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- - European weblog on food, health and environment
 

News - Week 26 - 2009


Low-fat diet helps genetically predisposed animals avoid liver cancer

In a study comparing two strains of mice, one susceptible to developing cancer and the other not, researchers found that a high-fat diet predisposed the cancer-susceptible strain to liver cancer, and that by switching to a low-fat diet early in the experiment, the same high-risk mice avoided the malignancy. The switched mice were lean rather than obese and had healthy livers at the end of the study. The findings, from a joint University of Pennsylvania School of Medicine and Case Western Reserve University study, appear online this month in Human Molecular Genetics. The investigators studied hepatocellular carcinoma (HCC), a type of liver cancer that is one of the leading causes of cancer death worldwide. Thirty percent of cases of this type of liver cancer are associated with obesity, type 2 diabetes, and related metabolic diseases, although a direct link between these and liver cell cancer has not been completely established. "The connection between obesity and cancer is not well understood at this point," says senior co-author John Lambris, PhD, the Dr. Ralph and Sallie Weaver Professor of Research Medicine at Penn. The researchers hope the results will lead to the development of blood tests that can detect precancerous conditions related to diet. The remaining seventy percent of HCC cases result from hepatitis B and C viral infections, exposure to the fungal toxin aflatoxin, chronic alcohol use, or genetic liver diseases. The usual outcome of hepatocellular carcinoma is poor, because only 10 to 20 percent of these tumors can be surgically removed. If the cancer cannot be completely removed, the disease is usually deadly within 3 to 6 months. Hepatocellular carcinoma causes close to 700,000 deaths worldwide per year, mostly outside the US. The researchers tested the long-term effects of high-fat and low-fat diets on males of two inbred strains of mice and discovered that one strain, named C57BL/6J, was susceptible to non-alcoholic steatohepatitis (NASH) and hepatocellular carcinoma on a high-fat, but not a low-fat diet. The other strain, called A/J, was not susceptible to disease on a high-fat diet. The mice were fed their respective diets for close to 500 days, weighed periodically, and then analyzed for the presence of disease.


Jumping genes discovery 'challenges current assumptions'

Jumping genes do most of their jumping, not during the development of sperm and egg cells, but during the development of the embryo itself. The research, published this month in Genes and Development, "challenges standard assumptions on the timing of when mobile DNA, so-called jumping genes, insert into the human genome," says senior author Haig H. Kazazian Jr., MD, Seymour Gray Professor of Molecular Medicine in Genetics at the University of Pennsylvania School of Medicine. Jumping genes – also called transposons – are sequences of DNA that can move or jump to different areas of the genome within the same cell. Jumping gene insertions do cause disease; however, it's not known how frequently diseases due to insertions can be inherited in the next generation. They are a rare cause of several genetic diseases, such as hemophilia and Duchenne muscular dystrophy. In addition, transposon insertion into the genome could play a role in the development of cancer. The current work alters thinking in the field of jumping genes, challenging standard assumptions that mobile DNA inserts only in eggs and sperm during their respective early development. In this study, the researchers found that insertions took place during embryogenesis after fertilization, at a time when nearly all of the changes can't be inherited. The researchers now purport, based on the study's findings, that many of those insertions occur in the early embryo, perhaps in the 4- or 8-cell stage. The study looked at retrotransposons, one class of jumping genes, with the L1 family the most abundant type of retrotransposon in the human genome. Retrotransposons move by having their DNA sequence transcribed or copied to RNA, and then instead of the genetic code being translated directly into a protein sequence, the RNA is copied back to DNA by the retrotransposon's own enzyme called reverse transcriptase. This new DNA is then inserted back into the genome. The process of copying is similar to that of retroviruses, such as HIV, leading scientists to speculate that retroviruses were derived from retrotransposons. The L1 family of retrotransposons comprises about 17 percent of the human genome. Eventually, continuous jumping by retrotransposons expands the size of the human genome and may cause shuffling of genome content. For example, when retrotransposons jump, they may take portions of nearby gene sequences with them, inserting these where they land, and thereby allowing for the creation of new genes. Even otherwise unremarkable insertions of L1 may cause significant effects on nearby genes, such as lowering their expression.


Waste disposal protein is mechanism behind cancer tumor suppression

"Taking out the trash" takes on a whole new meaning, as investigators at The Cancer Institute of New Jersey (CINJ) and Rutgers, The State University of New Jersey, have discovered that a waste disposal protein is the key to cancer tumor suppression in a process known as autophagy. CINJ is a Center of Excellence of UMDNJ-Robert Wood Johnson Medical School. Autophagy is a process in which cancer cells eat themselves. Previous study from the lab of Eileen White, PhD, associate director for basic science at CINJ, and a number of other groups has shown that autophagy is a pathway to cancer tumor suppression, but scientists did not know the mechanism behind it, until now. The latest research, which appears in this week's print and online editions of Cell, focuses on a protein known as p62. This protein is responsible for disposing of damaged proteins that accumulate in a cell when it is no longer receiving nourishment for growth and is under other environmental stress. In order for cells to prevent themselves from becoming a cancer tumor, they need to rid themselves of this waste. The p62 protein packages the damaged materials and prepares these materials, along with itself, to be degraded through the autophagy process. Disruption in the process or failure to dispose of p62 from the cell can result in toxicity, genome damage and inflammation, which in turn can promote tumor progression. Dr. White, who is an adjunct professor of surgery at UMDNJ-Robert Wood Johnson Medical School, and a professor of molecular biology and biochemistry at Rutgers University, is the senior author of the research publication. She notes this is the first time the disposal of p62 has been linked with tumor suppression, which can be key in cancer prevention. "This discovery is important, because we now have an opportunity to look at people at risk for cancer before it develops," she notes. "These latest findings show that p62 can act as a marker to identify certain cancers and that we can manipulate p62 levels to stimulate the process of autophagy and ultimately tumor suppression."


Researcher explores why smoking increases the risk of heart disease and strokes

Researchers at Charles Drew University of Medicine and Science in Los Angeles and Western University of Health Sciences in Pomona have discovered a reason why smoking increases the risk of heart disease and strokes. The study, which will be presented Thursday, June 11 at The Endocrine Society's 91st annual meeting in Washington, D.C., found that nicotine in cigarettes promotes insulin resistance, a pre-diabetic condition that raises blood sugar levels higher than normal. People with pre-diabetes are at greater risk of developing cardiovascular disease. Theodore Friedman, MD, Ph.D., chief of the endocrinology division at Charles Drew University, said the findings help explain a "paradox" that links smoking to heart disease. Smokers experience a high degree of cardiovascular deaths, Friedman said. "This is surprising considering both smoking and nicotine may cause weight loss and weight loss should protect against cardiovascular disease." The researchers studied the effects of twice-daily injections of nicotine on 24 adult mice over two weeks. The nicotine-injected mice ate less food, lost weight and had less fat than control mice that received injections without nicotine ."Our results in mice show that nicotine administration leads to both weight loss and decreased food intake," Friedman said. "Mice exposed to nicotine have less fat. In spite of this, mice have abnormal glucose tolerance and are insulin resistant (pre-diabetes)."


If You Do Good, You Look Good

In today's economy, it's increasingly difficult to elicit donations for charitable causes — but new research from Dr. Anat Bracha of the Eitan Berglas School of Economics at Tel Aviv University can provide fundraising organizations with a potent tool. A powerful spur to giving, Dr. Bracha's research demonstrates, is "image motivation," the positive recognition a giver gets from other members of the community. Her study, published in American Economic Review, can help organizations understand how to elicit maximum donor response in today's tough times.


Wii-hab may enhance Parkinson's treatment

The Nintendo Wii may help treat symptoms of Parkinson's disease, including depression, a Medical College of Georgia researcher says. Parkinson’s disease is a degenerative disease that impairs motor skills. Dr. Herz theorized that the popular computer game console, which simulates various sports and activities, could improve coordination, reflexes and other movement-related skills, but he found additional benefits as well. "The Wii allows patients to work in a virtual environment that's safe, fun and motivational," says Dr. Ben Herz, program director and assistant professor in the School of Allied Health Sciences Department of Occupational Therapy. "The games require visual perception, eye-hand coordination, figure-ground relationships and sequenced movement, so it's a huge treatment tool from an occupational therapy perspective."


New images may improve vaccine design for deadly rotavirus

Howard Hughes Medical Institute researchers are reporting the first detailed molecular snapshots of a deadly gastrointestinal virus as it is caught in the grasp of an immune system molecule with the capacity to destroy it. The images could help scientists design a more effective vaccine against rotavirus, a lethal infection that kills more than 500,000 children worldwide each year. The discovery is timely. Last week the World Health Organization recommended that rotavirus vaccination be included in all national immunization programs worldwide. Virtually every child in the world becomes infected with rotaviruses before developing natural immunity. But each year an estimated two million children are hospitalized because rotavirus infection results in severe dehydration caused by diarrhea and vomiting. Both natural and vaccine-induced immunity occur only after the immune system has "seen" the virus and generates neutralizing antibodies. These soldiers of the immune system seek out and attach to rotavirus particles, rendering them unable to infect cells. In the new experiments, Howard Hughes Medical Institute (HHMI) researchers have mapped the structure of an antiviral antibody clamped onto a protein called VP7 that stipples the surface of rotavirus. The structural map reveals intimate new details about how the antibody interferes with VP7, a protein that helps the virus infect cells. The information may be useful in designing a new generation of rotavirus vaccines that could be easier to store and administer than current vaccines, said the researchers. HHMI investigator Stephen C. Harrison and colleagues at Children's Hospital Boston and Harvard University published their findings in the June 12, 2009, issue of the journal Science.


Researchers at Case Western Reserve discover a new way the body fights fungal infection

A team of researchers led by Amy G. Hise, M.D., M.P.H., assistant professor at the Center for Global Health and Diseases, Case Western Reserve University School of Medicine, is the first to discover how the body fights off oral yeast infections caused by the most common human fungal pathogen, Candida. As fungal infections become more resistant to current drugs, this groundbreaking research may directly lead to the development of new drugs and therapies that will help limit and/or prevent Candida infections in the future for millions of sufferers. Candida albicans is the most common species of the Candida fungus and is the leading cause of vaginal and oral yeast infections, including thrush and denture stomatitis. It is the fourth most common hospital acquired bloodborne pathogen in the United States and surprisingly, it is present in the mouths of 30 to 50 percent of healthy adults. Because of the widespread nature of Candida, the potential for overgrowth and infection is common in the young, elderly, immuno-compromised and people receiving corticosteroid or chemotherapy treatments.


Diagnosis of arthritis 5 years earlier in childless women compared to those with children

Nulliparous women (those who have not given birth to children) are diagnosed with chronic arthritides (including ankylosing spondylitis, psoriatic arthritis and rheumatoid arthritis (RA) an average of 5.2 years before parous women (those who have given birth to children), according to a new study presented today at EULAR 2009, the Annual Congress of the European League Against Rheumatism in Copenhagen, Denmark. Previous studies have highlighted that pregnancy may be a protective factor against the development of RA, whereas this is the first study to assess the effect of pregnancy and having children on the development of chronic arthritic conditions in premenopausal women. Within the study, the mean age at time of diagnosis for nulliparous women was 26 years, compared with 31.2 years for parous women (p< 0.001). Rheumatoid factor (an autoantibody sometimes found in the immune systems of people with RA) was also present in 37.1% of the nulliparous women compared with 41.1% of the parous women (p=0.21), which, although not statistically significant, may indicate that the parous women studied may possess a higher disposition to developing arthritis than the nulliparous women. Dr Marianne Wallenius, of the Norwegian University of Science and Technology, Norway, who led the study, said: "Arthritic conditions tend to occur more commonly in women, particularly those of childbearing age. Some symptoms of RA, for example, can improve during pregnancy, but our study indicates that the processes of pregnancy and childbearing could delay the onset of arthritic conditions. Continued examination of the complex interactions between the female reproductive processes and the epidemiology of RA could yield further interesting insights." The retrospective study analysed 557 women aged 18-45 years from the Norwegian Disease Modifying Antirheumatic Drug (NOR-DMARD) study, who were all diagnosed with chronic arthritides before the age of 45 years. Information about parous status was confirmed through linking the NOR-DMARD patient cohort with the Medical Birth Registry of Norway (MBRN).


What are the risk factors of sporadic colorectal cancer?

Colorectal cancer (CRC) is one of the most common cancers in China. Although the association between the epidemiological factors and sporadic colorectal cancer has been studied, the relation between smoking, alcohol drinking, family history of cancer, body mass index (BMI) and sporadic colorectal cancer still remains uncertain. So it is important to investigate the role of these factors in the development of sporadic colorectal cancer. A research team led by Professor Jian-Ping Wang from the Gastrointestinal Institute of Sun Yat-Sen University addressed this question. Their study will be published on May 28, 2009 in the World Journal of Gastroenterology They conducted a hospital-based case-control study from July 2002 to December 2008 in Guangzhou city. There were 706 cases and 723 controls with their sex and age (within 5 years) matched. An unconditional logistic regression model was used to analyze the association between smoking, alcohol drinking, family history of cancer, BMI and sporadic colorectal cancer. They found that current alcohol drinking and greater BMI (? 24.0 kg/m2) are the independent risk factors for colon and rectal cancer, while former alcohol drinking and positive family history of cancer are the independent risk factors for colon cancer in southern Chinese. Their findings may contribute to the prevention and control of sporadic colorectal cancer. However, because of the uncontrolled bias in selection participants and retrospective design, their findings need to be further evaluated in well-designed larger epidemiological studies with different ethnic populations.


A breakthrough in gastric carcinogenesis

Checkpoint with forkhead and ring finger (CHFR) is a mitotic stress checkpoint gene whose promoter is frequently methylated in various kinds of cancer. In gastric cancer, CHFR promoter hypermethylation has been reported to lead to chromosome instability (CIN) and genetic instability is one of the hallmarks of human cancer. A research team led by Dr Eiji Oki from Kyushu University examined the methylation status of the promoter region of CHFR and microsatellite instability (MIN) status in primary gastric cancers. Their study will be published on May 28, 2009 in the World Journal of Gastroenterology They investigated the promoter methylation of CHFR in 59 cases of gastric cancer using methylation-specific PCR. Five microsatellite loci were analyzed using high-intensity microsatellite analysis reported previously, and p53 gene mutations were investigated by direct sequencing. They found that twenty cases (33.9%) showed promoter methylation and no relation was observed with the clinicopathological factors. The promoter methylation of CHFR was frequently accompanied with MIN. Seven of 20 (35.0%) cases showed MIN in hypermethylation of the CHFR tumor, while three of 39 (7.7%) cases showed MIN in the non-methylated CHFR tumor (P < 0.01). However, they failed to find any relationship between CHFR methylation and p53 mutation status. In conclusion, they demonstrated a correlation between the hypermethylation of CHFR and the MIN of gastric cancer patients. Both MIN and CHFR hypermethylation induce mitotic check point disruption and confer a survival advantage to the cells, however, this survival advantage does not lead to either p53 mutation or CIN in gastric cancer. This is the first study to show the striking relationship between CHFR silencing and microsatellite alteration in gastric cancer.


What is the relationship between hepatocellular carcinoma and type 2 diabetes mellitus?

Hepatocellular carcinoma (HCC) is the fifth most common malignancy worldwide and the third leading cause of cancer-related deaths. Type 2 diabetes mellitus has been associated with HCC. However, the relationship between type 2 diabetes mellitus and the underlying liver cirrhosis, and the effects of antidiabetic therapy on HCC risk have not yet been fully evaluated. A research team led by Dr. Valter Donadon from Pordenone Hospital addressed this question. Their study will be published on May 28, 2009 in the World Journal of Gastroenterology. Four hundred and sixty five HCC patients, 618 cirrhosis patients and 490 control subjects were enrolled in this study. They evaluated the odds ratio (OR) for HCC by univariate and multivariate analysis. Moreover, OR for HCC in diabetic subjects treated with insulin or sulphanylureas and with metformin were calculated. The prevalence of diabetes mellitus was 31.2% in HCC, 23.3% in cirrhotic patients and 12.7% in the Control group. By univariate and multivariate analysis, the OR for HCC in diabetic patients were respectively 3.12 (95%CI: 2.2-4.4, P < 0.001) and 2.2 (95%CI: 1.2-4.4, P = 0.01). In 84.9% of cases, type 2 diabetes mellitus was present before the diagnosis of HCC. Moreover, we report an OR for HCC of 2.99 (95%CI: 1.34-6.65, P = 0.007) in diabetic patients treated with insulin or sulphanylureas, and an OR of 0.33 (CI 0.1-0.7, P = 0.006) in diabetic patients treated with metformin. This study demonstrates that type 2 diabetes mellitus is an independent risk factor for HCC and pre-exists in the majority of HCC patients. In male HCC, patients with type 2 diabetes mellitus, their data shows a direct association of HCC risk with insulin and sulphanylureas treatment and an inverse relationship with metformin therapy.


A new 'idol' grabs the spotlight

Low-density lipoprotein (LDL) is the so-called "bad cholesterol" often linked to medical problems like heart disease and clogged arteries. Cells in the liver produce a specific receptor that sticks to LDL and removes it from the blood, lowering cholesterol levels. Statin drugs also reduce LDL cholesterol levels by boosting cells' production of the receptor. FINDINGS - Using a mouse model, UCLA scientists discovered a new mechanism that controls cells' production of LDL receptor. The team identified an enzyme called Idol that destroys the receptor, permitting more LDL cholesterol to circulate in the blood. In blocking Idol's activity, the researchers triggered cells to make more receptor and absorb more cholesterol from the body. "We only know of three pathways that regulate the LDL receptor. The first two are already targeted by existing drugs," explained Dr. Peter Tontonoz, professor of pathology and laboratory medicine at the David Geffen School of Medicine at UCLA and an investigator at the Howard Hughes Medical Institute. "Idol is the first mechanism discovered in several years that may lead to a new medication designed to control cholesterol levels."


Adults, especially women, have calorie-burning 'brown fat'

Keeping your baby fat turns out to be a good thing, as long as it is "brown fat"—the kind that burns calories, according to a study that found adults have much more of this type of fat than previously thought. The results, which suggest a new way to treat obesity, were presented at The Endocrine Society's 91st Annual Meeting in Washington, D.C. Brown fat burns off calories and generates heat in babies and small mammals. Most of our body fat is white fat, which also provides insulation but stores calories. It becomes "bad" fat when you have too much. The "good" fat—brown fat—was considered essentially nonexistent in human adults. "We now know that it is present and functional in adults," said the study's lead author, Aaron Cypess, MD, PhD, MMSc, of the Joslin Diabetes Center in Boston. "Three ounces of brown fat can burn several hundred calories a day." For the first time, the researchers were able to measure patches of brown adipose tissue—brown fat—in people, thanks to a high-tech imaging method that combines positron emission tomography and computed tomography, called PET/CT. By evaluating biopsy tissue of what appeared to be brown fat on PET/CT scans in some patients who had neck surgery, the authors confirmed that they were, indeed, looking at stores of brown fat. More than 1,970 study participants had PET/CT scans, from mid-skull to mid-thigh.


Successful weight loss with dieting is linked to vitamin D levels

Vitamin D levels in the body at the start of a low-calorie diet predict weight loss success, a new study found. The results, which suggest a possible role for vitamin D in weight loss, were presented at The Endocrine Society's 91st Annual Meeting in Washington, D.C. "Vitamin D deficiency is associated with obesity, but it is not clear if inadequate vitamin D causes obesity or the other way around," said the study's lead author, Shalamar Sibley, MD, MPH, an assistant professor of medicine at the University of Minnesota. In this study, the authors attempted to determine whether baseline vitamin D levels before calorie restriction affect subsequent weight loss. They measured circulating blood levels of vitamin D in 38 overweight men and women before and after the subjects followed a diet plan for 11 weeks consisting of 750 calories a day fewer than their estimated total needs. Subjects also had their fat distribution measured with DXA (bone densitometry) scans. On average, subjects had vitamin D levels that many experts would consider to be in the insufficient range, according to Sibley. However, the authors found that baseline, or pre-diet, vitamin D levels predicted weight loss in a linear relationship. For every increase of 1 ng/mL in level of 25-hydroxycholecalciferol—the precursor form of vitamin D and a commonly used indicator of vitamin D status—subjects ended up losing almost a half pound (0.196 kg) more on their calorie-restricted diet. For each 1-ng/mL increase in the active or "hormonal" form of vitamin D (1,25-dihydroxycholecalciferol), subjects lost nearly one-quarter pound (0.107 kg) more. Additionally, higher baseline vitamin D levels (both the precursor and active forms) predicted greater loss of abdominal fat. "Our results suggest the possibility that the addition of vitamin D to a reduced-calorie diet will lead to better weight loss," Sibley said.


Symptoms of depression in obese children linked to elevated cortisol

A new study connects abnormalities of the "stress" hormone cortisol with symptoms of depression in obese children, and confirms that obesity and depression often occur together, even in children. The results were presented at The Endocrine Society's 91st Annual Meeting in Washington, D.C. "There is evidence in adults that abnormal regulation of cortisol plays a role in both obesity and depression," said the study's lead author, Panagiota Pervanidou, MD, of Athens University Medical School in Athens, Greece. "Our study indicates that cortisol abnormalities may underlie obesity and depression starting in childhood." Cortisol is a steroid hormone that helps the body respond to stress but also has other functions, including converting fat, protein and carbohydrates into energy. Normally, levels of this hormone peak in the early morning, start to drop in late morning and reach their low point at night. However, depressed adults have slightly elevated cortisol levels at night—"the endocrine equivalent of chronic stress," Pervanidou said. This chronic elevation of cortisol contributes to development of the metabolic syndrome, which includes abdominal obesity and other risk factors for diabetes and cardiovascular disease. In this new study, Pervanidou and colleagues measured cortisol five times a day in the saliva of 50 obese children and teenagers as well as in their blood in the morning. The 20 boys and 30 girls, ages 8 to 15 years, were patients in the Athens University pediatric obesity clinic and did not have a prior diagnosis of depression. All subjects completed the Children's Depression Inventory (CDI), a questionnaire that assesses self-reported symptoms of depression.


Nicotine induces prediabetes, likely contributes to high prevalence of heart disease in smokers

Researchers have discovered a reason why smoking greatly increases the risk of heart disease and stroke. Nicotine promotes insulin resistance, also called prediabetes, which is a risk factor for cardiovascular disease, according to the new study, which was presented at The Endocrine Society's 91st Annual Meeting in Washington, D.C. Additionally, the study authors were able to partially reverse this harmful effect of nicotine in mice by treating them with the nicotine antagonist mecamylamine, a drug that blunts the action of nicotine. The study, which the National Institutes of Health funded, was conducted by researchers at Charles Drew University of Medicine and Science in Los Angeles and Western University of Health Sciences in Pomona, Calif. Their results may explain why cigarette smokers have a high cardiovascular death rate, even though "smoking causes weight loss, which should protect against heart disease," said the study's lead author, Theodore Friedman, MD, PhD, chief of the endocrinology division at Charles Drew University. Prediabetes and diabetes are known risk factors for cardiovascular disease. Past studies show that cigarette smokers tend to be insulin resistant, meaning that their hormone insulin does not work properly. To compensate, their blood glucose (sugar) levels become higher than normal but not yet high enough for diabetes. Smokers also have higher rates of diabetes, but it is not clear whether smoking is the cause, because they could have other risk factors, Friedman explained. Some studies demonstrate that nicotine and cigarette smoking induce high levels of the stress hormone cortisol. "As cortisol excess is known to induce insulin resistance, it has been suggested that glucocorticoids, such as cortisol, are the missing [causative] link between cigarette smoking and insulin resistance," Friedman said. The new study results suggest this theory is correct, he said. The researchers studied the effects, on 24 adult mice, of twice-daily injections of nicotine for 2 weeks. The mice ate less food than control mice that received injections without nicotine, and they also lost weight and had less fat. Despite this, the mice receiving nicotine developed prediabetes (insulin resistance), which subsequent mecamylamine treatment improved somewhat. These mice also had high cortisol levels in their blood and tissues, and mecamylamine blocked this effect.


Moderately reduced carbohydrate diet keeps people feeling full longer

A modest reduction in the amount of carbohydrates eaten, without calorie restriction and weight loss, appears to increase a sense of fullness, which may help people eat less, a preliminary study found. The results were presented at The Endocrine Society's 91st Annual Meeting in Washington, D.C. "There has been great public interest in low-carbohydrate diets for weight loss, but they are difficult to maintain, in part because of the drastic reduction in carbohydrates," said coauthor Barbara Gower, PhD, a professor in the Department of Nutrition Sciences, University of Alabama at Birmingham. In this study funded by the National Institutes of Health, Gower and her co-workers investigated whether a modest reduction in dietary carbohydrates, or "carbs," would improve feelings of fullness better than a carbohydrate level comparable to that of the typical U.S. diet. In a standard American diet, according to Gower, 55 percent of daily calories consumed come from carbohydrates: sugars, starches and fiber. The control diet used in their study contained 55 percent of daily calories from carbohydrates, in contrast to their "moderate-carb diet" which was 43 percent of calories from carbohydrates. The moderate-carb diet had more fat than their control diet—39 percent versus 27 percent of calories—so that protein intake could be the same percentage. The researchers matched the protein intake of both diets studied (18 percent of calories) because protein may influence both satiety ("fullness") and insulin secretion. The authors assigned the moderate-carb diet to 16 adults and the standard diet to 14 adults for a month. Subjects received enough calories to maintain their weight at what it was before the study. During the study they were weighed each weekday, and if a participant gained or lost weight, the amount of food was modified individually so weight could stay the same. After the subjects adjusted to their diet for 4 weeks, they ate a test meal, a breakfast that was specific to their diet.


UNC study suggests new approach to common cause of blindness

Researchers at the University of North Carolina at Chapel Hill School of Medicine in collaboration with lead investigators at the University of Kentucky have identified a new target for the diagnosis and treatment of age-related macular degeneration, the most common cause of blindness in older Americans. In a study published online June 14, 2009 by the journal Nature, the researchers demonstrate that blocking the activity of a specific protein – called CCR3 -- can reduce the abnormal blood vessel growth that leads to macular degeneration. Furthermore, targeting this new protein may prove to be safer and more effective than the current treatment for the disease, which is directed at a protein called vascular endothelial growth factor or “VEGF.” The discovery -- made in mouse models and cultured human cells -- may also enable physicians to catch the disease in its earliest stages, before blood vessels have fully infiltrated and destroyed the central portion of the eye’s retina -- an area known as the macula -- to cause vision loss. “It would be much better to prevent the disease in the first place,” said study co-author and principal investigator of the UNC study site, Mary Elizabeth Hartnett, M.D., a professor of ophthalmology in the UNC School of Medicine. “An exciting implication of this study was that the CCR3 protein could be detected in early abnormal blood vessel growth, giving us the opportunity to prevent structural damage to the retina and preserve vision.”


The Earth’s magnetic field remains a charged mystery

400 years of discussion and we’re still not sure what creates the Earth’s magnetic field, and thus the magnetosphere, despite the importance of the latter as the only buffer between us and deadly solar wind of charged particles (made up of electrons and protons). New research raises question marks about the forces behind the magnetic field and the structure of Earth itself. The controversial new paper published in New Journal of Physics (co-owned by the Institute of Physics and the German Physical Society), ‘Secular variation of the Earth’s magnetic field: induced by the ocean flow?’, will deflect geophysicists’ attention from postulated motion of conducting fluids in the Earth’s core, the twentieth century’s answer to the mysteries of geomagnetism and magnetosphere.


Is the sky the limit for wind power?

In the future, will wind power tapped by high-flying kites light up New York? A new study by scientists at the Carnegie Institution and California State University identifies New York as a prime location for exploiting high-altitude winds, which globally contain enough energy to meet world demand 100 times over. The researchers found that the regions best suited for harvesting this energy match with population centers in the eastern U.S. and East Asia, but fluctuating wind strength still presents a challenge for exploiting this energy source on a large scale.Using 28 years of data from the National Center for Environmental Prediction and the Department of Energy, Ken Caldeira of the Carnegie Institution's Department of Global Ecology and Cristina Archer of California State University, Chico, compiled the first-ever global survey of wind energy available at high altitudes in the atmosphere. The researchers assessed potential for wind power in terms of "wind power density," which takes into account both wind speed and air density at different altitudes.There is a huge amount of energy available in high altitude winds," said coauthor Ken Caldeira. "These winds blow much more strongly and steadily than near-surface winds, but you need to go get up miles to get a big advantage. Ideally, you would like to be up near the jet streams, around 30,000 feet." Jet streams are meandering belts of fast winds at altitudes between 20 and 50,000 feet that shift seasonally, but otherwise are persistent features in the atmosphere. Jet stream winds are generally steadier and 10 times faster than winds near the ground, making them a potentially vast and dependable source of energy. Several technological schemes have been proposed to harvest this energy, including tethered, kite-like wind turbines that would be lofted to the altitude of the jet streams. Up to 40 megawatts of electricity could be generated by current designs and transmitted to the ground via the tether."We found the highest wind power densities over Japan and eastern China, the eastern coast of the United States, southern Australia, and north-eastern Africa," said lead author Archer. "The median values in these areas are greater than 10 kilowatts per square meter. This is unthinkable near the ground, where even the best locations have usually less than one kilowatt per square meter."


‘Colossal’ Magnetic Effect Under Pressure

Millions of people today carry around pocket-sized music players capable of holding thousands of songs, thanks to the discovery 20 years ago of a phenomenon known as the “giant magnetoresistance effect,” which made it possible to pack more data onto smaller and smaller hard drives. Now scientists are on the trail of another phenomenon, called the “colossal magnetoresistance effect” (CMR) which is up to a thousand times more powerful and could trigger another revolution in computing technology. Understanding, and ultimately controlling, this effect and the intricate coupling between electrical conductivity and magnetism in these materials remains a challenge, however, because of competing interactions in manganites, the materials in which CMR was discovered. In the June 12, 2009, issue of the journal Physical Review Letters, a team of researchers report new progress in using high pressure techniques to unravel the subtleties of this coupling.


Gene evolution process discovered

One of the mechanisms governing how our physical features and behavioural traits have evolved over centuries has been discovered by researchers at the University of Leeds. Darwin proposed that such traits are passed from a parent to their offspring, with natural selection favouring those that give the greatest advantage for survival, but did not have a scientific explanation for this process. In research published this week, the Leeds team reports that a protein known as REST plays a central role in switching specific genes on and off, thereby determining how specific traits develop in offspring.The study shows that REST controls the process by which proteins are made, following the instructions encoded in genes. It also reveals that while REST regulates a core set of genes in all vertebrates, it has also evolved to work with a greater number of genes specific to mammals, in particular in the brain – potentially playing a leading role in the evolution of our intelligence. Says lead researcher Dr Ian Wood of the University's Faculty of Biological Sciences: "This is the first study of the human genome to look at REST in such detail and compare the specific genes it regulates in different species. We've found that it works by binding to specific genetic sequences and repressing or enhancing the expression of genes associated with these sequences. "Scientists have believed for many years that differences in the way genes are expressed into functional proteins is what differentiates one species from another and drives evolutionary change – but no-one has been able to prove it until now."


Hebrew University research leads to advanced trials of new cancer treatment

Research by a Hebrew University of Jerusalem professor has led to the development of a product that has been shown in clinical trials to be successful in halting the growth of various types of cancer cells. The research, conducted by Prof. Avraham Hochberg of the Silberman Institute of Life Sciences at the university, has won for him first prize among faculty members for this year's Kaye Innovations Awards, which was presented on June 9 during the annual Hebrew University Board of Governors meeting. Prof. Hochberg was successful in isolating the H19 gene in humans and determining that it is significantly expressed in over 33 different forms of cancer, including superficial bladder carcinoma and pancreatic, ovarian and metastatic liver cancer, while laying dormant and non-expressed in non-cancerous cells. Research has also demonstrated that the H19 gene plays a significant role in the tumor development process by enabling tumor cells to survive under stress conditions, such as low serum and low oxygen levels, that are typical conditions of the environment in which cancerous cells develop. This survival supports the growth of the tumor and the development of metastases.


GARP makes the difference

Scientists from the Helmholtz Center for Infection Research in Braunschweig, Germany and the Medical School Hannover, Germany have succeeded in treating immune cells in a way that enables them to inhibit unwanted immune reactions such as organ rejection. Their results have now been published in the current issue of the scientific journal Journal of Cellular and Molecular Medicine. The immune system keeps us healthy - day and night it protects us against invading and harmful pathogens. But this fulltime surveillance can also turn into a problem, for example after an organ transplant. The immune system recognizes the new organ as "foreign" and starts fighting it. In the end, the life-saving transplant will be rejected. Until now, only special drugs have managed to keep the immune system silent and thus inhibit organ rejection. Theoretically, these drugs are not necessary because the immune system has its own unique "peace makers": regulatory T cells (Tregs), a special group of helper T cells, an important cell type of the immune system. Tregs inhibit immune reactions and are thus of special medical interest. Until now, distinguishing between Tregs and helper T cells has represented a problem for scientists. Now, in co-operation with the Medical School Hannover, researchers from the Helmholtz Centre for Infection Research in Braunschweig have identified a molecular factor that plays an essential role in Treg function. This protein constitutes the key difference between Tregs and helper T cells. Furthermore, the scientists have also generated Tregs from helper T cells that permanently maintained their characteristics.


Novel discovery in dendritic cell signalling pathways pave the way for new therapeutic targets

Scientists from A*STAR's Singapore Immunology Network (SIgN) and the University of Milano-Bicocca, Italy, have discovered another signaling pathway for the activation and apoptosis, or programmed cell death, of dendritic cells[1] . This discovery was published in the advanced online publication of Nature on 15 Jun 2009. Led by Prof Paola Castagnoli, Scientific Director of SIgN and Associate Prof Francesca Granucci of the University of Milano-Bicocca, the team discovered that the well-studied immune receptor called CD14 in dendritic cells could be independently activated by bacterial fragments called liposaccharides or LPS. Once activated, the CD14 would initiate the NFAT[2] or nuclear factor of activated T-cells pathway, which would then activate the dendritic cells to trigger off the body's immune response. The scientists also discovered that the entire activation by CD14 was necessary to cause apoptosis. Dendritic cells are the frontline sentinels in the body's defence mechanisms and they are potent inducers of an immune response against invading pathogens. Activated dendritic cells have a short life span, and scientists have observed that they undergo apoptosis in order to protect the body from the over-stimulation of the immune system, which could result in autoimmunity. This behaviour is supported by Prof Castagnoli and Associate Prof Granucci's findings. "What is exciting is the link between CD14 activation and the NFAT pathway," explained Prof Castagnoli. "These findings have identified novel potential targets for the development of therapeutics against diseases that are involved with the CD14-NFAT pathway. For example, overexpression of CD14 has been associated with sepsis and chronic heart failure. New drugs that can modulate the CD14-NFAT pathway could provide treatments for such serious medical conditions."


Protein regulates movement of mitochondria in brain cells

Scientists have identified a protein in the brain that plays a key role in the function of mitochondria – the part of the cell that supplies energy, supports cellular activity, and potentially wards off threats from disease. The discovery, which was reported today in the Journal of Cell Biology, may shed new light on how the brain recovers from stroke. "Understanding the molecular machinery that helps distribute mitochondria to different parts of the cell has only recently begun to be understood," said University of Rochester Medical Center neurologist David Rempe, M.D., Ph.D., the lead author of the study. "We know that in some disease states that mitochondria function is modified, so understanding how their activity is modulated is important to understanding how the brain responds to a pathological state." Mitochondria are cellular power plants that generate most of the cell's supply of adenosine triphosphate (ATP), which is used as a source of chemical energy. While mitochondria are present in all of the body's cells, some cells – because of their size and purpose – need to transport mitochondria to distant sites within the cell to maintain proper function. A prominent example is neurons which have a complex cellular structure that consist of a main cell body and dendrites and axons that project out from the cell core and transmit signals to adjoining cells via synapses at their terminus. "Neurons are at a disadvantage in terms of their anatomy," said Rempe. "They put out enormous arms of axons and dendrites and they have to keep supplying nutrients and everything down these arms. The supply line is very long." The supply line includes mitochondria which the cell must also push down the axons and dendrites to provide these parts of the cell with energy, help with the transmission of signals, and generally maintain cellular health. Mitochondria are constantly cycling throughout the neuron. Some are stationary while others are moving down the arms of the cell to assume their proper position. Additionally, for reasons not completely understood, at any given time about half of the mobile mitochondria in the neuron are in the process of returning to the cell body – perhaps to be recycled or replenished in some form.


Depression Medications May Reduce Male Fertility

As many as half of all men taking the antidepressant medication paroxetine (trade names Seroxat, Paxil) may have increased sperm DNA fragmentation -- a predictor of compromised fertility. Research led by NewYork-Presbyterian Hospital/Weill Cornell Medical Center also found that the changes are reversible with normal levels of sperm returning after discontinuation of the drug. The study is currently published in the online edition of the journal Fertility & Sterility, and represents one of the first scientific investigations into the effect of antidepressants on sperm quality. "It's fairly well known that SSRI antidepressants negatively impact erectile function and ejaculation. This study goes one step further, demonstrating that they can cause a major increase in genetic damage to sperm," says Dr. Peter Schlegel, the study's senior author. "Although this study doesn't look directly at fertility, we can infer that as many as half of men taking SSRIs have a reduced ability to conceive. These men should talk with their physician about their treatment options, including non-SSRI depression medications." Dr. Schlegel is chairman of the Department of Urology and professor of reproductive medicine at Weill Cornell Medical College, and urologist-in-chief at NewYork-Presbyterian Hospital/Weill Cornell Medical College. The study followed 35 healthy male volunteers who were given paroxetine, a selective serotonin reuptake inhibitor (SSRI), for five weeks. The drug was used because of its relatively short half-life and because it has previously shown to exert the strongest effect in delaying ejaculation. DNA fragmentation, defined as missing pieces of genetic code in the sperm DNA, was measured using an assay called terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). Results showed that the percent of participants with abnormal DNA fragmentation rose from less than 10 percent to 50 percent while taking the drug. DNA fragmentation, the authors note, is known to correlate with poorer fertility and pregnancy outcomes, even when techniques such as in vitro fertilization and intracytoplasmic sperm injection are applied. It has also been linked with an increased risk for birth defects.


Researchers Identify DNA Mutation That Occurs At Beginning Point of T Cell Lymphoma

Researchers at the Keck School of Medicine of the University of Southern California (USC) have identified a key mechanism that causes chromosomes within blood cells to break—an occurrence that marks the first step in the development of human lymphoma. The study provides researchers with the clearest insight yet into why these breakages—called chromosomal translocations—occur at a specific points in the chromosome, says principal investigator Michael R. Lieber, M.D., Ph.D., Rita and Edward Polusky Professor in Basic Cancer Research at the Keck School of Medicine.The study appears as the featured cover article in the June 12 issue of the journal Molecular Cell. The study is the second led by Lieber to appear on the cover of a Cell journal in the past six months. “The new findings go to the heart of why cancers begin. This is an opportunity to see the very beginning step of human lymphoma,” Lieber says. “With this information, we can now begin to look at ways to interfere with this process in order to stop the lymphoma and to develop more targeted therapies for treatment.” There are two types of lymphoma: B cell lymphomas and T cell lymphomas. Both B cells and T cells perform vital functions in the immune system by creating antibodies and destroying virus-infected cells. However, the beginning point, or inception, of most human lymphomas occurs when two chromosomes break and the resulting fragments are reassembled in an exchange. Researchers specifically looked at T cell acute lymphoblastic lymphomas (ALL). ALL accounts for half of all childhood cancers under the age of five, and T cell ALL represents about 10 percent of ALL. The USC scientists identified a specific enzyme known as the RAG complex that occasionally cuts the chromosome at an off-target site, causing lymphocyte (blood) cells to proliferate uncontrollably. They showed that the RAG complex selects the wrong target largely because the proteins in which the wrong chromosome is wrapped (called chromatin) lures the RAG complex to the wrong site.


Laptops Linked to Male Infertility

While fatherhood might be far from the minds of most young men, behavior patterns they establish early on may impact their ability to become a dad later in life. Excessive laptop use tops this list of liabilities, according to one reproductive specialist at Loyola University Health System (LUHS). "Laptops are becoming increasingly common among young men wired into to the latest technology," said Suzanne Kavic, MD, director of the division of reproductive endocrinology at LUHS and associate professor in the department of obstetrics and gynecology and department of medicine at Loyola University Chicago Stritch School of Medicine. "However, the heat generated from laptops can impact sperm production and development making it difficult to conceive down the road." Kavic recommends placing laptops on desktops to prevent damaging sperm and decreasing counts and motility.


Chemical in Blood May Explain Susceptibility to Bladder Pain

Marker in the blood of both cats and humans that was identified in a recent study might signal both species' susceptibility for a painful bladder disorder called interstitial cystitis, a condition that is often difficult to diagnose. Follow-up studies of the chemicals that appeared in blood samples suggest that the way tryptophan, an essential amino acid, is processed in cats and humans with interstitial cystitis ultimately could affect the way signals are transmitted in the brain. The results, while preliminary, suggest that the disease is not just a malfunction of the bladder, but might instead have origins in the central nervous system, researchers say. Symptoms of interstitial cystitis, known as IC, include recurring discomfort or pain in the bladder and pelvis, and often both an urgent and frequent need to urinate. A diagnosis typically follows tests to rule out other diseases, such as infections or cancer. No diagnostic test currently exists for IC, and the cause is unknown. Treatments range from oral medications to exercise for humans, and maintaining a safe environment for cats."What we know now is that this testing method is very sensitive and specific for the disorder in both humans and domestic cats. So far it hasn't missed one diagnosis," said Tony Buffington, senior author of the study and professor of veterinary clinical sciences at Ohio State University.


Chronic Infection Now Clearly Tied to Immune-System Protein

The reason deadly infections like human immunodeficiency virus (HIV) and hepatitis C never go away is because these viruses disarm the body’s defense system. Researchers at the University of Alabama at Birmingham (UAB) have discovered that a key immunity protein must be present for this defense system to have a chance against chronic infection. Research up to now has tried but failed to decipher the cross-talk between ‘killer T-cells’ and ‘helper T-cells’ in the fight against viruses. The new UAB study finds this cross-talk can only happen in the presence of interleukin-21, a powerful immune system protein. If interleukin-21 is missing for whatever reason, then the immune system’s anti-viral efforts fail, said Allan Zajac, Ph.D., an associate professor in UAB's Department of Microbiology and lead author on the study. The findings are published in the journal Science. “Adding interleukin-21 back in stimulates the immune response and controls the infection,” Zajac said. “We demonstrate that the loss of this protein prevents the control of the infection and diminishes the function of the killer T-cells, specifically CD8 T-cells.” The study mice were treated for lymphocytic choriomeningitis, a viral infection of the membranes surrounding the brain and spinal cord. Measurements were taken for two types of T-cells, CD4 and CD8 T-cells, before and after the mice were treated with interleuikin-21.


Predicting Fatal Fungal Infections

In a study published in The Journal of Infectious Diseases, researchers from Albert Einstein College of Medicine of Yeshiva University have identified cells in blood that predict which HIV-positive individuals are most likely to develop deadly fungal meningitis, a major cause of HIV-related death. This form of meningitis affects more than 900,000 HIV-infected people globally—most of them in sub-Saharan Africa and other areas of the world where antiretroviral therapy for HIV is not available. A major cause of fungal meningitis is Cryptococcus neoformans, a yeast-like fungus commonly found in soil and in bird droppings. Virtually everyone has been infected with Cryptococcus neoformans, but a healthy immune system keeps the infection from ever causing disease.


Good news for some hard-to-treat hepatitis C patients

In a multi-center trial led by a Saint Louis University researcher, investigators found that a new combination therapy of daily consensus interferon and ribavirin helps some hepatitis C patients who have not responded to previous treatment. The findings, published in the June issue of Hepatology, offer a new option for hepatitis C patients, and may be effective even for those patients with factors that make their condition difficult to treat. "This represents an important advance for difficult to treat hepatitis C patients who have failed to respond to traditional therapy," said Bruce Bacon, M.D., director of the division of gastroenterology and hepatology at Saint Louis University School of Medicine and co-director of the Saint Louis University Liver Center . About 4 million people in the U.S. have been infected with hepatitis C; an estimated 10,000 to 12,000 people die from complications each year in this country. Hepatitis C is caused by a virus, transmitted by contact with blood, and may initially be asymptomatic. For patients who develop chronic hepatitis C infection, inflammation of the liver may develop, leading to fibrosis and cirrhosis (scarring of the liver), as well as other complications including liver cancer and death. For patients with chronic hepatitis C, the prognosis varies. About half fully recover after an initial course of pegylated interferon and ribavirin anti-viral therapy that may last from six months to a year.


Test detects molecular marker of aging in humans

In 2004, researchers at the University of North Carolina at Chapel Hill Lineberger Comprehensive Cancer Center announced a crucial discovery in the understanding of cellular aging. They found that as cells and tissues age, the expression of a key protein, called p16INK4a, dramatically increases in most mammalian organs. Because p16INK4a is a tumor suppressor protein, cancer researchers are interested in its role in cellular aging and cancer prevention. Now the team has proven that the same biomarker is present in human blood and is strongly correlated both with chronological age and with certain behaviors such as tobacco use and physical inactivity, which are known to accelerate the aging process. In a paper published online ahead of print in the journal Aging Cell, the researchers reported that they have solved technical hurdles to develop a simple blood test to detect p16INK4a expression, which is present in cells called T-lymphocytes, also known as T-cells. "This is a major step toward a practical tool to clinically determine a person's actual molecular, as opposed to just their chronological age," said UNC Lineberger member Norman Sharpless, M.D., the senior author of the study and associate professor of medicine and genetics at UNC's School of Medicine. They validated the test by obtaining blood from two groups of healthy human volunteers, totaling 170 subjects, who also filled out a questionnaire about current and past health status and health behaviors. They found that expression of the biomarker was strongly correlated with the donor's chronological age and, in fact, increased exponentially with age. In addition, increased levels were independently associated with tobacco use and physical inactivity as well as with biomarkers of human frailty.


RNA snippet suppresses spread of aggressive breast cancer

A low cellular level of a tiny fragment of RNA appears to increase the spread of breast cancer in mouse models of the disease, according to researchers at Whitehead Institute for Biomedical Research. Measuring levels of this so-called microRNA, which is also associated with metastatic breast cancer in humans, may more accurately predict the likelihood of metastasis (which accounts for 90% of cancer-related deaths) and ultimately help determine patient prognoses. In the study, whose results are reported in the June 12 issue of Cell, Scott Valastyan, a graduate student in Whitehead Member Robert Weinberg's laboratory, screened patient breast cancer samples for microRNAs with potential roles in metastasis. MicroRNAs are single strands of RNA about 21-23 nucleotides long. Within a cell, a single microRNA can fine-tune the expression of dozens of genes simultaneously. This capability could be particularly important in metastasis, a multi-step process that could be influenced by a single microRNA at several points. The screened samples were classified as either metastatic cancer or non-metastatic cancer. After analysis, the microRNA miR-31 stood out because of its inverse correlation with metastasis. In samples where a patient's original tumor had not metastasized, the cancer cells retained high levels of the microRNA. But where the tumor had metastasized, the cancer cells came to possess lower levels of miR-31. The functional role of miR-31 in metastasis regulation was then confirmed in mice. When Valastyan removed miR-31 from normally non-aggressive breast cancer cells and implanted those cells into mice, the cells formed highly aggressive tumors. Mice injected with the cancer cells lacking miR-31 had 6 to 10 times more cancer cells that metastasized to their lungs than did their counterparts implanted with unmodified cancer cells.To see how increasing miR-31 levels could affect metastasis, Valastyan introduced miR-31 into breast cancer cells that readily metastasize. After injecting these altered cells into mice, the mice had four to 40 times fewer metastases than mice injected with the unaltered cells. Valastyan says that quantifying miR-31 levels in a patient's cancer cells could one day support a more accurate prognosis. Currently, breast cancers are divided into three major categories, two of which are typically associated with poor prognoses. "This microRNA seems to be quite unique, in that it seems to provide some prognostic utility across these existing subclassifications [of cancers]," says Valastyan. A better-defined prognosis could help patients determine whether they might benefit from poorly tolerated cancer therapies.


The anti-consumption movement - Researchers examine resistance to global brands

What motivates people to rebel against global brands—or consumption in general? A new study in the Journal of Consumer Research examines the connection between nationalism and the anti-consumption movement in India. Authors Rohit Varman (Indian Institute of Management, Calcutta) and Russell W. Belk (York University, Toronto) examined a movement against Coca-Cola based in the village of Mehdiganj in the Indian state of Uttar Pradesh. They found that the movement employs a version of the nationalist ideology of swadeshi, an ideology that has been associated with Ghandhi and the overthrow of British colonialism. "According to swadeshi, indigenous goods should be preferred by consumers even if they are more expensive and inferior in quality," write the authors. "The contemporary processes of globalization have again unleashed a resurgence of opposition, this time involving neo-nationalism. As a result, the ideology of swadeshi continues to shape the ongoing debate about the concept of nationhood in India." The researchers examined the practices of organizations involved in the struggle against Coca Cola. They conducted interviews with activists, villagers, and Coca Cola workers and managers. They observed protest activities and analyzed written material on the movement.


The freebie dilemma - Consumers are skeptical about 'free' products

It's common for retailers to bundle two different products (like razors and blades) together and describe one as free. A new study in the Journal of Consumer Research shows that this strategy leads consumers to devalue the items when they're sold individually. Authors Michael A. Kamins (Stony Brook University-SUNY), Valerie S. Folkes (University of Southern California), and Alexander Fedorikhin (Indiana University) found that describing a bundled item as free decreases the amount consumers are willing to pay for each product when sold individually. They call this the "freebie devaluation" effect. "Why does a freebie decrease the price consumers are willing to pay for each individual product? Our research shows that consumers tend to make inferences about why they are getting such a great deal that detract from perceptions of product quality," the authors explain. "For example, consumers figure the companies can't sell the product without this marketing gimmick." The authors also found exceptions to the "freebie devaluation" rule. For example, when the researchers explained that the products were paired so consumers would become familiar with the freebies, they were willing to pay more.


'Shortcuts' of the mind lead to miscalculations of weight and caloric intake, says Penn study

Psychologists at the University of Pennsylvania have identified a cognitive shortcut, or heuristic, they call "Unit Bias," which causes people to ignore vital, obvious information in their decision-making process, points to a fundamental flaw in the modern, evolved mind and may also play a role in the American population's 30 years of weight gain. Researchers who focus on the cognitive aspects that contribute to obesity conducted several studies with college-age participants in which the subjects were asked to estimate the weight of adult women from either photographs or a live presentation by models. Other student participants were asked to estimate the calories in one of two actual meals. Both meals contained the same foods, but one had larger portion sizes than the other. The results demonstrated that when estimating the body weight of women, participants apparently disregard or ignore the provided height information and focus solely on the width of the model. In certain instances, researchers would inflate the provided height information of the models as much as 10 inches, though that did not alter participants' estimates of the models' weights. When estimating calories, study participants assumed portion sizes were culturally typical and guessed no caloric differences between small and large portions. The findings are akin to asking a room full of people to calculate the volume of a box when given only the height and width and no one asks for the length. Or, more accurately, the length is provided and no one pays attention to that one, crucial dimension, thereby making it impossible to arrive at the correct answer. The study suggests that there are situations where critical dimensions to understanding are devalued or ignored. The paper examines different circumstances discovered by researchers where single dimensions dominate multidimensional judgments. In these studies specifically, participants estimated body weight based on the model's shape even though height information was provided in the photographs or directly available with live models. Meanwhile, participants devalued or completely ignored other parameters critical to an accurate judgment.


Stress puts double whammy on reproductive system, fertility

University of California, Berkeley, researchers have found what they think is a critical and, until now, missing piece of the puzzle about how stress causes sexual dysfunction and infertility. Scientists know that stress boosts levels of stress hormones - glucocorticoids such as cortisol - that inhibit the body's main sex hormone, gonadotropin releasing hormone (GnRH), and subsequently suppresses sperm count, ovulation and sexual activity. The new research shows that stress also increases brain levels of a reproductive hormone named gonadotropin-inhibitory hormone, or GnIH, discovered nine years ago in birds and known to be present in humans and other mammals. This small protein hormone, a so-called RFamide-related peptide (RFRP), puts the brakes on reproduction by directly inhibiting GnRH. The common thread appears to be the glucocorticoid stress hormones, which not only suppress GnRH but boost the suppressor GnIH - a double whammy for the reproductive system. "We know stress affects the top-tier reproductive hormone, GnRH, but we show, in fact, that stress also affects another high-level hormone, GnIH, to cause reproductive dysfunction," said lead author Elizabeth Kirby, a graduate student at UC Berkeley's Helen Wills Neuroscience Institute. "This work provides a new target for researchers, a new way to think about infertility and dysfunction. The more we know, the more we can look for ways to treat it." The results will be published the week of June 15 in the Online Early Edition of the journal Proceedings of the National Academy of Sciences (PNAS)


New method separates cancer cells from normal cells

The vast majority of cancer deaths are due to metastasis, the spread of cancer cells from its primary site to other parts of the body. These metastatic cells tend to move more than their non-metastatic variants but this movement is poorly understood. Scientists are studying cancer cells intently with the hope they can learn to control the movements of the dangerous cells. Northwestern University researchers now have demonstrated a novel and simple method that can direct and separate cancer cells from normal cells. Based on this method, they have proposed that cancer cells possibly could be sequestered permanently in a sort of "cancer trap" made of implantable and biodegradable materials. The demonstrated device, which takes advantage of a physical principle called ratcheting, is a very tiny system of channels for cell locomotion. Each channel is less than a tenth of a millimeter wide. The asymmetric obstacles inside these channels direct cell movement along a preferred direction.Details are published online by the journal Nature Physics. "We have demonstrated a principle that offers an unconventional way to fight metastasis, a very different approach from other methods, such as chemotherapy," said Bartosz Grzybowski, the paper's senior author. "These are fundamental studies so the method needs to be optimized, but the idea has promise for a new approach to cancer therapy." Grzybowski is associate professor of chemical and biological engineering in the McCormick School of Engineering and Applied Science and associate professor of chemistry in the Weinberg College of Arts and Sciences. The researchers first discovered they could design channels of different geometries -- some a series of connected triangles -- through which cells can move in a single direction. (Live mammalian melanoma, breast cancer and normal cells were studied.) To create the channels, the researchers patterned cell-adhesive and cell-repellant chemical compounds onto a substrate. The cells stayed out of the repellant areas and localized onto the "ratchet" channels, which then directed the cells' movements.


Newborn weights affected by environmental contaminants

Recent epidemiological studies have revealed an increase in the frequency of genital malformations in male newborns (e.g., un-descended testes) and a decrease in male fertility. The role played by the growing presence in our environment of contaminants that reduce male hormone action could explain this phenomenon. It is known that the birth weight of males is higher than that of females due to the action of male hormones on the male fetus.If the exposure of pregnant women to environmental contaminants that diminish the action of male hormones has increased over the years, one would expect to see a decrease in the sex difference in birth weight. This is exactly what a new study published in the July 2009 issue of Epidemiology shows. Investigators analyzed the Public Health Agency of Canada's database on the birth weights of more than five million children born in Canada between 1981 and 2003. Using statistical methods that control for changes over time of mother's age and parity, the investigators effectively show a sustained decrease in birth weight differences between boys and girls, which supports the hypothesis of growing endocrine disruption related to environmental contaminants. Contaminants found in plastic materials represent lausible candidates, since they are known to diminish the action of male hormones. "Our study underlines the importance of probing the impact of environmental contaminants on the health of mothers and fetuses and on the reproductive potential of future generations," says lead researcher Dr. Guy Van Vliet, a pediatric endocrinologist and investigator at the Sainte-Justine University Hospital Research Center and a professor at the Department of Pediatrics of the Université de Montréal.


Pregnant women at high risk of complications from H1N1 influenza

With the H1N1 flu outbreak now elevated to pandemic level, a new article http://www.cmaj.ca/cgi/rapidpdf/cmaj.090866 in CMAJ (Canadian Medical Association Journal) reports that oseltamivir (Tamiflu®) and zanamivir (Relenza®) are relatively safe drugs for use in pregnant and breast-feeding women. Pregnant women, especially those in the third trimester, are at high risk of serious complications from the H1N1 A influenza virus. The study was conducted by researchers from the Motherisk Program at The Hospital for Sick Children (SickKids) in Toronto and the Japan Drug Information Institute in Pregnancy in Tokyo, Japan. For treatment or prevention during the current pandemic, "oseltamivir appears to be the drug of choice because there are more data on its safety in pregnancy," writes Dr. Shinya Ito, Head of the Division of Clinical Pharmacology and Toxicology at SickKids. Zanamivir can be used, although there is less data available about its safety in pregnant women. Neither drug appears to affect the growth and development of the fetus, although ongoing data collection is important. The groups at high risk of flu-related complications from the novel H1N1 influenza are the same as those for seasonal flu – pregnant women, children under 5 years, the elderly and others such as those with chronic lung conditions. Only small amounts of oseltamivir and zanamivir are excreted into human milk. If an infant is breastfed by the mother on these drugs and needs treatment, the recommended dose of oseltamivir or zanamivir should be given to the infant.


Questions and answers on the new biocides regulation

The new regulation on the use and placing on the market of biocidal products will repeal and replace the current directive on biocides (98/8/EC). It will enter into force on 1 January 2013.

What are biocidal products?

Biocidal products contain or generate active substances and are used against harmful organisms such as pests and bacteria. They are used both to protect human and animal health. They include household products such as disinfectants, rodenticides, repellents, and insecticides. Others are used in more industrial applications as wood and material preservatives, anti-fouling paints, and embalming products to avoid damage to natural or manufactured products.

Due to their intrinsic properties and uses, biocidal products may themselves pose health risks and be harmful to the environment. It is vital therefore to ensure that only biocidal products safe for use are placed on the market.

What are the main differences between the current directive and the new regulation?

The new regulation increases the protection of health and environment, while being more efficient at the same time, notably through the active involvement of ECHA. It will retain the two-step authorisation process brought in by the current directive, whereby active substances are first tested and approved and included in a Community list (known as the Annex I), with subsequent authorisation of a product containing the active substance.

Scope

The scope has been extended to cover articles and materials treated with biocidal products, including furniture and textiles. The regulation will also apply to active substances generated in situ, and to biocidal products used in materials that come into contact with food. But other products that are sufficiently covered by existing legislation (including food and feed, food and feed additives and processing aids) are excluded from the scope of the new regulation. Biocidal products approved under the International Convention for the Control and Management of Ships' Ballast Water and Sediments are considered as authorised.

Product authorisation and mutual recognition

Under the current Directive, all biocidal products are authorised at Member State level. This will change for two types of biocidal products – biocidal products based on new active substances and low-risk biocidal products – which will have access to a Community authorisation allowing them to be placed on the market throughout the Community. All other biocidal products will still be subject to national authorisations issued by Member States.

There will also be further changes to the rules on mutual recognition, the process whereby an authorisation in one Member State may be recognised by another Member State. Under the regulation, it will be possible to apply either for a mutual recognition of an existing authorisation, or for a mutual recognition which runs in parallel to the first authorisation process. The new regulation will also clarify the conditions for obtaining a parallel trade permit.

Data requirements

Under the current directive, the same set of data must be submitted for all biocidal products, not all of which is always necessary.

Under the proposed regulation, data requirements will be more aligned with the actual needs of the evaluating authorities. It will become possible to waive requirements if data is not scientifically necessary, if it is technically impossible to supply, or if it is not relevant (there is no need for marine toxicity studies, for example, if a product is reserved for use on dry land). It will no longer be possible to repeat tests that have already been carried out on vertebrate animals, and information gained from such tests must be shared, in exchange for fair compensation.

What active substances will be phased out?

The proposed regulation sets out 'exclusion criteria' to prevent authorisation of active substances with very poor hazard profiles, including substances that can cause cancer, mutations, reproductive problems and hormonal imbalances.

In future, such substances will only be allowed for use provided that:

human exposure to the active substance in the biocidal product is negligible

the active substance is necessary to control a serious danger to public health such as an epidemic of particular insects

the negative effects of banning the active substance would be disproportionate to the impacts on human health or the environment, and no alternatives are available.

Biocidal products with problematic active substances will also be compared to ensure that only the products with the lower risk remain on the market.

How will the rules on the inclusion of active substances change?

There is a need to ensure equality of treatment for active substances evaluated before and after the entry into force the new regulation. It is therefore proposed that substances still being evaluated under the old rules on 1 January 2013 should continue to be evaluated under the same rules.

The changes introduced by the new regulation, including the data requirements, data waiving, obligatory sharing of vertebrate animal data and so forth will only apply to active substances whose evaluation starts after 1 January 2013.

The new proposal will not affect the rules on the examination of existing active substance (those on the market on 14 May 2000) laid down under Regulation (EC) No 1451/2007.

How will the rules on Community-wide authorisation work?

Community authorisation will be available for two types of biocidal products: those based on new active substances, and low-risk biocidal products. Such authorisations will be granted by the European Commission, and will allow products to be placed on the market across the EU without any need to apply for separate national authorisations or the mutual recognition process.

Applications for a Community authorisation will be submitted to the European Chemicals Agency (ECHA) and to a competent authority of the applicant's choice. The competent authority will evaluate the application and send its conclusions to ECHA for an opinion. The Commission will then decide whether a Community authorisation can be granted, and if so under which conditions.

Community-wide authorisations should stimulate innovation and the development of new and improved products.

What will be the impacts on animal?

The proposal strives to minimise animal testing as far as possible Vertebrate tests may not be repeated, and a new obligation to share data involving vertebrate animal tests will come into force. This means that data owners will be obliged to share their data, in exchange for fair compensation.

The regulation will also encourage the sharing of data from other types of animal tests, with a view to reducing the overall costs and avoiding the duplication of tests..

What will be the tasks of ECHA under the new Regulation?

The European Chemicals Agency (ECHA) will coordinate the active substance evaluation for new and existing active substances, the re-assessments of the already approved active substances in light of available new information, and some related evaluation work.

The agency will also play a key role in the centralised authorisation of products. ECHA will be in charge of coordinating the technical and scientific work of this new centralised authorisation process. In the event of any disputes between over mutual recognition between the Member States or the Member States and applicants, ECHA will provide the Commission with technical and scientific support.

ECHA will intervene in cases of disagreements about data sharing from vertebrate animal tests. ECHA will also be responsible for maintaining the relevant databases and other administrative and scientific tasks, such as coordinating the meeting of experts reviewing the draft risk assessments reports prepared by the Member States in the context of the review programme of the biocidal active substances.

What are the costs and benefits of this proposal?

Compared with the existing rules, the only change involving additional costs to the industry concerns the extension of the scope to treated articles and materials. These costs will mainly result from the inclusion of further active substances in Annex I and the compliance with the labelling obligations. But it should be noted that according to the impact assessment carried out to evaluate the proposal, the environmental and human health benefits of extending the scope to treated articles and materials will easily outweigh the costs.

The other measures introduced by the proposal, such as improved authorisation procedures, including the Community authorisation, obligatory data sharing for vertebrate animal data and streamlining the data requirements, will result in significant cost savings. The reduction of financial and administrative burden was also one of the main objectives of this proposal. However, this proposal shows that these savings can be achieved without compromising the high level of environmental and human health protection.

Further information:

European Commission:

http://ec.europa.eu/environment/biocides/revision.htm

ECHA:

http://echa.europa.eu/


Rosemoor announces its Herbal Medicine Week

RHS Garden Rosemoor is celebrating the National Herbal Medicine Week from 20 - 27 June. A fascinating workshop on the wonderful world of plant remedies is set to take place on Tuesday 23 June.

Link

Ditta


Scientists Find Faster, Cheaper Way to Identify Cancer-Causing Genes

Researchers at the University of Virginia Health System have found a new way to study how genes function in living organisms, and their approach could substantially cut the time and costs that drug makers spend in searching for potential targets for new cancer therapies. “A big problem in biology is that there are many thousands of genes. Testing the function of any one of them in a living organism, such as a mouse, has traditionally been slow and very expensive,” notes Ian Macara, PhD, professor of microbiology at UVA’s School of Medicine and co-author of a study published in the June 15 issue of Genes & Development. “The new technology is hundreds of times cheaper and many times faster than traditional approaches. While we used it to study the function of a specific breast-developing gene, our method can be replicated in screening for genes that can suppress tumors or cause cancer.” In Genes & Development, UVA researchers describe how they isolated mammary gland stem cells from mice and then infected the cells with a virus that enabled the scientists to manipulate a particular gene and cause it to glow green. When transplanted in mice that had undergone mastectomies, the altered stem cells regenerated entire new breasts within a few months. Because the target gene glowed green, researchers could monitor its role in the development of the new breast.


Fibromyalgia Patients Show Decreases in Gray Matter Intensity

Previous studies have shown that fibromyalgia is associated with reductions in gray matter in parts of the brain, but the exact cause is not known. Using sophisticated brain imaging techniques, researchers from Louisiana State University, writing in The Journal of Pain, found that alterations in levels of the neurotransmitter dopamine might be responsible for gray matter reductions. For the study, magnetic imaging resonance data from 30 female fibromyalgia patients were compared with 20 healthy women of the same age. The primary objective of the study was to confirm original findings about reduced gray matter density in a larger sample of fibromyalgia patients. They explored whether there is a correlation between dopamine metabolic activity and variations in the density of gray matter in specific brain regions. Results showed there were significant gray matter reductions in the fibromyalgia patients, which supports previous research. In addition, the fibromyalgia patients showed a strong correlation of dopamine metabolism levels and gray matter density in parts of the brain in which dopamine controls neurological activity. The authors concluded that the connection between dopamine levels and gray matter density provide novel insights to a possible mechanism that explains some of the abnormal brain morphology associated with fibromyalgia.


Study Pinpoints Links of Depression with Chronic Pain

It is well known that chronic pain and clinical depression go together, but a study in The Journal of Pain, published by the American Pain Society, shows that the connection between pain and depression is strongest in middle-age women and African Americans.


Discovery of the cell's water gate may lead to new cancer drugs

The flow of water into and out from the cell may play a crucial role in several types of cancer. Scientists at the University of Gothenburg have now found the gate that regulates the flow of water into yeast cells. The discovery, which will be published in the journal PLoS Biology, raises hopes of developing a drug that inhibits the spread and growth of tumours. All living organisms must be able to regulate the flow of water into and out from cells, in order to maintain cell form and size. This regulation is carried out by special proteins known as "aquaporins". These act as water channels and control the flow of water into and out from the cell.


Crustacean shell with polyester creates mixed-fiber material for nerve repair

In the clothing industry it's common to mix natural and synthetic fibers. Take cotton and add polyester to make clothing that's soft, breathable and wrinkle free. Now researchers at the University of Washington are using the same principle for biomedical applications. Mixing chitosan, found in the shells of crabs and shrimp, with an industrial polyester creates a promising new material for the tiny tubes that support repair of a severed nerve, and could serve other medical uses. The hybrid fiber combines the biologically favorable qualities of the natural material with the mechanical strength of the synthetic polymer. "A nerve guide requires very strict conditions. It needs to be biocompatible, stable in solution, resistant to collapse and also pliable, so that surgeons can suture it to the nerve," said Miqin Zhang, a UW professor of material science and engineering and lead author of a paper now available online in the journal Advanced Materials. "This turns out to be very difficult."After an injury that severs a peripheral nerve, such as one in a finger, nerve endings continue to grow. But to regain control of the nerve surgeons must join the two fragments. For large gaps surgeons used to attempt a more difficult nerve graft. Current surgical practice is to attach tiny tubes, called nerve guides, that channel the two fragments toward each other. Today's commercial nerve guides are made from collagen, a structural protein derived from animal cells. But collagen is expensive, the protein tends to trigger an immune response and the material is weak in wet environments, such as those inside the body. The strength of the nerve guide is important for budding nerve cells.


Research Uncovers Clues to Virus-Cancer

In a series of recently-published articles, a research team from the University of North Carolina at Chapel Hill Lineberger Comprehensive Cancer Center has uncovered clues to the development of cancers in AIDS patients.In an April article published in the journal PLoS Pathogens, Dirk Dittmer, Ph.D., associate professor of microbiology and immunology at UNC’s School of Medicine, demonstrated that the Kaposi sarcoma associated herpesvirus (KSHV) is not only present in every tumor cell, but that the cells also transcribe microRNAs (miRNA) from the virus. This represents a collaborative effort between UNC researchers and clinicians at Beth Israel Hospital, the University of Miami and the Federal University in Bahia, Brazil. MicroRNAs are small molecules that regulate gene expression. Scientists have hypothesized that viruses can cause cancer through a mechanism where the viral genes take over the cell and induce cancerous growth through alteration of cell miRNA, since certain kinds of miRNA are responsible for putting the ‘brakes’ on uncontrolled cell growth. Dittmer’s team examined samples of tissue provided with the consent of Kaposi’s sarcoma patients and found that specific miRNA biomarkers accurately identify stages of tumor progression. They found that certain miRNAs were lost as the tumors progressed, effectively accelerating the cancer’s growth. More aggressive tumor stages expressed higher levels of KSHV miRNA.


New Cortex Study Uncovers How We Recognize What is True and What is False

A recent neuroimaging study reveals that the ability to distinguish true from false in our daily lives involves two distinct processes. Previous research relied heavily on the premise that true and false statements are both processed in the left inferior frontal cortex. Carried out by researchers from the Universities of Lisbon and Vita-Salute, Milan, the June Cortex study found that we use two separate processes to determine the subtle distinctions between true and false in our daily lives. Deciding whether a statement is true involves memory; determining one is false relies on reasoning and problem-solving processes.


The bitter side of sweeteners

Sewage treatment plants fail to remove artificial sweeteners completely from waste water. What's more, these pollutants contaminate waters downstream and may still be present in our drinking water. Thanks to their new robust analytical method, which simultaneously extracts and analyses seven commonly used artificial sweeteners, Marco Scheurer, Heinz-Jürgen Brauch and Frank Thomas Lange from the Water Technology Center in Karlsruhe, Germany, were able to demonstrate the presence of several artificial sweeteners in waste water. Their findings are published online this week in Springer's journal Analytical and Bioanalytical Chemistry. A range of artificial sweeteners are commonly used in food and drinks, as well as drugs and sanitary products. The potential health risks of artificial sweeteners have been debated for some time. Until now, only sucralose has been detected in aquatic environments. Through the use of a new analytical method, the researchers were able to look for seven different artificial sweeteners (cyclamate, acesulfame, saccharin, aspartame, neotame, neohesperidin dihydrochalcone and sucralose) simultaneously, and show, for the first time, that a number of commonly used artificial sweeteners are present in German waste and surface water.


We have discovered the first genes intervening in brain metastasis

Joan Massagué (Barcelona, Spain, 1953) is the first winner of the BBVA Foundation Frontiers of Knowledge Awards in the Biomedicine category. The Frontiers of Knowledge Awards are intended to recognize and promote research of excellence. The breadth of disciplines addressed and their monetary amount – a combined purse of 3.2 million euros spread over eight prize categories – place them among the world’s foremost award schemes. Massagué is Spain’s most widely cited working scientist, with his papers referred to on more than 62,000 occasions. His studies, with great potential for clinical application, are opening up fundamental new pathways in the fight against cancer. He has conducted pioneering research into the genetic and cellular bases of metastasis and remains an acknowledged leader in this field. His group’s latest findings, published in the May edition of Nature, explain how tumor cells manage to enter the brain and form a new tumor. Until now, scientists were baffled as to how cancer cells were able to breach the blood-brain barrier which normally protects the brain from harmful substances. Massagué has identified three genes that intervene in the process, but the list will go on and work will continue to determine which is most important in each type of cancer.


Protein in the envelope enclosing the cell nucleus - a new piece of the puzzle in research on cancer and stem cells?

A research team led by Professor Einar Hallberg at the Department of Life Sciences at Södertörn University in Sweden has discovered a new protein in the inner membrane of the cell nucleus. This protein may play an important role in cell division and now provides a new piece of the puzzle to study in cancer research. All living organisms are made up of cells. The cell consists of different "compartments" that have different functions. In one of the compartments, the cell nucleus, there is genetic information about how the organism's proteins should look like, and when they should be produced. The cell nucleus is enclosed by a double lipid membrane that is called the nuclear envelope. All transports in and out of the nucleus take place through pores in the nuclear envelope. It is estimated that there are some 100 different proteins in the nuclear envelope, but today scientists do not yet know precisely how they function.


How much chronic depression with medical disorders affect work performance?

A group of Australian researchers investigated in medical disorders the effects of comorbid dysthymic disorder as compared to major depressive disorder (MDD) on health-related quality of life (HR-QoL) and disability days in the general population. In a population-based study 4,181 individuals were assessed for the presence of dysthymic disorder and depression, utilizing the Composite International Diagnostic Interview. Each participant received a thorough medical examination to assess the presence of comorbid somatic conditions. HR-QoL was evaluated using the Medical Outcomes Survey Short-Form 36 (SF-36) and disability days were provided by self-report. Descriptive statistics, analysis of variance and multivariable logistic regression were used. Comorbidity with illnesses from a maximum of 6 somatic disease groups was more prevalent in persons with dysthymic disorder (78.7%) than in those with MDD (70.4%). Persons with dysthymic disorder had a significantly lower mental health summary score in the SF-36 and more disability days than those with MDD. The physical health summary scores were not significantly different between participants with dysthymic disorder and MDD (after Bonferroni correction), suggesting that limitations in physical functioning due to comorbid medical conditions were similar in both affective disorder groups.


Histamine affects alcohol-related behaviour

The histamine-3 receptor is important in terms of alcohol-related behaviour, and a drug affecting that receptor may have qualities that alter alcohol-related behaviour. This appears in the study headed by Pertti Panula entitled “Tuberomamillary nucleus neurons, histamine and H3 receptor in hypothalamic regulation of alcohol addiction” which is part of the Substance Use and Addictions research programme of the Academy of Finland. “Whether these histamine-3 receptor drugs help in the treatment of human alcoholism will probably be clear when the results of the currently ongoing clinical trials become public. The drugs are currently being tested for the treatment of conditions such as observation disorders, sleep disorders and narcolepsy,” says Professor Panula. In addition to the well-known dopamine and serotonin, neurotransmitters that are important to the functioning of the brain also include histamine, which is better known for the regulation of allergies and stomach functioning. The histamine system of the brain is important in the regulation of the sleep-waking rhythm. There is also an extensive histamine system in the human brain.


What the Immune System Reveals about Breast Cancer

Researchers working with Dr Marcus Schmidt in the Department of Obstetrics and Gynecology at the University Medical Center Mainz have unlocked the key to the immune system's significance in cases of breast cancer, thus identifying its long-neglected role in the prognosis of the disease. Their research results, published in the renowned Cancer Research journal, show that patients with certain breast tumors have a better prognosis when more immune cells are present in the tumor. These results permitted the scientists to extend the "coordinate system" in case of breast tumors to include the immune system as the third important reference point for the prognosis of this disease, in addition to the long-established prognostic factors of estrogen receptor expression and proliferative activity (Cancer Research, 1 July 2008; Cancer Research, 1 April 2009).


Farmed fish may pose risk for mad cow disease

University of Louisville neurologist Robert P. Friedland, M.D., questions the safety of eating farmed fish in today’s Journal of Alzheimer’s Disease, adding a new worry to concerns about the nation’s food supply. University of Louisville neurologist Robert P. Friedland, M.D., questions the safety of eating farmed fish in the June issue of the Journal of Alzheimer’s Disease, adding a new worry to concerns about the nation’s food supply. Friedland and his co-authors suggest farmed fish could transmit Creutzfeldt Jakob disease--commonly known as mad cow disease--if they are fed byproducts rendered from cows. The scientists urge government regulators to ban feeding cow meat or bone meal to fish until the safety of this common practice can be confirmed. “We have not proven that it’s possible for fish to transmit the disease to humans. Still, we believe that out of reasonable caution for public health, the practice of feeding rendered cows to fish should be prohibited,” Friedland said. “Fish do very well in the seas without eating cows,” he added.


Disclosing your feelings may help the course of rheumatoid arthritis

The health and physiological effects of an intervention which facilitates the opening of feelings are described in a paper published in the current issue of Psychotherapy and Psychosomatics. The efficacy of emotional disclosure in alleviating psychological and physical stress has been well documented in controlled laboratory studies. A next step is to evaluate its clinical utility in 'real world' settings. A group of Dutch investigators adapted the emotional disclosure intervention for use in home-based settings by stimulating the suggested effective ingredients of cognitive-emotional processing, and evaluated its psychological and clinical effectiveness. Reviews indicated the need to examine the physiological changes brought about by emotional disclosure, which may be particularly relevant in immune-mediated diseases. This study was the first to examine neuroendocrine and immune changes after emotional disclosure in patients with rheumatoid arthritis. Sixty-eight patients were randomly assigned to four weekly oral emotional disclosure or time management sessions.


Roux-en-Y weight loss surgery raises kidney stone risk

The most popular type of gastric bypass surgery appears to nearly double the chance that a patient will develop kidney stones, despite earlier assumptions that it would not, Johns Hopkins doctors report in a new study. The overall risk, however, remains fairly small at about 8 percent. As rates of morbid obesity have climbed in recent years, so has the popularity of various weight-loss operations, with more than 200,000 patients expected to have one of these procedures this year. The most common type of weight loss, or bariatric, surgery, called Roux-en-Y in a nod to the Y-shape of the surgical connections that go around part of the bowel, accomplishes weight loss by decreasing the size of the stomach and allowing food to bypass part of the small intestine. While other bariatric procedures have been shown to decrease calcium absorption and increase the risk of kidney stones, doctors have long assumed that the Roux-en-Y procedure did not. To test the assumption, researchers led by Brian Matlaga, M.D., assistant professor of urology at the Johns Hopkins University School of Medicine and director of stone diseases and ambulatory care at Hopkins' James Buchanan Brady Urological Institute, used an insurance claims database to identify 4,639 patients who had undergone Roux-en-Y surgery between 2002 and 2006. The researchers identified a second set of 4,639 patients who had similar characteristics—including age, gender, and body mass indices that indicate obesity—but not the surgery. Using medical information encoded in the database for both patient populations, the researchers looked to see which patients were either diagnosed with kidney stones or had treatment for this condition. Their results showed that while only 8 percent of the Roux-en-Y patients developed kidney stones, they were nearly twice as likely to get this condition as the patients with similar characteristics who didn't have weight loss surgery. The researchers published these findings in the June Journal of Urology. "Our study is not an indictment of bariatric surgery—the benefits of this surgery are well known," says Matlaga. "Rather, we'd like to help physicians understand that their bariatric patients could be at risk for kidney stones, a condition that could be avoidable with proper preventative care."


Study supports validity of test that indicates widespread unconscious bias

In the decade since the Implicit Association Test was introduced, its most surprising and controversial finding is its indication that about 70 percent of those who took a version of the test that measures racial attitudes have an unconscious, or implicit, preference for white people compared to blacks. This contrasts with figures generally under 20 percent for self report, or survey, measures of race bias. A new study published this week validates those findings, showing that the Implicit Association Test, a psychological tool, has validity in predicting behavior and, in particular, that it has significantly greater validity than self-reports in the socially sensitive topics of race, gender, ethnicity, sexual orientation and age. The research, published in the Journal of Personality and Social Psychology, is an overview and analysis of 122 published and unpublished reports of 184 different research studies. In this analysis, 85 percent of the studies also included self-reporting measures of the type generally used in surveys. This allowed the researchers, headed by University of Washington psychology Professor Anthony Greenwald, to compare the test's success in predicting social behavior and judgment with the success of self-reports.


'Life force' linked to body's ability to withstand stress

Our ability to withstand stress-related, inflammatory diseases may be associated, not just with our race and sex, but with our personality as well, according to a study published in the July issue of the journal Brain, Behavior and Immunity. Especially in aging women, low levels of the personality trait extraversion may signal that blood levels of a key inflammatory molecule have crossed over a threshold linked to a doubling of risk of death within five years. An emerging area of medical science examines the mind-body connection, and how personality and stress contribute to disease in the aging body. Long-term exposure to hormones released by the brains of people under stress, for instance, takes a toll on organs. Like any injury, this brings a reaction from the body's immune system, including the release of immune chemicals that trigger inflammation in an attempt to begin the healing process. The same process goes too far as part of diseases from rheumatoid arthritis to Alzheimer's disease to atherosclerosis, where inflammation contributes to clogged arteries, heart attacks and strokes. The current study found that that extroverts, and in particular those high "dispositional activity" or engagement in life, have dramatically lower levels of the inflammatory chemical interleukin 6 (IL-6). Swiss psychiatrist Carl Jung defined extroverts as focused on the world around them and most happy when active and surrounded by people. Introverts looked inward and were shy. The definitions of extraversion and other personality traits were refined by American psychologist Gordon Allport beginning in the 1930s. He reviewed all adjectives in the dictionary used to describe personality, and attempted to group them into clusters. Over the next several decades, researchers statistically analyzed these dictionary terms and discovered that they tended to cluster into five general dimensions: extraversion vs. introversion, emotional stability vs. neuroticism, openness vs. closed-minded, agreeable vs. hostile, and conscientiousness vs. unreliability. These dimensions, known as the "Five Factor Model" of personality, served to organize hundreds of specific traits like "activity" for psychologists, similar to the way the Periodic Table organizes elements for physicists.


Wrong type of help from parents could worsen child's OCD

For most parents, soothing a child's anxiety is just part of the job. But for a parent whose child has obsessive-compulsive disorder, soothing anxiety and helping with behaviors linked to the disease could lead to more severe symptoms, University of Florida researchers say. Often, parents of children with OCD will help their children complete rituals related to their obsessions and compulsions, such as excessive bathing or checking things like door locks, according to findings recently published in the Journal of Consulting and Clinical Psychology. These accommodations can be anything that makes the symptoms of OCD less impairing, from reassuring a child that his hands are clean and his baby brother is OK to even doing his homework for him or buying objects that make the child feel safe. "Parents do that because that is what a parent whose child doesn't have OCD would do," said Lisa Merlo, Ph.D., a UF assistant professor of psychiatry and the lead author of the study. "If your child is upset, you try to comfort them. But what we know is, for patients with OCD, if they get an accommodation, that reinforces the OCD to them.


Structures from the human immune system's oldest branch shed light on a range of diseases

How molecules of the oldest branch of the human immune system have interconnected has remained a mystery. Now, two new structures, both involving a central component of an enzyme important to the complement system of the immune response, reveal how this system fights invading microbes while avoiding problems of the body attacking itself. The structures may pave the way to more efficient therapeutics for such complement-mediated diseases as age-related macular degeneration, rheumatoid arthritis, or systemic lupus erythematosus, as well as give insight into the pathogenesis of other immune and inflammatory diseases. The complement system, an evolutionarily old arm of the immune system, comprises a network of proteins that "complement" the work of antibodies in destroying foreign invaders. They serve as a rapid defense mechanism in most species, from primitive sponges to humans. When complement proteins are triggered into action by a microbe, the proteins ultimately form a complex enzyme called C3 convertase, initiating a cascade of immune and inflammatory reactions. In order to avoid self-attack, regulatory proteins such as factor H bind with C3b, a central component of C3, to help the immune system recognize the body's own tissue and keep complement in check. Researchers at the University of Pennsylvania School of Medicine, in collaboration with colleagues at Utrecht University in the Netherlands, have determined the structure of C3 convertase and of the C3b fragment in complex with factor H. The work appears this month in two companion papers in Nature Immunology.


Jumping Genes Discovery “Challenges Current Assumptions,” Say Penn Researchers

Jumping genes do most of their jumping, not during the development of sperm and egg cells, but during the development of the embryo itself. The research, published this month in Genes and Development, “challenges standard assumptions on the timing of when mobile DNA, so-called jumping genes, insert into the human genome,” says senior author Haig H. Kazazian Jr., MD, Seymour Gray Professor of Molecular Medicine in Genetics at the University of Pennsylvania School of Medicine.


Europeans target better pesticide protection

With the annual spread of some 80 000 tonnes of pesticides, farmers are bound to get hit. However, the context for pesticide spraying has changed considerably over the years, and Europe has outlined new requirements related to the safety of operators, the general public, and the environment.In 2005 alone, a total of 800 000 French farmers were exposed to pesticides. French public research institute Cemagref's Technologies for Farm-Equipment Safety and Performance Research unit is working to gain knowledge on the exposure of operators to phytosanitary products. The latest project is building on a 2006 experimental study that centred on apple tree orchards needing some 30 phytosanitary treatments every year. The main objectives of the study were to obtain data on the phytosanitary exposure and contamination of operators, and to enhance the performance of protection cabs used during the spraying process. For this study, Sonia Grimbuhler, the project manager, and her team evaluated 250 apple farmers on their use of pesticides, and assessed their perception of the risks involved. According to a number of typologies already identified, Ms Grimbuhler established scenarios by considering the most common practices and those resulting in the highest number of contaminations. The researchers were innovative in their approach in that they took measurements that were as physically close as possible to the operator's actual exposure to products: through contact and inhalation.


SSRIs Prescribed for Autistic Children Make Them Worse

Despite the fact the U.S. Food and Drug Administration (FDA) has not approved any prescription medications to treat the symptoms of autism and related disorders, drugs are frequently -- and increasingly -- being given to autistic children, according to a study in the June issue of Archives of General Psychiatry. An especially popular medication for autistic kids is the antidepressant citalopram, sold under the brand name Celexa, a selective serotonin reuptake inhibitor (SSRI), which interferes with the way the brain regulates the neurotransmitter serotonin.


Powerful Nutrient Cocktail Can Put Kids with Crohn's into Remission

Treating children with inflammatory bowel disease (IBD) usually involves the same steroids-based medication prescribed to adults. But such treatments can have negative side effects for kids and teens dealing with IBD. Dr. Raanan Shamir of Tel Aviv University's Sackler School of Medicine and Schneider Children's Medical Centre shows that there is another path to treating IBD in children: a nutritional formula that was first developed for astronauts. This supplement puts 60-70% of children with Crohn's disease, a common IBD disorder, into remission — a success rate similar to that of traditional steroid-based drugs, but without side effects like malnutrition and growth retardation.


Study finds reproductive health effects from low doses of bisphenol-A

New research from North Carolina State University and the National Institute of Environmental Health Sciences (NIEHS) shows significant reproductive health effects in rats that have been exposed to bisphenol-A (BPA) at levels equivalent to or below the dose that has been thought not to produce any adverse effects. BPA is a chemical found in baby bottles, water bottles, canned foods and an array of other consumer products. The potential health effects of BPA are currently the subjects of intense debate. The study found that female rats exposed to a BPA dose of 50 micrograms per kilogram of body weight (µg /kg) in their first four days of life experienced early onset of puberty. Female rats exposed to 50 milligrams per kilogram of body weight (mg/kg) during their first four days of life developed significant ovarian malformations and premature loss of their estrus cycle. "The 50 mg/kg level is important," says lead researcher Dr. Heather Patisaul, "because it is equivalent to the U.S. Environmental Protection Agency's 'Lowest Observable Adverse Effect Level' for BPA. So, by definition, we should not have seen significant effects at or below this level, but we did." Patisaul, an assistant professor of biology at NC State, explains that the 50 µg /kg level is also significant because it is EPA's listed reference dose for BPA – meaning it is the level of BPA that EPA says a person can be exposed to on a daily basis without expecting any adverse effects after a lifetime of exposure. Patisaul stresses that the research was done on rats, making it difficult to determine its applicability to humans, but notes that "this adds to a growing body of evidence that exposure to low doses of BPA during development can impact female reproductive health." The female rats in the study were exposed during the first four days of life because that is a sensitive developmental window for the rats, similar to a sensitive developmental stage that takes place for humans when they are still in the womb. While exposure to the lowest dose, 50 µg /kg, resulted in early onset of puberty in the rats, exposure to higher dose had more complicated results.


Brain detects happiness more quickly than sadness

People make value judgements about others based on their facial expressions. A new study, carried out be Spanish and Brazilian researchers, shows that – after looking at a face for only 100 milliseconds – we can detect expressions of happiness and surprise faster than those of sadness or fear. Our brains get a first impression of people's overriding social signals after seeing their faces for only 100 milliseconds (0.1 seconds). Whether this impression is correct, however, is another question. Now an international group of experts has carried out an in-depth study into how we process emotional expressions, looking at the pattern of cerebral asymmetry in the perception of positive and negative facial signals. The researchers worked with 80 psychology students (65 women and 15 men) to analyze the differences between their cerebral hemispheres using the "divided visual field" technique, which is based on the anatomical properties of the visual system. "What is new about this study is that working in this way ensures that the information is focused on one cerebral hemisphere or the other", J. Antonio Aznar-Casanova, one of the authors of the study and a researcher at the University of Barcelona (UB), tells SINC.


Researchers make progress toward early identification of muscular dystrophy

The saying "Knowing is half the battle" is never more true than when discussing early treatment of disease. Muscular dystrophy is one such disease where patients can benefit from early treatment. Now, new research is moving doctors and scientists closer to disease diagnosis in advance of patient symptoms. A team of University of Birmingham researchers used mice as model animals to study the key proteins involved in two types of muscular dystrophy (MD): the most severe MD form, Duchenne Muscular Dystrophy (DMD), and a more mild form, Limb Girdle MD (LGMD-1c). As described in their new report published in Disease Models & Mechanisms (DMM), dmm.biologists.org, the researchers found disrupted stem cell function and delays of skeletal muscle formation in embryos of MD-like mice. .The severity of these embryonic abnormalities closely corresponded to the severity of symptoms seen in DMD or Limb Girdle MD. This study demonstrates that there are prenatal signs for muscular dystrophy, and suggests that both types of MD might be detected in utero or shortly after birth. This work has the potential to create a better quality of life for DMD children. It is now clear that early treatment significantly improves life expectancy and quality of life for DMD children. However, diagnosis is often delayed until the disease is well under way, around ages 3-5 years, and treatment thus often begins between ages 4-8 years, when the disease is already established. This new research indicates that understanding these MD-associated proteins can lead to earlier diagnoses and treatment for DMD/LGMD patients. This in turn leads to longer life and enhanced quality of life for individuals affected by these diseases.


Statins don't lower risk of pneumonia in elderly

Taking popular cholesterol-lowering statin drugs, such as Lipitor® (atorvastatin), does not lower the risk of pneumonia. That's the new finding from a study of more than 3,000 Group Health patients published online on June 16 in advance of the British Medical Journal's June 20 print issue. "Prior research based on automated claims data had raised some hope—and maybe some hype—for statins as a way to prevent and treat infections including pneumonia," said Sascha Dublin, MD, PhD, a physician at Group Health and assistant investigator at Group Health Center for Health Studies. "But when we used medical records to get more detailed information about patients, our findings didn't support that approach." In fact, Dublin's population-based case-control study found that pneumonia risk was, if anything, slightly higher (26%) in people using a statin than in those not using any; and this extra risk was even higher (61%) for pneumonia severe enough to require being hospitalized. "As a doctor, I'm a fan of statins for what they've been proven to do: lowering cholesterol and risk of heart disease and stroke in people who've had either disease or are at risk for them," said Dublin. Statins are HMG coenzyme A reductase inhibitors, which also include Zocor® (simvastatin) and Mevacor® (lovastatin). This class of medications lessens inflammation, which plays a role in infections. "But now we and some others have found that statins may have gotten some unearned credit for health benefits that they don't actually have, including preventing pneumonia," Dublin said.Suggestions from prior research had led to calls for expensive randomized controlled trials of statins to prevent or treat infection. "But our study indicates that such trials would be an ill-advised use of limited research funds at this time," she added.


Putting a name to a face may be key to brain's facial expertise

Our tendency to see people and faces as individuals may explain why we are such experts at recognizing them, new research indicates. This approach can be learned and applied to other objects as well."This new research adds to the evidence that the brain processes faces differently because of our expertise with them. It also tells us what it is about our experience with faces that leads us to treat them holistically," Isabel Gauthier, associate professor of psychology at Vanderbilt University and one of the study's co-authors, said. "This knowledge may be useful in the development of training protocols for individuals with difficulties in face perception, such as individuals with autism spectrum disorders." The research is currently in press at Psychological Science. Gauthier's co-authors are Alan Wong, who completed the study as his doctoral thesis in psychology at Vanderbilt, and Thomas Palmeri, associate professor of psychology. Wong is now an assistant professor at Chinese University of Hong Kong. "Our findings suggest that facial expertise does not just develop with any type of experience," Wong said. "Learning to recognize a set of objects as individuals may work, but categorizing them at a more general level, or learning to manipulate them, would not. We develop different types of expertise in recognizing different objects not just due to their unique appearance, but also because of the types of experience we have had with them."For decades, scientists have debated whether we are better able to recognize faces because we have evolved a brain system dedicated to this task or because we have extensive practice recognizing faces. Researchers agree that we recognize faces holistically, which is not how we generally recognize other objects. For example, we find it almost impossible to attend to only one part of a face and ignore the rest, while we might recognize a car by its grill, taillights or branding.


Another McGill/JGH breakthrough opens door to early Alzheimer's diagnosis

A new diagnostic technique which may greatly simplify the detection of Alzheimer's disease has been discovered by researchers at McGill University and the affiliated Lady Davis Institute for Medical Research at Montreal's Jewish General Hospital (JGH). Their results were published June 8 in the Journal of Alzheimer's Disease. There is currently no accepted blood test for Alzheimer's, and the diagnosis is usually based on expensive and labour-intensive neurological, neuropsychological and neuroimaging evaluations. Dr. Hyman Schipper and colleagues at the Lady Davis Institute and McGill University utilized a new minimally-invasive technique called near-infrared (NIR) biospectroscopy to identify changes in the blood plasma of Alzheimer's patients, changes which can be detected very early after onset, and possibly in pre-clinical stages of the disease. Biospectroscopy is the medical form of spectroscopy, the science of detecting the composition of substances using light or other forms of energy. In NIR spectroscopy, different substances emit or reflect light at specific, detectable wavelengths.


Novel light-sensitive compounds show promise for cancer therapy

Chemists at the University of California, Santa Cruz, have developed novel compounds that show promise for photodynamic cancer therapy, which uses light-activated drugs to kill tumor cells. The new compounds, called dye-sensitized ruthenium nitrosyls, are absorbed by cancer cells and respond to specific wavelengths of light by releasing nitric oxide, which triggers cell death. "For cancer treatment, you want localized delivery of a very high concentration of nitric oxide. We've designed these molecules to do just that," said Pradip Mascharak, professor of chemistry and biochemistry at UCSC. Nitric oxide is a simple molecule with a wide range of biological effects. Long known for its role in regulating blood pressure, it has attracted the attention of cancer researchers in recent years. According to Mascharak, one advantage of nitric oxide for cancer treatment is that it induces an orderly type of cell death known as apoptosis. Also known as "programmed cell death," apoptosis does not lead to the inflammation, pain, and swelling normally associated with damage to cells and tissues in the body. The drugs currently used in photodynamic therapy, called photosensitizers, produce a highly reactive form of oxygen when activated by light. The reactive oxygen kills cells in a way that tends to cause local swelling and inflammation. Mascharak and graduate student Michael Rose have synthesized several different ruthenium nitrosyls in their lab. They described these compounds in detail in a recent paper published in Inorganic Chemistry (published online May 29, 2009). In another paper published last year in the Journal of the American Chemical Society, the researchers reported that the compounds were effective against breast cancer cells in laboratory experiments. "We know it works in cancer cells, so now we're very confident about taking it to the next level," Mascharak said. "The idea for cancer therapy would be to embed the compounds in a matrix that you can place in the treatment site, then shine light on it to produce a high concentration of nitric oxide."


Trans fats hinder multiple steps in blood flow regulation pathways

Partially hydrogenated vegetable oils in processed foods contain trans fatty acids that interfere with the regulation of blood flow. A new report reveals a new way in which these "trans fats" gum up the cellular machinery that keeps blood moving through arteries and veins. In the August 2009 issue of the international journal Atherosclerosis, University of Illinois emeritus veterinary biosciences professor Fred Kummerow reports for the first time that trans fats interfere with more than one key enzyme in the regulation of blood flow. Kummerow begins by describing the two main causes of heart disease – sudden blood clots in the coronary arteries, and atherosclerosis, the buildup of plaque in the arteries to the point where it interferes with blood flow. "The arteries of someone who dies from atherosclerosis look like old scrub boards as a result of the formation of plaques," Kummerow said. "They look corrugated, and this plaque buildup continues to the point where it will stop blood flow." Trans fats contribute to both of these causes of heart disease, Kummerow said. Trans fats are made through hydrogenation, which involves bubbling hydrogen through hot vegetable oil, changing the arrangement of double bonds in the essential fatty acids in the oil and "saturating" the "unsaturated" carbon chain with hydrogen. Because double bonds are rigid, altering them can straighten or twist fat molecules into new configurations that give the fats their special qualities, such as the lower melting point of margarine that makes it creamy at room temperature. Kummerow, 94, has spent nearly six decades studying lipid biochemistry, and is a long-time advocate for a ban on trans fats in food.


UCF researcher's nanoparticles could someday lead to end of chemotherapy

Nanoparticles specially engineered by University of Central Florida Assistant Professor J. Manuel Perez and his colleagues could someday target and destroy tumors, sparing patients from toxic, whole-body chemotherapies. Perez and his team used a drug called Taxol for their cell culture studies, recently published in the journal Small, because it is one of the most widely used chemotherapeutic drugs. Taxol normally causes many negative side effects because it travels throughout the body and damages healthy tissue as well as cancer cells. The Taxol-carrying nanoparticles engineered in Perez's laboratory are modified so they carry the drug only to the cancer cells, allowing targeted cancer treatment without harming healthy cells. This is achieved by attaching a vitamin (folic acid) derivative that cancer cells like to consume in high amounts. Because the nanoparticles also carry a fluorescent dye and an iron oxide magnetic core, their locations within the cells and the body can be seen by optical imaging and magnetic resonance imaging (MRI). That allows a physician to see how the tumor is responding to the treatment. The nanoparticles also can be engineered without the drug and used as imaging (contrast) agents for cancer. If there is no cancer, the biodegradable nanoparticles will not bind to the tissue and will be eliminated by the liver. The iron oxide core will be utilized as regular iron in the body.


Study finds autistics better at problem-solving

Autistics are up to 40 percent faster at problem-solving than non-autistics, according to a new Université de Montréal and Harvard University study published in the journal Human Brain Mapping. As part of the investigation, participants were asked to complete patterns in the Raven's Standard Progressive Matrices (RSPM) – test that measures hypothesis-testing, problem-solving and learning skills. "While both groups performed RSPM test with equal accuracy, the autistic group responded more quickly and appeared to use perceptual regions of the brain to accelerate problem-solving," says lead author Isabelle Soulières, a post-doctoral fellow at Harvard University who completed the experiment at the Université de Montréal. "Some critics agued that autistics would be unable to complete the RSPM because of its complexity, yet our study shows autistics complete it as efficiently and have a more highly developed perception than non-autistics." Fifteen autistics and 18 non-autistics were recruited for the study. Participants were 14 to 36 years old and matched according to their preliminary results on the Wechsler Adult Intelligence Scale. All subjects underwent magnetic resonance imaging to explore their neural activity during RSPM problem-solving. While autism is a common neurodevelopmental disability characterized by profound differences in information processing and analysis, this study showed that autistics have efficient reasoning abilities that build on their perceptual strengths. "This study builds on our previous findings and should help educators capitalize on the intellectual abilities of autistics," says senior researcher Laurent Mottron, the new Marcel & Rolande Gosselin Research Chair in Autism Cognitive Neuroscience of the Université de Montréal and psychiatry professor. "The limits of autistics should constantly be pushed and their educational materials should never be simplified."


Research proves tai chi benefits for arthritis

A new study by The George Institute for International Health has found Tai Chi to have positive health benefits for musculoskeletal pain. The results of the first comprehensive analysis of Tai Chi suggest that it produces positive effects for improving pain and disability among arthritis sufferers. The researchers are now embarking on a new trial to establish if similar benefits can be seen among people with chronic low back pain. "This is the first robust evidence to support the beneficial effects of Tai Chi. Our study proves that Tai Chi relieves pain and disability among people with arthritis and shows a positive trend towards effects for overall physical health. We now want to see if these benefits are the same for people suffering from low back pain", said author Dr Chris Maher at The George Institute. Musculoskeletal pain, such as that experienced by people with arthritis, places a severe burden on the patient and community and is recognised as an international health priority. Arthritis is the major cause of disability and chronic pain in Australia, with 3.85million Australians affected. Low back pain is the most prevalent and costly musculoskeletal condition in Australia, estimated to cost up to $1billion per annum with indirect costs exceeding $8billion.


Antitrust: Commission statement on Microsoft Internet Explorer announcement

The European Commission notes with interest Microsoft's announcement of its plans for Windows 7, and in particular of the apparent separation of Internet Explorer (IE) from Windows in the EEA. The Commission will shortly decide in the pending browser tying antitrust case whether or not Microsoft’s conduct from 1996 to date has been abusive and, if so, what remedy would be necessary to create genuine consumer choice and address the anticompetitive effects of Microsoft’s long-standing conduct. In terms of potential remedies if the Commission were to find that Microsoft had committed an abuse, the Commission has suggested that consumers should be offered a choice of browser, not that Windows should be supplied without a browser at all.

At the level of both computer manufacturers and retail sales, the Commission's Statement of Objections (SO) suggested that consumers should be provided with a genuine choice of browsers. Given that over 95% of consumers acquire Windows pre-installed on a PC, it is particularly important to ensure consumer choice through the computer manufacturer channel.

As for retail sales, which amount to less than 5% of total sales, the Commission had suggested to Microsoft that consumers be provided with a choice of web browsers. Instead Microsoft has apparently decided to supply retail consumers with a version of Windows without a web browser at all. Rather than more choice, Microsoft seems to have chosen to provide less.

As for sales to computer manufacturers, Microsoft's proposal may potentially be more positive. It is noted that computer manufacturers would appear to be able to choose to install Internet Explorer – which Microsoft will supply free of charge - another browser or multiple browsers. Were the Commission to conclude that Microsoft’s behaviour has been abusive, it would have to consider whether this proposal would in itself be sufficient to create genuine consumer choice on the web browser market. The Commission would inter alia take into account the long standing nature of Microsoft's conduct. It would also have to consider whether this initial step of technical separation of IE from Windows could be negated by other actions by Microsoft.

Consumer Choice and Innovation

The development of new online services makes web browsers an increasingly important tool for businesses and consumers, and a lack of real consumer choice on this market would undermine innovation.

The Commission’s preliminary concerns are set out in detail in a Statement of Objections sent to Microsoft in January. The specific circumstances of Microsoft’s tying of IE to Windows in this case would appear to lead to significant consumer harm.

The SO sets out the preliminary view that, should the Commission conclude that Microsoft’s conduct was abusive, any remedy would need to restore a level-playing field and enable genuine consumer choice between Internet Explorer and third-party web browsers, in order to bring the infringement effectively to an end. A potential remedy to these concerns, which the Commission considered in the SO and which would not require Microsoft to provide Windows to end-users without a browser, would be to allow consumers to choose from different web browsers presented to them through a 'ballot screen' in Windows.

Background

The Commission sent a Statement of Objections (SO) to Microsoft on 15 January 2009 (see MEMO/09/15 ).

A Statement of Objections is a formal step in Commission antitrust investigations in which the Commission informs the parties concerned in writing of the objections raised against them. The addressee of a Statement of Objections can reply in writing to the Statement of Objections, setting out all facts known to it which are relevant to its defence against the objections raised by the Commission.

Microsoft replied to the SO on 28 April 2009. The Commission is currently considering Microsoft’s reply, and additional evidence in the case, and has not yet reached any conclusion.

The Commission's assessment would be guided in particular by the principles laid down by the Court of First Instance in its judgment of September 2007 in the Microsoft case regarding the tying of Windows Media Player (see MEMO/07/359 ) and the Commission's experience with the remedy in that case, while taking account of the specific circumstances of the present case.


Aussie and Kiwi researchers make double MS genetic discovery

Australian and New Zealand researchers have accelerated research into Multiple Sclerosis by discovering two new locations of genes which will help to unravel the causes of MS and other autoimmune disease. Their findings will be published today in the prestigious journal Nature Genetics. "For decades the cause of MS has remained a mystery. This discovery reveals important new insights into the genetic susceptibility to the disease, "says Professor Trevor Kilpatrick, Director for Neurosciences at the University of Melbourne, who with Dr Justin Rubio of Florey Neurosciences Institutes coordinated the international study. "The newly discovered gene locations in chromosomes 12 and 20, offer very promising targets which indicate susceptibility to MS," says Professor Kilpatrick. "They also reveal a link between genetic susceptibility to MS and other autoimmune diseases including Type 1 diabetes, Rheumatoid Arthritis and Graves' Disease and the also the potential involvement of Vitamin D metabolism in the risk of developing these diseases." "These results are like the key in the door – leading us to where to look for MS susceptibility," explains Professor Trevor Kilpatrick. The research was conducted by members of the ANZgene consortium, more than 40 investigators from 11 institutions in Australia and New Zealand. The three year study utilized the MS Research Australia (MSRA) Gene Bank and involved scanning the DNA of 1,618 people with MS and 3,413 people without MS (controls). Using a genome-wide association scan (GWAS), researchers scanned the entire human genome in broad brushstrokes; looking at genetic landmarks in the genome and then progressively narrowing down their search to individual genes. Dr Justin Rubio who coordinated the GWAS says these genetic discoveries are a major advance for the field.


NYU Langone Medical Center researchers identify key gene in deadly inflammatory breast cancer

Aggressive, deadly and often misdiagnosed, inflammatory breast cancer (IBC) is the most lethal form of primary breast cancer, often striking women in their prime and causing death within 18 to 24 months. Now, scientists from The Cancer Institute at NYU Langone Medical Center have identified a key gene—eIF4G1—that is overexpressed in the majority of cases of IBC, allowing cells to form highly mobile clusters that are responsible for the rapid metastasis that makes IBC such an effective killer. The new findings, Essential Role for eIF4G1 Overexpression in Inflammatory Breast Cancer Pathogenesis, scheduled for advance online publication on Nature Cell Biology's website (Embargoed for June 14th, 2009 at 1:00PM EST) could lead to the identification of new approaches, therapies and a new class of drugs to target and treat IBC. This would be a critical development in the fight against IBC, which respond poorly to chemotherapy, radiation or any other current treatments for breast cancer, according to the study's lead authors Dr. Robert Schneider, associate director for translational research at The Cancer Institute, co-director of breast cancer research, and the Albert B. Sabin Professor of Molecular Pathogenesis at NYU School of Medicine, and Dr. Deborah Silvera, a postdoctoral research fellow. "The tragedy of IBC is that it is often misdiagnosed and misclassified. Rather than presenting as a 'typical' lump, IBC looks like an inflammation of the breast and is frequently mistaken for an infection. Physicians often prescribe antibiotics, losing valuable time for treating this fast-moving killer," says Dr. Schneider, noting that IBC accounts for several percent of all breast cancer cases but takes a high toll on mortality, with an incidence that is 50 percent higher in African American women. He adds that there has been little progress in treating IBC over the past two decades, and there are no drugs specifically for this form of cancer. "In fact, IBC has only recently been recognized as a unique, genetically distinct form of breast cancer."


Huntington's disease deciphered

Researchers at the University of Illinois at Chicago College of Medicine have discovered how the mutated huntingtin gene acts on the nervous system to create the devastation of Huntington's disease. The report of their findings is available in Nature Neuroscience online. The researchers were able to show that the mutated huntingtin gene activates a particular enzyme, called JNK3, which is expressed only in neurons and, further, to show what effect activation of that enzyme has on neuron function. Huntington's disease is an adult onset neurodegenerative disease marked by progressive mental and physical deterioration. It has been known for more than a decade that everyone who develops the disease has mutations in a particular gene, called huntingtin, according to Scott Brady, professor and head of anatomy and cell biology at the UIC College of Medicine. "There are several puzzling aspects of this disease," said Brady, who is co-principal investigator on the study. "First, the mutation is there from day one. How is it that people are born with a perfectly functioning nervous system, despite the mutation, but as they grow up into their 30s and 40s they start to develop these debilitating symptoms? We need to understand why the protein is bad at 40 but it wasn't bad at 4." The second problem, according to Brady, is that the gene is expressed not just in the nervous system but in other parts of the body. However, the only part of the body that is affected is the nervous system. Why are neurons being affected? Brady, Gerardo Morfini, assistant professor of anatomy and cell biology at UIC and co-principal investigator of the study, and their colleagues began looking for a mechanism that could explain all the pieces of the puzzle. They found that at extremely low concentrations, huntingtin was a potent inhibitor of axonal transport, the system within the neuron that shuttles proteins from the cell body where they are synthesized to the synaptic terminals where they are needed. A neuron's critical role in making connections may require it to make the cellular trunk, called an axon, between the cell body and the synaptic terminal to be very long. Some cells have axons that reach half the body's length -- for a tall person, a meter or more. But even in the brain, axonal projections are very long compared to other cells. In addition to the challenge of distance, neurons are very complex cells with many specialized areas necessary to carry out synaptic connections, requiring a robust transport system. "Inhibition of neuronal transport is enough to explain what is happening in Huntington's," said Brady. Loss of delivery of materials to the terminals results in loss of transmission of signals from the neuron. Loss of signal transmission causes the neurons to begin to die back, leading to reduced transmissions, more dying back and eventual neuronal cell death. This mechanism also explains the late onset of the disease, Brady said. Activation of JNK3 reduces transport but does not eliminate it. Young neurons have a robust transport system, but transport gradually declines with age.


Tracking levels of key biomarkers reflects disease activity and progression of rheumatoid arthritis

New research has identified biomarkers associated with inflammation and progression in joint erosion in individuals with early rheumatoid arthritis (RA), according to the results of a new study presented today at EULAR 2009, the Annual Congress of the European League Against Rheumatism in Copenhagen, Denmark. The researchers suggest a potential role for these biomarkers in the monitoring of ongoing disease activity through assessing inflammation and joint destruction, two important targets for the treatment of early RA.Over the 12-month study period, levels of the serological biomarkers sYKL-40 and sMMP3 were consistently associated with three measures of disease activity: MRI (RAMRIS (RA MRI score) synovitis score and RAMRIS bone marrow oedema score) and clinical scores (DAS28*) of inflammation (p<0.05), when the analyses were corrected for age, gender, c-reactive protein (CRP, a marker for inflammation) levels and treatment type. The bone marker sCTX1 and the cartilage marker uCTXII were also shown to be predictors of erosive progression (RAMRIS erosion score; beta 2.42 (95%CI 0.48-4.36)). Dr Silje Syversen of Diakonhjemmet Hospital, Norway, who led the study, said: "Disease monitoring in RA can be problematic and patients 'at-risk' of future irreversible joint destruction can go undetected. Current predictors of joint destruction such as radiographic abnormalities are signs of later-stage disease development. Biomarkers could offer a novel, more sensitive, rapid and reliable approach to disease monitoring and prediction, and importantly could be useful predictors of bone and cartilage damage before such abnormalities have occurred." In the study, 84 patients with early RA (disease duration <1 year, mean age 58.4 years, 73.9% females, 55% anti-cyclic citrullinated peptide antibodies (ACPA) positive) were assessed at baseline, 3, 6 and 12 months including clinical examination, conventional radiographs (CR) of the hands and MRI scans of the dominant wrist. RAMRIS score (erosions range 0-150, synovitis range 0-9 and bone marrow oedema range 0-45) was used to evaluate MRI images and the van der Heijde modified Sharp score (vdHSS) was used for for the CRs.


Increased levels of certain cytokines and chemokines predict onset of rheumatoid arthritis

Up-regulation of certain cytokines and chemokines (signaling molecules involved in the functioning of the immune system) can predict the development of rheumatoid arthritis (RA) three years before the onset of symptoms, according to the results of a new study presented today at EULAR 2009, the Annual Congress of the European League Against Rheumatism in Copenhagen, Denmark. The results of the study showed that up-regulation of certain cytokines (specifically Th1, Th2 and Treg) involved in the growth and proliferation of various cells integral to the immune system, predicted which individuals go on to develop RA. Interestingly, post-disease onset, chemokines, stromal cell and angiogenic-related markers were important in differentiating up-regulation in those who had developed RA compared to findings in the same individual before symptoms of RA. Cytokines and chemokines are small signalling molecules which are integral to the immune system, as they mediate and regulate immunity, inflammation, and the development of blood cells (haematopoiesis). In this study, several of these molecules, as well as some cytokine receptors, showed significantly increased levels before disease onset compared with controls (median 3.3 years before symptoms), indicating general immune activation (p<0.05-0.001)* and therefore a progression of disease activity. The levels were seen to be particularly elevated in individuals identified as being ACPA- (anti-citrullinated peptide antibody) and RF- (rheumatoid factor) positive (both known risk factors for RA), and most of the concentrations increased further after disease onset. Notably, the concentration of interleukin 17 (IL-17, a cytokine which acts as a regulator of multiple immune functions) was found to be significantly higher before onset compared with post-diagnosis (p>0.01). Prof Solbritt Rantapää Dahlqvist, of the University Hospital Umeå, Sweden, who led the study said: "Our findings add another important piece to the complex puzzle of pathophysiological processes responsible for the occurrence of RA. Understanding more about what happens in the body, to precipitate the onset of RA, could potentially contribute to the development of new strategies for the treatment and even prevention of this debilitating disease."


Females are usually at higher risk than males in a maternal history of non-GCs

Gastric cancer (GC) is a major clinical challenge because of its frequency, and poor prognosis. The etiology of GC is still uncertain, but its familial aggregation in a variable but significant proportion of cases suggests the importance of genetic predisposition. Previous studies on family history of GC, the association of familial risk of GC with the age of onset GC, with family member genders, or with family history of non-GCs, usually yielded contrasting results. Although GC is prevalence in China, scanty information about its family history is available. A research article to be published on June 7,2009 in the World Journal of Gastroenterology addresses this question. The research team led by Professor Yu-Long He from The First Affiliated Hospital, Sun Yat-Sen University, investigated 2260 GC population in Guangdong, China and found 256 with oncological family history. Among the 256 families, 112 were the families with history for gastric and 144 were the families with history for non-gastric cancer. The category and overall ranking of associated tumors in the families, gender of the affected members and their relationship to the probands were analyzed. Through comparison of the features between the 2 kinds of families, this study is believed that the overall ranking of associated non-GCs in the family history of GC may depends on geographical variation; familial predisposition to GC may be related to compound genetic and/or local environmental factors; and a certain subtype of GC may be inherited in a female-influenced fashion. These results represent important data about familial predisposition to GC in a part of the world with a high prevalence, and will add to the available body of knowledge about GC hereditary and aid in future research into this important disease. The results, especially females are usually at higher risk than males when reporting a maternal history of non-GCs, also help to guide genetic counseling for the relatives of GC patients.


Individuals who apply pesticides are found to have double the risk of blood disorder

A study involving 678 individuals who apply pesticides, culled from a U.S. Agricultural Health Study of over 50,000 farmers, recently found that exposure to certain pesticides doubles one's risk of developing an abnormal blood condition called MGUS (monoclonal gammopathy of undetermined significance) compared with individuals in the general population. The disorder, characterized by an abnormal level of a plasma protein, requires lifelong monitoring as it is a pre-cancerous condition that can lead to multiple myeloma, a painful cancer of the plasma cells in the bone marrow. The study will appear in the June 18 issue of Blood, the official journal of the American Society of Hematology. "Previously, inconclusive evidence has linked agricultural work to an increased multiple myeloma risk. Our study is the first to show an association between pesticide exposure and an excess prevalence of MGUS," said lead author Ola Landgren, MD, PhD, of the National Cancer Institute (NCI), which is part of the National Institutes of Health, U.S. Department of Health and Human Services. "This finding is particularly important given that we recently found in a large prospective cancer screening study that virtually all multiple myeloma patients experienced a MGUS state prior to developing myeloma." "As several million Americans use pesticides, it's important that the risks of developing MGUS from the use of pesticides is known," added senior study author and NCI investigator Michael Alavanja, DrPH. The blood of study participants, who were individuals licensed to apply restricted-use pesticides, was assessed for MGUS prevalence. The median age of participants was 60 years (range 30-94 years), and all lived in either Iowa or North Carolina. Participants also completed questionnaires providing comprehensive occupational exposure information for a wide range of pesticides, including information such as the average number of days of pesticide use per year, years of use, use of protective gear while applying pesticides, and pesticide application methods. Information on smoking and alcohol use, cancer histories of the participants' first-degree relatives, and other basic demographic and health data were also obtained. Individuals with prior histories of lymphoproliferative malignancies (such as multiple myeloma or lymphoma) were excluded. Cancer incidence and mortality were monitored annually, and, after five years, follow-up interviews were conducted to update the information about participants' occupational exposures, medical histories, and lifestyle factors.


Blocking a muscle growth-limiting hormone protects against obesity and atherosclerosis

Knockout of myostatin, a growth factor that limits muscle growth, can decrease body fat and promote resistance against developing atherosclerosis, or "hardening" of the arteries, according to a new study conducted in mice. The results will be presented Thursday at The Endocrine Society's 91st Annual Meeting in Washington, D.C. "Obesity increases the risk of atherosclerosis, which accounts for 75% of all cardiovascular events, such as heart attacks and strokes," said study co-author Shalender Bhasin, MD, professor of medicine at Boston University School of Medicine and chief of the Section of Endocrinology, Diabetes, and Nutrition at Boston Medical Center. "Current strategies aimed at preventing heart disease consist primarily of lowering cholesterol levels, but patients reaching the desired cholesterol levels are still at risk for atherosclerosis if they have other risk factors, such as obesity." Humans and animals with a mutation in the myostatin gene are extremely muscular and have little fat, past research shows. Also, when the gene encoding myostatin is knocked out in mice, their muscle mass increases. Bhasin and his co-workers wanted to find out if inhibiting myostatin in mice could resist the development of diet-induced obesity and of atherosclerosis, the buildup of lipid deposits called plaque that can narrow and clog coronary arteries. The researchers took mice that were genetically altered to develop atherosclerosis and then cross-bred them with myostatin knockout mice. Ten generations later, they had mice who were genetically predisposed to both atherosclerosis and inactivation of myostatin. For controls, they studied mice with a genetic predisposition for atherosclerosis but with intact myostatin gene. All mice received a high-fat diet for 12 weeks, to spur the development of atherosclerosis.


A natural hormone may protect muscle from atrophy

Researchers have found a potential new treatment for the common problem of muscle atrophy. Results of the animal study were presented at The Endocrine Society's 91st Annual Meeting in Washington, D.C. Muscular atrophy is a debilitating process that results in an extensive loss of muscle mass and function, which greatly worsens quality of life. It occurs in diseases such as cancer, diabetes, AIDS and heart failure, negatively affecting the patients' prognosis. Also, muscular atrophy can occur with aging, inadequate food intake such as in anorexia nervosa, or disuse (in those who are bedridden or who must keep a limb immobile) or as a side effect of glucocorticoid steroid therapy. Nerve injury also triggers severe muscular atrophy. Currently, there are few options to treat the problem. Some of the treatments, such as anabolic steroids (testosterone) and insulin-like growth factor 1 (IFG-1), raise concerns about safety and effectiveness, said study co-author Andrea Graziani, PhD. He is a molecular biologist with the Department of Clinical and Experimental Medicine and the Biotechnology Center for Applied Medical Research, University of Piemonte Orientale, Novara, Italy. "Because of the wide impact of muscular atrophy on public health, it is of pivotal importance to find new and better drug strategies to treat it," Graziani said.


Stress makes your hair go gray

Those pesky graying hairs that tend to crop up with age really are signs of stress, reveals a new report in the June 12 issue of Cell, a Cell Press publication. Researchers have discovered that the kind of "genotoxic stress" that does damage to DNA depletes the melanocyte stem cells (MSCs) within hair follicles that are responsible for making those pigment-producing cells. Rather than dying off, when the going gets tough, those precious stem cells differentiate, forming fully mature melanocytes themselves. Anything that can limit the stress might stop the graying from happening, the researchers said. "The DNA in cells is under constant attack by exogenously- and endogenously-arising DNA-damaging agents such as mutagenic chemicals, ultraviolet light and ionizing radiation," said Emi Nishimura of Tokyo Medical and Dental University. "It is estimated that a single cell in mammals can encounter approximately 100,000 DNA damaging events per day." Consequently, she explained, cells have elaborate ways to repair damaged DNA and prevent the lesions from being passed on to their daughter cells. "Once stem cells are damaged irreversibly, the damaged stem cells need to be eliminated to maintain the quality of the stem cell pools," Nishimura continued. "We found that excessive genotoxic stress triggers differentiation of melanocyte stem cells." She says that differentiation might be a more sophisticated way to get rid of those cells than stimulating their death. Nishimura's group earlier traced the loss of hair color to the gradual dying off of the stem cells that maintain a continuous supply of new melanocytes, giving hair its youthful color. Those specialized stem cells are not only lost, they also turn into fully committed pigment cells and in the wrong place. Now, they show in mice that irreparable DNA damage, as caused by ionizing radiation, is responsible. They further found that the "caretaker gene" known as ATM (for ataxia telangiectasia mutated) serves as a so-called stemness checkpoint, protecting against MSCs differentiation. That's why people with Ataxia-telangiectasia, an aging syndrome caused by a mutation in the ATM gene, go gray prematurely.


Lost molecule is lethal for liver cancer cells in mice

Scientists at Johns Hopkins have discovered a potential strategy for cancer therapy by focusing on what's missing in tumors. Noticing the conspicuous absence of single-stranded genetic snippets called microRNAs in cancer cells, a team of researchers from Johns Hopkins and Nationwide Children's Hospital delivered these tiny regulators of genes to mice with liver cancer and found that tumor cells rapidly died while healthy cells remained unaffected. Publishing results of the study June 12 in Cell, the researchers say they have provided one of the first demonstrations that microRNA replacement provides an effective therapy in an animal model of human disease. "This work suggests that microRNA replacement may be a highly effective and nontoxic treatment strategy for some cancers or even other diseases," says Josh Mendell, M.D., Ph.D., an associate professor in the McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine. "We set out to learn whether tumors in a mouse model of liver cancer had reduced levels of specific microRNAs and to determine the effects of restoring normal levels of these microRNAs to these cancer cells. We were very excited to see that the tumors were, in fact, very vulnerable to microRNA replacement." His team had considered the possibility that the replacement of a single small RNA might have little if any effect, especially in the setting of all the complex changes that drive the aberrant behavior of a cancer cell. But the tumor cells in the mouse were indeed sensitive to the restoration of the microRNA—so much so that they died, rapidly. "This concept of replacing microRNAs that are expressed in high levels in normal tissues but lost in diseases hasn't been explored before," Mendell says. "Our work raises the possibility of a more general therapeutic approach that is based on restoring microRNAs to diseased tissues."


Snoring pregnant women at higher risk for gestational diabetes

If you are pregnant and your mate complains your frequent snoring is rattling the bedroom windows, you may have bigger problems than an annoyed, sleep-deprived partner. A new study from researchers at the Northwestern University Feinberg School of Medicine has found that women who reported frequent snoring during their pregnancy were more likely to develop gestational diabetes -- a condition than can cause health problems for the mother and baby. The study also found pregnancy increases the likelihood that a woman will snore. This is the first study to report a link between snoring and gestational diabetes. For the study, 189 healthy women completed a sleep survey at the time of enrollment (six to 20 weeks gestation) and in the third trimester. Pregnant women who were frequent snorers had a 14.3 percent chance of developing gestational diabetes, while women who did not snore had a 3.3 percent chance. Even when researchers controlled for other factors that could contribute to gestational diabetes such as body mass index, age, race and ethnicity, frequent snoring was still associated with the disease. Principal investigator Francesca Facco, M.D., a fellow at Northwestern's Feinberg School, will present her findings at the SLEEP 2009 23rd Annual Meeting of the Associated Professional Sleep Societies June 11.


A red-wine polyphenol called resveratrol demonstrates significant health benefits

The benefits of alcohol are all about moderation. Low to moderate drinking – especially of red wine – appears to reduce all causes of mortality, while too much drinking causes multiple organ damage. A mini-review of recent findings on red wine's polyphenols, particularly one called resveratrol, will be published in the September issue of Alcoholism: Clinical & Experimental Research; the review is also available at Early View. "Reports on the benefits of red wine are almost two centuries old," said Lindsay Brown, associate professor in the School of Biomedical Sciences at The University of Queensland and corresponding author for the study. "The media developed the more recent story of the French paradox in the early 1990s. However, studies on the actions of resveratrol, one of the active non-alcoholic ingredients, were uncommon until research around 1997 showed prevention of cancers. This led to a dramatic interest in this compound." (See attached figure.) Red wine contains a complex mixture of bioactive compounds, including flavonols, monomeric and polymeric flavan-3-ols, highly colored anthocyanins, as well as phenolic acids and the stilbene polyphenol, resveratrol. Brown said that some of these compounds, particularly resveratrol, appear to have health benefits. "The breadth of benefits is remarkable – cancer prevention, protection of the heart and brain from damage, reducing age-related diseases such as inflammation, reversing diabetes and obesity, and many more," said Brown. "It has long been a question as to how such a simple compound could have these effects but now the puzzle is becoming clearer with the discovery of the pathways, especially the sirtuins, a family of enzymes that regulate the production of cellular components by the nucleus. 'Is resveratrol the only compound with these properties?' This would seem unlikely, with similar effects reported for other components of wine and for other natural products such as curcumin. However, we know much more about resveratrol relative to these other compounds."


Extended or shortened sleep duration linked to weight gain

Body Mass Index (BMI) varies as a function of habitual sleep duration, according to a research abstract that will be presented on Thursday, June 11, at SLEEP 2009, the 23rd Annual Meeting of the Associated Professional Sleep Societies. Results indicate that twins who slept between 7 and 8.9 hours each night had a lower mean BMI (25.0 kg/m2) compared to those who regularly slept either more (25.2 kg/m2) or less (26.4 kg/m2) per night. The relationship between sleep duration and BMI remained after controlling for genetics and shared environment. According to the lead author of the story, Nathaniel Watson, MD, co-director at the University of Washington Sleep Institute, in Seattle, sleep habits have a significant impact on weight and BMI. "Findings of the study point towards an environmental cause of the relationship between sleep duration and BMI," said Watson. "Results were robust enough to be present when the sample was limited to identical twins." The study included data from 1,797 twins, including 634 twin pairs (437 monozygotic, 150 dizygotic and 47 indeterminate pairs) and 529 individual twins with a mean age of 36.8. Habitual sleep duration was obtained by self-reported length of sleep per night and BMI was calculated by self-reported height and weight. Of the sample, 68.3 percent female, 88.2 percent were Caucasian. Results persisted in a co-twin control analysis of within twin pair differences in sleep duration and BMI.


Spanish researchers advance Natural Computing and Synthetic Biology techniques for treating diseases

Researchers from the Artificial Intelligence Group (LIA) at the Universidad Politécnica de Madrid's School of Computing have designed a biomolecular automaton and several genetic circuits with potential future applications in the field of vanguard medicine. Depending on how it is programmed, the molecular automaton detects DNA or RNA signals in vitro. In the future, though, provided it passes all the experimental tests, it will be able to operate inside the human organism. The ultimate aim of a molecular automaton is to detect and treat diseases in situ inside a human organism. Fitted inside the organism, the automaton detects anomalies and dispenses the right medicine at the right time. Biomolecular automata are artificial devices built with biomolecules and designed to operate inside a living organism.


Transparent solar cells

Offering a view of the garden and an adjacent field, it looks like any other window. But this window offers an additional feature: it also produces electricity. The facades of the house, too, harness solar energy to supply the occupants with electrical power. This is what the domestic power supply of the future could look like. The surface area used to produce energy would increase greatly with transparent solar cells. To translate the vision of see-through solar cells and transparent electronics into reality, two different transparent coatings would be required – one to conduct the electricity via electrons, the n-conductors, and one in which electron holes enable the electricity to flow, the p-conductors. To produce these coatings the engineers dope the base material with a few other atoms. Depending on which atoms they use, they obtain the differently conducting coatings. N-conducting transparent materials are state of the art, but the p-conductors are problematic. Their conductivity is too low and often their transparency is poor. Manufacturers need a transparent base material which is amenable to both n- and p-doping.


Greenland ice sheet larger contributor to sea-level rise

The Greenland ice sheet is melting faster than expected according to a new study led by a University of Alaska Fairbanks researcher and published in the journal Hydrological Processes. Study results indicate that the ice sheet may be responsible for nearly 25 percent of global sea rise in the past 13 years. The study also shows that seas now are rising by more than 3 millimeters a year--more than 50 percent faster than the average for the 20th century. UAF researcher Sebastian H. Mernild and colleagues from the United States, United Kingdom and Denmark discovered that from 1995 to 2007, overall precipitation on the ice sheet decreased while surface ablation--the combination of evaporation, melting and calving of the ice sheet--increased. According to Mernild’s new data, since 1995 the ice sheet lost an average of 265 cubic kilometers per year, which has contributed to about 0.7 millimeters per year in global sea level rise. These figures do not include thermal expansion--the expansion of the ice volume in response to heat--so the contribution could be up to twice that. The Greenland ice sheet has been of considerable interest to researchers over the last few years as one of the major indicators of climate change. In late 2000/early 2001 and in 2007, major glacier calving events sent up to 44 square miles of ice into the sea at a time. Researchers are studying these major events as well as the less dramatic ongoing melting of the ice sheet through runoff and surface processes.


New study reveals structure of the HIV protein shell

New research by scientists at The Scripps Research Institute and other institutions provides a close-up look at the cone-shaped shell that is the hallmark of human immunodeficiency virus (HIV), revealing how it is held together—and possible ways to break it apart. Previously, scientists had known that the genetic material within HIV is enclosed within a shell called the capsid, which is formed by a honeycomb arrangement of about 250 hexagonal protein building blocks. For HIV to infect human cells, the virus binds to cell surface receptors, and then the capsid is delivered into the cytoplasm of the cell. Now, in an advance, online issue of the journal Cell published on June 11, 2009, Professor Mark Yeager and colleagues at The Scripps Research Institute, the University of Virginia, and the University of Utah describethe first high-resolution molecular structure of the hexagonal protein building block, called CA, that makes up the HIV capsid. This detailed description may help scientists identify new ways to block HIV infection.


Scripps Research Team Creates Simple Chemical System that Mimics DNA

A team of Scripps Research scientists has created a new analog to DNA that assembles and disassembles itself without the need for enzymes. Because the new system comprises components that might reasonably be expected in a primordial world, the new chemical system could answer questions about how life could emerge. The work, reported in the June 11, 2009 issue of Science Express, an advance, online publication of the journal Science, might also be a starting point on the way to exotic new materials that repair themselves or transform in response to their environment. Scientists are both bemused and fascinated by the question of how life could have arisen on Earth. One of the most prominent theories is that, before the emergence of DNA, the earliest forms of life used RNA to transmit their genetic codes. The late Leslie Orgel, a co-author of the new paper, first suggested this idea, known as the "RNA World." One of the theory's challenges is that RNA is still so complex that many researchers believer something still simpler must have preceded it. "I have been working for years to learn what replicators and genetic systems might have come before the advent of the RNA World," says team leader of the new research Professor Reza Ghadiri, a Scripps Research chemist.


Texas wines fight cancer growth

Research now shows that wines produced in the Lone Star State share the anti-cancer traits known to exist in wines from other producing regions. Extracts from two Texas red wines decreased cancer cell growth in a comparable magnitude as other wines previously studied, according to Dr. Susanne Talcott, Texas AgriLife Research food and nutrition scientist. Her study, which concluded in May, showed decreased growth of colon and breast cancer cells treated with port and syrah (or shiraz) wine. It was the first such study of the health components of Texas wines, she said. "These results could definitely be projected to all Texas wines containing similar amounts of bioactive compounds," Talcott said. "And this will be the basis for a continued intensive study of all the health benefits of wines made in this state." Talcott presented her findings at the recent Texas Viticulture and Enology Research Symposium. She said the findings suggest that people who consume regular, moderate amounts of Texas wine daily -- up to a glass and a half -- may profit from similar health benefits ascribed to wines from other regions. "In general, studies show that wine may either prevent cells from mutating into cancer cells, or stop existing cancer cells from growing and causing them to die," Talcott noted.


Children At Risk in Hot Cars

With summer approaching, the danger of children dying from being left unattended in vehicles increases, a Texas AgriLife Extension Service specialist warns. "The problem is that temperatures in parked vehicles rise very quickly," said Bev Kellner, AgriLife Extension passenger safety specialist. In just 10 minutes the temperature can increase by almost 20 degrees, according to figures from San Francisco State University's department of geosciences. A child’s body temperature rises three to five times faster than an adult making children more vulnerable to a deadly condition known as hyperthermia or heat stroke, Kellner noted. Heat stroke can occur at body temperatures above 104 degrees.


Appetite-stimulating hormone is first potential medical treatment for frailty in older women

Older women suffering from clinical frailty stand to benefit from the first potential medical treatment for the condition, according to a study presented today by Penn Medicine researchers at ENDO, The Endocrine Society's 91st Annual Meeting. Ghrelin, a hormone that stimulates appetite, was administered to older women diagnosed with frailty, a common geriatric syndrome characterized by unintentional weight loss, weakness, exhaustion and low levels of anabolic hormones which increases risk of falls, hospitalizations, disability, and death. Those who received ghrelin infusions consumed 51 percent more calories than the placebo group, with an increase in carbohydrate and protein intake, not fat. Their growth hormone levels were also higher throughout the ghrelin infusion. "As Americans are increasingly living into their 80s and 90s, we need to identify ways to prevent or treat common geriatric conditions, such as unexplained weight loss and frailty, which have serious health consequences," said senior author Anne Cappola, MD, ScM, Assistant Professor of Medicine in Endocrinology, Diabetes, and Metabolism at the University of Pennsylvania School of Medicine. "We're gaining a better understanding of the hormonal changes that occur as we get older and, with treatments like ghrelin, we can start intervening to prevent some of the common health problems that keep elderly people from living their most productive lives." In the pilot study, funded by the National Institutes of Health and Penn's Institute on Aging, five frail women and five healthy women, all over the age of seventy, were randomized to receive an infusion of the hormone ghrelin or placebo. After a ghrelin transfusion, frail women in the study had a stronger, healthy appetite and increased anabolic hormone activity. The only side effect reported during the treatment was a transient sense of warmth that occurred in four women who received the ghrelin transfusion. Now that safety and initial efficacy has been proven in this pilot study, larger follow-up studies will look at the potential therapeutic role of ghrelin or ghrelin mimetic agents in the frail population. At this time, these agents are only available for research use.


Over half of people with rheumatoid arthritis have periodontitis

Over half (56%) of people with rheumatoid arthritis (RA) also have periodontitis (a chronic inflammatory disease of the gum and surrounding ligaments and bones that hold the teeth in place), displaying fewer teeth than healthy matched controls, high prevalence of oral sites presenting dental plaque and advanced attachment loss (the extent of periodontal support that has been destroyed around a tooth) (chi square p<0.05), according to the results of a new study presented today at EULAR 2009, the Annual Congress of the European League Against Rheumatism in Copenhagen, Denmark. In addition, these patients were found to have significantly higher RA disease activity and anti-CCP (cyclic citrullinated peptide) antibody levels than others with RA who did not exhibit periodontitis (r=0.84, p<0.05; r=0.78, p<0.05). The study also showed that, after six months of anti-TNF therapy (prescribed to control RA inflammation and destruction), a statistically significant improvement in periodontal status was seen in 20 (80%) of the 25 participants (mean age 41.5+3.7 years; mean disease duration 7.2+4.8 years), suggesting that the biological therapy may also be able to modulate the inflammatory process in the periodontium (the tissues investing and supporting the teeth, including the cementum, periodontal ligament, alveolar bone, and gingival / gums). Dr Codrina Ancuta of the Grigore T Popa University of Medicine and Pharmacy, Rehabilitation Hospital, Iasi, Romania, who led the study, said: "There is a growing body of evidence to demonstrate an association between periodontal disease and systemic conditions involving inflammatory rheumatic disease (especially RA), cardiovascular disease and diabetes. However, further cross-disciplinary research among rheumatologists and periodontologists is required to fully understand the underlying mechanisms that link RA and periodontitis, and to explore how patients can be managed more holistically using treatments such as anti-TNFs and some lifestyle approached that may simultaneously address both conditions."


Anxiety and depression lower quality of life in majority of systemic lupus erythematosus patients

92.8% of patients with systemic lupus erythematosus (SLE) suffer anxiety and depression which significantly affects both their physical and emotional quality of life (QoL), according to the results of a new study presented today at EULAR 2009, the Annual Congress of the European League Against Rheumatism in Copenhagen, Denmark. Logistic regression analysis revealed that depression was the most significant factor shown to affect QoL (p=0.015; OR=0.18; CI 95%:0.045-0.72). In the study, 92.8% (52 of 56) of the patients who were diagnosed with SLE had an element of confirmed neuropsychiatric (NP) involvement (including anxiety, depression, mild cognitive deficits and major NP involvement).


Dual role in breast tissue for a protein involved in leukemia

A protein known to play a role in growth of some types of leukemia appears to have a mixed function in breast cancer development, say researchers from the Lombardi Comprehensive Cancer Center at Georgetown University Medical Center (GUMC). The findings, presented at the annual meeting of the Endocrine Society in Washington, DC, indicate that the function of this protein, known as Stat5a, may be different in developing breast cancer cells that are estrogen receptor-positive as compared to estrogen receptor-negative. When estrogen receptor levels were overexpressed, loss of Stat5a reduced development of a lobular type of preneoplasia. However, when estrogen receptor levels were normal, loss of Stat5a not only had no effect on reducing preneoplasia, but increased susceptibility to carcinogen-induced breast cancer. The results illustrate the importance of breast cancer heterogeneity when testing new therapeutic targets. The researchers say Stat5a could be a target for treatment of leukemia, but add, "If Stat5a is to be used as a drug target for leukemia or other cancers, it is important to fully understand how altering its function impacts the breast, especially since it appears it may play different roles in different types of breast cancer," says the study's lead author, Anne Miermont, MS, a doctoral graduate student in tumor biology at Georgetown University Medical Center. Stat5a is a member of the STAT family of proteins, which are key to regulating cell growth and differentiation. Because they have been found to be over-expressed in leukemia, Miermont and Priscilla Furth, MD, a professor of oncology, sought to see if they were important in breast cancer development. Estrogen receptors are over-expressed in more than half of human breast cancers, so the investigators set up studies to test if the function of Stat5a was the same or different in cells with estrogen receptor overexpression.


Protein Linked to Change in Tissue That Surround and Support Breast Tumors

A protein known to be overly active in breast cancer can exist in a form that seems to change the structural composition of mammary tissue, potentially making it more conducive to tumor progression, say researchers from the Lombardi Comprehensive Cancer Center at Georgetown University Medical Center (GUMC). At the annual meeting of the Endocrine Society in Washington, DC, the scientists report that the protein, AIB1 (Amplified in Breast Cancer 1), has a shorter form known as AIB1delta3 which turns breast tissue more fibrous. The researchers say this shorter form may contribute to the dense breast tissue that is a known risk factor for breast cancer. “We found that AIB1delta3 alters the stroma, or environment that surrounds and supports cancer cells, producing excessive fibrosis,” says the study’s lead author, Priscilla Furth, MD, Professor of Oncology and Medicine. “This is significant, because disordered interactions between the epithelial and stromal compartments are being increasingly recognized as an important component of breast cancer risk.”


USC researchers identify DNA mutation that occurs at beginning point of T-cell lymphoma

Researchers at the Keck School of Medicine of the University of Southern California (USC) have identified a key mechanism that causes chromosomes within blood cells to break—an occurrence that marks the first step in the development of human lymphoma. The study provides researchers with the clearest insight yet into why these breakages—called chromosomal translocations—occur at a specific points in the chromosome, says principal investigator Michael R. Lieber, M.D., Ph.D., Rita and Edward Polusky Professor in Basic Cancer Research at the Keck School of Medicine. The study appears as the featured cover article in the June 12 issue of the journal Molecular Cell. The study is the second led by Lieber to appear on the cover of a Cell journal in the past six months. "The new findings go to the heart of why cancers begin. This is an opportunity to see the very beginning step of human lymphoma," Lieber says. "With this information, we can now begin to look at ways to interfere with this process in order to stop the lymphoma and to develop more targeted therapies for treatment." There are two types of lymphoma: B cell lymphomas and T cell lymphomas. Both B cells and T cells perform vital functions in the immune system by creating antibodies and destroying virus-infected cells. However, the beginning point, or inception, of most human lymphomas occurs when two chromosomes break and the resulting fragments are reassembled in an exchange. Researchers specifically looked at T cell acute lymphoblastic lymphomas (ALL). ALL accounts for half of all childhood cancers under the age of five, and T cell ALL represents about 10 percent of ALL. The USC scientists identified a specific enzyme known as the RAG complex that occasionally cuts the chromosome at an off-target site, causing lymphocyte (blood) cells to proliferate uncontrollably. They showed that the RAG complex selects the wrong target largely because the proteins in which the wrong chromosome is wrapped (called chromatin) lures the RAG complex to the wrong site.


Gene therapy technique thwarts cancer by cutting off tumor blood supply

University of Florida researchers have come up with a new gene therapy method to disrupt cancer growth by using a synthetic protein to induce blood clotting that cuts off a tumor's blood and nutrient supply. In mice implanted with human colorectal cancer cells, tumor volume decreased 53 percent and cancer cell growth slowed by 49 percent in those treated with a gene that encodes for the artificial protein, compared with those that were untreated. The research team, led by Dr. Bradley S. Fletcher, an assistant professor of pharmacology and therapeutics in the College of Medicine, created the so-called fusion protein to target another protein called tumor endothelial marker 8, or TEM8, which was recently found to be preferentially expressed in the inner lining of tumor vessels. Such differences in protein expression enable delivery of drug molecules to the cells that harbor these proteins. "The protein we created did a very good job of homing to the tumor and binding," said Stephen Fernando, who recently completed his doctoral studies. "By targeting TEM8, we can potentially create a therapy against cancer." The Fletcher group is the first to target cancer cells through protein binding to TEM8. The findings, now available online, are featured on the cover of the June 15 edition of Cancer Research. "If you can cut off the blood supply, then you can inhibit the tumor from growing -- there have been many attempts," said Brad St. Croix, director of the National Cancer Institute's Tumor Angiogenesis Section, whose group first identified the TEM genes that over-express in tumor endothelial cells. "The concept of targeting tumor blood vessels has been around for many years, but it's good that we're finally getting around to the stage where we can see the vessels being targeted therapeutically -- it's pretty exciting, I think."


Majority won't have access to antivirals in pandemic but generic drugs could help prevent deaths

Almost 90 per cent of the world's population will not have timely access to affordable supplies of vaccines and antiviral agents in the current influenza pandemic, but it is possible that inexpensive generic drugs that are readily available, even in developing countries, could save millions of lives. That's the conclusion reached by an extensive review and analysis by immunisation expert Dr David Fedson, published online by Influenza and Other Respiratory Viruses within hours of the World Health Organization declaring a pandemic. Dr Fedson points out that seasonal flu resistance to antiviral drugs like Tamiflu may make them ineffective in the pandemic and maintains that without effective drugs some countries will have to rely on 19th century public health measures to see them through the outbreak. He is calling for urgent and sharply focused research to determine whether drugs that reduce inflammation or modify the host response - the way that the body responds to infection or injury - could be used to manage the pandemic. And he believes that a lot could be learnt from the work done on these commonly available generic drugs - which include drugs to lower cholesterol and treat diabetes - by scientists not involved in influenza research. "Despite the best efforts of influenza scientists, pharmaceutical companies and health officials, the stark reality is that although studies of the molecular characteristics of influenza viruses have been enormously informative, they have failed to explain the system-wide effects that flu has on people who contract it. "For example we still don't understand why so many young adults died in the 1918 pandemic, while the death rate for children was much lower. I believe this is because researchers have focused on studying the actual virus rather than how these particular hosts – the children and young people – responded to the virus.


UK tops the list of 213 countries at extreme risk to the spread of swine flu

A Warwick Business School professor and one of the founders of global risks specialist, Maplecroft, has released three new maps and indices revealing the countries most at risk from an influenza pandemic.Each index generates a list of countries most at risk and which require a tailored policy response on the part of government and business. Maplecroft's research focuses on global risks to business. The map of Risk of Spread shows the UK most at risk to the spread of an influenza pandemic, ranking number 1 out of 213 countries. The Netherlands, Germany, Italy, Russia, Canada and Japan are also categorised as extreme risk because of their high population density, urbanisation and busy airports.


A research group focus on neurobiology of Parkinson's disease an the early detection of the disease

A research group based at the University of Granada, in cooperation with the Neurology Unit of the San Cecilio Hospital of Granada and the Department of Experimental Sciences of the University of Jaen, is studying the Neurobiology of Parkinson's disease (PD). They have developed a non-invasive method for serological diagnosis of Parkinson's disease, which is being patented by the University of Granada. To this end, the scientists analyzed and purified proteins associated with this disease, such as aminopeptidase. However, it is not an easy task: "there are thousands of proteins in the blood, and only a few are related to neurodegenerative diseases." Francisco Vives, Head of the Institute the Neurosciences of Granada and coordinator of the University of Granada's research group for the "Study of neurodegenerative diseases in Andalusia" says that "so far, there is not effective treatment" for Parkinson's disease so, at the moment the only solution is palliative treatment. Therefore, "finding plasma specific proteins in patients before the first symptoms of Parkinson's disease appear, will allow us to use drugs that either stop or at least slow down the disease. An early diagnose is important to PD medication"


 


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