News 12 march 2009


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News 12 march 2009


Survey explores medical care for children with autism using complementary alternative medicine

Primary care physicians more likely to ask about CAM use when caring for autistic children. In a national survey conducted by the University of Minnesota, primary care physicians report that they are more likely to ask patients with autism about complementary alternative medicine (CAM) use. These physicians also desire more CAM education for this population. The study¹ of 539 U.S. physicians, published this week in Springer’s Journal of Autism and Developmental Disorders, explores the attitudes and practices of primary care physicians caring for children with autism using CAM treatments.

The Navel - a Single, Safe Surgical Access Route for Kidney Extraction

The team of Dr. Antoni Alcaraz of Hospital Clínic de Barcelona has removed a kidney from a woman diagnosed with kidney cancer, through a single opening. This is the first operation of this type carried out in Spain and one of very few performed throughout the world. Recovery time is reduced by half and the surgical results are far better than those of conventional laparoscopy. The operation was carried out with material specially designed to be able to work from the navel, access that requires control and precision. Successful surgery that leaves no scars has become the main objective of the most daring and innovative surgeons. Since conventional open surgery gave way to laparoscopy-assisted surgery, which requires 3, 4 or even 5 incisions, surgeons operating on the pelvic and abdominal cavity, together with experts in robotics, are investigating new ways of entering the body to explore structures, diagnose diseases and extract organs. Hospital Clínic, Barcelona is committed to minimally invasive surgery, particularly as the navel has now been shown to be a safe and effective single access route for extracting kidneys. The operation – the first of its kind to be performed in Spain – was carried out by the team of Dr. Alcaraz of the Hospital Clínic urology department on 17 February on an 85-year-old woman who had been diagnosed with cancer. Three days after the operation, the woman was discharged home with no symptoms.

Estrogen activates critical lung genes to improve lung function

Estrogen may be a new postnatal therapy to improve lung function and other outcomes in preterm infants, researchers at UT Southwestern Medical Center have found in an animal study. “Ironically, a hormone that has received great attention as a potential means to optimize the health of older women may be a beneficial treatment for humans during the earliest stages of life,” said Dr. Philip Shaul, professor of pediatrics at UT Southwestern and the study’s senior author.The study, conducted in preterm primates, appears in the March issue of the American Journal of Respiratory and Critical Care Medicine. The study was performed at the Southwest Foundation for Biomedical Research Primate Center in San Antonio as part of a National Institutes of Health-funded consortium investigating causes and treatments for bronchopulmonary dysplasia (BPD), a devastating primary complication of premature birth that develops in the preterm lung following ventilation and oxygen support. Sufficient production of nitric oxide in fetal and newborn lungs is necessary for the lungs to develop and function properly. During the latter part of pregnancy the placenta produces large amounts of estrogen that enters the fetal circulation. Another spike of estrogen occurs during labor. In prior studies in cultured cells the investigators found that estrogen activates the genes in lung cells encoding nitric oxide synthases, enzymes that produce nitric oxide. That research suggested treatment with the hormone may achieve the same results in the intact lung. Premature infants — nearly 50,000 are born in the U.S. each year — miss out on this exposure to estrogen in the womb and, as a consequence, may experience respiratory problems because they lack nitric oxide.

A diet rich in calcium aids weight loss

Boosting calcium consumption spurs weight loss, according to a study published in the most recent issue of the British Journal of Nutrition, but only in people whose diets are calcium deficient. Angelo Tremblay and his team at Université Laval’s Faculty of Medicine made the discovery in a 15-week weight loss program they conducted on obese women. The participants consumed on average less than 600 mg of calcium per day, whereas recommended daily intake is 1000 mg. In addition to following a low calorie diet, the women were instructed to take two tablets a day containing either a total of 1200 mg of calcium or a placebo. Those who took the calcium tablets lost nearly 6 kg over the course of the program, the researchers found, compared to 1 kg for women in the control group. “Our hypothesis is that the brain can detect the lack of calcium and seeks to compensate by spurring food intake, which obviously works against the goals of any weight loss program,” said Angelo Tremblay, holder of the Canada Research Chair in Environment and Energy Balance. “Sufficient calcium intake seems to stifle the desire to eat more,” he added.

Patients who gave up smoking before surgery had half as many complications afterwards

More than a third of patients who took part in an eight-week smoking cessation programme before and after planned surgery were able to give up and most of them were still smoke free after a year, according to research in the March issue of Anaesthesia. They also experienced half as many complications after surgery as the patients who did not receive help to give up smoking, with 21 per cent experiencing problems as opposed to 41 per cent. Researchers randomly assigned 117 patients who were due to undergo general or orthopaedic surgery to an intervention and control group. "The intervention group attended weekly meetings or received telephone support and were provided with free nicotine replacement therapy, while the control group just received standard pre-operative care" says lead author Dr Omid Sadr Azodi from the Karolinska Institute in Stockholm, Sweden. "Patients were then assessed at regular intervals before and after surgery and after 12 months. "One interesting thing to emerge from the study was the high refusal rate. A further 76 patients declined to take part in our research because they were unwilling to give up smoking or were stressed by their forthcoming surgery."

Well-known enzyme is unexpected contributor to brain growth

An enzyme researchers have studied for years because of its potential connections to cancer, diabetes, heart disease, hypertension and stroke, appears to have yet another major role to play: helping create and maintain the brain. When scientists at Washington University School of Medicine in St. Louis selectively disabled the enzyme AMP-activated protein kinase (AMPK) in mouse embryos, overall brain size was reduced by 50 percent, the cerebrum and cerebellum were shrunken, and the mice died within three weeks of birth. Researchers showed that the version of AMPK they disabled was essential to the survival of neural stem cells that create the central nervous system. Many scientists believe these same cells also regularly produce new brain cells essential for learning and memory and the general upkeep of the adult brain. "For years, scientists have showed how AMPK regulates multiple metabolic processes, and revealed how that influence can affect cancer, diabetes, and many other diseases," says senior author Jeffrey Milbrandt, M.D., Ph.D., the David Clayson Professor of Neurology. "Now, for the first time, we've shown that AMPK can cause lasting changes in cell development. That's very exciting because it opens the possibility of modifying AMPK activity to improve brain function and health." The study was the featured paper in the February issue of Developmental Cell.

Discovery may lead to development of safer immunosuppressants

Immunosuppressive treatment is necessary to prevent rejection of an organ after transplant and has great potential for treating chronic inflammatory diseases. However, currently available immunosuppressant drugs can pose serious health risks, restricting their long-term use. Now, new research findings may lead to the development of immunosuppressant drugs that have fewer adverse side effects. The study, published by Cell Press in the March 13th issue of the journal Molecular Cell, reveals detailed information about how drugs commonly used to prevent transplant rejection interact with their target.Calcineurin (CN) is a highly conserved protein that plays a multitude of roles in diverse biological processes. Previous work has shown that CN regulates a protein called nuclear factor of activated T cells (NFAT) in mammals and that this regulation involves a docking interaction between CN and NFAT. The CN-NFAT pathway is known to play a critical role in processes such as inflammation, diabetes and cardiac hypertrophy.CN is the target of the immunosuppressant drugs cyclosporine A (CsA) and FK506 which are used to prevent rejection after a transplant. These drugs have also been used to treat atopic dermatitis, severe asthma, and refractory rheumatoid arthritis. "CsA and FK506 each form complexes with a specific immunophilin binding proteins and it is these complexes, called IS-IP complexes, that inhibit CN activity," says senior study author Dr. Juan Miguel Redondo from the Department of Vascular Biology and Inflammation at the Centro Nacional de Investigaciones Cardiovasculares in Madrid.Dr. Redondo and colleagues designed a series of experiments to investigate how IS-IP complexes and substrates like NFAT interact with CN. They identified a "pocket" within the CN molecule that mediated binding to NFAT and other substrates. Their analyses also provided insights into the mechanisms by which immunosuppressants inhibit CN. "We showed that IS-IP complexes compete for binding to the same docking surface in CN that mediates interactions with natural substrates, thereby blocking CN signaling," explains Dr. Redondo.The discovery of a common CN docking pocket for substrates and IS-IP complexes reveals a promising target for development of less toxic immunosuppressive drugs. "Many of the severe side effects of FK506 and CsA, such as neurotoxicity, diabetes, kidney dysfunction and hypertension, are at least partly independent of CN," says Dr. Redondo. "Identifying selective CN inhibitors that avoid these secondary effects is of high interest."

Parkinson's-linked mutation makes neurons vulnerable to calcium-induced death

A new study reveals the mechanism by which a genetic mutation linked with Parkinson's disease (PD) renders dopamine neurons particularly vulnerable to cell injury and death. The research is published by Cell Press in the March 13th issue of the journal Molecular Cell. PD is a neurodegenerative disease characterized by a specific loss of dopamine neurons. Several genes have been linked with inherited forms of PD. Many of these genes encode proteins that are targeted to mitochondria, tiny intracellular "power plants" that metabolize oxygen and generate energy. Mitochondria also play a major role in maintaining appropriate calcium levels inside of cells. Abnormal calcium levels can be toxic to neurons and are associated with a range of neurodegenerative diseases. Mutations in the PINK1 gene cause an inherited form of PD and research has shown that PINK1 is localized to mitochondria. "We previously demonstrated that PINK1 deficiency results in an age related loss of neuronal viability, and an increased sensitivity to mitochondrial dysfunction. However, the mechanisms underlying this mitochondrial pathophysiology remained unknown," explains senior study author Dr. Andrey Y. Abramov from the Institute of Neurology in London. Dr. Abramov and colleagues used a sophisticated and dynamic imaging technique to explore the mitochondrial pathophysiology of PINK1-dependent PD. They found that loss of PINK1 resulted in an aberrant calcium overload inside the mitochondria. This overload stimulated production of dangerous reactive oxygen species that interfered with the ability of the mitochondria to transport sugar needed for energy production. This phenomenon could be reversed by providing substrates for energy production. "These data strongly suggest that the respiratory complexes in PINK1 deficiency are still intact and that their functional inhibition is in fact secondary to reduced substrate supply," offers Dr. Abramov. Importantly, adult dopamine-producing neurons are frequently exposed to large influxes of calcium that must be buffered by the mitochondria. Mitochondria dysfunction and an inability to process these calcium loads are likely to make the dopamine neurons quite vulnerable to injury "Our findings define a mechanism whereby PINK1 dysfunction may cause the death of dopamine neurons," concludes Dr. Abramov.

Unraveling the roots of dyslexia

By peering into the brains of people with dyslexia compared to normal readers, a study published online on March 12th in Current Biology, a Cell Press publication, has shed new light on the roots of the learning disability, which affects four to ten percent of the population. The findings support the notion that the reading and spelling deficit—characterized by an inability to break words down into the separate sounds that comprise them—stems in part from a failure to properly integrate letters with their speech sounds. "The adults with dyslexia in the study had enough reading experience to match letters and their speech sounds correctly," said Vera Blau of the University of Maastricht, The Netherlands "Still, the results show that the way their brain integrates letters and speech sounds is very different from normal readers. It's quite astonishing." The researchers examined activity in the brains of dyslexic and normal adult readers by using functional magnetic resonance imaging (fMRI) as they were presented with letters, speech sounds, or a matching or non-matching combination of the two. While undergoing that task, dyslexic adults showed lower activation of a brain region known as the superior temporal cortex than the more typical readers did. The findings point to a neural deficit in letter-speech sound integration as a fundamental mechanism that might distinguish poor from good readers, Blau said. Such a difficulty in integrating the most basic units of written and spoken language could offer a promising link between well-documented difficulties in processing the sounds of language (phonology) and the actual reading problem itself, she added. Her team, led by Leo Blomert at the University of Maastricht, is currently conducting further studies in children as they are learning to read to help identify whether the difficulty to integrate letters with speech sounds begins in early school years and whether it comes before or after deficits in processing the sounds of language.

Genes identified that are linked to spinal disc degeneration

Lumbar disc degeneration is an uncomfortable condition that affects millions of people, but two University of Alberta researchers have identified some of the genes that are causing problems. Michele Crites-Battie? and Tapio Videman, in the Faculty of Rehabilitation Medicine, have discovered eight genes that are directly related to disc degeneration. "We found more genes associated with disc degeneration than was discovered in 30 prior studies," said Videman. "This is very exciting." The pair started by studying 25 specific genes they thought could be linked to the disease. They picked these "candidate" genes based on the views of two leading experts in the field who Crites-Battie? and Videman have collaborated with through the years. They narrowed their search down using state-of-the-art DNA analyzers, then applying statistical methods and analyzing MRIs of twins' spines. "Identifying genes involved can provide important insights into the biological mechanisms behind disc degeneration and a better understanding of what is going wrong in the system," said Crites-Battie?. "This can eventually lead to effective interventions for the problem." The pair will now look at the interaction between these eight genes and their environment. This will help them identify what gene forms indicate susceptibility. "This will tell us who should avoid physical loading, and in which people obesity could be a risk factor for spine problems," said Videman.

New therapy protects lungs from runaway inflammation

A novel anti-inflammatory therapy designed by Vanderbilt University Medical Center investigators prevents acute lung injury in mice exposed to an inflammation-causing toxin, the researchers report in the journal Molecular Therapy. The new therapy may offer a way to protect the lungs from the "runaway inflammation" that can accompany bacterial or viral pneumonia, said Jacek Hawiger, M.D., Ph.D., the leader of the research team that has pioneered the new approach. "Lung inflammation is an extremely perplexing problem," noted Hawiger, chair of the Department of Microbiology & Immunology. The immune system sometimes overreacts to lung infection and produces excessive concentrations of inflammatory signals (cytokines and chemokines), which can damage the fine architecture of the lungs and lead to life-threatening acute respiratory distress syndrome (ARDS). Such damage is most likely when pneumonia has both viral and bacterial causes – for example from combined influenza and Staphylococcus aureus infections. "We believe that in addition to controlling the infection with antibacterial and antiviral agents, we need therapies that reduce this inflammation-induced collateral damage to the lung tissue," Hawiger said. "This would allow both faster clearance of the infecting organisms and faster healing of the lung." Several years ago, Hawiger and colleagues began searching for new targets for anti-inflammatory therapy. They reasoned that a protein called NF-kappa-B – the "master regulator" of genes that encode mediators of inflammation – might make a good target. The researchers knew that NF-kappa-B moves from the cell cytoplasm to the nucleus (where it is active) in response to cellular injury or microbial agents, and they decided to try to block this nuclear translocation. They designed a small protein fragment – a peptide – that mimicked the nuclear transport "signal," hoping that it would compete with, and block, NF-kappa-B's movement to the nucleus. To get the peptide into cells, the team took advantage of the cellular mechanism that proteins use to cross membranes and engineered a membrane-crossing motif onto the therapeutic peptide. "To our delight, we found that this peptide crossed the cell membrane and stopped NF-kappa-B in its tracks, blocking it from going to the nucleus in response to conditions which cause inflammation," Hawiger said.

University of Miami physicist develops battery using new source of energy

Researchers at the University of Miami and at the Universities of Tokyo and Tohoku, Japan, have been able to prove the existence of a "spin battery," a battery that is "charged" by applying a large magnetic field to nano-magnets in a device called a magnetic tunnel junction (MTJ). The new technology is a step towards the creation of computer hard drives with no moving parts, which would be much faster, less expensive and use less energy than current ones. In the future, the new battery could be developed to power cars. The study will be published in an upcoming issue of Nature and is available in an online advance publication of the journal. The device created by University of Miami Physicist Stewart E. Barnes, of the College of Arts and Sciences and his collaborators can store energy in magnets rather than through chemical reactions. Like a winding up toy car, the spin battery is "wound up" by applying a large magnetic field --no chemistry involved. The device is potentially better than anything found so far, said Barnes. "We had anticipated the effect, but the device produced a voltage over a hundred times too big and for tens of minutes, rather than for milliseconds as we had expected," Barnes said. "That this was counterintuitive is what lead to our theoretical understanding of what was really going on." The secret behind this technology is the use of nano-magnets to induce an electromotive force. It uses the same principles as those in a conventional battery, except in a more direct fashion. The energy stored in a battery, be it in an iPod or an electric car, is in the form of chemical energy. When something is turned "on" there is a chemical reaction which occurs and produces an electric current. The new technology converts the magnetic energy directly into electrical energy, without a chemical reaction. The electrical current made in this process is called a spin polarized current and finds use in a new technology called "spintronics."

Study shows Human Sounds may Kill Fish

Anthropogenic, or human generated, sounds have the potential to significantly affect the lives of aquatic animals - from the individual animal's well-being, right through to its reproduction, migration and even survival of the species. According to a study entitled "The effects of human-generated sound on fish", published in Integrative Zoology by Wiley-Blackwell, marine animals could suffer detrimental effects ranging from a loss of hearing to increased stressed levels as a result of environmental noise - in ways not dissimilar to humans and land animals. The study also describes some recent well-controlled experimental studies while highlighting areas for future study. "Human generated sounds in the marine environment may result in only small shifts in behavior for some animals, but immediate death in others. With the vast increase in production of sound in the marine environment due to human activity such as oil exploration, shipping and construction, the effect of human-generated sounds on the aquatic life becomes a growing issue", said Dr. Arthur Popper from the University of Maryland, USA. Marine animals use sounds to communicate and to glean information about their environment. Unlike the "visual scene" developed by the animal's sense of sight, the "auditory scene" derived from sounds provides marine animals with a three dimensional view of the world and extends far beyond the visual scene. Dr. Popper added, "The detection of the auditory scene plays a critical role in sound detection - along with the detection of communication signals. Anything in the environment that alters the organism's ability to detect and analyze its auditory scene has the potential to cause a detrimental impact on the life of the animal as well as the survival of the species".


 

 


 


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