Although his research is still exploring the fundamentals, his progress so far suggests computer-adapted electrical stimulation could one day help the estimated 700,000 Americans who suffer from strokes and the 11,000 who suffer from cord injuries annually. “It’s an adaptive scheme to do electrical stimulation more efficiently, with less fatigue and more accuracy,” said Warren Dixon, an associate professor of mechanical and aerospace engineering, explaining that existing techniques do little more than apply a set current to a designated muscle. Stroke victims may be among the first to benefit. Dixon said stroke sufferers who work at regaining the ability to walk often unconsciously drag their toes, causing them to stumble. He said his goal is to develop techniques for a wearable, pacemaker-sized device. The device would deliver just the right stimulation to the calf at just the right moment in a person’s gait, lifting the toe just enough to avoid a stumble and walk naturally.

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Greenpeace Success: Polish Coal Mine Expansion Suspended

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Lab-on-a-Chip Homes in on How Cancer Cells Break Free

Johns Hopkins engineers have invented a method that could be used to help figure out how cancer cells break free from neighboring tissue, an "escape" that can spread the disease to other parts of the body. The new lab-on-a-chip, described in the March issue of the journal Nature Methods, could lead to better cancer therapies. "Studying cell detachment at the subcellular level is critical to understanding the way cancer cells metastasize," says principal investigator Peter Searson, Reynolds Professor of Materials Science and Engineering. "Development of scientific methods to study cell detachment may guide us to prevent, limit or slow down the deadly spreading of cancer cells." His team's research focuses on a missing puzzle piece in the common but unfortunate events that can occur in cancer patients. For example, cancer that starts in the breast sometimes spreads to the lungs. That's because tumor cells detach and travel through the bloodstream to settle in other tissues. Scientists have learned much about how cancer cells attach to these surfaces, but they know little about how these insidious cells detach because no one had created a simple way to study the process.

Study finds how brain remembers single events

Single events account for many of our most vivid memories – a marriage proposal, a wedding toast, a baby’s birth. Until a recent UC Irvine discovery, however, scientists knew little about what happens inside the brain that allows you to remember such events. In a study with rats, neuroscientist John Guzowski and colleagues found that a single brief experience was as effective at activating neurons and genes associated with memory as more repetitive activities. Knowing how the brain remembers one-time events can help scientists design better therapies for diseases such as Alzheimer’s in which the ability to form such memories is impaired. “Most experiences in life are encounters defined by places, people, things and times. They are specific, and they happen once,” says Guzowski, UCI neurobiology and behavior assistant professor. “This type of memory is what makes each person unique.

Penn Researchers Identify New Protein Important in Breast Cancer Gene’s Role in DNA Repair

For years, researchers have known that under normal conditions, the breast cancer protein BRCA1 orchestrates the repair of damaged DNA, but the details of just how BRCA1 moves to the damaged site and recruits the right nuclear repairmen for DNA restoration remains a mystery. Now, a new study from the University of Pennsylvania School of Medicine has identified genes associated with the BRCA1 protein and their involvement in the DNA repair pathway, helping to clear the way for researchers to better understand what goes wrong when the BRCA1 gene is mutated and the repair pathway goes haywire. Identifying patients with mutations in these BRCA1-associated genes may help better fight breast cancer.

Study finds biological clue in brain tumour development

Scientists at The University of Nottingham have uncovered a vital new biological clue that could lead to more effective treatments for a children’s brain tumour that currently kills more than 60 per cent of young sufferers. Clinician –scientists at the University’s Children’s Brain Tumour Research Centre, working on behalf of the Children’s Cancer and Leukaemia Group (CCLG), have studied the role of the WNT biological pathway in central nervous system primitive neuroectodermal tumours (CNS PNET), a type of brain tumour that predominantly occurs in children and presently has a very poor prognosis.
In a paper published in the British Journal of Cancer, they have shown that in over one-third of cases, the pathway is ‘activated’, suggesting that it plays a role in tumour development. The research also highlighted a link between WNT pathway activation and patient survival — patients who had a CNS PNET tumour that was activated survived for longer than those without pathway activation.

Vitamin D may not be the answer to feeling SAD

A lack of Vitamin D, due to reduced sunlight, has been linked to depression and the symptoms of Seasonal Affective Disorder (SAD), but research by the University of Warwick shows there is no clear link between the levels of vitamin D in the blood and depression. Exposure to sunlight stimulates vitamin D in the skin and a shortage of sunlight in the winter has been put forward as one possible cause of SAD. However Warwick Medical School researchers, led by Dr Oscar Franco, have discovered low levels of vitamin D in the blood may not be connected to depression. In a study published in the Journal of Affective Disorders, the team recruited more than 3,000 people and tested levels of vitamin D (25-hydroxyvitamin D) in the blood. They then carried out a questionnaire with the participants to assess the prevalence of depressive symptoms.
Vitamin D deficiency exists when the concentration of 25-hydroxy-vitamin D (25-OH-D) in the blood serum occurs at 12ng/ml (nanograms/millilitre) or less. The normal concentration of 25-hydroxy-vitamin D in the blood serum is 25-50ng/ml. The researchers found there was no clear association between depressive symptoms and the concentration of vitamin D in the blood.

Fish Health Claims May Cause More Environmental Harm than Good

The health benefits of fish consumption have been over-dramatized and have put increased pressure on wild fish, according to a new research published today in the Canadian Medical Association Journal (CMAJ). In an innovative collaboration, medical scientists from St. Michael’s Hospital and the University of Toronto have teamed up with researchers from the University of British Columbia’s Fisheries Centre and author Farley Mowat to closely examine the effects of health claims with regard to seafood. For years, international agencies concerned with health and nutrition have promoted seafood consumption. “Our concern is that fish stocks are under extreme pressure globally and that studies are still urgently required to define precisely who will benefit from fish oil,” says Dr. David J. A. Jenkins, a doctor at St. Michael’s Hospital and a professor at the University of Toronto Faculty of Medicine’s Department of Nutritional Sciences. “Further, if we decide that fish oil supplementation is necessary for good health, then unicellular sources of ‘fish oil’ like algae, yeasts, etc, should now be used, as they are in infant formula,” adds Dr. Jenkins. While many studies show healthy benefits of consuming omega-3 fatty acids, found in fish oils, some other studies fail to show significant benefits. But these negative studies are often ignored and the result is that there is increasing demand for seafood by consumers in the developed world, often at the expense of food security in developing nations.

Depressed People Have Trouble Learning 'Good Things In Life'

While depression is often linked to negative thoughts and emotions, a new study suggests the real problem may be a failure to appreciate positive experiences. Researchers at Ohio State University found that depressed and non-depressed people were about equal in their ability to learn negative information that was presented to them.
But depressed people weren’t nearly as successful at learning positive information as were their non-depressed counterparts. “Since depression is characterized by negative thinking, it is easy to assume that depressed people learn the negative lessons of life better than non-depressed people – but that’s not true,” said Laren Conklin, co-author of the study and a graduate student in psychology at Ohio State.

Regular exercise reduces depressive symptoms, improves self esteem in overweight children

Less than an hour of daily exercise reduces depressive symptoms and improves self esteem in overweight children, Medical College of Georgia researchers say. The study included 207 overweight, typically sedentary children ages 7-11 randomly assigned to either continue their sedentary lifestyle or exercise for 20 or 40 minutes every day after school for an average of 13 weeks. The 40-minute group sustained the most psychological benefit, according to research published online in the Journal of Pediatric Psychology. The MCG researchers were the first to demonstrate this dose response benefit of exercise – meaning the more the better – on depressive symptoms and self worth in these children. Benefits came despite the fact that the children's weight did not change much over the three months. "Just by getting up and doing something aerobic, they were changing how they felt about themselves," says the study's first author, Dr. Karen Petty, postdoctoral fellow in psychology at MCG's Georgia Prevention Institute. "Hopefully these children are taking home the idea: Hey, when we do this stuff, we feel better."

Liking sweets makes sense for kids

As any parent knows, children love sweet-tasting foods. Now, new research from the University of Washington and the Monell Center indicates that this heightened liking for sweetness has a biological basis and is related to children's high growth rate. "The relationship between sweet preference and growth makes intuitive sense because when growth is rapid, caloric demands increase. Children are programmed to like sweet taste because it fills a biological need by pushing them towards energy sources," said Monell geneticist Danielle Reed, PhD, one of the study authors. Across cultures, children prefer higher levels of sweetness in their foods as compared to adults, a pattern that declines during adolescence. To explore the biological underpinnings of this shift, Reed and University of Washington researcher Susan Coldwell, PhD, looked at sweet preference and biological measures of growth and physical maturation in 143 children between the ages of 11 and 15. The findings, reported in the journal Physiology & Behavior, suggest that children's heightened liking for sweet taste is related to their high growth rate and that sweet preferences decline as children's physical growth slows and eventually stops.
Based on the results of sensory taste tests, children were classified according to their sweet taste preference into a 'high preference' or 'low preference' group. Children in the 'low preference' group also had lower levels of a biomarker (type I collagen cross-linked N-teleopeptides; NTx) associated with bone growth in children and adolescents.

Paul Stamets: 6 ways mushrooms can save the world

Entrepreneurial mycologist Paul Stamets seeks to rescue the study of mushrooms from forest gourmets and psychedelic warlords. The focus of Stamets' research is the Northwest's native fungal genome, mycelium, but along the way he has filed 22 patents for mushroom-related technologies, including pesticidal fungi that trick insects into eating them, and mushrooms that can break down the neurotoxins used in nerve gas.

Unique nerve-stimulation device proves effective against epilepsy

Epilepsy is a common medical condition characterized by convulsions and short periods of confusion. It affects more than 50 million people worldwide. But intractable epilepsy, which affects more than 1 million Americans and is often resistant to drug treatment and surgery, is arguably worse. But in a just completed clinical trial, a unique nerve-stimulation treatment for intractable epilepsy reduced the number of seizures by more than 50 percent. In the March edition of the journal Neurology, UCLA neurology professor Christopher M. DeGiorgio and colleagues report the results of the long-term pilot trial, which demonstrated the effectiveness of the new treatment, called trigeminal nerve stimulation (TNS). The results, though preliminary, are very encouraging, DeGiorgio said. Those participating in the trial for three months saw a 66 percent reduction in the number of seizures, those participating for six months saw a 56 percent reduction and those who completed one year saw a 59 percent reduction in seizures. One of the subjects who participated for a full year had a 90-percent reduction in seizures. The trigeminal nerve extends into the brain from the face and forehead and is known to play a role in seizure inhibition. The stimulator, about the size of a large cell phone, attaches to a belt or can slip into a pocket. Two wires from the stimulator are passed under the clothing and connected to electrodes attached to the forehead by adhesive. The electrodes, which can be covered by a cap or scarf, transmit an electrical current to the nerve. "People with intractable epilepsy who have continuing seizures are often drug-resistant," DeGiorgio said. "In addition, anti-seizure drugs can have significant side effects on thinking and alertness."

Researchers identify genetic markers for aggressive head and neck cancer

Scientists at Albert Einstein College of Medicine of Yeshiva University have identified genetic markers that signal poor outcomes for patients with head and neck cancer. These findings could one day lead to a genetic test that could help select or predict successful treatment options for patients with this type of cancer. The results were published in the American Journal of Pathology. Head and neck cancer refers to tumors in the mouth, throat or larynx (voice box). Each year, about 40,000 men and women in the U.S. develop head and neck cancer, making it the sixth most common cancer in the U.S. Surgery, chemotherapy and/or radiation are the main treatment options but cause serious side effects: surgery may involve removing large areas of the tongue, throat, or neck and can affect appearance, and any type of therapy can cause swallowing or speech problems that can significantly affect quality of life. Despite curative treatment attempts, on average only about half of patients survive beyond five years after treatment. This is greatly affected by the size and location of the tumor. The Einstein study focuses on microRNAs, a recently identified class of short RNA molecules that play key roles in regulating gene expression. Abnormal microRNA levels have been associated with all types of cancer yet examined. In previous research, the Einstein scientists and other groups reported that approximately 50 specific microRNAs were expressed at higher or lower levels in head and neck tumor cell lines compared with normal cells. In this study, the Einstein researchers, for the first time, have linked levels of specific microRNAs with tumor recurrence and poorer survival in head and neck cancer. The Einstein team analyzed samples from 104 head and neck cancer patients from Montefiore Medical Center, The University Hospital and Academic Medical Center for Einstein. The patients were treated and followed over five years. At the time of cancer diagnosis and before any therapy, researchers removed samples tumor tissue from patients, as well as normal tissue adjacent to their tumor, and measured microRNA levels in the two types of tissue.
Patients who fared worst had the lowest levels of two particular microRNAs?miR-205 and let-7d?in their tumor tissue. Specifically, these patients were four times more likely to have an earlier metastasis or local-regional recurrence of their cancer than patients with higher levels of miR-205 and let-7d in tumor tissue.

Einstein Researchers Develop Novel Antibiotics That Don't Trigger Resistance

Bacterial resistance to antibiotics is one of medicine's most vexing challenges. In a study described in Nature Chemical Biology, researchers from Albert Einstein College of Medicine of Yeshiva University are developing a new generation of antibiotic compounds that do not provoke bacterial resistance. The compounds work against two notorious microbes: Vibrio cholerae, which causes cholera; and E. coli 0157:H7, the food contaminant that each year in the U.S. causes approximately 110,000 illnesses and 50 deaths. Most antibiotics initially work extremely well, killing more than 99.9% of microbes they target. But through mutation and the selection pressure exerted by the antibiotic, a few bacterial cells inevitably manage to survive, repopulate the bacterial community, and flourish as antibiotic-resistant strains.Vern L. Schramm, Ph.D., professor and Ruth Merns Chair of Biochemistry at Einstein and senior author of the paper, hypothesized that antibiotics that could reduce the infective functions of bacteria, but not kill them, would minimize the risk that resistance would later develop. Dr. Schramm's collaborators at Industrial Research Ltd. earlier reported transition state analogues of an enzyme that interferes with "quorum sensing" — the process by which bacteria communicate with each other by producing and detecting signaling molecules known as autoinducers. These autoinducers coordinate bacterial gene expression and regulate processes — including virulence — that benefit the microbial community. Previous studies had shown that bacterial strains defective in quorum sensing cause less-serious infections.

New Jefferson Research Suggests Common Anti-Seizure Medications May Increase Risk of Cardiovascular Problems

An important clinical repercussion in the treatment of epilepsy has been discovered by a research team led by Scott Mintzer, M.D., assistant professor in the Department of Neurology at Jefferson Medical College of Thomas Jefferson University. The team has determined that two of the most commonly prescribed anti-seizure medications may lead to significantly increased levels of cholesterol, C-reactive protein and other markers of cardiovascular disease risk. The finding – set to appear in the April issue of Annals of Neurology – may help doctors manage the care of patients with seizures more effectively by prescribing different anti-seizure medications that will not adversely affect cardiovascular health. The study involved two of the most widely-prescribed anticonvulsants – phenytoin (Dilantin®) and carbamazepine (Tegretol®, Carbatrol®) – which have potent effects on many enzymes in the body involved in different areas of metabolism. The researchers recruited 34 epilepsy patients taking either one of those two drugs who were being switched over to one of two newer anti-seizure drugs which do not widely affect enzymes – lamotrigine (Lamictal®) or levetiracetam (Keppra®). The goal was to determine if the change affected the patients’ cholesterol levels and other key markers of cardiovascular disease. Just 6 weeks after the patients’ drugs were switched, there were significant declines in total cholesterol, non-high-density lipoprotein (commonly referred to as ‘bad’) cholesterol, triglycerides and C-reactive protein, suggesting the older, commonly-used drugs might substantially increase the risk of cardiovascular disease.

Mechanism of Alzheimer's suggests combination therapy needed

Researchers at the University of Illinois at Chicago College of Medicine have discovered a mode of action for mysterious but diagnostic protein snarls found in the brains of Alzheimer's patients that suggests a one-two punch of therapy may be needed to combat the neurodegenerative disease. Alzheimer's disease, which may affect as many as 5 million Americans and is among the most costly diseases to society in the United States and Europe, is characterized by two distinctive protein malformations: amyloid plaques and tau tangles. Amyloid plaques are sticky deposits made up of a short protein called amyloid beta, and tau tangles are made of short filaments of the tau protein.
So far no one has been able to explain how amyloid beta and the tau tangles wreak their damage on the nervous system. "We have known for a long time that amyloid beta was bad," said Scott Brady, professor and head of anatomy and cell biology at the UIC College of Medicine. "What we haven't understood is why it's bad." The findings, reported in a new study appearing in the Proceedings of the National Academy of Sciences Online Early Edition for March 16-20, suggest promising new targets for combination therapy. In previous work, published earlier this year, the researchers suggested how tau tangles work together with amyloid beta to create a perfect storm that destroys neural function and memory. "Cell death occurs at a very late stage of the disease," said Brady, principal investigator of the study. "Long before the cells die they lose function, and that function is critical for the symptoms that we see." Brady and his colleagues found that when short assemblies of amyloid -- rather than the long-chain plaques -- get inside neurons, they interfere with the cells' transport system. This limits their ability to send vital proteins and vesicles to where they are needed within the cell and interferes with the synaptic connections to other nerve cells.

Obese women play cancer roulette

Obese women may be putting themselves at greater risk of breast cancer by not undergoing regular screening. According to new research by Dr. Nisa Maruthur and her team from The John Hopkins University School of Medicine in Baltimore, USA, seriously obese women are significantly less likely to say they have undergone a recent mammography than normal weight women, especially if they are white. Maruthur’s findings are published online this week in Springer’s Journal of General Internal Medicine.Breast cancer is the second leading cause of cancer death among women in the US. Mammography screening has been proven to reduce the number of deaths from breast cancer; current guidelines recommend that women over the age of 40 undergo a mammography every couple of years. Obesity is also an important risk factor for both the development of, and death from, postmenopausal breast cancer.

Master Molecular Switch May Prevent the Spread of Cancer Cells to Distant Sites in the Body, According to Penn Study

Researchers at the University of Pennsylvania School of Medicine have identified a master switch that might prevent cancer cells from metastasizing from a primary tumor to other organs. The switch is a protein that, when in the “on” position, maintains the normal character of cells that line the surface of organs and body cavities. These epithelial cells are the type of cell from which most solid tumors arise. However, when the switch is turned “off” or absent, epithelial cells acquire characteristics of another cell type, called mesenchymal cells, and gain the ability to migrate and move away from the primary tumor. The researchers report their findings in this month’s issue of Molecular Cell.Understanding how this switch works may one day lead to a drug that controls cancer cell metastasis and tissue fibrosis. This change in cell motility is called the epithelial to mesenchymal transition, or EMT, and is an important process during the development of embryos. But when the transition is aberrantly reactivated in adults it can have dire physiological consequences, leading to cancer metastasis as well as other disease processes such as tissue fibrosis. Fibrotic tissue is a hallmark of organ failure, as in liver cirrhosis or kidney failure.

Synthesizing the most natural of all skin creams

Even after nine months soaking in the womb, a newborn’s skin is smooth – unlike an adult’s in the bath. While occupying a watery, warm environment, the newborn manages to develop a skin fully equipped to protect it in a cold, dry and bacteria-infected world. A protective cream called Vernix caseosa (VC), which covers the fetus and the newborn, aids in the growth of skin both before and after birth. VC provides ‘waterproofing’ in utero, allowing skin to grow in wet conditions, while after birth it hydrates and cleanses, even healing when applied to ulcers. Prof. Joke Bouwstra, a specialist in the skin barrier and its synthesis at Leiden University, and her colleague Robert Rißmann set out to study VC in detail and has produced a synthetic version of this natural buttery ointment which shows the same structure and unique properties. As well as helping pre-term babies develop essential protection against temperature changes, dehydration and infection, artificial VC could also benefit sufferers of skin disease. Like most moisturising creams, VC is mostly water. Its outstanding properties come from the addition of just 10% each of lipid molecules and dead skin cells (corneocytes), so the exact composition of the mixture is important. For the lipids, X-ray diffraction measurements at the Dutch/Flemish DUBBLE beamline at the ESRF (European Synchrotron Radiation Facility) allowed the Leiden researchers to find the proportions of the various forms in the cream, even distinguishing between complex molecules differing in chain length.

Researchers clone key sperm-binding proteins

New treatments for infertility could be closer to reality, thanks to a discovery from scientists at the Université de Montréal and Maisonneuve-Rosemont Hospital Research Centre. According to a study published in the journal Molecular Human Reproduction, the researchers have become the first to clone, produce and purify a protein important for sperm maturation, termed Binder of Sperm (BSP), which may have implications for both fertility treatments and new methods of male contraception."We have previously isolated and characterized BSPs from many species, such as bulls and boars," says Dr. Puttaswamy Manjunath, senior author and a professor in the departments of medicine and of biochemistry at the Université de Montréal and a member of the Maisonneuve-Rosemont Hospital Research Centre. "We know from these studies that if this protein is missing or defective in these species, fertility is compromised. We believe that BSP is equally important in humans."

Studies show that nice guys finish first in business world

When it comes to leading a team tasked with developing new products and bringing them to market, new research from North Carolina State University shows that being nice and playing well with others gives you a very real competitive advantage. One new study shows that project managers can get much better performance from their team when they treat team members with honesty, kindness and respect. A second study shows that product development teams can reap significant quality and cost benefits from socializing with people who work for their suppliers. The first study, co-authored by NC State's Dr. Jon Bohlmann, focused on cross-functional product development teams, which bring together engineers, researchers and business personnel. The diverse backgrounds of the team members means there is a focus on finance and marketing, as well as design and functionality, from the beginning of the product-development process. But that diversity also makes effective communication essential, in order to ensure that team members are collaborating rather than working at cross-purposes. The Bohlmann study finds that "interactional fairness perception" affects "cross-functional communication." In other words, Bohlmann explains, "If you think you are being treated well, you are going to work well with others on your team." Bohlmann, an associate professor of marketing at NC State, says that the study evaluated whether team members felt they were being well treated by their project leader. This evaluation included questions as to whether team members felt their leader was honest, kind and considered the viewpoints of team members. Bohlmann says the results of the study show that if a team's leader was perceived as "basically being a nice guy," then "team members showed a significant increase in commitment to the team's success and to the project they were working on." This increase in commitment is important, Bohlmann explains, because it leads to enhanced performance in meeting team goals.

Oil spill clean-up kills more fish than spills themselves, says Queen’s biologist

A new Queen's University study shows that detergents used to clean up spills of diesel oil actually increase its toxicity to fish, making it more harmful. "The detergents may be the best way to treat spills in the long term because the dispersed oil is diluted and degraded," says Biology professor Peter Hodson. "But in the short term, they increase the bioavailability and toxicity of the fuel to rainbow trout by 100-fold." The detergents are oil dispersants that decrease the surface tension between oil and water, allowing floating oil to mix with water as tiny droplets. Dr. Hodson and his team found that dispersion reduces the potential impacts of oil on surface-dwelling animals, While this should enhance biodegradation, it also creates a larger reservoir of oil in the water column. This increases the transfer of hydrocarbons from oil to water, Dr. Hodson explains. The hydrocarbons pass easily from water into tissues and are deadly to fish in the early stages of life. "This could seriously impair the health of fish populations, resulting in long-term reductions in economic returns to fisheries," he says.

Nanoscopic probes can track down and attack cancer cells

A researcher has developed probes that can help pinpoint the location of tumors and might one day be able to directly attack cancer cells. Joseph Irudayaraj, a Purdue University associate professor of agricultural and biological engineering, developed the nanoscale, multifunctional probes, which have antibodies on board, to search out and attach to cancer cells. A paper detailing the technology was released last week in the online version of Angewandte Chemie, an international chemistry journal. "If we have a tumor, these probes should have the ability to latch on to it," Irudayaraj said. "The probe could carry drugs to target, treat as well as reveal cancer cells." Scientists have developed probes that use gold nanorods or magnetic particles, but Irudayaraj's nanoprobes use both, making them easier to track with different imaging devices as they move toward cancer cells. The magnetic particles can be traced through the use of an MRI machine, while the gold nanorods are luminescent and can be traced through microscopy, a more sensitive and precise process. Irudayaraj said an MRI is less precise than optical luminescence in tracking the probes, but has the advantage of being able to track them deeper in tissue, expanding the probes' possible applications.

Alzheimer's Disease Neuroimaging Initiative announces completion of genome-wide analysis

Researchers announced today that a high-density genome wide analysis of participants in the Alzheimer's Disease Neuroimaging Initiative (ADNI; www.adni-info.org) is more than 95% complete and that data will be shared with scientists around the world for further analysis. The ADNI data will be used by researchers to search for genes that contribute to the development of Alzheimer's disease, which currently affects up to 5 million people in the United States alone. ADNI, an ongoing $60 million project, is a public-private partnership supported primarily by the National Institutes of Health (NIH) with pharmaceutical and related industries and not-for-profit organizations providing support through the Foundation for the National Institutes of Health (FNIH). One of the largest scale neuroimaging projects ever undertaken, ADNI involves longitudinal magnetic resonance imaging (MRI) and positron emission tomography (PET) brain imaging and blood, urine and spinal fluid biomarker studies of more than 800 individuals, half of whom have mild cognitive impairment, a condition placing them at high risk for developing Alzheimer's disease or another dementia. The primary goal of ADNI is to determine whether brain imaging, other biological markers, and clinical and neuropsychological assessment can accurately measure the progression of mild cognitive impairment and early Alzheimer's disease. The identification of specific biomarkers of early Alzheimer's disease and disease progression will provide a useful tool for researchers and clinicians in both the diagnosis of early Alzheimer's disease and in the development, assessment and monitoring of new treatments. One major Alzheimer's disease risk gene, APOE, has been consistently shown to be associated with the form of the disease arising later in life that accounts for approximately 95 percent of all cases. It is widely suspected that variants in an ensemble of other genes play a role in susceptibility to the disease and may influence the age of onset, expression and rate of progression of neurodegenerative changes in the brain. "This new data set provides a unique opportunity to evaluate the associations between a highly comprehensive dataset based on brain imaging, clinical examinations and other biomarkers and the entire genome or selected candidate genes," said Andrew Saykin, Psy.D., director of the IU Center for Neuroimaging at the Indiana University School of Medicine, who leads the genetics research team.

Less of a stink in diabetes patients?

Hydrogen sulfide (H2S) is commonly associated with smell of rotten eggs, stink bombs and blocked drains but lower blood levels of the gas are possibly linked to cardiovascular complications in some male patients with type II diabetes, according to research recently presented by researchers at the Peninsula Medical School in the South West of England at the Annual Diabetes UK Professional Conference in Glasgow this week and published in Diabetic Medicine. H2S is produced naturally within our bodies, along with other chemical compounds such as nitric oxide, where it is believed to help regulate blood pressure. Research shows that a balance between these compounds relates to good health, whereas an imbalance could indicate disease. In the case of diabetes, common complications of the disease are high blood pressure and microvascular dysfunction, which leads to damage of the tiny blood vessels (microvessels) that deliver blood, oxygen and nutrients to the eyes, skin, nerves and kidney. Dr. Matt Whiteman of the Peninsula Medical School and colleagues from the Peninsula National Institute for Health Research (NIHR) Clinical Research Facility have compared the levels of H2S in blood samples taken from healthy people and male patients with type II diabetes and found markedly decreased levels of H2S in the diabetes patients. Lower H2S levels were associated with clinical markers of impaired microvessel function suggesting that a loss of this blood pressure lowering gas could be a contributing factor in the development of vascular complications in patients with diabetes.

Dendritic cells ensure immune tolerance

One of the most important tasks of the immune system is to identify what is foreign and what is self. If this distinction fails, then the body's own structures will be attacked, the result of which could be an autoimmune disease such as diabetes mellitus type 1 or multiple sclerosis. The only way to protect against these afflictions is to destroy all immune factors that turn against the body’s own tissue – in other words: immune tolerance. A team working with LMU researcher Dr. David Vöhringer has now investigated exactly what role dendritic cells play in this process. There has long been suspicion that these cells, which are important for the body’s defenses, are also essential for the establishment and maintenance of immune tolerance. “We investigated mice that lacked this cell type from birth,” reports Vöhringer. “It turned out that immune cells that attack the body’s own tissue survive in these animals, and thereby trigger an autoimmune response. It follows that dendritic cells play a major part in protecting against autoimmune disease.” T cells are a type of white blood cell that are key actors in the body's immune defenses. Each T cell has a receptor on its surface for recognizing just one single antigen. Antigens are molecular structures, mostly fragments of proteins. T cells do not dock onto free antigens, however: they rely on other cells which can present antigens to them. It is the dendritic cells that are primarily responsible for this job. They present the T cells with various antigens, and if an antigen matches a receptor, then that T cell will trigger an immune response from the body. This is how the body defends itself against pathogens and other intruders. But behind this tactic lies an element of danger to the organism: what happens if the antigen is not foreign, but originates from the body’s own tissue instead? A wrongly induced immune response can lead to a severe autoimmune disease that, if left untreated, could lead to destruction of organs or even death. So-called autoreactive T cells, which recognize the body’s own structures, must be eradicated or pacified to avoid that they can cause harm. A T cell screening process therefore takes place in the thymus, the bilobular organ in the upper thorax, to distinguish the good from the bad of these dangerous lone mavericks. Each individual T cell is tested, and the autoreactive ones destroyed.

Stress may cause the brain to become disconnected

The new paper by Hajszan and colleagues at Yale University suggests that in learned helplessness, an animal model for depression and PTSD, stress-related reductions in synapses in the hippocampus are directly related to the emergence of depression-like behavior. These data help to make the case that stress-related changes in the structure of nerve cells may have important behavioral consequences, explains Dr. Hajszan. "The importance of our findings is derived from the well-known fact that synapses have a great potential for rapid changes, which may underlie sudden mood swings. More importantly, it is feasible to restore hippocampal synapses in a very short period of time (hours or even minutes), which opens up exciting new avenues for developing rapid-acting antidepressants that may provide immediate relief from depressive symptoms."  It cannot yet be said that reductions in cortical volumes in patients with PTSD reflect reductions in the number of synapses. However, these findings underscore the potential importance of studying post-mortem human tissue to determine whether humans also show this pattern of neural changes. Dr. Krystal notes that "settling this issue could help us to better understand recent epidemiologic data suggesting that most of the adjustment problems of soldiers returning from Iraq and Afghanistan with mild traumatic brain injury (TBI) or post-concussive syndrome are attributable to PTSD." He adds, "We have tended to think of PTSD and mild TBI as unrelated at the neural level. However, with growing evidence from animal studies that PTSD may be associated with loss of neural connections, it may turn out that PTSD and mild TBI are two distinct, but interacting, ways that soldiers might be affected by their combat experience. " Research is ongoing in the authors' lab and in others as they continue to make progress in understanding how the brain is affected by depression and stress, and in developing targeted medications.

University of Pennsylvania Researchers Find that the Unexpected Is a Key to Human Learning

The human brain’s sensitivity to unexpected outcomes plays a fundamental role in the ability to adapt and learn new behaviors, according to a new study by a team of psychologists and neuroscientists from the University of Pennsylvania. Using a computer-based card game and microelectrodes to observe neuronal activity of the brain, the Penn study, published this week in the journal Science, suggests that neurons in the human substantia nigra, or SN, play a central role in reward-based learning, modulating learning based on the discrepancy between the expected and the realized outcome. “This is the first study to directly record neural activity underlying this learning process in humans, confirming the hypothesized role of the basal ganglia, which includes the SN, in models of reinforcement including learning, addiction and other disorders involving reward-seeking behavior,” said lead author Kareem Zaghloul, postdoctoral fellow in neurosurgery at Penn’s School off Medicine. “By responding to unexpected financial rewards, these cells encode information that seems to help participants maximize reward in the probabilistic learning task.” Learning, previously studied in animal models, seems to occur when dopaminergic neurons, which drive a larger basal ganglia circuit, are activated in response to unexpected rewards and depressed after the unexpected omission of reward. Put simply, a lucky win seems to be retained better than a probable loss.

Researchers develop DNA 'patch' for canine form of muscular dystrophy

Using a novel genetic technology that covers up genetic errors, researchers funded in part by the National Institutes of Health have developed a successful treatment for dogs with the canine version of Duchenne muscular dystrophy, a paralyzing, and ultimately fatal, muscle disease. The technology, known as "exon skipping" uses tailor-made snippets of DNA-like molecules as molecular "patches." These patches cover up mutant DNA sequences that code for making an important muscle protein. The mutant sequences occur in portions of the gene known as exons, which contain the information needed to make the muscle protein. By covering up the mutant regions, the DNA patches allowed the dogs to make an imperfect—but functional—version of the protein, and significantly improve their muscle functioning. Earlier studies showed that it was possible to inject the patches into the bloodstream of mice and deliver them throughout the animals' bodies. The current finding shows that the DNA patches could be delivered by injection throughout the entire body in a much larger animal than a mouse, raising the possibility that they might be successfully delivered throughout the body to human muscles as well. Moreover, the current study represents an advance over the earlier efforts in that it was able to use several different kinds of DNA patches. A combination of different patches, known as a cocktail, would be needed to treat most of the human cases of the disease, which can involve many different exons. The canine version of Duchenne muscular dystrophy occurs naturally in dogs, and affects the same gene that is affected in the human form of the disease. "This is a promising finding," said Duane Alexander, M.D., director of the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), one of the NIH institutes that provided partial funding for the study. "It's an important step toward realizing the goal of developing a treatment that could alleviate the symptoms of this disorder."

Music tuition can help children improve reading skills

Children exposed to a multi-year programme of music tuition involving training in increasingly complex rhythmic, tonal, and practical skills display superior cognitive performance in reading skills compared with their non-musically trained peers, according to a study published today in the journal Psychology of Music, published by SAGE. According to authors Joseph M Piro and Camilo Ortiz from Long Island University, USA, data from this study will help to clarify the role of music study on cognition and shed light on the question of the potential of music to enhance school performance in language and literacy. Studying children the two US elementary schools, one of which routinely trained children in music and one that did not, Piro and Ortiz aimed to investigate the hypothesis that children who have received keyboard instruction as part of a music curriculum increasing in difficulty over successive years would demonstrate significantly better performance on measures of vocabulary and verbal sequencing than students who did not receive keyboard instruction.
Several studies have reported positive associations between music education and increased abilities in non-musical (eg, linguistic, mathematical, and spatial) domains in children. The authors say there are similarities in the way that individuals interpret music and language and "because neural response to music is a widely distributed system within the brain…. it would not be unreasonable to expect that some processing networks for music and language behaviors, namely reading, located in both hemispheres of the brain would overlap." The aim of this study was to look at two specific reading subskills – vocabulary and verbal sequencing – which, according to the authors, are "are cornerstone components in the continuum of literacy development and a window into the subsequent successful acquisition of proficient reading and language skills such as decoding and reading comprehension."

Important new model shows how proteins find the right DNA sequences

Researchers at Uppsala University and Harvard University have collaboratively developed a new theoretical model to explain how proteins can rapidly find specific DNA sequences, even though there are many obstacles in the way on the chromosomes. The findings are being published today in the scientific journal Nature Physics. In living cells, DNA-binding proteins regulate the activity of various genes so that different cells carry out the right tasks at the right time. For this to work, the DNA-binding proteins need to find the right DNA site sufficiently quickly. The research team behind the new study has previously succeeded in determining that it takes only a few minutes for an individual protein molecule to look through the millions of nearly identical binding alternatives and find the right place to bind. This is nevertheless slower than what is predicted by the established theoretical model for how DNA-binding proteins find their way to the proper place by alternating between diffusing in the cell cytoplasm and along DNA strands. "By also taking into consideration the fact that there are many obstacles in the way when proteins are to diffuse along DNA strands, we can now calculate more exactly how long it takes them to find their way," says Johan Elf, associate professor of molecular biotechnology at the Center for Bioinformatics.

Gladstone scientists reveal key enzyme in fat absorption

Scientists at the Gladstone Institutes of Cardiovascular Disease (GICD) have found that a key enzyme involved in absorbing fat may also be a key to reducing it. The enzyme, acyl CoA: monoacylglycerol acyltransferase 2 or Mgat2 is found in the intestines and plays an important part in the uptake of dietary fat by catalyzing a critical step in making triglyceride, a kind of fat. Triglyceride accounts for nearly one-third of the fat eaten by people in developed countries. Researchers in the laboratory of Robert V. Farese, Jr. MD, found that mice that were genetically modified to lack Mgat2 remain normal on a low-fat diet. However, when fed a high-fat diet that is similar to that eaten by many Americans, the mice do not get fat and do not develop other symptoms of obesity, such as glucose intolerance, hypercholesterolemia, and fatty livers. The mice eat the same number of calories as other mice, and the calories are fully absorbed. Results of their study were published in the current issue of the journal Nature Medicine. "Because mice that lack this enzyme do not gain weight on a high-fat diet, it is an intriguing target for future interventions to prevent weight gain and the problems associated with that extra weight," said Dr. Farese. The mechanism of action, the researchers identified was that the lack of Mgat2 may reduce the uptake of fat in the small intestine and delay its entry into the blood. This process may dissociate fat from carbohydrate absorption and insulin secretion and ultimately lower the amount of fat stored and used. How this happens is not clear. One possibility is that the absorbed fat is partitioned more to tissues where it is burned up. "Differences in Mgat2 expression may contribute to the propensity of some people to gain weight from diets rich in fat," said Eric Yen, PhD, lead author of the study. "Our findings suggest that inhibiting this enzyme in the small intestine might be an effective way to treating metabolic diseases that result from excessive fat intake."

Blocking protein may help ease painful nerve condition

Scientists have identified the first gene that pulls the plug on ailing nerve cell branches from within the nerve cell, possibly helping to trigger the painful condition known as neuropathy. The condition is a side effect of some forms of chemotherapy and can also afflict patients with cancer, diabetes, kidney failure, viral infections, neurodegenerative disorders and other ailments. Researchers at Washington University School of Medicine in St. Louis showed that blocking the dual leucine zipper kinase (DLK) gene inhibits degeneration of ailing nerve cell branches, possibly preventing neuropathy. "Neuropathy can become so extraordinarily painful that some patients stop taking their chemotherapy, regardless of the consequences in their fight against cancer," says co-senior author Aaron DiAntonio, M.D., Ph.D., associate professor of developmental biology. "So we're very excited about the possibilities this gene may offer for reducing that pain." Scientists have known since 1850 that nerve cells have ways to prune branches (also known as axons) that are injured. Although axon pruning is also a normal part of early human development, inappropriate loss of axons in the adult nervous system causes painful sensations that have been compared to burning, freezing or electric shock and have come to be known as neuropathy. DiAntonio's lab previously revealed that the fruit fly's version of DLK helps establish synapses, junctures where two nerve cells communicate. But they found the gene doesn't do the same thing in mice. Curious about DLK's role in mammals, Bradley Miller, an M.D./Ph.D. student in DiAntonio's lab, consulted with co-senior author Jeffrey Milbrandt, M.D., Ph.D., the David Clayson Professor of Neurology. Milbrandt studies the role of various proteins in neurodegeneration. With support from the University's Hope Center for Neurological Disorders, they showed that the long axons of the sciatic nerve in mice with a mutated DLK gene resisted degeneration after it was surgically cut.

A sticky business -- how cancer cells become more 'gloopy' as they die

The viscosity, or 'gloopiness', of different parts of cancer cells increases dramatically when they are blasted with light-activated cancer drugs, according to new images that provide fundamental insights into how cancer cells die, published in Nature Chemistry today (15 March).The images reveal the physical changes that occur inside cancer cells whilst they are dying as a result of Photodynamic Therapy (PDT). This cancer treatment uses light to activate a drug that creates a short-lived toxic type of oxygen, called singlet oxygen, which kills cancerous cells.The research team behind the study says that revealing what happens to viscosity within a dying cancer cell is important because it helps give a better understanding of how cells function and which factors are important for controlling reactions inside cells. Ultimately this could help scientists design more efficient drugs for Photodynamic Therapy and other treatments.The research is also of wider significance because these are the first ever real-time maps showing viscosity changing over a period of time inside a cell during a biologically important process like cell death.Previous studies have shown that the viscosity of human cells and organs also changes in patients with diseases including diabetes and atherosclerosis, says lead author Dr Marina Kuimova from Imperial College London's Department of Chemistry.She explains - "We're still not quite sure exactly what the relationship is between increased stickiness inside cells and disease, but we expect that the two are related."

Iron is involved in prion disease-associated neuronal demise

Imbalance of iron homeostasis is a common feature of prion disease-affected human, mouse, and hamster brains, according to a new study by Dr. Neena Singh and colleagues at Case Western Reserve University School of Medicine, alongside collaborators from Creighton University. These findings, published March 13 in the open-access journal PLoS Pathogens, provide new insight into the mechanism of neurotoxicity in prion disorders, and novel avenues for the development of therapeutic strategies. Unlike other neurodegenerative conditions, prion disorders are sporadic, inherited, and infectious, and affect both humans and animals; common examples are mad cow disease in cattle, scrapie in sheep, and Creutzfeldt-Jakob disease in humans. The causative agent is a misfolded protein referred to as PrP-scrapie that replicates itself by changing the conformation of neighboring copies of the same protein, namely the prion protein. Aggregates of PrP-scrapie are toxic to brain cells and cause a spongy-like appearance in diseased brains. Research from the Singh laboratory suggests that accumulation of PrP-scrapie alters the metabolism of iron in diseased brains. The imbalance of brain iron homeostasis worsens with disease progression, and is not an outcome of end-stage disease. Since iron is highly toxic when mismanaged, this condition is likely to contribute significantly to prion-disease-associated neurotoxicity. The likely cause of this condition is loss of normal function of the prion protein in cellular iron metabolism demonstrated recently by Singh and colleagues, combined with gain of toxic function by the redox-active PrP-scrapie complex as shown in this report.

New strategy to weaken traumatic memories

Imagine that you have been in combat and that you have watched your closest friend die in front of you. The memory of that event may stay with you, troubling you for the rest of your life. Posttraumatic stress disorder (PTSD) is among the most common and disabling psychiatric casualties of combat and other extremely stressful situations. People suffering from PTSD often suffer from vivid intrusive memories of their traumas. Current medications are often ineffective in controlling these symptoms and so novel treatments are needed urgently. In the February 1st issue of Biological Psychiatry, published by Elsevier, a group of basic scientists shed new light on the biology of stress effects upon memory formation. In so doing, they suggest new approaches to the treatment of the distress related to traumatic memories. Their work is based on the study of a drug, RU38486, that blocks the effects of the stress hormone cortisol. Using an animal model of traumatic memory, investigators at the Mount Sinai School of Medicine show that treatment with RU38486 selectively reduces stress-related memories, leaving other memories unchanged. They also found that the effectiveness of the treatment is a function of the intensity of the initial "trauma." Although this particular study was performed in rats, their findings help to set the stage for trials in humans. Cristina Alberini, Ph.D., corresponding author on this article, explains how their findings will translate into developing clinical parameters: "First, the drug should be administered shortly before or after recalling the memory of the traumatic event. Second, one or two treatments are sufficient to maximally disrupt the memory. Third, the effect is long lasting and selective for the recalled memory. Finally, the time elapsing between the traumatic experience and the treatment seems to be an important parameter for obtaining the most efficacious treatment."

Study tracks increasing use of CT on pregnant women

Researchers have found that over a 10-year period radiologic exams on pregnant women have more than doubled, according to a study published in the online edition of Radiology. "Imaging utilization has not been previously studied in the pregnant population," said Elizabeth Lazarus, M.D., assistant professor of diagnostic imaging at the Warren Alpert School of Medicine at Brown University and a radiologist at Rhode Island Hospital in Providence, R.I. "This population may be vulnerable to the adverse effects of radiation." Dr. Lazarus and colleagues conducted a retrospective review of nuclear medicine, CT, fluoroscopy and plain-film x-ray imaging examinations performed at Rhode Island Hospital and Women and Infants' Hospital from 1997 through 2006 to determine how often these imaging exams were performed on pregnant women and the estimated radiation dose to the fetus. Data were then compared to the number of infant deliveries per year for that same time period. The researchers found that from 1997 to 2006, the total number of imaging studies performed on pregnant women at their institution increased by 10.1 percent per year, but the number of CT exams increased by 25.3 percent per year. CT delivers a higher amount of radiation than many other radiologic procedures. CT exams are not routinely ordered for pregnant women, but may be necessary to detect suspected life-threatening conditions such as bleeding in the brain, blood clots in the lungs or appendicitis. Since CT exposes the developing fetus to radiation, concerns are often raised regarding overuse. The majority of CT examinations (approximately 75 percent) analyzed in the study were performed in areas of the mother's body separate from the uterus, so the fetus was not exposed to any direct radiation. Still, low levels of radiation have been shown to carry a small risk of harm to a developing fetus. "Women should know that imaging is generally safe during pregnancy and is often used to detect potentially life-threatening problems," Dr. Lazarus said. "However, this study should raise awareness about imaging trends in pregnant patients and help us continue in our efforts to minimize radiation exposure," Dr. Lazarus said.

Preventium is 'where the prevention of breast and prostate cancer begins'

Dr. Ercole Cavalieri and Dr. Eleanor Rogen of the University of Nebraska Medical Center, Eppley Institute for Research in Cancer, located in Omaha, Nebraska, have identified the triggering mechanism by which breast and prostate cancer cells begin. Preventium™ http://www.preventium.org is a recently developed dietary supplement that promises to reduce people's risk for breast and prostate cancer. Ercole Cavalieri, D.Sc. and research collaborator Eleanor Rogen, Ph.D. say: "We have found the first step that starts a cell down the road to becoming a cancer cell. By blocking this first step from happening, we feel we can stop the development of breast and prostate cancer." The researchers have discovered that certain estrogen derivates (metabolites) can react with deoxyribonucleic acid (DNA) to cause damage that may initiate the start of breast and prostate cancer. Estrogen can initiate cancer when natural protective mechanisms do not function properly in the body, which then allows estrogen metabolites to react with DNA. Since both men and women have naturally occurring estrogen, the triggering mechanism for breast and prostate cancer is identical. This research has been funded in part by nearly $40 million in direct funding from the National Cancer Institute and the U.S. Defense Department.

UH sociologist has different perspective on obesity 'epidemic'

Headlines tell us the nation is getting fatter, and that obesity has become an epidemic. But there is more to the story, according to one University of Houston sociologist. While she acknowledges that there has been a shift in body weight over the years, assistant sociology professor Samantha Kwan looks at obesity from a different perspective. The term obesity was constructed by the medical community, Kwan says. And the use of the Body Mass Index, which measures obesity, as the main factor to define obesity, has resulted in the media greatly overstating the rise of the condition. "This epidemic has been constructed to the benefit of the medical industry that has in part medicalized the treatment of obesity over the years," Kwan says. "While there may be a rise in 'obesity,' the BMI is not always accurate. Some scholars describe this epidemic more as a moral panic. While there may be some truths to rising rates, they have been overstated." Kwan, who has been studying gender and body image since 2001, examines how cultural beauty messages about fat interact with other cultural messages about fat, such as health discourses. This is summarized in her article "Framing the Fat Body: Contested Meanings between Government, Activists and Industry," published in February's Sociological Inquiry. "I am trying to get students and audiences to understand that there are competing cultural meanings about the fat body," Kwan says. "Fat does not, in itself, signify unhealthy and unattractive. These are cultural constructions. We as a society say what it means to be fat, and right now cultural discourses say it's ugly and unhealthy to be fat. … It's also assumed that the body is a reflection of the psyche, including one's moral fiber." Kwan has found that women's self-esteem is more closely tied to weight than men's.

First sister study results reinforce the importance of healthy living

Women who maintain a healthy weight and who have lower perceived stress may be less likely to have chromosome changes associated with aging than obese and stressed women, according to a pilot study that was part of the Sister Study. The long-term Sister Study is looking at the environmental and genetic characteristics of women whose sister had breast cancer to identify factors associated with developing breast cancer. This early pilot used baseline questionnaires and samples provided by participants when they joined the Sister Study. Two recent papers published in Cancer Epidemiology Biomarkers and Prevention looked at the length of telomeres, or the repeating DNA sequences that cap the ends of a person's chromosomes. Telomere length is one of the many measures being looked at in the Sister Study. Telomeres protect the ends of chromosomes and buffer them against the loss of important genes during cell replication. Over the course of an individual's lifetime, telomeres shorten, gradually becoming so short that they can trigger cell death. The papers show that factors such as obesity and perceived stress may shorten telomeres and accelerate the aging process. "Together these two studies reinforce the need to start a healthy lifestyle early and maintain it," said Linda Birnbaum, Ph.D., the director of the National Institute of Environmental Health Sciences (NIEHS), part of the National Institutes of Health. The researchers who published these papers are from the NIEHS which sponsors the Sister Study. The papers are the first findings coming out of the Sister Study. The Sister Study is just completing its enrollment of 50,000 women aged 35-74 to prospectively study risk factors for breast cancer. "We anticipate a wealth of information to come out of the Sister Study," said Dale Sandler, Ph.D., chief of the Epidemiology Branch at NIEHS and principal investigator of the Sister Study. "Not only do we hope to find out more about the environmental and genetic factors that might lead to breast cancer, we also want to learn more about how factors such as stress, diet and exercise might impact cancer and other disease risks." One of the studies published this week found that women who were obese for a long time had reduced telomere length. The researchers looked at the relationship between various measures of current and past body size and telomere length in 647 women enrolled in the Sister Study. They found that women who had an overweight or obese body mass index (BMI) before or during their 30s, and maintained that status since those years, had shorter telomeres than those who became overweight or obese after their 30s. "This suggests that duration of obesity may be more important than weight change per se, although other measures of overweight and obesity were also important," said Sangmi Kim, Ph.D., epidemiologist and lead author on the paper. "Our results support the hypothesis that obesity accelerates the aging process," said Kim.

Search for blood pressure secrets reveals a surprising new syndrome

Yale researchers investigating the genetic causes of blood pressure variation have identified a previously undescribed syndrome associated with seizures, a lack of coordination, developmental delay and hearing loss.
The findings, published this week in Proceedings of the National Academy of Sciences, illustrate the power of genetic studies not only to find causes of chronic ailments, but also to identify a common cause in a seemingly unrelated set of symptoms in different parts of the body. "Our ability to unequivocally and rapidly define new syndromes and their underlying disease genes has progressed dramatically in recent years," said Richard Lifton, chair of the Department of Genetics at the Yale School of Medicine and senior author of the study. "A study like this would have taken years in the past, but was accomplished in a few weeks by a single fellow in the lab." The discovery of the new syndrome was made by Ute Scholl, a post-doctoral fellow in Lifton's lab, who was conducting a genetic analysis of 600 patients for causes of salt-handling defects of the kidney, which lead to high or low blood pressure. She identified a group of five patients from four families in Afghanistan, Turkey, Great Britain and Canada who had, in addition to a salt-handling defect, diverse neurologic problems. The similar clinical features of these patients suggested that all might be caused by a single defect, and in a matter of weeks she found that all five had inherited mutations in the gene KCNJ10, a potassium channel that is expressed in the brain, inner ear and kidney.

Emotions can help predict future eating disorders

A PhD thesis at the University of the Basque Country (UPV/EHU) has analysed the role played by a number of emotional variables, such as the way in which negative emotions are controlled or attitudes to emotional expression, and to use these variables as tools to predict the possibility of suffering an eating disorder. The author of the thesis, Ms. Aitziber Pascual Jimeno, presented her work under the title, Emotions and emotional control in eating disorders: predictor role and emotional profiles. Ms Pascual is a graduate in Psychology and carried out her thesis under Ms Itziar Etxebarria Bilbao and Ms Marķa Soledad Cruz Sįez, from the Department of Basic Psychological Processes and their Development at the Faculty of Psychology of the UPV/EHU. She is currently working as a lecturer at the University. In order to undertake the study, 433 women took part; 143 of these suffered from some kind of eating disorder and 145 in risk of contracting one. The results of the study show that, in general, the majority of the variables put forward can be used as predictive of suffering an eating disorder. The variables which, above all, alert to greater risk of developing an eating disorder are when the emotional state of the person is excessively influenced by diet, weight and body shape, when self-esteem is low, and when, in anxiety situations, emotions are not expressed and the person tends to act in an impulsive manner. These results have important implications, above all when drawing up prevention programmes for eating disorders. With the data obtained, it can be said that many of the emotional variables dealt with in Ms Pascual’s work should be taken into account when drawing up these prevention programmes.

Brain abnormality found in boys with attention deficit hyperactivity disorder

Researchers trying to uncover the mechanisms that cause attention deficit hyperactivity disorder and conduct disorder have found an abnormality in the brains of adolescent boys suffering from the conditions, but not where they expected to find it. Boys with either or both of these disorders exhibited a different pattern of brain activity than normally developing boys when they played a simple game that sometimes gave them a monetary reward for correct answers, according to a new study by a University of Washington research team. The research focused on two brain areas, the striatum and anterior cingulate cortex. The striatal region is a network of structures in the mid brain that motivates people to engage in pleasurable or rewarding behavior. The anterior cingulate is higher in the brain and normally activates when an expected reward stops. However, this process, called extinction, doesn't occur, at least as quickly, in boys with attention deficit hyperactivity or conduct disorders. Instead, the striatal region continues to be activated, said Theodore Beauchaine, a UW associate professor of psychology and senior author of the paper. "When children engage in impulsive behavior they are looking to stimulate themselves and have fun. Children with attention deficit hyperactivity disorder are always looking to have fun and that is what gets them in trouble," he said. "A behavior should stop when the reward stops. When you stop the reward for children with these disorders, they continue to focus on the reward long afterward and the anterior cingulate does not appear to become activated." Attention deficit hyperactivity disorder is one of the most common mental disorders among children, affecting between 3 and 5 percent of school-age youngsters, or an estimated 2 million. The researchers used functional magnetic resonance imaging to compare brain activity in 19 boys with either or both disorders and 11 normally developing boys. The adolescents ranged in age from 12 to 16. Their brains were scanned while they played the game. The boys looked at a screen and there was a button under each of their thumbs. When a light flashed on the left or right side of the screen they were instructed to press the button on that side. The screen lit up very fast, up to 100 times a minute. The boys received five cents for each correct response and could win up to $50. They were not penalized for wrong answers and their accumulated winnings showed up on the screen.

The Notch gene accelerates colon carcinogenesis

Professor Daniel Louvard (1) (CNRS Research Director and Director of the Curie Institute Research Centre) and his group, working in close partnership with Spyros Artavanis-Tsakonas (2), recently discovered how the Notch gene is involved in the pathogenic process leading to colon cancer. The Notch and Wnt signalling pathways play an important role in normal gut development and homeostasis. In mice, abnormal activation of these two signalling pathways increases the number of benign tumours-adenomas-in the intestine by a factor of over twenty compared with activation of the Wnt pathway alone. Moreover, these tumours grow extremely fast in the colon, mimicking the pathogenic process observed in humans. Cooperative action between these two pathways creates a favourable environment for malignant transformation. These findings (published online in PNAS) show that Notch acts as an "accelerator" in the development of colon cancer in humans, constituting an essential component of the pathogenic process. The question now is to find a "brake" that can counter this.
The gut, which represents a surface area equivalent to that of a tennis court, is in constant turnover completely renewing itself every five days. This turnover depends on the presence of stem cells and progenitor cells found in the crypts between intestinal villi. The stem cells give rise to progenitor cells which can in turn differentiate, over successive division cycles, to give the various different cell types that populate and form the gut. The key factor is to maintain a balance between differentiation and proliferation in the intestinal epithelium.

Cancer - Another step towards medication - Austrian Scientists identify a potential tumor suppressor

The gene Myc is an important factor for the growth of organisms by cell division. It causes the production of a protein which, as a transcription factor, controls the expression of up to 15 % of all human genes. When this gene mutates to an oncogene, the cell proliferates excessively and apoptosis is inhibited. Thereby the gene plays a decisive role in the development of many tumors. The problem is that pharmacological substances do not target Myc as it does not have enzymatic activity of its own. Thus, scientists worldwide are trying to find alternative ways to inhibit this oncogene. A team of scientists led by Klaus Bister and Markus Hartl of the Institute of Biochemistry and the Centre for Molecular Biosciences of the University of Innsbruck may have made an important step towards achieving this goal. For the first time, the scientists have shown that Myc suppresses the expression of the gene BASP1. This evidence prompted them to test the effect of BASP1 on the oncogene. In cell experiments they proved that BASP1 specifically inhibits the uncontrolled proliferation of Myc. „Until now the precise biochemical function of BASP1 is unknown“, Prof. Bister explains. „However, in our experiments we have found clear evidence that Myc-induced cell transformation can be specifically inhibited by BASP1, and consequently, the gene functions as a tumor suppressor.“ This finding may facilitate the development of new drugs which keep the development of tumors under control.

Study finds biological clue in brain tumour development

Scientists at The University of Nottingham have uncovered a vital new biological clue that could lead to more effective treatments for a children’s brain tumour that currently kills more than 60 per cent of young sufferers. Clinician –scientists at the University’s Children’s Brain Tumour Research Centre, working on behalf of the Children’s Cancer and Leukaemia Group (CCLG), have studied the role of the WNT biological pathway in central nervous system primitive neuroectodermal tumours (CNS PNET), a type of brain tumour that predominantly occurs in children and presently has a very poor prognosis. In a paper published in the British Journal of Cancer, they have shown that in over one-third of cases, the pathway is ‘activated’, suggesting that it plays a role in tumour development. The research also highlighted a link between WNT pathway activation and patient survival — patients who had a CNS PNET tumour that was activated survived for longer than those without pathway activation. The reason for the link between WNT pathway activation and better patient prognosis is as yet unclear. It could be that these tumours represent a less aggressive subset or that pathway activation itself actually harms the tumour. However, the pathway could represent an important new target for the treatment of more effective drugs, with fewer side effects.

Study finds extensive patient sharing among hospitals; could impact spread of infectious diseases

Findings from the first in-depth study of patient sharing show that hospitals share large numbers of patients with other acute care facilities without knowing it. In the new study released today at the annual meeting of the Society for Healthcare Epidemiology of America (SHEA), researchers found that only one in nine shared patients is directly transferred from one hospital to another, whereas most patients were discharged before being readmitted to another hospital. This high underestimation of patient sharing has important implications for handling the potential spread of infectious disease among acute care facilities, since patient sharing could be an avenue of transmission if a major disease outbreak were to occur. "We were surprised to find extensive interlinking of all the hospitals included in the study," said Susan S. Huang, MD, MPH, assistant professor and hospital epidemiologist, University of California Irvine School of Medicine and SHEA member. "The level of patient sharing among hospitals is grossly underestimated because patients often don't transfer directly between hospitals." The study included nearly 240,000 patient admissions. Researchers assessed direct and indirect transfers among all 31 acute care hospitals in Orange County, CA, a large metropolitan county of three million people, using a retrospective evaluation of 2005 California Hospital Discharge Data. Huang and colleagues examined the likelihood that adult patients admitted to each hospital in 2005 would subsequently be transferred or admitted to another hospital in the county in the 365 days following their discharge. This research did not include skilled nursing homes, psychiatric hospitals or rehabilitation facilities, which according to Huang could mean that the amount of patient sharing among all healthcare facilities is even higher than their study found. A large number of people (22 percent) who are discharged from acute care facilities are readmitted elsewhere within one year. Huang attributed the intricate and broad connections among hospitals to three primary factors: patient choice, insurer agreements among hospitals and immediacy of needing care.

Why we have difficulty recognizing faces in photo negatives

Humans excel at recognizing faces, but how we do this has been an abiding mystery in neuroscience and psychology. In an effort to explain our success in this area, researchers are taking a closer look at how and why we fail. A new study from MIT looks at a particularly striking instance of failure: our impaired ability to recognize faces in photographic negatives. The study, which appears in the Proceedings of the National Academy of Sciences this week, suggests that a large part of the answer might lie in the brain's reliance on a certain kind of image feature. The work could potentially lead to computer vision systems, for settings as diverse as industrial quality control or object and face detection. On a different front, the results and methodologies could help researchers probe face-perception skills in children with autism, who are often reported to experience difficulties analyzing facial information. Anyone who remembers the days before digital photography has probably noticed that it's much harder to identify people in photographic negatives than in normal photographs. "You have not taken away any information, but somehow these faces are much harder to recognize," says Pawan Sinha, an associate professor of brain and cognitive sciences and senior author of the PNAS study. Sinha has previously studied light and dark relationships between different parts of the face, and found that in nearly every normal lighting condition, a person's eyes appear darker than the forehead and cheeks. He theorized that photo negatives are hard to recognize because they disrupt these very strong regularities around the eyes. To test this idea, Sinha and his colleagues asked subjects to identify photographs of famous people in not only positive and negative images, but also in a third type of image in which the celebrities' eyes were restored to their original levels of luminance, while the rest of the photo remained in negative.

Research yields potential target for cancer, wound healing and fibrosis

Research conducted by Allison Berrier, PhD, Assistant Professor of Oral and Craniofacial Biology at the LSU Health Sciences Center New Orleans School of Dentistry, and colleagues, provides insights that may help scientists design novel approaches to control wound healing and fight diseases such as cancer and fibrosis. The paper, ?1 Integrin Cytoplasmic Domain Residues Selectively Modulate Fibronectin Matrix Assembly and Cell Spreading through Talin and Akt-1, will be published in the March 20, 2009 issue of the Journal of Biological Chemistry. The research team also included Drs. J. Angelo Green and Kenneth Yamada at the National Institute of Dental and Craniofacial Research, as well as Dr. Roumen Pankov at Sofia University in Sofia, Bulgaria. The research concerns the regulation of integrins – proteins on the surface of cells that serve dual roles of anchoring cells within tissues and controlling cell behavior. Integrins anchor to extracellular proteins found outside the cell and this contact regulates important cellular activities that are critical for survival, proliferation and differentiation in both healthy tissues and tumors. Integrins are involved in the cellular response to injury and infection and are needed to repair damaged tissue. Of the many integrins that exist, the beta-1 integrin is of great interest because it is involved in nearly every cell in the body. Its importance is demonstrated by the fact that mice, which are typically used as models for disease, cannot survive without the beta-1 integrin gene. Beta-1 integrin is a cell surface protein that spans the membrane and has a portion of the protein outside the cell and a portion of the protein inside the cell. The beta-1 integrin tail is the portion found inside the cell. The beta-1 integrin tail has two functions -- it connects integrins to the cellular infrastructure and to signaling pathways. This study advances earlier research on the beta-1 integrin tail, that revealed the ability of this integrin tail to provide a scaffold for signaling proteins that control cell survival. The extracellular matrix is a complex mixture containing proteins such as fibronectin and collagen that provide structural support to cells and traction for cell movement. If cells are placed on top of extracellular matrix proteins the cells become activated by their integrins and trigger signaling for the cell to expand or spread over the matrix. Cell spreading is an intermediate step during cell migration on matrix proteins. Prior to the current study it was not clear whether the beta-1 integrin tail recruits the same or different proteins inside the cell to control two different integrin receptor functions outside the cell, namely, formation of fibronectin fibrils and cell spreading.

Conflicts of interest in clinical research

Although paying finder's fees to researchers and clinicians to identify study participants could compromise the recruitment process and harm human lives, many medical schools fail to address this conflict of interest in their Institutional Review Board (IRB) policies. Leslie Wolf, an associate professor of law at Georgia State University, studied the IRB policies posted on the Web sites of 117 medical schools that received National Institutes of Health funding. Among the study's findings, Wolf revealed that less than half of the IRB policies discuss finder's fees or bonus payments as conflicts of interest, where research sponsors pay members of the research team or clinicians to identify potential participants or for meeting predetermined enrollment targets. "Since IRBs must review research protocols, and also are in a position to educate investigators about these issues, I thought their policies were an important place to look," Wolf said. "I thought they would have tried to address it more frequently than they did. That's a gap in IRB guidance." Finder's fees raise concern because researchers and their colleagues may be tempted to enroll individuals in studies for which they are ineligible, Wolf said. Wolf is also concerned that only 26 of the IRBs in the study mentioned potential conflicts when physicians recruit their own patients and that only four percent ask doctors to tell their patients that they are not obligated to participate. "It was talked about much less frequently than either the employer/employee or the teacher/student role conflict. It's been in the literature and patients may be particularly vulnerable," Wolf said. Concerns about conflicts of interest are only continuing to grow as more stories appear in the news, Wolf said. For instance, Ellen Roche, a healthy 24-year-old who died from lung failure in 2002, while in a study sponsored by her employer, the Johns Hopkins Asthma and Allergy Center. Roche became ill after she inhaled an experimental compound as part of a study to understand the cause of asthma. An external committee that reviewed the circumstances of the death expressed concerns that there were "subtle coercive pressures" on employees to enroll in the Center's studies. Employees who participated in the study not only received compensation for participation, but were given time off from the workday to undergo study procedures. "There have been situations that people have talked about in the media that undermine our confidence in research and could prevent important research from going forward," Wolf said. "We need to have a trustworthy research enterprise so that we can get good research that hopefully improves the lives of the rest of us."

Preterm Birth Rate Drops

The nation’s preterm birth rate declined slightly in 2007 – a finding that the March of Dimes hopes will prove to be the start of a new trend in improved maternal and infant health. The preterm birth rate declined for babies born at 34-36 weeks gestation (late preterm) and among babies born to African American and white women. “We’re encouraged by this drop in the preterm birth rate, and hope that the emphasis we’ve put on the problem of late preterm birth is beginning to make a difference,” said Jennifer L. Howse, Ph.D., president of the March of Dimes. “Through our Prematurity Campaign, we can build on this success and begin to give more babies a healthy start in life.” The rate of preterm births (less than 37 weeks gestation) dropped to 12.7 percent from 12.8 percent in 2006, a small but statistically significant decrease, according to preliminary birth data for 2007 released by the National Center for Health Statistics.

Barriers to diabetes care include restaurants and high-risk lifestyles, says international review

Eating out, lack of social support and high-risk lifestyles are just some of the barriers that stop patients with type 2 diabetes from controlling their condition, according to a research review that covered 8,900 patients and 4,550 healthcare providers from 28 countries. The study, published in the March issue of the Journal of Nursing and Healthcare of Chronic Illness, shows that psychosocial, socioeconomic, physical, environmental and cultural factors can provide major barriers to effective care. Researchers from Hong Kong and Northern Ireland (UK) studied research carried out between 1986 and 2007 to try and identify how treatment regimes could be improved. Their findings have enabled them to come up with a three-point plan for nurses involved in diabetes care. “Diabetes is a chronic condition and patients need to modify their lifestyle on a long-term basis to cope with it” says Sandra Pun from the School of Nursing at The Hong Kong Polytechnic University.

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