Honest Signals: How They Shape Our World

How can you know when someone is bluffing? Paying attention? Genuinely interested? The answer, writes Sandy Pentland in Honest Signals, is that subtle patterns in how we interact with other people reveal our attitudes toward them. These unconscious social signals are not just a back channel or a complement to our conscious language; they form a separate communication network. Biologically based "honest signaling," evolved from ancient primate signaling mechanisms, offers an unmatched window into our intentions, goals, and values. If we understand this ancient channel of communication, Pentland claims, we can accurately predict the outcomes of situations ranging from job interviews to first dates. Professor Alex ("Sandy") Pentland, is a leading figure at the MIT Media Lab and is a pioneer in the fields of organizational engineering, mobile information systems, and computational social science. He co-directs the Digital Life Consortium, a group of more than twenty multinational corporations exploring new ways to innovate, and oversees the Next Billion Network, established to support aspiring entrepreneurs in emerging markets. In 1997 Newsweek magazine named him one of the 100 Americans likely to shape this century.

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New genes involved in Acute Lymphoblastic Leukemia play fundamental role in prognosis of the disease

The inactivity or silence of certain genes plays a fundamental role in the prognosis of acute lymphoblastic leukemia (ALL) as well as in response to treatment, according to the results of research involving a team made up of specialists from the University Hospital of Navarra and the Centre for AppliedMedical Research (CIMA) at the same University of Navarra, as well as the Reina Sofi­a Hospital in Cardoba, Andalusia.

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Cognitive training can alter the biochemistry of the brain

Researchers at the Swedish medical university Karolinska Institutet have shown for the first time that the active training of the working memory brings about visible changes in the number of dopamine receptors in the human brain. The study, which is published in the prestigious scientific journal Science,was conducted with the help of PET scanning and provides deeper insight into the complex interplay between cognition and the brain's biological structure.

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Pathologically Elevated Blood Fat Levels in Obesity

Scientists at the German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ) have discovered a mechanism in liver metabolism that is responsible for pathologically elevated blood fat levels found in severe metabolic disorders. Mice suffering from metabolic syndrome or type 2 diabetes produce only small amounts of a molecule called LSR in the liver, as reported by researchers headed by Dr. Stephan Herzig of DKFZ in the specialist journal Diabetes. As a result, only small amounts of fat are transported from the blood into the liver and blood fat levels rise immensely. Stephan Herzig heads the Research Group "Molecular Metabolic Control" at DKFZ.

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Long-Sought Protein Structure May Help Reveal How ‘Gene Switch’ Works

The bacterium behind one of mankind's deadliest scourges, tuberculosis, is helping researchers at the Commerce Department's National Institute of Standards and Technology (NIST) and the Department of Energy's Brookhaven National Laboratory (BNL) move closer to answering the decades-old question of what controls the switching on and off of genes that carry out all of life's functions. In a Journal of Biological Chemistry paper* posted online today, the NIST/BNL team reports that it has defined—for the first time—the structure of a "metabolic switch" found inside most types of bacteria—the cyclic AMP (cAMP) receptor protein, or CRP—in its "off" state. CRP is the "binding site" (attachment point) for cAMP, a small molecule that, once attached, serves as the signal to throw the switch. This "on" state of CRP then turns on the genes that help a microbe survive in a human host.The researchers hope that once the switching mechanism is understood the data can be used to develop new methods for preventing tuberculosis and other pathogenic bacterial diseases.

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Study questions effectiveness of $80 million per year 'brain exercise' products industry

A new study from Lifespan evaluated the research to date on the impact of cognitive training on the healthy elderly population. Their review of all relevant randomized, controlled trials shows no evidence that structured cognitive interventions or "brain exercise" programs delay or slow progression of cognitive changes in healthy elderly. Such programs are now an $80 million per year industry. The study appeared in Alzheimer's & Dementia. There is much research on the benefits of cognitive rehabilitation strategies among elderly who already experience mild cognitive impairment (MCI) or Alzheimer's disease, as well as on the positive impact of physical exercise. The researchers, however, wanted to evaluate current research that would focus on the impact of cognitive interventions in the healthy elderly population. With this in mind, they established three objectives for their study: to systematically review the available literature on cognitive training and the healthy elderly, to assess and compare the efficacy of different cognitive interventions and to provide recommendations for future research. According to senior author Peter J. Snyder, PhD, vice president of research for Lifespan, and a professor of clinical neurosciences (neurology) at the Warren Alpert Medical School of Brown University, the researchers determined that the last meta-analysis performed on studies of healthy elderly and memory training was published in 1992. Since then, the definition of cognitive training has expanded and media attention has sparked an increase in public awareness with more and more Americans trying to curtail the effects of aging. As a result, Americans are now expected to spend $80 million this year on brain exercise products, compared to $2 million in 2005.

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Unexplained chest pain can be due to stress

Each year, many people seek emergency treatment for unexplained chest pains. A thesis from the Sahlgrenska Academy, University of Gothenburg, Sweden, indicates several common factors among those affected, including stress at work, anxiety, depression and a sedentary lifestyle.Chest pain is a common reason for patients to seek emergency treatment. A considerable number of patients are diagnosed with unexplained chest pain, which means that the pain cannot be linked to biomedical factors such as heart disease, or some other illness. The patient group is significant in size, with just over 20,000 patients seeking hospital treatment in 2006, and so far researchers have been unable to identify specific causes for unexplained chest pain. "Many suffer from recurring bouts of pain over several years, while the healthcare services are unable to find out what's causing it," says Registered nurse Annika Janson Fagring, the author of the thesis. In her thesis, Annika Janson Fagring describes and analyses symptoms among patients with unexplained chest pain. The results show that most of them are middle-aged, and that over a third of those affected were born outside Sweden. The chest pain had a negative impact on the patients' daily life in the form of tiredness, anxiety and fear of death. "The main difference between women and men with unexplained chest pain is that men were more likely to perceive their lives and jobs as being stressful, while women tended more to suffer from symptoms of depressions and anxiety," says Annika Janson Fagring. The patients, both men and women, experienced more symptoms of depression and anxiety, and work-related stress when compared with a reference group of people who were not suffering from heart disease. The male patients were more physically active in their spare time than the female patients, but compared with the reference group, both the men and the women with unexplained chest pain led a more sedentary lifestyle.

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Ketogenic Diet-Mayo Clinic

You might have heard the term "brain food" used to describe food that's good for you. Doctors at Mayo Clinic say there really is a diet that benefits the brain. But this diet is not for everybody. It's for kids who have epilepsy, and it's based on extremely high fats and very few carbs. More on how the ketogenic diet is helping some kids with epilepsy become seizure free.

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Marijuana use linked to increased risk of testicular cancer

Frequent and/or long-term marijuana use may significantly increase a man's risk of developing the most aggressive type of testicular cancer, according to a study by researchers at Fred Hutchinson Cancer Research Center. The study results were published online Feb. 9 in the journal Cancer.The researchers found that being a marijuana smoker at the time of diagnosis was associated with a 70 percent increased risk of testicular cancer. The risk was particularly elevated (about twice that of those who never smoked marijuana) for those who used marijuana at least weekly and/or who had long-term exposure to the substance beginning in adolescence.The results also suggested that the association with marijuana use might be limited to nonseminoma, a fast-growing testicular malignancy that tends to strike early, between ages 20 and 35, and accounts for about 40 percent of all testicular-cancer cases. Since the 1950s, the incidence of the two main cellular subtypes of testicular cancer, nonseminoma and seminoma – the more common, slower growing kind that strikes men in their 30s and 40s – has increased by 3 percent to 6 percent per year in the U.S., Canada, Europe, Australia and New Zealand. During the same time period, marijuana use in North America, Europe and Australia has risen accordingly, which is one of several factors that led the researchers to hypothesize a potential association. "Our study is not the first to suggest that some aspect of a man's lifestyle or environment is a risk factor for testicular cancer, but it is the first that has looked at marijuana use," said author Stephen M. Schwartz, M.P.H., Ph.D., an epidemiologist and member of the Public Health Sciences Division at the Hutchinson Center. Established risk factors for testicular cancer include a family history of the disease, undescended testes and abnormal testicular development. The disease is thought to begin in the womb, when some fetal germ cells (those that eventually make sperm in adulthood) fail to develop properly and become vulnerable to malignancy. Later, during adolescence and adulthood, it is thought that exposure to male sex hormones coaxes these cells to become cancerous."Just as the changing hormonal environment of adolescence and adulthood can trigger undifferentiated fetal germ cells to become cancerous, it has been suggested that puberty is a 'window of opportunity' during which lifestyle or environmental factors also can increase the risk of testicular cancer," said senior author Janet R. Daling, Ph.D., an epidemiologist who is also a member of the Center's Public Health Sciences Division. "This is consistent with the study's findings that the elevated risk of nonseminoma-type testicular cancer in particular was associated with marijuana use prior to age 18."

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While focusing on heart disease, researchers discover new tactic against fatal muscular dystrophy

Based on a striking similarity between heart disease and Duchenne muscular dystrophy, researchers at Columbia University Medical Center have discovered that a new class of experimental drugs for heart failure may also help treat the fatal muscular disorder. At first glance, heart failure and the muscle-wasting Duchenne disease couldn't appear more dissimilar. Duchenne affects boys usually before the age of 6, destroying their muscle cells. The boys become progressively weaker through their teens and usually die in their twenties. In people without Duchenne, heart failure typically starts much later in life, robbing the heart's pumping ability in the 7th, 8th or 9th decade of life. But the new study found that the muscle cells affected in both diseases have sprung the same microscopic leak that ultimately weakens skeletal muscle in Duchenne and cardiac muscle in heart failure. The leak lets calcium slowly seep into the skeletal muscle cells, which are damaged from the excess calcium in Duchenne. In people with chronic heart failure, a similar calcium leak continuously weakens the force produced by the heart and also turns on a protein-digesting enzyme that damages its muscle fibers.

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That gut feeling may actually reflect a reliable memory

You know the feeling. You make a decision you're certain is merely a "lucky guess." A new study from Northwestern University offers precise electrophysiological evidence that such decisions may sometimes not be guesswork after all. The research utilizes the latest brain-reading technology to point to the surprising accuracy of memories that can't be consciously accessed. During a special recognition test, guesses turned out to be as accurate or more accurate than when study participants thought they consciously remembered. "We may actually know more than we think we know in everyday situations, too," said Ken Paller, professor of psychology at Northwestern. "Unconscious memory may come into play, for example, in recognizing the face of a perpetrator of a crime or the correct answer on a test. Or the choice from a horde of consumer products may be driven by memories that are quite alive on an unconscious level." The study links lucky guesses to valid memories and suggests that people need to be more receptive to multiple types of knowledge, Paller said. Paller and Joel L. Voss, who received his Ph.D. at Northwestern and is now at the Beckman Institute, are co-investigators of the study. "An Electrophysiological Signature of Unconscious Recognition Memory" will be published online Feb. 8 by the journal Nature Neuroscience. During the first part of the memory test, study participants were shown a series of colorful kaleidoscope images that flashed on a computer screen. Half of the images were viewed with full attention as participants tried to memorize them.

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International study identifies gene variants associated with early heart attack

The largest study ever completed of genetic factors associated with heart attacks has identified nine genetic regions – three not previously described – that appear to increase the risk for early-onset myocardial infarction. The report from the Myocardial Infarction Genetics Consortium, based on information from a total of 26,000 inviduals in 10 countries, will appear in Nature Genetics and is receiving early online release. "For several decades, it has been known that the risk for heart attack – the leading cause of death and disability in the U.S. – clusters in families and that some of this familial clustering is due to differences in DNA sequence," says Sekar Kathiresan, MD, director of Preventive Cardiology at Massachusetts General Hospital (MGH) and corresponding author of the Nature Genetics report. "We set out to find specific, single-letter differences in the genome, what are called single-nucleotide polomorphisms (SNPs), that may be responsible for an increased familial risk for heart attack." Groundwork for the current study was laid more than 10 years ago when co-author Christopher O'Donnell, MD, now based at the Framingham Heart Study, began to gather data on patients treated at the MGH for early-onset heart attack – men under 50 and women under 60. Kathiresan soon joined the project, and in 2006 they formed the Myocardial Infarction Genetics Consortium along with David Altshuler, MD, PhD, of the MGH Center for Human Genetic Research and the Broad Institute of MIT and Harvard, eventually involving six groups around the world that had collected samples on a total of about 3,000 early-onset heart attack patients and 3,000 healthy controls. The current study took advantage of several scientific tools developed over the past decade. These include the International Haplotype Map, a comprehensive map of SNPs across the genome; genotyping arrays that allow screening of hundreds of thousands of SNPs at once; and a gene chip developed by Altshuler's team that can simulaneously screen for SNPs and for copy-number variants – deletions or duplications of gene segments, a type of change associated with several disease categories. After analysis of the consortium's samples identified SNPs that could be associated with heart attack risk, the researchers ran replication screens in three independent groups of samples, resulting in a total of 13,000 heart attack patients and 13,000 controls.

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Growth factor protects key brain cells in Alzheimer's models

Memory loss, cognitive impairment, brain cell degeneration and cell death were prevented or reversed in several animal models after treatment with a naturally occurring protein called brain-derived neurotrophic factor (BDNF). The study by a University of California, San Diego-led team – published in the February 8, 2009 issue of Nature Medicine – shows that BDNF treatment can potentially provide long-lasting protection by slowing, or even stopping the progression of Alzheimer's disease in animal models. "The effects of BDNF were potent," said Mark Tuszynski, MD, PhD, professor of neurosciences at the UC San Diego School of Medicine and neurologist at the Veterans Affairs San Diego Health System. "When we administered BDNF to memory circuits in the brain, we directly stimulated their activity and prevented cell death from the underlying disease." BDNF is normally produced throughout life in the entorhinal cortex, a portion of the brain that supports memory. Its production decreases in the presence of Alzheimer's disease. For these experiments, the researchers injected the BDNF gene or protein in a series of cell culture and animal models, including transgenic mouse models of Alzheimer's disease; aged rats; rats with induced damage to the entorhinal cortex; aged rhesus monkeys, and monkeys with entorhinal cortex damage. In each case, when compared with control groups not treated with BDNF, the treated animals demonstrated significant improvement in the performance of a variety of learning and memory tests. Notably, the brains of the treated animals also exhibited restored BDNF gene expression, enhanced cell size, improved cell signaling, and activation of function in neurons that would otherwise have degenerated, compared to untreated animals. These benefits extended to the degenerating hippocampus where short-term memory is processed, one of the first regions of the brain to suffer damage in Alzheimer's disease.

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Case Western Reserve research finds that the lack of specific gene plays role in autism

It is estimated that three to six out of every 1,000 children in the United States have autism – and the number of diagnosed cases is rising. Autism is one of a group of series developmental problems called autism spectrum disorders (ASD) that appear in early childhood, usually before age 3. Through symptoms and severity vary, all autism disorders affect a child's ability to communicate and interact with others. It's not clear whether this is due to better detection and reporting of autism, a real increase in the number of cases, or both. That's why researchers at Case Western Reserve University, led by Gary Landreth, a professor of neurosciences and neurology at the School of Medicine, have pulled together a number of recent findings that link a common genetic pathway with a number of human syndromes and a newly-recognized genetic form of autism, publishing them in the January 29, 2009, issue of the prestigious journal Neuron. Landreth, whose research team is made up of partners from the Cole Eye Institute at the Cleveland Clinic, the Louis Stokes Cleveland VA Medical Center and the University of Pennsylvania, says his lab in particular has been researching the class of enzymes called ERKs (extracellular signal regulated kinase), which are the central elements of a major intracellular signal transduction pathway. His research team has found that in animal models the ERKs – known as ERK 1 and ERK 2 – are required for normal brain, heart and facial development. This common genetic pathway that acts to regulate the ERK signaling cascade is particularly important in brain development, learning, memory and cognition. It has been recently reported that mutation or deletion of elements within this signaling pathway leads to developmental syndromes in humans that are associated with impaired cognitive function and autism.

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Team led by Scripps Scientists increases understanding of two types of blindness

Though based on mouse studies, the research bolsters the idea that humans suffering from these and other eye conditions may be able to help preserve function by adding antioxidants to their diet, and explains why this would work. The team also devised a new cell-based gene therapy technique that could eventually offer another option for arresting vision loss from these diseases. The work, led by Scripps Research Professor Martin Friedlander, M.D., Ph.D., was reported in an advance, online edition of the Journal of Clinical Investigation on February 2, 2009. The research is also likely to apply to a range of other neurodegenerative conditions, including vision loss from Huntington's and Alzheimer's diseases and inherited retinal degenerations, such as retinitis pigmentosa. Many forms of blinding degenerative eye conditions are tied to the abnormal proliferation of new blood vessels in the eyes, or neovascularization. Treatment of these conditions has generally focused on blocking continued neovascularization, but this typically only slows disease progression because new growth eventually wins out, leading to continued damage and vision loss. For many of these conditions, vision loss has been definitively attributed to the blinding effect of fluid leakage and hemorrhage from newly grown blood vessels. But the cause of vision loss in certain diseases such as MacTel has been more elusive.

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For Patients With Cirrhosis, Inflammation May Be Common Thread Behind Nervous And Heart Rhythm Problems

Liver cirrhosis is the seventh leading cause of death in the United States, taking 25,000 lives per year. It is often the result of alcohol over-consumption or exposure to hepatitis C, either of which can damage the liver and prevent it from filtering toxins. These toxins then accumulate in the blood stream and eventually reach the brain where they disrupt neurological and mental performance, a condition known as hepatic encephalopathy. Individuals with cirrhosis are also susceptible to a change in heart rhythm (decreased heart rate variability). Since cirrhosis, hepatic encephalopathy and heart rate variability are known to be associated with inflammation, researchers have examined what role cytokines (inflammatory molecules) play. A new study from The American Physiological Society suggests that these cytokines can lead to both the neurological and cognitive abnormalities and changes in heart rhythm in patients with cirrhosis. The results of the study may also apply to other conditions where heart rate variability is also decreased, such as bipolar disorder and post-menopausal depression.

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MRI shows brain atrophy pattern that predicts Alzheimer's

Using special MRI methods, researchers have identified a pattern of regional brain atrophy in patients with mild cognitive impairment (MCI) that indicates a greater likelihood of progression to Alzheimer's disease. The findings are published in the online edition of Radiology. "Previously, this pattern has been observed only after a diagnosis of probable Alzheimer's disease," said the study's lead author, Linda K. McEvoy, Ph.D., assistant project scientist in the Department of Radiology at the University of California San Diego School of Medicine in La Jolla. "Our results show that some individuals with MCI have the atrophy pattern characteristic of mild Alzheimer's disease, and these people are at higher risk of experiencing a faster rate of brain degeneration and a faster decline to dementia than individuals with MCI who do not show that atrophy pattern."According to the Alzheimer's Association, more than five million Americans currently have Alzheimer's disease. One of the goals of modern neuroimaging is to help in early and accurate diagnosis, which can be challenging. There is no cure for Alzheimer's disease, but when it is diagnosed early, drug treatment may help improve or stabilize patient symptoms. In Alzheimer's disease, nerve cell death and tissue loss cause areas of the brain to atrophy. Structural MRI allows radiologists to visualize subtle anatomic changes in the brain that signal atrophy. MCI is associated with an increased risk of progression to Alzheimer's disease. Rates of progression vary. Some patients progress rapidly, while others remain stable for relatively long periods of time.

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Stroke Therapy Window Might Be Extended Past Nine Hours for Some

Some patients who suffer a stroke as a result of a blockage in an artery in the brain may benefit from a clot-busting drug nine or more hours after the onset of symptoms. The findings are published in the online edition of Radiology. "Stroke is the third leading cause of death in the U.S.," said the study's lead author, William A. Copen, M.D., Director of Advanced Magnetic Resonance Neuroimaging at Massachusetts General Hospital (MGH) in Boston. "Every hour that we can add to the treatment window would allow vastly more stroke patients to be treated with potentially life-saving therapy." The most common type of stroke is called ischemic stroke. These strokes occur when a blood clot blocks a blood vessel supplying blood to the brain. Some ischemic strokes can be treated with thrombolytic, or clot-busting, therapy using tissue plasminogen activator (t-PA), which helps dissolve the blockage. However, the window of opportunity to safely administer the medication is generally considered to be just three hours. Because few patients get to the hospital to be diagnosed and treated within that time frame, fewer than seven percent of patients receive the drug.

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Body’s Defenses May Worsen Chronic Lung Diseases in Smokers

Although the immune system is designed to protect the body from harm, it may actually worsen one of the most difficult-to-treat respiratory diseases: chronic obstructive pulmonary disorder (COPD), according to new University of Cincinnati (UC) research. In a preclinical research study, UC environmental health scientists have identified a link between cigarette smoke and activation of a specific cellular receptor (NKG2D) critical to immune system activation. They say the finding is key to understanding COPD disease progression and developing future interventional drug therapies. “People have historically believed that if you smoke, you suppress the immune system. We’ve shown that you actually activate certain parts of the immune system and it could potentially work against you,” explains Michael Borchers, PhD, lead investigator of the study and UC assistant professor of environmental health.

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The Future of Food

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Give the foie gras a miss

Another reason not to eat pate de foie gras is discussed by Michael Greger of The Humane Society of the United States, Washington DC in a forthcoming issue of the International Journal of Food Safety, Nutrition and Public Health. Harmful proteins fragments known as amyloid fibrils associated with damage to brain cells in Alzheimer's disease and to pancreatic cells in Type II diabetes can be present in the meat of poultry and mammals. These amyloids are not destroyed even with high-temperature cooking process. Greger, who is the Director of Public Health and Animal Agriculture at the Humane Society of the United States is concerned with this discovery and the transmissibility of amyloid fibrils. Researchers have recently demonstrated in the laboratory that these compounds, when ingested, can enter the organs of laboratory rats fed affected meat. Greger explains that a biochemical mechanism akin to the replication of similar protein fragments in the brain diseases Creutzfeldt-Jakob Disease (CJD), scrapie, and Bovine Spongiform Encephalopathy (BSE), also known as mad cow disease, might occur when amyloid fibrils enter brain tissue or the pancreas. He points out that high levels of these materials can be found in pâté de foie gras, fatty liver pate, produced by force-feeding poultry. Stressed poultry birds are known to undergo spontaneous amyloidosis due to a chronic inflammatory response that causes amyloid fibrils to form non-functioning deposits of this protein-like material in their organs. In laboratory tests amyloidosis is found to be accelerated by injection of tiny quantities of amyloid fibrils, which induce production of the malformed proteins strands. Greger points out that pâté de foie gras is the only food stuff currently known to contain high levels of amyloid fibrils and no demonstration of it affecting people has been seen. However, the suggestion from laboratory research is that amyloid fibrils may be transmitted in a similar way to prion diseases like BSE/CJD is cause for concern.

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First brain study reveals benefits of exercise on quitting smoking

Research from the University of Exeter reveals for the first time, that changes in brain activity, triggered by physical exercise, may help reduce cigarette cravings. Published in the journal Psychopharmacology, the study shows how exercise changes the way the brain processes information among smokers, thereby reducing their cravings for nicotine. For the first time, researchers used functional Magnetic Resonance Imaging (fMRI) to investigate how the brain processes images of cigarettes after exercise. The study adds weight to a growing body of evidence that exercise can help manage addiction to nicotine and other substances. It backs up previous studies, which have shown that just one short burst of moderate exercise can significantly reduce smokers' nicotine cravings. Ten regular smokers were asked to cycle at a moderate pace for ten minutes, after 15 hours of abstinence from nicotine. They were then given an fMRI scan while they viewed a series of 60 images. Some visuals featured cigarettes and would normally induce cravings in a smoker. On a second occasion, the same group was given an fMRI scan and shown the same series of images without having undertaken exercise. They were also asked to report on their cravings for nicotine during both phases of the study. The brain images captured by the fMRI show a difference between the two conditions. After no exercise the smokers showed heightened activity in response to the images in areas of the brain associated with reward-processing and visual attention. After exercise the same areas of activation were not observed, which reflected a kind of 'default mode' in the brain. The smokers also reported lower cravings for cigarettes after exercise compared with when they had been inactive. The researchers do not know exactly what caused the difference in brain activity following exercise. One suggestion is that completing exercise raises mood (possibly through increases in dopamine) which reduces the salience or importance of wanting a cigarette. Another possibility is that exercise causes a shift in blood flow to areas of the brain less involved in anticipation of reward and pleasure generated by smoking images.

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Eosinophils as markers for asthma -The largest scale study so far on asthma genetics sheds light on disease mechanisms

In the study, the Icelandic company Decode Genetics together with Helmholtz Zentrum München and a number of other international research institutes performed a genome-wide association scan of more than 50,000 test persons. The researchers found several sequence variants associated with asthma. “Two of the detected sequence variants are of significance for a biochemical pathway in the interleukin-1 cluster,” explained Dr. Matthias Wjst, who was one of the initiators of the study at the Institute of Inhalation Biology of Helmholtz Zentrum München. This finding confirms the results of a research group at Helmholtz Zentrum München from 2004, which showed that the IL-1 gene cluster is associated with asthma.

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Higher blood sugar levels linked to lower brain function in diabetics, study shows

Results of a recent study conducted by researchers at Wake Forest University Baptist Medical Center and colleagues show that cognitive functioning abilities drop as average blood sugar levels rise in people with type 2 diabetes. The ongoing Memory in Diabetes (MIND) study, a sub-study of the Action to Control Cardiovascular Risk in Diabetes Trial (ACCORD), found a statistically significant inverse relationship between A1C levels (average blood glucose levels over a period of two to three months) and subjects' scores on four cognitive tests. No association, however, was found between daily blood glucose levels (measured by the fasting plasma glucose test) and test scores. For the study, researchers at 52 of the 77 ACCORD sites throughout the United States and Canada administered a 30-minute battery of cognitive tests to nearly 3,000 individuals ages 55 years and older. "The tests used in the study measured several aspects of memory function," said Jeff Williamson, M.D., M.H.S., principal investigator for the study at the Wake Forest clinical site. "For example, we tested one's ability to switch back and forth between memory tasks or to 'multitask,' an important skill for people needing to manage their diabetes." The results showed that a 1 percent increase in A1C corresponded to slightly lower scores on tests of psychomotor speed, global cognitive function, memory and multiple task management. "One of the little known complications of type 2 diabetes is memory decline leading to dementia, particularly Alzheimer's dementia," said Williamson, a professor of internal medicine, director of gerontology and geriatrics research, and director of the Roena Kulynych Center for Memory and Cognition Research at Wake Forest Baptist. "This study adds to the growing evidence that poorer blood glucose control is strongly associated with poorer memory function and that these associations can be detected well before a person develops severe memory loss."

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Louis Armstrong - What A Wonderful World

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Smokers putting their loved ones at risk of heart attacks

Researchers at University College London and St George's, University of London measured recent exposure to tobacco smoke in non-smoking middle-aged men taking part in the British Regional Heart Study by measuring the levels of cotinine - a compound carried in the blood - at two time points 20 years apart. A blood cotinine level above 0.7ng/mL is associated with a 40% increase in the risk of a heart attack (2), and other studies have suggested that even a level of 0.2ng/mL may increase the risk (3). The researchers found that while in 1978-80, 73% of men had a cotinine level above 0.7ng/mL, by 1998-2000 that proportion had fallen to 17%. However, despite the number of non-smoking men at risk having fallen, half of those who still had a high cotinine level (above 0.7 ng/ml) in 1998-2000 lived with a partner who smoked. Non-smoking men who had a partner who smoked had average cotinine levels of 1.39ng/mL, almost twice the level associated with an increased risk of a heart attack. Their cotinine levels were nearly eight times higher than the cotinine levels of men whose partner did not smoke. During the period the study looked at, national data shows that the prevalence of smoking amongst adults across the UK declined from 40% to 27% and the number of cigarettes consumed by smokers fell from 114 to 97 per week. Restrictions on smoking in public spaces and workplaces were also introduced, although the study period was before the national legislative bans on smoking in public places introduced between 2006 and 2007.

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Dangerous printer particles identified

The identity and origin of tiny, potentially hazardous particles emitted from common laser printers have been revealed by a new study at Queensland University of Technology. Professor Lidia Morawska from QUT's International Laboratory for Air Quality and Health led the study which aimed to answer questions raised by earlier findings that almost one third of popular laser printers emitted large numbers of ultrafine particles. These tiny particles are potentially dangerous to human health because they can penetrate deep into the lungs. Professor Morawska said the latest study found that the ultrafine particles formed from vapours which are produced when the printed image is fused to the paper. "In the printing process, toner is melted and when it is hot, certain compounds evaporate and those vapours then nucleate or condense in the air, forming ultrafine particles," she said. "The material is the result of the condensation of organic compounds which originate from both the paper and hot toner."

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Scientists at Scripps Research identify a mutation that causes inflammatory bowel disease

A team of scientists at The Scripps Research Institute has linked a mouse mutation to an increased susceptibility for developing inflammatory bowel disease -- represented in humans as Crohn's disease and ulcerative colitis, which together are estimated to affect more than a million people in the United States. The findings may one day lead to new and better treatments for the disease. The work was published in the February 6, 2009 Early Edition of the Proceedings of the National Academy of Sciences (PNAS). Humans have a gene that is very similar to the mouse gene, called Mbtps1, and in certain rare instances, mutations of this gene may contribute to IBD in humans. The disease is associated with painful ulcers and bleeding in people's intestines and can place them at greater risk for colon cancer. Although common, the disease is still somewhat mysterious. The Scripps Research study sheds light on a major mechanism through which it may develop. "We are just beginning to get a sense of the complexity of inflammatory bowel disease as far as humans are concerned," says Bruce Beutler, M.D., who is the chair of the Scripps Research Department of Genetics. Scientists have known for a long time that IBD is linked to genetics—it runs in families, for instance. However, there seems to be no single gene responsible. More likely, says Beutler, mutations in many different genes have additive effects and cause people to develop variably severe forms of the disease. One of the long-term goals of his laboratory is to identify these genes and the main biological processes they control.

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NCI-Penn Collaboration Finds Targeted Immune Cells Shrink Tumors in Mice

Researchers have generated altered immune cells that are able to shrink, and in some cases eradicate, large tumors in mice. The immune cells target mesothelin, a protein that is highly expressed, or translated in large amounts from the mesothelin gene, on the surface of several types of cancer cells. The approach, developed by researchers at the University of Pennsylvania School of Medicine and the National Cancer Institute (NCI), shows promise in the development of immunotherapies for certain tumors. The study appears online this week in the Proceedings of the National Academy of Sciences. Expression of mesothelin is normally limited to the cells that make up the protective lining (mesothelium) of the body’s cavities and internal organs. However, the protein is abundantly expressed by nearly all pancreatic cancers and mesotheliomas and by many ovarian and non-small-cell lung cancers. Although the biological function of mesothelin is not known for certain, it is thought to play a role in the growth and metastatic spread of the cancers that express it.

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Study reveals high level of adverse drug reactions in hospitals

In a study of more than 3,000 patients, researchers at the University of Liverpool have found that one in seven admitted to hospital experience adverse drug reactions to medical treatment. Adverse drug reactions (ADRs) are a major cause of hospital admissions, but recent data on ADRs that develop following hospital treatment is lacking. To further understanding of the clinical characteristics of ADRs, researchers at Liverpool assessed drug reactions of patients on 12 hospital wards over a six-month period. Researchers found that 15% of patients admitted to hospital experienced one or more adverse reactions, which included constipation, confusion, renal problems, bleeding and infection with Clostridium difficle. Drugs most commonly associated with ADRs were anticoagulants, analgesics and diuretics. The team also found that ADRs increased the length of a patient's hospital stay by an average of 0.25 days, and that those most susceptible were elderly patients on a number of different medications. Professor Munir Pirmohamed, from the University's School of Biomedical Sciences, said "We previously found that approximately a quarter of a million people are admitted to hospital in the UK each year following adverse drug reactions to a variety of commonly prescribed drugs, but we had very little data on ADRs experienced as a result of hospital treatment. We studied patients admitted to wards in Merseyside hospitals and analysed suspected ADRs for causality and severity.

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Fish Oil Alternatives to Farmed Fish Feed May Alleviate Global Seafood Shortage

Fish oil replacements for farmed fish feeds may help reduce the aquaculture industry’s dependence on wild fisheries for their essential omega-3 requirements. This move may also help overcome existing barriers that impede the industry’s expansion. A study published in the inaugural issue of Reviews in Aquaculture by Wiley-Blackwell provides a review and discussion of research activities conducted to evaluate alternative lipid sources. It focuses on the effects of fish oil replacement in finfish nutrition on feed quality, fish performance, feed efficiency, lipid metabolism, final eating quality and related economic aspects. “There is heavy emphasis for aquaculture to meet the global shortage of fish and seafood created by unsustainable fishing practices. However, dietary fish oil is required for the production of omega-3-rich farmed fish and this commodity, in a vicious circle, is at present derived solely from wild fisheries”, said Dr. Giovanni Turchini from the School of Life and Environmental Science, Deakin University, Australia.

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Stubborn Belly Fat

Slow metabolizing fat in the belly is hard to get rid of, because hormones prevent the fat tissue from breaking down. Diet guru Ori Hofmekler has more details.

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Iron-containing nanomaterials can damage skin

Iron-containing nanomaterials can cause inflammation and other cell damage if it touches skin, conclude the researchers who tested the particles on engineered skin, human skin cells and mice skin. The particles may be a health risk for workers who make or use the tiny single-walled carbon nanotubes (SWCNT), as well as consumers of the final products that contain them. Development of new electronic devices, circuits and computers using these particular materials is underway. Because they are very, very small, nanomaterials have vast potential applications in industry, engineering and medicine. However, their small size -- usually less than 200 nanometers -- also presents unique potentials for toxicity.

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Wintertime Blues or Lack of Vitamin B12?

Not receiving adequate amounts of vitamin B12, or cobalamin as it is also known, may leave you feeling tired, dizzy, or lightheaded.

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Spain withdraws cervical cancer shot after illnesses

Spanish health authorities have withdrawn tens of thousands of doses of a vaccine against cervical cancer after two teenagers who received the shots were hospitalised, regional authorities said on Tuesday.

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Doctors fear children eat too little fat

Psychiatrist Annemarie van Elburg says parents who are obsessed about healthy eating are suffering from an eating disorder known as orthorexia and forget that their children need fats for proper brain development.

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Obesitas, dat zal ons niet overkomen

Ook vindt Van Strien dat ouders zich, helemaal bij de heel jonge kinderen, verre moeten houden van light producten. ,,Al was het maar vanwege de aspartaam die er vaak aan is toegevoegd. Dat is een ronduit schadelijk middel.’’ Maar light producten brengen voor kinderen nog een ander risico met zich mee. Van Strien: ,,Kinderen weten precies wanneer ze genoeg hebben gegeten. Wie zijn kinderen te lichte producten geeft, brengt ze in de war. Ze eten en ze eten en het verzadigingspunt wordt simpelweg niet bereikt. Light producten geven een verkeerd signaal af aan een lichaam dat nog volop in ontwikkeling is.’’

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How to Lose Weight with Chia Seeds

What are chia seeds? What we know as chia seeds are the seeds from the Chia plant, which is a member of the mint family of plants. They do not have a minty taste, in fact they don`t taste of much at all. The benefits of chia lie in its nutritional value; it`s high in omega-3 fatty acid (ref: http://www.therawfoodworld.com/prod...), has plenty of fiber, and is abundant in various other vitamins and minerals. It can be added to just about anything you want to eat: salad, smoothies, deserts or savory foods. And that`s not all; chia can actually help you lose weight.

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Mental workout alters brain biochemistry

Actively training the working memory leads to demonstrable changes in the number of dopamine receptors in the brain, new Swedish research reveals. The study, published in the journal Science, is the first to demonstrate how mental activity can affect brain biochemistry in humans. The findings have implications for the treatment of conditions such as stroke and chronic fatigue syndrome, in which working memory is impaired. Working memory refers to the ability to retain information for short periods of time, for example when problem solving. The messenger molecule dopamine plays a key role in this type of memory. As a neurotransmitter, dopamine's role is to ferry messages from one nerve cell to another. Disruptions to the dopamine system can damage the working memory. Impaired working memory is associated with a number of neurological and psychiatric disorders as well as normal ageing. This latest study was led by Professor Torkel Klingberg of the Karolinska Institute in Sweden. He and his team had previously demonstrated that intensive training can lead to improvements in the working memory in just a few weeks.

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Growth hormone 'could help reverse autism-like condition'

A new study has revealed that a hormone which promotes brain development could help reverse an autism-like condition in girls.

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New cold virus linked with childhood asthma

A study by researchers at the Monroe Carell Jr. Children's Hospital at Vanderbilt implicates a new virus in an old, but growing problem: childhood asthma. Lead author Kathryn Miller, M.D., and colleagues surveyed young children hospitalized for respiratory illness and fever over two years and two geographic locations. The study, published online this month by the Journal of Allergy and Clinical Immunology, documented a newly described group of rhinoviruses (the cause of the "common cold") called HRV-C and found it accounted for almost half of rhinovirus-related asthma.

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A new window into hormone-altering chemicals

A new interactive database, including a timeline showing how human fetuses develop, displays scientific data about controversial chemicals in a graphic way. An electronic database going public on Tuesday has gathered the latest science on some of the most controversial chemicals in use today, offering a handy look into potential health effects when babies are exposed while developing in the womb.The interactive website, called “Critical Windows of Development,” has compiled an array of data from hundreds of scientists studying low doses of endocrine-disrupting chemicals.

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Mayo Clinic Researchers Discover Drug can Prevent Colon Cancer Development in Mice

Researchers at the Mayo Clinic campus in Florida have found that a drug now being tested to treat a range of human cancers significantly inhibited colon cancer development in mice. Because the agent appears to have minimal side effects, it may represent an effective chemopreventive treatment in people at high risk for colon cancer, the investigators say. Their study, published in the Feb. 15 issue of Cancer Research, found that use of the agent, enzastaurin, significantly reduced development of cancerous colon tumors in treated animals. Furthermore, the tumors that did develop in the mice were of a lower grade, which meant they were less advanced and aggressive than the tumors seen in animals not given the drug. "There is need for an agent that has a proven ability to reduce colon cancer risk, and this study suggests that enzastaurin could be uniquely effective," says the study's senior investigator, Nicole Murray, Ph.D., of the Department of Cancer Biology.

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New lab evidence suggests preventive effect of herbal supplement in prostate cancer

DHEA is a natural circulating hormone and the body's production of it decreases with age. Men take DHEA as an over-the-counter supplement because it has been suggested that DHEA can reverse aging or have anabolic effects since it can be metabolized in the body to androgens. Increased consumption of dietary isoflavones is associated with a decreased risk of prostate cancer. Red clover (Trifolium pretense) is one source of isoflavones. Both supplements may have hormonal effects in the prostate and little is known about the safety of these supplements. In a recent report in Cancer Prevention Research, a journal of the American Association for Cancer Research, researchers report that DHEA levels can be manipulated in cells in the laboratory to understand its effects. Julia Arnold, Ph.D., a staff scientist at the National Center for Complementary and Alternative Medicine (NCCAM) at the National Institutes of Health, said more research is necessary in an environment where men and women concerned about health problems tend to self-prescribe based on information they find on the Internet. Towards this end, the NCCAM laboratory is studying signaling between human prostate cancer cells and their supporting stromal cells as they grow together in laboratory culture. "DHEA effects in the prostate tissues may depend on how these two cells types 'talk to each other' and further, it may be potentially harmful in tissues containing inflammation or with early cancer lesions because the cells can induce DHEA to become more androgenic," said Arnold.

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Gaza strip families give first clue to condition causing blindness and tooth decay

Scientists studying an inherited condition resulting in blindness and crumbling teeth have found a single defective gene can affect both eye function and normal tooth development. A previously undiscovered and unexpected link between the formation of teeth and eyes has been uncovered by researchers from the University of Leeds, through studies in two families living in a village in the war-torn Gaza strip. Funded by the Wellcome Trust and Yorkshire Eye Research, the project team sought to identify the cause of a condition they named Jalili syndrome, in which related individuals suffered loss of eyesight, almost from birth, and poorly developed teeth. Chris Inglehearn, Professor of Molecular Ophthalmology at Leeds Institute of Molecular Medicine, said: "What interested us was the idea that there might be a single process or protein essential in both teeth and eyes, not something you'd normally think of as having much in common. "Working with colleagues in the Leeds Dental Institute, genetic changes were found that disrupt the function of a protein called CNNM4 and that are passed on from one generation to the next in these families. This protein is present in the cells that lay down tooth enamel and also in the various layers of the retina, the light sensitive 'film' at the back of the eye."

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Stem cells Deathly awakening by interferon

After injuries with blood loss, the body quickly needs to restore the vital blood volume. This is accomplished by a special group of stem cells in the bone marrow. These hematopoietic stem cells remain dormant throughout their lives and are only awakened to activity in case of injury and loss of blood. Then they immediately start dividing to make up for the loss of blood cells. This has recently been shown by a group of scientists headed by Professor Andreas Trumpp of DKFZ. Dormancy is an important protection mechanism of stem cells. First, it protects their genetic material from genetic alterations, which happen primarily during cell division. In addition, dormancy helps them escape attacks of many cytotoxins, which act only on dividing cells. Scientists were still puzzling over which signaling molecules actually wake up stem cells from their dormancy. Andreas Trumpp and Marieke Essers from his team have now reported in Nature that interferon-alpha, a messenger substance of the immune system, acts like an alarm clock for hematopoietic stem cells. The scientists have thus shown for the first time that interferon-alpha can have a direct influence on the function of stem cells. Interferon-alpha is released by immune cells when the organism is threatened by bacteria or viruses. The scientists triggered interferon production in mice by administering a substance that simulates a viral infection to the animals. Subsequently, there was a great increase in the division rate of hematopoietic stem cells. In control animals that were unable to process the interferon signals, the substance did not lead to an awakening of the stem cells.

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Durability of dental fillings improves if the enzyme activity of teeth is inhibited

Composite dental fillings have one problematic feature, in that the bond between the filling and the dental tissue deteriorates over time – in fact, sometimes by as much as 50 per cent in one year. As the bond deteriorates, it may allow bacteria to enter and this brings a high risk of further tooth decay. Professor Tjäderhane has researched the occurrence of certain enzymes, matrix metalloproteinases (MMPs), in the dental tissue and their role in dental conditions. The MMPs break down the extracellular matrix, including collagen, which is a major component of dentin. As a result of international research collaboration, Professor Tjäderhane's research team has shown that human dentin contains the key MMP for breaking down collagen. The bonding of composite resins with dental tissue is based on the use of collagen bonds, and the tooth's own MMPs are responsible in part for the deterioration of the bond over time. By inhibiting the activity of these enzymes, the research team has succeeded in significantly slowing down the deterioration of the bond between dental tissue and a composite filling, and in some cases to prevent deterioration completely. The best results have been obtained in clinical trials, where deterioration of the bond has been more or less completely prevented. MMP enzyme activity in the tooth can be rapidly and easily inhibited when a filling is put in place by using chlorhexidine, a substance which is already on hand at all dental practices. This means that the research results are immediately applicable in dental care for the best benefit of the patients. The research in question also strongly indicates that MMP inhibitors might help slow down tooth decay. These observations are based only on animal testing so far, so further research on the subject will be needed before pratical applications can be made available.

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Groundbreaking study on complex movements of enzymes

A groundbreaking study has revealed in great detail how enzymes in the cell cooperate to make fat. These enzymes are integrated into a single molecular complex known as fatty acid synthase. This complex is regarded as a potential target for developing new anti-obesity and anti-cancer drugs. Dr. Stuart Smith, at Children's Hospital Oakland Research Institute, collaborated with Drs. Edward Brignole and Francisco Asturias from The Scripps Research Institute in La Jolla, Calif. in a study published in the February 2009 edition of Nature Structural and Molecular Biology and featured on the cover of the journal. "Fatty Acid Synthase is a remarkably complex structure. It contains all of the components needed to convert carbohydrates into fat," Dr. Smith explained. "We have suspected for some time that the enzyme complex is extremely flexible, which makes it difficult to analyze using X-ray crystallography. Last year the X-ray structure of the complex was solved by a group in Switzerland, but this structure provided only a snapshot of the complex in one of its many poses. We were able to use state-of-the-art electron microscopy to obtain images of the complex in many of its different conformations and assemble these images into a movie that displays the full range of motion of the components of the complex." The results reveal how enzymes that appear distantly located in the X-ray structure are able to make the contacts with each other needed for catalysis. The extraordinary swinging, swiveling and rolling motions of fatty acid synthase are represented on the cover of the journal in the form of a flamenco dancer. Some pharmaceutical companies are focusing on inhibitors of fatty acid synthase because they are known to block the conversion of carbohydrates into fat and suppress appetite as well as slow the growth of cancer cells. Structural information garnered from X-ray and electron microscope images may aid in the design of more effective inhibitors that could be used therapeutically.

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New method to stimulate immune system may be effective at reducing amyloid burden in Alzheimer’s

Researchers at NYU Langone Medical Center have discovered a novel way to stimulate the innate immune system of mice with Alzheimer's disease (AD) - leading to reduced amyloid deposits and the prevention of Alzheimer's disease related pathology - without causing toxic side effects. The study entitled "Induction of Toll-like Receptor 9 Signaling as a Method for Ameliorating Alzheimer's Disease Related Pathology" was published in The Journal of Neuroscience. NYU Langone researchers stimulated the innate immune system via the Toll-like 9 receptor (TLR9) via treatment with cytosine-guanosine containing DNA oligodeoxynucleotides (CpG ODNs) in Tg2576 AD model transgenic mice. This treatment produced a 66% and 80% reduction in the cortical and vascular amyloid burden, when compared with non-treated AD mice. Also, vaccinated Tg2576 mice performed similarly to non-treated mice on a radial arm maze used in the study, showing improvements in behavior and reduced amyloid burden. "Our results indicate that stimulation of the innate immune system through TLR9 with CpG ODNs is an effective and apparently non-toxic method to reduce the amyloid burden in the brain," said Thomas Wisniewski, MD, professor of neurology, pathology and psychiatry at NYU Langone Medical Center. "Furthermore we found that amyloid reduction was associated with significant cognitive benefits in an AD mouse model. This approach has significant implications for future human immunomodulatory approaches to prevent AD in humans." The deposition of amyloid ? (A?) in the central nervous system in the form of amyloid plaques is a hallmark of Alzheimer's disease. A? accumulation destroys neurons in the brain, leading to deficits in cognitive abilities. Immunomodulation or vaccination for AD is emerging as an effective means of shifting the equilibrium from A? accumulation to clearance; however, excessive cell mediated inflammation and cerebral microhemorrhages - two forms of toxicity- were shown to occur in previous vaccination studies targeting the adaptive immune system.

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New method to eliminate ibuprofen from polluted waters using ultrasound

An international team of scientists, in which researchers from the University of Barcelona (UB) have participated, has applied ultrasound treatment that enables ibuprofen to be eliminated from waters polluted with this drug. This method could be used in water purification plants, which would avoid the emission of pharmaceutical pollutants into rivers, lakes, seas and other surface waters. The team of scientists at the laboratories of the Federal Polytechnic School in Lausanne, Switzerland has developed a novel method for eliminating pharmaceutical products from water. The substance chosen for the study was ibuprofen, as it is one of the drugs that appears with the most frequency in the analyses of waste waters due to its high consumption as an anti-inflammatory and analgesic.

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Periodontitis and myocardial infarction - A shared genetic predisposition

A mutual epidemiological relationship between aggressive periodontitis and myocardial infarction has already been shown in the past. Scientists at the universities of Kiel, Dresden, Amsterdam and Bonn have now presented the first evidence of a shared genetic variant on chromosome 9, which maps to a genetic region that codes for the "antisense RNA" Anril, as reported in the latest edition of the specialist journal PLoS Genetics. The first author, Dr Arne Schaefer from the Institute for Clinical Molecular Biology at Kiel University, sees clear similarities in the genetic predisposition: "We have examined the aggressive form of periodontitis, the most extreme form of periodontitis which is characterized by a very early age of onset. The genetic variation associated with this clinical picture is identical to that of patients who suffer from cardiovascular disease and have already had a myocardial infarction." Because it has to be assumed that there is a causal connection between periodontitis and myocardial infarction, periodontitis should be taken seriously by dentists and diagnosed and treated at an early stage. "Aggressive periodontitis has shown itself to be associated not only with the same risk factors such as smoking, but it shares, at least in parts, the same genetic predisposition with an illness that is the leading cause of death worldwide.," warned Schaefer. Knowledge of the risk of heart attacks could also induce patients with periodontitis to keep the risk factors in check and take preventive measures.

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Cheap love costs the Earth

cology and conservation biologist at the University of Leicester, Dr David Harper, who has conducted research for over 25 years at Lake Naivasha in Kenya, today warned that cut-price Valentine roses exported for sale in the UK were 'bleeding that country dry'. Dr Harper, of the University's Department of Biology where he is a senior lecturer, claimed that cheap roses grown by companies that had no concern for the environment were having a devastating effect on the ecology of Lake Naivasha- the centre of Kenya's horticultural industry. Instead, Dr Harper urged UK shoppers to buy Fair Trade roses, produced by companies that were conscientious and had a transparent supply chain.Dr Harper said "Roses that come cheap are grown by companies that have no concern for the environment, who cut corners and avoid legislation, who sell their flowers into the auction in Amsterdam so that all the buyer knows is the flowers "come from Holland"."In reality, they have come from Kenya where the industry is - literally - draining that country dry." However, some companies took a more responsible approach and sold direct to British supermarkets - many of them being "Fair Trade" certified. Said Dr Harper - "These companies want a sustainable future for the wildlife and the environment, as well as the people, where they grow their roses. Sadly, there are not enough of them. "At Lake Naivasha, the good companies make up about half of the total. That is not enough; together, the industry is sucking the lake dry. The country's legislation is strong, but its enforcement is weak so companies whose only interest is profit take advantage of that." Dr Harper said the demand for the ten thousand tonnes of roses sold in the UK for Valentine's Day and for Mother's Day had contributed to the devastation of the ecosystem at the lake. Almost half a million people now live around the shores of the lake - drawn there by the flower trade. The shanty towns that have emerged around the lake have no sanitation- water comes from the lake and sewage returns to it. This pressure - from people - is destroying the lake that supports their jobs lives and their livelihoods. David and his colleagues from other UK - and Dutch - universities first raised the alarm about the situation in 2002, just as the new Kenyan Water Act was passed.

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Engineers create intelligent molecules that seek-and-destroy diseased cells

Current treatments for diseases like cancer typically destroy nasty malignant cells, while also hammering the healthy ones. Using new advances in synthetic biology, researchers are designing molecules intelligent enough to recognize diseased cells, leaving the healthy cells alone. "We basically design molecules that actually go into the cell and do an analysis of the cellular state before delivering the therapeutic punch," said Christina Smolke, assistant professor of bioengineering who joined Stanford University in January. "When you look at a diseased cell (e.g. a cancer cell) and compare it to a normal cell, you can identify biomarkers—changes in the abundance of proteins or other biomolecule levels—in the diseased cell," Smolke said. Her research team has designed molecules that trigger cell death only in the presence of such markers. "A lot of the trick with developing effective therapeutics is the ability to target and localize the therapeutic effect, while minimizing nonspecific side effects," she said. Smolke will present the latest applications of her lab's work at the American Association for the Advancement of Science (AAAS) meeting in Chicago on Friday, Feb. 13. These designer molecules are created through RNA-based technologies that Smolke's lab developed at the California Institute of Technology. A recent example of these systems, developed with postdoctoral researcher Maung Nyan Win (who joined Smolke in her move to Stanford), was described in a paper published in the Oct. 17, 2008, issue of Science. "We do our design on the computer and pick out sequences that are predicted to behave the way we like," Smolke said. When researchers generate these sequences inside the operating system of a cell, they reprogram the cell and change its function. "Building these molecules out of RNA gives us a very programmable and therefore powerful design substrate," she said. Smolke's team focuses on well-researched model systems in breast, prostate and brain cancers, including immunotherapy applications based on reprogramming human immune response to different diseases. The researchers work directly with clinicians at the City of Hope Cancer Center (a National Cancer Institute designated Comprehensive Cancer Center in Duarte, Calif.) that have ongoing immunotherapy trials for treating glioma, a severe type of brain cancer.

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Researchers find new biomarker for fatal prostate cancer

New research findings out of Wake Forest University School of Medicine and the University of Wisconsin may help provide some direction for men diagnosed with prostate cancer about whether their cancer is likely to be life-threatening. In a study that appears in the February issue of Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research, researchers confirmed their earlier findings that men who have too much calcium in their bloodstreams subsequently have an increased risk of fatal prostate cancer. Now researchers have also identified an even more accurate biomarker of the fatal cancer - high levels of ionized serum calcium."Scientists have known for many years that most prostate cancers are slow-growing and that many men will die with, rather than of, their prostate cancer," said Gary G. Schwartz, Ph.D., senior author of the study and an associate professor of cancer biology at the School of Medicine, a part of Wake Forest University Baptist Medical Center. "The problem is, how can we determine which cancers pose a significant threat to life and need aggressive treatment versus those that, if left alone, are unlikely to threaten the patient's life? These findings may shed light on that problem." This was the first study to examine fatal prostate cancer risk in relation to prediagnostic levels of ionized serum calcium, and researchers found that men in the highest third of ionized serum calcium levels are three times more likely to die of prostate cancer than those with the least amount of ionized serum calcium. Researchers also confirmed a previous finding of a doubling of risk for fatal prostate cancer among men whose level of total serum calcium falls in the highest third of the total serum calcium distribution. Ionized serum calcium is the biologically active part of total serum calcium. About 50 percent of total serum calcium is inactive, leaving only the ionized serum calcium to directly interact with cells. The findings have both scientific and practical implications, said Halcyon G. Skinner, Ph.D., of the University of Wisconsin, the study's lead author. From a scientific standpoint, it helps focus research on what it is about calcium that may promote prostate cancer. On a practical level, the finding may offer some guidance to men trying to decide whether or not to seek treatment for a recent prostate cancer diagnosis. If confirmed, the findings could also lead to the general reduction of over-treatment of prostate cancer. "Many men with this diagnosis are treated unnecessarily," Schwartz said. "Within months of initial diagnosis of prostate cancer, many men opt to undergo either radiation or radical surgery. The problem is, we don't know who needs to be treated and who doesn't, so we treat most men, over-treating the majority. These new findings, if confirmed, suggest that men in the lower end of the normal distribution of ionized serum calcium are three times less likely than men in the upper distribution to develop fatal disease.

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Gladstone scientists reveal that fat synthesizing enzyme is key to healthy skin and hair

Scientists at the Gladstone Institutes of Cardiovascular Disease (GICD) have found that an enzyme associated with the synthesis of fat in the body is also an element in healthy skin and hair. The enzyme is acyl CoA;diacylglycerol acyltransferase 1 or DGAT1. Mice that lack DGAT1 have many interesting characteristics. For example, they are lean, resistant to diet-induced obesity, are more sensitive to insulin and leptin, and have abnormalities in mammary gland development and skin. When Gladstone researchers in the laboratory of Robert V. Farese, Jr. used genetic engineering to delete the enzyme in mice, they found that lack of DGAT1 caused levels of retinoic acid (RA) to be greatly increased in skin and resulted in the loss of hair. Their findings were reported in The Journal of Biological Chemistry. "For some time, we have been studying the enzymes that make triglycerides," said Robert V. Farese, Jr., senior investigator and senior author on the study. "We found that one of these enzymes is a major regulator of retinoic acid actions in the skin." RA, which comes from vitamin A (retinol) has been used to treat skin disorders, such as acne and psoriasis, and certain cancers, but it is fairly toxic and must be carefully controlled.

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Stem cell research uncovers mechanism for type 2 diabetes

Taking clues from their stem cell research, investigators at the University of California San Diego (UC San Diego) and Burnham Institute for Medical Research (Burnham) have discovered that a signaling pathway involved in normal pancreatic development is also associated with type 2 diabetes. Their findings, published online January 9 in Experimental Diabetes Research, could provide a potential new target for therapy. Pamela Itkin-Ansari, Ph.D., assistant adjunct professor at the UC San Diego School of Medicine and Burnham; Fred Levine, M.D., Ph.D., professor and director of the Sanford Children's Health Research Center at Burnham, and colleagues showed that the Wnt signaling pathway is up-regulated in insulin producing cells of pancreases from adults with type 2 diabetes. "It is now clear that progenitor cells, with the capacity to become insulin producing cells, reside in the adult pancreas," said Dr. Itkin-Ansari. "The key to harnessing those cells to treat diabetes is to understand the signaling pathways that are active in the pancreas under both normal and disease conditions. In the course of that research we found that Wnt signaling activity, which plays a critical role in the development of the pancreas, re-emerges in type 2 diabetes." The Wnt signaling pathway – a series of protein interactions that control several genes –plays a role in normal development, as well as cancer, in many tissues. In this study, the scientists compared the expression of different proteins in the Wnt pathway in the pancreas from adults with type 2 diabetes and those from healthy individuals. The researchers discovered that cells from those without the disease had low levels of beta-catenin, a protein that enters cell nuclei and activates certain genes. Beta cells from people with type 2 diabetes had increased levels of the protein. Activation of the Wnt pathway also up-regulates the expression of c-myc, which has been implicated in the destruction of insulin-producing beta cells. Significantly, Wnt signaling was also apparent in obese mice well before they developed symptoms, indicating that Wnt may be an important factor leading to Type 2 diabetes.

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Fructose-sweetened drinks increase nonfasting triglycerides in obese adults

Obese people who drink fructose-sweetened beverages with their meals have an increased rise of triglycerides following the meal, according to new research from the Monell Center. "Increased triglycerides after a meal are known predictors of cardiovascular disease," says Monell Member and study lead author Karen L. Teff, PhD, a metabolic physiologist. "Our findings show that fructose-sweetened beverages raise triglyceride levels in obese people, who already are at risk for metabolic disorders such as cardiovascular disease and diabetes." Triglycerides are manufactured by the body from dietary fat and are the most common form of fat transported in blood. Although normal levels of triglycerides are essential for good health, high levels are associated with increased risk for atherosclerosis and other predictors of cardiovascular disease. In the study, published online by the Journal of Clinical Endocrinology and Metabolism, Teff and her collaborators studied 17 obese men and women. Each was admitted two times to the Clinical and Translational Research Center at the University of Pennsylvania. On each admission, the subjects were given identical meals and blood was collected from an intravenous catheter over a 24-hour period. The only difference was the sweetener used in the beverages that accompanied the meals; beverages were sweetened with glucose during one admission and with fructose during the other. Blood triglyceride levels were higher when subjects drank fructose-sweetened beverages with their meals compared to when they drank glucose-sweetened beverages. The total amount of triglycerides over a 24-hour period was almost 200 percent higher when the subjects drank fructose-sweetened beverages. Although fructose increased triglyceride levels in all of the subjects, this effect was especially pronounced in insulin-resistant subjects, who already had increased triglyceride levels. Insulin resistance is a pre-diabetic condition often associated with obesity. "Fructose can cause even greater elevations of triglyceride levels in obese insulin-resistant individuals, worsening their metabolic profiles and further increasing their risk for diabetes and heart disease," said Teff.Fructose and glucose are forms of sugar found in both table sugar (sucrose) and high fructose corn syrup. Both fructose and glucose are present in lower concentrations in many fruits and vegetables. Although fructose tastes much sweeter than either glucose or sucrose, it typically is not used alone as a sweetener. Future work will seek to determine how much fructose is needed to cause an increase of triglyceride levels when it is combined with glucose in beverages. Additional studies will explore the metabolic and health effects of long-term fructose intake.

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Omega-3 fatty acids prevent medical complications of obesity

According to a recent study published online in The FASEB Journal, diets rich in omega-3 fatty acids protect the liver from damage caused by obesity and the insulin resistance it provokes. This research should give doctors and nutritionists valuable information when recommending and formulating weight-loss diets and help explain why some obese patients are more likely to suffer some complications associated with obesity. Omega-3 fatty acids can be found in canola oil and fish. "Our study shows for the first time that lipids called protectins and resolvins derived from omega-3 fatty acids can actually reduce the instance of liver complications, such as hepatic steatosis and insulin resistance, in obese people," stated Joan Claria, a professor from the University of Barcelona and one of the researchers involved in the work.The scientists found that two types of lipids in omega-3 fatty acids—protectins and resolvins—were the cause of the protective effect. To reach this conclusion, they studied four groups of mice with an altered gene making them obese and diabetic. One group was given an omega-3-enriched diet and the second group was given a control diet. The third group was given docosahexaenoic acid, and the fourth received only the lipid resolvin. After five weeks, blood serum and liver samples from the test mice were examined. The mice given the omega-3-rich diet exhibited less hepatic inflammation and improved insulin tolerance. This was due to the formation of protectins and resolvins from omega-3 fatty acids.

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Nanoparticle "Smart Bomb" Targets Drug Delivery to Cancer Cells

Researchers at North Carolina State University have successfully modified a common plant virus to deliver drugs only to specific cells inside the human body, without affecting surrounding tissue. These tiny "smart bombs" - each one thousands of times smaller than the width of a human hair - could lead to more effective chemotherapy treatments with greatly reduced, or even eliminated, side effects. Drs. Stefan Franzen, professor of chemistry, and Steven Lommel, professor of plant pathology and genetics, collaborated on the project, utilizing the special properties of a fairly common and non-toxic plant virus as a means to convey drugs to the target cells.The researchers say that the virus is appealing in both its ability to survive outside of a plant host and its built-in "cargo space" of 17 nanometers, which can be used to carry chemotherapy drugs directly to tumor cells. The researchers deploy the virus by attaching small proteins, called signal peptides, to its exterior that cause the virus to "seek out" particular cells, such as cancer cells. Those same signal peptides serve as "passwords" that allow the virus to enter the cancer cell, where it releases its cargo. "We had tried a number of different nanoparticles as cell-targeting vectors," Franzen says. "The plant virus is superior in terms of stability, ease of manufacture, ability to target cells and ability to carry therapeutic cargo."

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