Protein Linked to Learning also Induces Cocaine Addiction: Researchers

The study describes how the learning-related protein works with other proteins to forge new pathways in the brain in response to a drug-induced rush of the "pleasure" molecule dopamine.

By adding important detail to the process of addiction, the researchers, led by a group at Johns Hopkins, said that the work may point the way to new treatments.

"The broad question was why and how cocaine strengthened certain circuits in the brain long term, effectively re-wiring the brain for addiction," Paul Worley, M.D., a professor in the Solomon H. Snyder Department of Neuroscience at the Johns Hopkins University School of Medicine, said.

"What we found in this study was how two very different types of systems in the brain work together to make that happen," he said.

The study is published in the journal Cell.

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Researchers Restore Immune Function in Spinal Injured Mice

The researchers are from The Center for Brain and Spinal Cord Repair at The Ohio State University Wexner Medical Center. People with spinal cord injury often are immune compromised, which makes them more susceptible to infections. Why these people become immune-suppressed is not known, but the Ohio State study found that a disorder called autonomic dysreflexia can cause immune suppression.

Autonomic dysreflexia is a potentially dangerous complication of high-level spinal cord injury characterized by exaggerated activation of spinal autonomic (sympathetic) reflexes. This can cause an abrupt onset of excessively high blood pressure that can cause pulmonary embolism, stroke and in severe cases, death.

"Our research offers an explanation for why people with spinal cord injuries develop a condition referred to as 'central immune depression syndrome.' Their immune systems, which are required to fight off infection, are suppressed due to damage or malfunction in regions of the spinal cord that help control immune function," said principal investigator Phillip G. Popovich, Ph.D., Professor of Neuroscience in Ohio State's College of Medicine and Director of Ohio State's Center for Brain and Spinal Cord Repair.

The study is published in the Journal of Neuroscience.

Researchers found that autonomic dysreflexia develops spontaneously in spinal cord injured mice, and becomes more frequent as time passes from the initial spinal cord injury.

They also found that simple, everyday occurrences that activate normal spinal autonomic reflexes, such as having bowel movements or emptying the bladder, become hyperactive and suppress immune function in people with spinal cord injury.

In the study, Popovich and colleagues were able to restore immune function in mice with spinal cord injuries using drugs that inhibit norepinephrine and glucocorticoids, immune modulatory hormones that are produced during the onset and progression of AD. They also observed in a patient with a high-level spinal cord injury that briefly inducing autonomic dysreflexia impaired immune function, confirming that their findings in mice have relevance to humans.

"Although we don't know how to fix this yet, we also show that it is possible to restore immune function in spinal injured mice," Popovich said. "After spinal cord injury, the ability of the spinal cord to control the immune system is impaired. As result, these individuals become susceptible to infection, and often die from these infections. For those that survive, the infections can impair what little function they have left after the spinal cord injury."

The study found that autonomic dysreflexia causes immune suppression in part by releasing into blood and immune organs high levels of immune modulatory hormones that non-selectively kill mature and immature white blood cells in the spleen, said first author Yi Zhang, a post-doctoral neuroscience researcher at Ohio State.

"Our research is laying the groundwork for potential therapeutic targets for reversing central immune depression syndrome," Zhang said, adding that further research is needed.

Source-Eurekalert

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Researchers: Childhood Economic Status Affects Substance Use Among Young Adults

by Rukmani Krishna on? August 02, 2013 at 12:09 AM Lifestyle News According to researchers at Duke Medicine, children who grow up in poverty are more likely than wealthier children to smoke cigarettes, but they are less likely to binge drink and are no more prone to use marijuana.
The researchers also found that economic strains in early life - including family worries about paying bills or needing to sell possessions for cash - independently erode a child's self-control, regardless of strong parenting in adolescence. Lack of self-control often leads to substance use.

The findings, appearing July 30, 2013, in the Journal of Pediatric Psychology, debunk common assumptions about who abuses substances, and provide a basis for better approaches to prevent young people from falling into drug and alcohol addiction.

"Poverty during childhood not only appears to affect child development, but can have lasting effects on the types of health choices made during adolescence and early adulthood, especially as it relates to cigarette smoking," said senior author Bernard Fuemmeler, Ph.D., MPH, MS, associate professor in Community and Family Medicine at Duke University School of Medicine. "Economic strains may shape an individual''s capacity for self-control by diminishing opportunities for self-regulation, or affecting important brain structures."

Fuemmeler and colleagues at Duke set out to examine the direct effect of childhood economic strains on smoking, binge drinking, and marijuana use in young adults. They also sought to determine how financial difficulties impact self-control, and how positive parenting might mitigate the tendency to use drugs and alcohol.

The group analyzed data from 1,285 children and caregivers included in a representative sample of U.S. families studied from 1986-2009. Economic status was measured by annual family income, plus a survey with questions about economic problems such as difficulty paying bills or postponing medical care. Additional information was gathered to gauge childhood self-control and parental interactions.

Among the study participants who were transitioning to adulthood, young people who lived in poverty as children were far more likely to become regular cigarette smokers than children who grew up in wealthier households. The impoverished children also scored low on self-control measures.

"Poor self-control may be a product of limited learning resources and opportunities for developing appropriate behaviors," Fuemmeler said.

Binge drinking, however, was much more common among the wealthier young people. And surprisingly, those who had good self-control as children were more likely to engage in heavy episodic drinking as young adults.

Neither wealth nor poverty appeared to influence marijuana use, although positive parenting did reduce the use of this drug. Parents who were nurturing and accepting, in fact, diminished the likelihood of young people using any of the substances.

The researchers also found no correlation between economic hardship and poor parenting - a contradiction to some other studies.

"We suspected we'd find a relationship between parenting and economic problems - the idea that economic strains may cause parents to have less capacity to deal with their children, but that relationship wasn't there," Fuemmeler said. "That means it's not necessarily poverty that affects the parenting strategy, but poverty that affects the children's self-control."

Fuemmeler said the findings are important given the increase in U.S. children living in poverty. The U.S. Census Bureau reported 22 percent of children lived in poverty in 2010, compared to 18 percent in 2000.

"Continued work is needed to better understand how economic strains may influence the development of self-control, as well as to identify other potential mediators between economic strains and substance use outcomes," Fuemmeler said.

In addition to Fuemmeler, study authors include Chien-Ti Lee, Joseph McClernon, Scott H. Kollins and Kevin Prybol.

The National Institutes of Health (RO1 DA030487), the National Cancer Institute (K07CA124905) and the National Institute on Drug Abuse (K24DA023464) funded the study.

Source-Newswise

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Researchers Uncover Clue About Hearing Loss

Dr Justin Tan of the University of Melbourne and lead author of the study said individuals who lack both copies of this good gene were reported to lose their hearing from 20 years of age.

"This is unusual because most people show gradual signs of age-related hearing loss from 60 years of age onwards but mutations in SERPINB6 accelerate this process. It is not yet clear how this mutation causes hearing loss."

Working with animal models induced with the condition, mice started to lose their hearing at three weeks of age, which is comparable to teenage years in humans. Hearing loss continued to worsen as the mice aged, a trend that was also noticed in humans. When the inner ears of these mice were examined under the microscope, the Melbourne team uncovered that tiny, specialised cells in the inner ear, responsible for hearing, had died.

These cells include, not only the sensory hair cells that detect sound vibrations, but also neighbouring cells that belong to a group of cells called fibrocytes.

Both types of cells are required to transform sound into electrical signals in our hearing nerve. Mutations affecting the sensory hair cells have been known for decades to cause hearing loss in humans but mutations affecting the fibrocytes remain uncommon.

"This is an exciting discovery for our hearing because the role of SERPINB6 as an inhibitor is now being unraveled," said Dr Tan.

Source-Eurekalert

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Researchers Find Way to Multiply Insulin-Producing Cells

Efforts to make this treatment possible have been limited by a dearth of insulin-producing beta cells that can be removed from donors after death, and by the stubborn refusal of human beta cells to proliferate in the laboratory after harvesting.

The new technique uses a cell conditioning solution originally developed to trigger reproduction of cells from the lining of the intestine.

"Until now, there didn't seem to be a way to reliably make the limited supply of human beta cells proliferate in the laboratory and remain functional. We have not only found a technique to make the cells willing to multiply, we've done it in a way that preserves their ability to make insulin," said Michael McDaniel, PhD, professor of pathology and immunology.

Lead author Haytham Aly, PhD, a postdoctoral research scholar, reported on his work with beta cells and was approached by Thaddeus Stappenbeck, MD, PhD, associate professor of pathology and immunology, who studies autoimmune problems in the gut.

Stappenbeck had developed a medium that causes cells from the intestine's lining to proliferate in test tubes.

The ability to produce large quantities of human beta cells in the laboratory gives the researchers hope that they could one day be transplanted into patients with type 1 diabetes.

If the new availability of laboratory-grown beta cells makes it possible to treat patients with transplants from one donor instead of multiple donors, Stappenbeck noted, that might reduce the risk of immune system rejection of the transplants.

The findings are now available online in PLOS ONE.

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Free Bus Travel for Teens Curbs Road Traffic Injuries and Benefits Environment: Researchers

by Rukmani Krishna on? June 15, 2013 at 12:32 AM Lifestyle News The findings show that it also seems to boost the number of short journeys taken by bus, which might otherwise have been cycled or walked.
The researchers wanted to assess the public health impact of giving teens in London free bus travel. The scheme was introduced for 12 to 16 year olds in 2005, and for 17 year olds in 2006.

They therefore used data from the London Area Transport Survey and London Travel Demand Surveys to calculate the number of journeys made in London?as well as distance and principal mode of travel?before (2001-4) and after (2005-9) the scheme was introduced.

And they looked at official data on traffic injuries and hospital admissions to see if the scheme had any noticeable effects on personal safety.

The analysis showed that the proportion of short journeys teens took by bus doubled from 2% to 5%, although the overall number of journeys they took did not increase.

The number of short trips walked also fell in tandem with an increase in this length of journey taken by bus, although there was no appreciable impact on total distance walked.

But there was clear evidence of a fall in the number of short journeys cycled and in distances cycled by young people, although this mode of travel was not hugely popular among this age group before the introduction of the scheme.

Rates of road traffic casualties had started falling before the introduction of the scheme, and continued to fall afterwards, but at a greater rate in young people, largely among passengers and cyclists. Pedestrian casualty rates remained the same.

Hospital admission rates for assaults had been rising among teens before 2005, but were higher among this age group after the scheme's introduction.

The number of daily car journeys taken by young people and adults fell, and the average distance travelled by car also shrank, suggesting that free bus travel prompts a shift away from car use and may therefore be a greener option.

There didn't seem to be any fall in the use of buses by older people after the scheme's introduction either.

"The findings suggest, unsurprisingly, a good uptake in use of buses for fulfilling travel needs, including for short journeys," write the authors.

"One disadvantage appears to be some reduction in the proportion of short trips by walking, and in the (already) low level of cycling; these might be detrimental to the establishment of future travel habits bringing regular physical activity," they suggest.

"On the other hand, the increase in the use of public transport may help to establish travel behaviour for later life that entails some physical activity, as well as helping to reduce car use," they say.

Source-Eurekalert

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2-step Mechanism of Inner Ear Tip Link Regrowth Discovered By Researchers

The discovery offers a possible mechanism for potential interventions that could preserve hearing in people whose hearing loss is caused by genetic disorders related to tip link dysfunction. The work was supported by the National Institute on Deafness and Other Communication Disorders (NIDCD), a component of the National Institutes of Health.

The findings appear in the June 11, 2013 online edition of PLOS Biology. The senior author of this study is Gregory I. Frolenkov, an associate professor in the College of Medicine at the University of Kentucky, Lexington, and his fellow, Artur A. Indzhykulian, Ph.D., is the lead author.

Stereocilia are bundles of bristly projections that extend from the tops of sensory cells, called hair cells, in the inner ear. Each stereocilia bundle is arranged in three neat rows that rise from lowest to highest like stair steps. Tip links are tiny thread-like strands that link the tip of a shorter stereocilium to the side of the taller one behind it. When sound vibrations enter the inner ear, the stereocilia, connected by the tip links, all lean to the same side and open special channels, called mechanotransduction channels. These pore-like openings allow potassium and calcium ions to enter the hair cell and kick off an electrical signal that eventually travels to the brain where it is interpreted as sound.

The findings build on a number of recent discoveries in laboratories at NIDCD and elsewhere that have carefully plotted the structure and function of tip links and the proteins that comprise them. Earlier studies had shown that tip links are made up of two proteins -- cadherin-23 (CDH23) and protocadherin-15 (PCDH15) - that join to make the link, with PCDH15 at the bottom of the tip link at the site of the mechanotransduction channel, and CDH23 on the upper end. Scientists assumed that the assembly was static and stable once the two proteins bonded.

Tip links break easily with exposure to noise. But unlike hair cells, which can't regenerate in humans, tip links repair themselves, mostly within a matter of hours. The breaking of tip links, and their regeneration, has been known about for many years, and is seen as one of the causes of the temporary hearing loss you might experience after a loud blast of sound (or a loud concert). Once the tip links regenerate, hair cell function returns usually to normal levels. What scientists didn't know was how the tip link reassembled.

To study tip link assembly, the researchers treated young, postnatal (5-7 days) mouse sensory hair cells with BAPTA - a substance that, like loud noise, damages and disrupts tip links. To image the proteins, the group pioneered an improved scanning electron microscopy (SEM) technique of immunogold labeling that uses antibodies bound to gold particles that attach to the proteins. Then using SEM they imaged the cells at high resolution to determine the positions of the proteins before, during, and after BAPTA treatment.

What the researchers found was that after a tip link is chemically disrupted, a new tip link forms, but instead of the normal combination of CDH23 and PCDH15, the link is made up of PCDH15 proteins at both ends. Over the next 24 hours, the PCDH15 protein at the upper end is replaced by CDH23 and the tip link is back to normal.

Why tip links regenerate using a two-step instead of a neat one-step process is not known. For reasons that are still unclear, CDH23 disappears from stereocilia after noise damage while PDCH15 stays around. Looking to regenerate quickly, the lower PDCH15 latches onto another PDCH15, forming a shorter and functionally slightly weaker tip link. Later, at some time during the 36 hours after the damage, when CDH23 returns, PDCH15 gives up its provisional partner and latches onto its much stronger mate in CDH23. In other words, PDCH15 prefers to be with CDH23, but in a pinch it will bond weakly with another bit of PDCH15 until CDH23 shows up.

The researchers coupled the SEM observations with electrophysiology studies to show how the functional properties of the tip links changed throughout this two-step process. The temporary PCDH15/PCDH15 tip link has a slightly different functional response than the permanent PDCH15/CDH23 combination. Researchers were able to correlate the differences in function with the protein combinations that make up the tip link.

Additional experiments revealed that when hair cells develop, the tip links use the same two-step process.

Previous research has shown that both CDH23 and PCDH15 are required for normal hearing and vision. In fact, NIDCD scientists in earlier studies have shown that mutations in either of these genes can cause the hearing loss or deaf-blindness found in Usher Syndrome types 1D and 1F.

"In the case of deaf individuals who are unable to make functional CDH23, knowledge of this new temporary alliance of PCDH15 proteins to form a weaker, but still functional, tip link could inform treatments that would encourage the double PCDH15 bond to become permanent and maintain at least limited hearing," said Tom Friedman, Ph.D., chief of the Laboratory of Molecular Genetics at NIDCD where the research began.

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Researchers Explain How Brain Stops Us from Being Impulsive

by Rukmani Krishna on? July 06, 2013 at 12:00 AM Research News Researchers have found that your feelings about something and the value you put on it are calculated similarly in a specific area of the brain. The researchers who are from Duke University study how the brain values things-a field called neuroeconomics.
The region is small area right between the eyes at the front of the brain. It's called the ventromedial prefrontal cortex, or vmPFC for short.

Scott Huettel, director of Duke's Center for Interdisciplinary Decision Science, said scientists studying emotion and neuroeconomics had independently singled out this area of the brain in their research but neither group recognized that the other's research was focused on it too.

Now, after a series of experiments in which subjects were asked to modify how they felt about something either positively or negatively, the Duke group is arguing that emotional and economic calculations are more closely related than brain scientists had realized.

"The neuroscience fits with your intuitive understanding," Amy Winecoff, a graduate student in psychology and neuroscience who led the research, said.

"Emotions appear to be relying on the same value system," she said.

The study is published in the Journal of Neuroscience.

Source-ANI

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Researchers Develop Sugar Solution That Turns Tissues Transparent in 3 Days

Combined with fluorescence microscopy, this technique enabled researchers at the RIKEN Center for Developmental biology to obtain detailed images of a mouse brain at an unprecedented resolution.

Over the past few years, teams in the USA and Japan have reported a number of techniques to make biological samples transparent, that have enabled researchers to look deep down into biological structures like the brain.

"However, these clearing techniques have limitations because they induce chemical and morphological damage to the sample and require time-consuming procedures," explains Dr. Takeshi Imai, who led the study.

SeeDB, an aqueous fructose solution that Dr. Imai developed with colleagues Drs. Meng-Tsen Ke and Satoshi Fujimoto, overcomes these limitations.

Using SeeDB, the researchers were able to make mouse embryos and brains transparent in just three days, without damaging the fine structures of the samples, or the fluorescent dyes they had injected in them.

They could then visualize the neuronal circuitry inside a mouse brain, at the whole-brain scale, under a customized fluorescence microscope without making mechanical sections through the brain.

They describe the detailed wiring patterns of commissural fibers connecting the right and left hemispheres of the cerebral cortex, in three dimensions, for the first time.

Dr. Imai and colleagues report that they were also able to visualize in three dimensions the wiring of mitral cells in the olfactory bulb, which is involved the detection of smells, at single-fiber resolution.

IMAGE: Japanese researchers have developed a new sugar and water-based solution called SeeDB that turns tissues transparent in just three days, without disrupting the shape and chemical nature of the samples....

"Because SeeDB is inexpensive, quick, easy and safe to use, and requires no special equipment, it will prove useful for a broad range of studies, including the study of neuronal circuits in human samples," explain the authors.

The study was recently published in the journal Nature Neuroscience.

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Alzheimer's Disease Protein Controls Movement in Mice: Researchers

Alzheimer's disease is the most common form of dementia found in older adults. The World Health Organization estimates that approximately 18 million people worldwide have Alzheimer's disease. The number of people affected by the disease may increase to 34 million by 2025. Scientists know that the protein beta-secretase-1 or Bace1, a protease enzyme that breaks down proteins into smaller molecules, is involved in Alzheimer's disease. Bace1 cleaves the amyloid precursor protein and generates the damaging Abeta peptides that accumulate as plaques in the brain leading to disease. Now scientists have revealed in more detail how Bace1 works.

"Our results show that mice that lack Bace1 proteins or are treated with inhibitors of the enzyme have difficulties in coordination and walking and also show reduced muscle strength," remarked Carmen Birchmeier, one of the authors of the paper, Professor at the Max-Delbr?ck-Center for Molecular Medicine in Berlin, Germany, and an EMBO Member. "In addition, we were able to show that the combined activities of Bace1 and another protein, neuregulin-1 or Nrg1, are needed to sustain the muscle spindles in mice and to maintain motor coordination."

Muscle spindles are sensory organs that are found throughout the muscles of vertebrates. They are able to detect how muscles stretch and convey the perception of body position to the brain. The researchers used genetic analyses, biochemical studies and interference with pharmacological inhibitors to investigate how Bace1 works in mice. "If the signal strength of a specific form of neuregulin-1 known as IgNrg1 is gradually reduced, increasingly severe defects in the formation and maturation of muscle spindles are observed in mice. Furthermore, it appears that Bace1 is required for full IgNrg1 activity. The graded loss of IgNrg1 activity results in the animals having increasing difficulties with movement and coordination," says Cyril Cheret, the first author of the work.

Drug developers are interested in stopping the Bace1 protein in its tracks because it represents a promising route to treat Alzheimer's disease. If the protein were inhibited, it would interfere with the generation of the smaller damaging proteins that accumulate in the brain as amyloid plaques and would therefore provide some level of protection from the effects of the disease. "Our data indicate that one unwanted side effect of the long-term inhibition of Bace1 might be the disruption of muscle spindle formation and impairment of movement. This finding is relevant to scientists looking for ways to develop drugs that target the Bace1 protein and should be considered," says Birchmeier. Several Bace1 inhibitors are currently being tested in phase II and phase III clinical trials for the treatment of Alzheimer's disease.

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Potentially Life-saving Cooling Treatment Rarely Used for In-hospital Cardiac Arrests: Researchers

by Rukmani Krishna on? June 25, 2013 at 12:13 AM Heart Disease News Researchers from the Perelman School of Medicine at the University of Pennsylvania report in the June issue of Critical Care Medicine that the brain-preserving cooling treatment known as therapeutic hypothermia is rarely being used in patients who suffer cardiac arrest while in the hospital, despite its proven potential to improve survival and neurological function. The authors suggest that scarce data about in-hospital cardiac arrest patients and guidelines that only call for health care providers to consider use of therapeutic hypothermia, rather than explicitly recommending it, may explain the study's results.
In a prospective study between 2003 and 2009 of over 530 hospitals in the United States, the Penn team found that 98 percent of over 67,000 patients who went into cardiac arrest in the hospital received only conventional post-resuscitation care--leaving just 2 percent who received therapeutic hypothermia, which has been credited with saving the lives of a growing number of patients who arrest outside hospitals.

"We know it's being used in patients who went into cardiac arrest in their homes, at work, or anywhere else outside of a hospital, but little was known about how often it's used in patients who arrest in the hospital," said Mark E. Mikkelsen, MD, MSCE, assistant professor in the division of Pulmonology, Critical Care and Allergy at Penn Medicine. "We found that even though most hospitals have the capability to treat these patients with therapeutic hypothermia, it's not being used. And even when it was used, in nearly half the cases, the correct target temperature was not being achieved.

"Several factors could explain this: there is little data, which is often conflicting, to support its use for patients in the hospital, and we have national guidelines that only have clinicians considering its use, which may lead to hesitation and lack of institutional protocol."

Cooling the body down to about 89.6 degrees after cardiac arrest protects it against neurological damage initiated by the lack of blood flow and oxygenation, several studies of out-of-hospital cardiac arrest patients have shown. It has also been shown to improve survival--a welcome development, since cardiac arrest survival statistics remain grim, with less than 10 percent of patients surviving in most cities across the U.S.

More than 300,000 people who go into cardiac arrest out of the hospital die each people each year in the United States; thousands of others are left neurologically devastated.

About 210,000 patients a year go into cardiac arrest while in the hospital--many of those patients may have other conditions that point to a poor prognosis, and a substantial portion may be terminally ill patients who are not candidates for hypothermia.

National recommendations established in 2005 call for out-of-hospital cardiac arrest patients to be treated with hypothermia when they remain comatose after resuscitation. In-hospital recommendations, however, are less direct. The International Liaison Committee on Resuscitation guidelines recommend providers to "consider its use," while the American Heart Association recommends that therapeutic hypothermia "may be considered" for a patient who goes into cardiac arrest caused by non-shockable rhythms.

For the study, the team analyzed treatments of 67,498 patients at 538 hospitals participating in the American Heart Association's Get With the Guidelines-Resuscitation database from 2003 to 2009. Of those patients, 1,367 patients were given therapeutic hypothermia. The use of therapeutic hypothermia increased slightly, from 0.7 percent in 2003 to 3.3 percent in 2009.

Younger patients and patients who were treated in a non-ICU location and a teaching hospital were more likely to get therapeutic hypothermia. Even when it was used, however, target temperature (32-34o Celsius, or 89.6-93.2 degrees Fahrenheit ) was not achieved in 44.3 percent of the patients within 24 hours, and 17.6 percent were overcooled.

"These rates are particularly important to examine, given that the incidence of in hospital events appears to be increasing," said Dr. Mikkelsen. "I believe there is potential for therapeutic hypothermia to benefit this population, but traction can only be made after clinical trials investigating safety and effectiveness are initiated-which are certainly warranted. Results of those studies could strengthen the case for stronger recommendations and increase use."

Source-Eurekalert

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Researchers Conduct Genomic Survey of Human Skin Fungal Diversity

In the first study of human fungal skin diversity, National Institutes of Health researchers sequenced the DNA of fungi at skin sites of healthy adults to define the normal populations across the skin and to provide a framework for investigating fungal skin conditions.

Human skin surfaces are complex ecosystems for microorganisms, including fungi, bacteria and viruses, which are known collectively as the skin microbiome. Although fungal infections of the skin affect about 29 million people in the United States, fungi can be slow and hard to grow in laboratories, complicating diagnosis and treatment of even the most common fungal skin conditions, such as toenail infections.

The research team from the National Human Genome Research Institute (NHGRI) and the National Cancer Institute (NCI), both parts of NIH, extended their recent genome sequencing study of skin bacteria, using DNA sequencing techniques optimized for identifying fungi. The study appears in the May 22, 2013 early online issue of Nature.

The researchers found that a single type of fungus, belonging to the genus Malassezia, is predominant on the head and trunk. Hands, which harbor a great diversity of bacteria, are home for relatively few types of fungi. In contrast, feet, including toenails, heels and toe webs contain tremendous diversity.

"Applying DNA sequencing to a study of the skin's fungi is the natural progression in understanding microbial life that co-exists on our bodies," said NHGRI Scientific Director Daniel Kastner, M.D., Ph.D. "Along with recent genome sequencing to define bacterial diversity, this analysis of fungal diversity provides a more complete human microbiome picture."

"Fungal communities occupy complex niches, even on the human body," said Heidi Kong, M.D., co-senior author and an investigator in the dermatology branch of NCI's Center for Cancer Research. "By gaining a more complete awareness of the fungal and bacterial ecosystems, we can better address associated skin diseases, including skin conditions which can be related to cancer treatments."

The researchers collected samples at 14 body sites from 10 healthy adults. DNA sequencing of the fungi in the samples identified fragments of DNA, called phylogenetic markers, which can be counted and used to distinguish one type of fungus from another. The sequencing efforts generated more than 5 million markers, from the samples, representing more than 80 fungal types, or genera. In contrast, traditional culturing methods produced 130 colonies of fungi that represented only 18 fungal genera.

In 20 percent of the study participants, the researchers observed problems such as heel and toe web scaling or toenail changes consistent with possible fungal infections. From genome sequencing analysis, the researchers found that different individuals with heel site infections have common fungal communities at that site, while those with toenail infections display tremendously different fungal communities.

"DNA sequencing reveals the great diversity of fungi, even those that are hard to grow in culture," said Julie Segre, Ph.D., co-senior author and senior investigator, NHGRI Genetics and Molecular Biology Branch. Her expertise is the development of microbial DNA sequencing technology. "DNA sequencing enabled us to learn immeasurably more about where fungi predominate as a part of the human skin microbiome."

The researchers identified fungi from two phyla, Ascomycetes and Basidiomycetes, as part of the normal fungal census at the 14 skin sites. The most common genus Malassezia was present in 11 of 14 sites sampled on the body. The researchers found Malassezia fungus on every skin surface of healthy volunteers, whether on the back of the head, behind the ears, in nostrils and on the heels. Heels were also home to many additional fungi, including the genera Aspergillus, Cryptococcus, Rhodotorula, and Epicoccum.

"DNA sequence-based methods of identification enabled us to differentiate among species of fungi and to conclude that the diversity of fungi is highly dependent on the body site rather than the person who is sampled," said Dr. Kong. A dermatologist, Dr. Kong explained why these sites were selected for exploration: "Our study focused on areas of the skin where we commonly find skin diseases that have been associated with fungi."

The most complex site, the heel, is home to about 80 genus-level types of fungi. The researchers found about 60 types in toenail swab samples and 40 types in samples from the webs of the toes. Sites with moderate fungal diversity are inside the bend of the arm, inside of the forearm and palm, with each location supporting 18 to 32 genera of fungi. Surprisingly, head and trunk body sites ? including the back, back of the neck, inside the ears, behind the ears, and between the eyebrows? have far fewer fungi types, with just two to 10 genera each.

The research team compared fungal diversity data with the skin bacteria on the same healthy adults. They found that while arms have high measures of bacterial diversity, they have lower fungal diversity. They found the reverse to be true for sites on the feet. Core body sites had neither a high bacterial diversity nor a high fungal diversity. The researchers had previously shown that bacterial diversity can be predicted by whether skin is moist, dry or oily. Fungal diversity, instead, seems to depend upon where a particular skin site is on the body.

The researchers observed, in addition, that there is greater similarity in the fungal community structure on the left and right sides of the same person's body compared to the same body parts on any two individuals. Fungal communities also appear to be quite stable over time, with little change when tested on two separate occasions, up to three months apart.

"The data from our study gives us a baseline about normal individuals that we never had before," Dr. Segre said. "The bottom line is your feet are teeming with fungal diversity, so wear your flip flops in locker rooms if you don't want to mix your foot fungi with someone else's fungi."

Source-Eurekalert

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Newly Identified Immune Protein Could Stop Diabetes in Its Tracks: Melbourne Researchers

The discovery has wider repercussions, as the protein is responsible for protecting the body against excessive immune responses, and could be used to treat, or even prevent, other immune disorders such as multiple sclerosis and rheumatoid arthritis.

Professor Len Harrison, Dr Esther Bandala-Sanchez and Dr Yuxia Zhang led the research team from the Walter and Eliza Hall Institute's Molecular Medicine division that identified the immune protein CD52 as responsible for suppressing the immune response, and its potential for protecting against autoimmune diseases.

So-called autoimmune diseases develop when the immune system goes awry and attacks the body's own tissues. Professor Harrison said CD52 held great promise as a therapeutic agent for preventing and treating autoimmune diseases such as type 1 diabetes.

"Immune suppression by CD52 is a previously undiscovered mechanism that the body uses to regulate itself, and protect itself against excessive or damaging immune responses," Professor Harrison said.

"We are excited about the prospect of developing this discovery to clinical trials as soon as possible, to see if CD52 can be used to prevent and treat type 1 diabetes and other autoimmune diseases. This has already elicited interest from pharmaceutical companies," he noted.

Type 1 diabetes is an autoimmune disease that develops when immune cells attack and destroy insulin-producing beta cells in the pancreas.

Professor Harrison said that T cells that have or release high levels of CD52 are necessary to maintain normal balance in the immune system.

"In a preclinical model of type 1 diabetes, we showed that removal of CD52-producing immune cells led to rapid development of diabetes. We think that cells that release CD52 are essential to prevent the development of autoiummune disease, and that CD52 has great potential as a therapeutic agent," he said.

CD52 appears to play a dominant role in controlling or suppressing immune activity in the early stages of the immune response, Professor Harrison said.

"We identified a specialised population of immune cells (T cells) that carry high levels of CD52, which they release to dampen the activity of other T cells and prevent uncontrolled immune responses," Professor Harrison said.

"The cells act as an early 'braking' mechanism," he added.

Professor Harrison said his goal is to prevent and ultimately cure type 1 diabetes.

He revealed that they can prevent and cure type 1 diabetes in animal models and he's hopeful that these results will be translatable into humans, hopefully in the not-too-distant future.

The research was published today in the journal Nature Immunology.

Source-ANI

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A Step to Unlocking Mystery of Ageing Taken By Swiss Researchers

by Rukmani Krishna on? May 25, 2013 at 11:28 PM Genetics & Stem Cells News A step closer to unlocking the mystery of ageing was taken by Swiss researchers after discovering the impact of a longevity gene in mice and then managing to extend the life-span of worms by 60 percent thanks to a basic antibiotic treatment.
"They were not only living longer, but were also more fit," said Johan Auwerx ion a video released by the Ecole Polytechnique Federale de Lausanne (EPFL), a cutting-edge Swiss research institute.

The findings of Auwerx's team have been published in the scientific journal Nature.

The goal of the research was to work out why certain individuals of the same species can have a far longer life-span than others.

"Our lab has for some time been using a complex genetic reference population of mice, which mimic the human population, to study ageing," said Auwerx.

The scientists started by examining mice's mitochondria -- a cell's version of a power plant -- and uncovered a group of three genes that affected the animals' life-span via their speed of functioning.

Those whose genes were 50 percent slower lived some 250 days longer, or about 30 percent of a mouse's lifetime.

"Based on this observation, we switched model, and started validating this experimentally in a worm," said Auwerx.

"Knocking down the same proteins, we could see an up to 60 percent extension of worm life-span," he added.

Auwerx underlined that since mitochondria are bacteria living within cells, his team then experimented with antibiotics, which target bacteria.

"We could see that treating the worms with the antibiotics also mimicked the genetic effects, and they also lived 60 percent longer," from 19 days to 30, he explained.

Mitochondria transform nutrients into various kinds of protein, and several previous studies have suggested that they may be the motor of ageing.

The Swiss team, working with counterparts in the Netherlands and United States, managed to identify the specific gene involved in the process and work out how variations in protein could affect life-span.

They worked out that so-called MRPs -- for mitochondrial ribosomal proteins -- had an inversely proportional impact on longevity.

In addition, they found that a lack of MRPs at key moments of an individual's early development caused stress on mitochondria.

This has short-term negative impacts such as a fall in fertility, but in the long term appeared to result in a better muscle structure as well as a longer life.

The researchers underlined that further studies would be needed to confirm whether antibiotics could be used to rein in ageing in mammals.

Source-AFP

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Largest Genetic Sequencing Study of Human Disease Completed By Researchers

The exact cause of these diseases - autoimmune thyroid disease, coeliac disease, Crohn's disease, psoriasis, multiple sclerosis and type 1 diabetes- is unknown, but is believed to be a complex combination of genetic and environmental factors. In each disease only a proportion of the heritability is explained by the identified genetic variants. The techniques used to date, have generally identified common (in the population) variants of weak effect.

In this study, using high-throughput sequencing techniques,a global team of scientists sought to identify new variants, including rare and potentially high risk ones, in 25 previously identified risk genes in a sample of nearly 42,000 individuals (24,892 with autoimmune disease and 17,019 controls).

It has been suggested - in the 'rare-variant synthetic genome-wide association hypothesis' - that a small number of rare variants in risk genes are likely to be a major cause of the heritability of these conditions.

However, the study published today in the journal Nature, suggests that the genetic risk of these diseases more likely involves a complex combination of hundreds of weak-effect variants which are each common in the population.

The authors estimate that rare variants in these risk genes account for only around three per cent of the heritability of these conditions that can be explained by common variants.

David van Heel, Professor of Gastrointestinal Genetics at Barts and The London School of Medicine and Dentistry at Queen Mary and director of the Barts and The London Genome Centre, led the study. He said: "These results suggests that risk for these autoimmune diseases is not due to a few high-risk genetic variations but seems rather due to a random selection from many common genetic variants which each have a weak effect.

"For each disease there are probably hundreds such variants and the genetic risk is likely to come from inheriting a large number of these variants from both parents. If this is the case then it may never be possible to accurately predict an individual's genetic risk of these common autoimmune diseases. However, the results do provide important information about the biological basis of these conditions and the pathways involved, which could lead to the identification new drug targets."

The research utilized high-throughput sequencing techniques performed at the Barts and The London Genome Centre and demonstrated for the first time that the sequencing can call genotypes as accurately as 'gold standard techniques' such as genotyping array platforms.

Additional laboratory work was carried out at the Blizard institute at Queen Mary.

Professor Richard Trembath, Vice Principal and Executive Dean for Health at Barts and The London School of Medicine and Dentistry, Queen Mary, and a co-author on the paper said: "The results prompt a re-assessment of the genetic architecture that determines risk for development of common auto-immune disorders and will fuel future careful assessment of regions of the human genome beyond those presently known to confer susceptibility to these important medical conditions."

Source-Eurekalert

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