ScienceDaily (July 3, 2012) — searchers from the University of Maryland School of Maryland report promising results from using adult stem cells from bone marrow in mice to help create tissue cells of other organs, such as the heart, brain and pancreas — a scientific step they hope may lead to potential new ways to replace cells lost in diseases such as diabetes, Parkinson’s or Alzheimer’s.

The research in collaboration with the University of Paris Descartes is published online in the June 29, 2012 edition of Comptes Rendus Biologies, a publication of the French Academy of Sciences.

"Finding stem cells capable of restoring function to different damaged organs would be the Holy Grail of tissue engineering," says lead author David Trisler, PhD, assistant professor of neurology at the University of Maryland School of Medicine.

He adds, “This research takes us another step in that process by identifying the potential of these adult bone marrow cells, or a subset of them known as CD34+ bone marrow cells, to be ‘multipotent,’ meaning they could transform and function as the normal cells in several different organs.”

University of Maryland researchers previously developed a special culturing system to collect a select sample of these adult stem cells in bone marrow, which normally makes red and white blood cells and immune cells. In this project, the team followed a widely recognized study model, used to prove the multipotency of embryonic stem cells, to prove that these bone marrow stem cells could make more than just blood cells. The investigators also found that the CD34+ cells had a limited lifespan and did not produce teratomas, tumors that sometimes form with the use of embryonic stem cells and adult stem cells cultivated from other methods that require some genetic manipulation.

"When taken at an early stage, we found that the CD34+ cells exhibited similar multipotent capabilities as embryonic stem cells, which have been shown to be the most flexible and versatile. Because these CD34+ cells already exist in normal bone marrow, they offer a vast source for potential cell replacement therapy, particularly because they come from a person’s own body, eliminating the need to suppress the immune system, which is sometimes required when using adults stem cells derived from other sources," explains Paul Fishman, MD, PhD, professor of neurology at the University of Maryland School of Medicine.

The researchers say that proving the potential of these adult bone marrow stem cells opens new possibilities for scientific exploration, but that more research will be needed to see how this science can be translated to humans.

Source: Science Daily

ScienceDaily (July 3, 2012) — As the United States confronts the growing epidemic of obesity among children and adults, a team of University of Colorado School of Medicine obesity researchers concludes that what the nation needs is a new battle plan — one that replaces the emphasis on widespread food restriction and weight loss with an emphasis on helping people achieve “energy balance” at a healthy body weight.

In a paper published in the July 3 issue of the journal Circulation, James O. Hill, PhD. and colleagues at the Anschutz Health and Wellness Center take on the debate over whether excessive food intake or insufficient physical activity cause obesity, using the lens of energy balance — which combines food intake, energy expended through physical activity and energy (fat) storage — to advance the concept of a “regulated zone,” where the mechanisms by which the body establishes energy balance are managed to overcome the body’s natural defenses towards preserving existing body weight. This is accomplished by strategies that match food and beverage intake to a higher level of energy expenditure than is typical in America today, enabling the biological system that regulates body weight to work more effectively. Additional support for this concept comes from many studies showing that higher levels of physical activity are associated with low weight gain whereas comparatively low levels of activity are linked to high weight gain over time.

"A healthy body weight is best maintained with a higher level of physical activity than is typical today and with an energy intake that matches," explained Hill, professor of pediatrics and medicine and executive director of the Anschutz Health and Wellness Center at the University of Colorado Anschutz Medical Campus and the lead author of the paper. "We are not going to reduce obesity by focusing only on reducing food intake. Without increasing physical activity in the population we are simply promoting unsustainable levels of food restriction. This strategy hasn’t worked so far and it is not likely to work in the future.

As Dr. Hill explains, “What we are really talking about is changing the message from ‘Eat Less, Move More” to ‘Move More, Eat Smarter.’ “

The authors argue that preventing excessive weight gain is a more achievable goal than treating obesity once it is present. Here, the researchers stress that reducing calorie intake by 100 calories a day would prevent weight gain in 90 percent of the adult population and is achievable through small increases in physical activity and small changes in food intake.

People who have a low level of physical activity have trouble achieving energy balance because they must constantly use food restriction to match energy intake to a low level of energy expenditure. Constant food restriction is difficult to maintain long-term and when it cannot be maintained, the result is positive energy balance (when the calories consumed are greater than the calories expended) and an increase in body mass, of which 60 percent to 80 percent is usually body fat. The increasing body mass elevates energy expenditure and helps reestablish energy balance. In fact, the researchers speculate that becoming obese may be the only way to achieve energy balance when living a sedentary lifestyle in a food-abundant environment.

Using an exhaustive review of the energy balance literature as the basis, the researchers also refuted the popular theory that escalating obesity rates can be attributed exclusively to two factors — the change in the American diet and the rise in overall energy intake without a compensatory increase in energy expenditure. Using rough estimates of increases in food intake and decreases in physical activity from 1971 to 2000, the researchers calculated that were it not for the physiological processes that produce energy balance, American adults would have experienced a 30 to 80 fold increase in weight gain during that period, which demonstrates why it is not realistic to attribute obesity solely to caloric intake or physical activity levels. In fact, energy expenditure has dropped dramatically over the past century as our lives now require much less physical activity just to get through the day. The authors argue that this drop in energy expenditure was a necessary prerequisite for the current obesity problem, which necessitates adding a greater level of physical activity back into our modern lives.

"Addressing obesity requires attention to both food intake and physical activity, said co-author John Peters, PhD., assistant director of the Anschutz Health and Wellness Center. "Strategies that focus on either alone will not likely work."

In addition, the researchers conclude that food restriction alone is not effective in reducing obesity, explaining that although caloric restriction produces weight loss, this process triggers hunger and the body’s natural defense to preserve existing body weight, which leads to a lower resting metabolic rate and notable changes in how the body burns calories. As a result, energy requirements after weight loss can be reduced from 170 to 250 calories for a 10 percent weight loss and from 325 to 480 calories for a 20 percent weight loss. These findings provide insight concerning weight loss plateau and the common occurrence of regaining weight after completing a weight loss regimen.

Recognizing that energy balance is a new concept for to the public, the researchers call for educational efforts and new information tools that will teach Americans about energy balance and how food and physical activity choices affect energy balance.

Source: Science Daily

ScienceDaily (July 3, 2012) — Scientists at Arizona State University have discovered that older honey bees effectively reverse brain aging when they take on nest responsibilities typically handled by much younger bees. While current research on human age-related dementia focuses on potential new drug treatments, researchers say these findings suggest that social interventions may be used to slow or treat age-related dementia.

Old bees collect nectar and pollen. Most bees start doing this job when they are 3-4 weeks old, and after that they age very quickly. Their bodies and wings become worn and they loose the ability to learn new things. Most food collector bees die after about 10 days. (Credit: Christofer Bang)

In a study published in the scientific journal Experimental Gerontology, a team of scientists from ASU and the Norwegian University of Life Sciences, led by Gro Amdam, an associate professor in ASU’s School of Life Sciences, presented findings that show that tricking older, foraging bees into doing social tasks inside the nest causes changes in the molecular structure of their brains.

"We knew from previous research that when bees stay in the nest and take care of larvae — the bee babies — they remain mentally competent for as long as we observe them," said Amdam. "However, after a period of nursing, bees fly out gathering food and begin aging very quickly. After just two weeks, foraging bees have worn wings, hairless bodies, and more importantly, lose brain function — basically measured as the ability to learn new things. We wanted to find out if there was plasticity in this aging pattern so we asked the question, ‘What would happen if we asked the foraging bees to take care of larval babies again?"

During experiments, scientists removed all of the younger nurse bees from the nest — leaving only the queen and babies. When the older, foraging bees returned to the nest, activity diminished for several days. Then, some of the old bees returned to searching for food, while others cared for the nest and larvae. Researchers discovered that after 10 days, about 50 percent of the older bees caring for the nest and larvae had significantly improved their ability to learn new things.

Amdam’s international team not only saw a recovery in the bees’ ability to learn, they discovered a change in proteins in the bees’ brains. When comparing the brains of the bees that improved relative to those that did not, two proteins noticeably changed. They found Prx6, a protein also found in humans that can help protect against dementia — including diseases such as Alzheimer’s — and they discovered a second and documented “chaperone” protein that protects other proteins from being damaged when brain or other tissues are exposed to cell-level stress.

In general, researchers are interested in creating a drug that could help people maintain brain function, yet they may be facing up to 30 years of basic research and trials.

"Maybe social interventions — changing how you deal with your surroundings — is something we can do today to help our brains stay younger," said Amdam. "Since the proteins being researched in people are the same proteins bees have, these proteins may be able to spontaneously respond to specific social experiences."

Amdam suggests further studies are needed on mammals such as rats in order investigate whether the same molecular changes that the bees experience might be socially inducible in people.

Source: Science Daily

July 3, 2012

Scientists at The University of Nottingham are leading research that will develop the world’s first ‘atlas’ of the Asian brain.

Working in collaboration with colleagues in South Korea, the project aims to build a detailed picture of how the Asian brain develops normally, taking into account the differences and variations which occur from person to person.

The resulting road-map of the brain could be used to help doctors in countries like South Korea, Japan and China to develop new diagnostic tools for age-related neurodegenerative diseases such as Alzheimer’s, Parkinson’s and dementia, allowing them to spot illnesses at a much earlier stage, thereby improving treatment options and outcomes.

The two-year project will marry the expertise of Nottingham academics in advanced brain imaging techniques, including ultra high field magnetic resonance imaging (MRI), with the clinical expertise and specialist computer software development skills of researchers at Korea University in Seoul.

Stephen Jackson, Professor of Cognitive Neuroscience in the University’s School of Psychology, said: “Developing this atlas of the Asian brain will be a major step forward in furthering the field of neuroscience, which is developing rapidly in the East.

"We hope this two-year project will also act as a template for further UK-South Korean collaboration and knowledge transfer, which has been highlighted by Government as a strategic priority."

The project, initially funded with a Global Partnership Fund grant from the British Foreign and Commonwealth Office (BIS), will see the Nottingham academics working with colleagues in the College of Medicine, Biomedical Engineering, and Psychology at Korea University, to scan the brains of healthy Asian adults using advanced MRI techniques.

Data from the hundreds of images produced will then be analysed and computer modelling techniques used to build up a detailed picture of how a normal Asian brain develops in adults, taking into account the slight variations that occur from person to person.

There are subtle differences in the size and genetics of the Asian brain compared to its Western cousin and the research will allow for the development of new diagnostic aids for age-related neuro-degenerative diseases which are specifically tailored to Asian patients.

The research will build on The University of Nottingham’s reputation as a world-leader in MRI research — the technique was invented there by Professor Sir Peter Mansfield, whose work jointly earned him the Nobel Prize for Medicine in 2003.

Biomedical imaging remains a strategic research priority for Nottingham through its Sir Peter Mansfield Magnetic Resonance Centre, which hosts the UK’s only 7 Tesla MRI scanner.

The University has recently established a UK Centre for Child Neuroimaging, a core theme of Nottingham’s Impact Campaign, the biggest fundraising campaign in The University of Nottingham’s 130 year history. It aims to raise £150m to transform research, enrich the student experience and enable the institution to make an even greater contribution to the global communities it serves.

The work to map the Asian brain will also involve collaboration with academics at other UK and European institutions, including University College London, the Institute of Neurology, Institute of Psychiatry, Imperial College and the University of Aachen in Germany.

The collaboration between The University of Nottingham and Korea University is the latest in a long-running relationship between the two higher education institutions and follows the signing of a Memorandum of Understanding, along with 12 other universities in the Universitas 21 group, in 2009 that aimed to offer postdoc students international opportunities through a joint PhD programme.

Provided by University of Nottingham

Source: medicalxpress.com

ScienceDaily (July 2, 2012) — Watching 3D movies can “immerse” you in the experience — but can also lead to visual symptoms and even motion sickness, reports a study — “Stereoscopic Viewing and Reported Perceived Immersion and Symptoms,” in the July issue of Optometry and Vision Science, official journal of the American Academy of Optometry.

The journal is published by Lippincott Williams & Wilkins, a part of Wolters Kluwer Health.

Symptoms related to 3D viewing are affected by where you sit while watching, and even how old you are. “Younger viewers incurred higher immersion but also greater visual and motion sickness symptoms in 3D viewing,” according to the authors, led by Shun-nan Yang, PhD, of Pacific University College of Optometry, Forest Grove, Ore. “Both [problems] will be reduced if a farther distance and a wider viewing angle are adopted.”

Greater ‘Immersion’ in 3D Also Associated With Increased Symptoms

The researchers performed experiments in which adults, from young adult to middle-aged, were invited to watch a movie (Cloudy with a Chance of Meatballs) in 2D or 3D while sitting at different angles and distances. Visual and other symptoms were assessed — including the role of factors including age, seating position, and level of “immersion” in the movie.

Twenty-one percent of participants reported symptoms while watching the movie in 3D, compared to twelve percent with 2D viewing. For younger study participants blurred vision, double vision, dizziness, disorientation, and nausea were all more frequent and severe when watching the movie in 3D.

3D viewing also led to a greater sense of immersion — “a greater sense of object motion and motion of the viewer in space” — compared to 2D viewing. Subjects sitting in more central or closer positions reported greater immersion as well as increased symptoms of motion sickness — that is, nausea. Sitting at an angle to the screen was associated with less immersion as well as reduced motion symptoms.

There were some differences by age, including a lower rate of blurred vision in older viewers (age 46 and older). Older viewers had more visual and motion sickness symptoms in 2D viewing, while younger viewers (age 24 to 34) had more symptoms in 3D viewing. The same age-related changes leading to lower rates of blurred vision in older viewers may also explain their lower rates of symptoms during 3D vision.

As 3D movies become more common, including on home screens, there are reports of visual and other symptoms among 3D viewers. Vision and orientation symptoms related to 3D viewing may be related to a “mismatch” between focusing and converging the eyes. Anthony Adams, OD, PhD, Editor-in-Chief of Optometry and Vision Science notes “the technology for reducing mismatch between where the eyes converge and where they focus is likely to improve rapidly.”

The study identifies several factors associated with symptoms during 3D viewing. “3D viewing is quite specific in causing blurred vision and double vision, and the resultant symptoms are greater for younger adults,” Dr Yang and colleagues write. 3D produces a greater sense of immersion than 2D viewing, which leads to more symptoms of motion sickness — especially for younger adults and when viewing from a closer distance and a more direct angle.

The study will help optometrists and other eye care professionals in talking to patients about visual and other symptoms related to today’s sophisticated 3D video setups.

Source: Science Daily

ScienceDaily (July 2, 2012) — Using an in vitro cell model of Huntington’s disease (HD), researchers at Florida Atlantic University’s Charles E. Schmidt College of Medicine have discovered a novel mechanism and potential link between mutant huntingtin, cell loss and cell death or apoptosis in the brain, which is responsible for the devastating effects of this disease. Apoptosis has been proposed as one of the mechanisms leading to neuronal death in HD.

Dr. Jianning Wei, Ph.D., assistant professor of biomedical science in the Schmidt College of Medicine, has received a $428,694 grant from the National Institutes of Health (NIH) for a project titled “Regulation of BimEL phosphorylation in the pathogenesis of Huntington’s disease.” With this grant, she will further her research and investigation of the molecular and physiological functions of BimEL, a protein known to promote cell death, in a rodent HD model to better understand the pathogenesis of this disease and develop treatments and therapies to prevent or slow down its progression. Wei’s previous findings may also represent a universal mechanism in the pathogenesis of neurodegenerative diseases that are involved with protein misfolding and aggregation — a phenomenon that occurs in many highly debilitating disorders including neurodegenerative diseases.

HD is a fatal, inherited disease caused by abnormal repeats of a small segment in an individual’s DNA or genetic code. The production of malfunctioning proteins in the body are results of this mutation, and the more repeat the protein contains, the worse the disease. A person who has the disease carries one normal copy of the gene and one mutated copy in his or her cells. Although the mutated forms of these genes are known for their devastating effects, their normal forms are critical for nerve function, embryonic development and other bodily processes. Similar mutations in other proteins are involved in several other neurodegenerative diseases.

"HD is a highly complex genetic, neurological disorder that causes certain nerve cells in the brain to waste away, and the underlying molecular mechanism of this disease still remains elusive," said Wei. "We are continuing our research to identify the pathways in the brain that are altered in response to mutant proteins, as well as to understand the cellular processes impacted by the disease in order to facilitate the development of effective pharmacological interventions."

Named after American physician George Huntington, HD is characterized by a selective loss of neurons in the brain and affects the basal ganglia, which controls motor control, cognition, learning and emotions. It also affects the outer surface of the brain or the cortex, which controls thought, perception, and memory. It is estimated that more than 250,000 Americans have HD or are at risk of inheriting the disease from an affected parent.

"The vital research that Dr. Wei and her colleagues are conducting at Florida Atlantic University will help to shed light on a very devastating and difficult disease for which there are currently no treatments available to stop or reverse its course," said Dr. David J. Bjorkman, M.D., M.S.P.H., dean of FAU’s Charles E. Schmidt College of Medicine.

Source: Science Daily

ScienceDaily (July 2, 2012) — Research published July 2 in Biomed Central’s open access journal Journal of Neuroinflammation suggests that chronic inflammation can predispose the brain to develop Alzheimer’s disease.

To date it has been difficult to pin down the role of inflammation in Alzheimer’s disease (AD), especially because trials of NSAIDs appeared to have conflicting results. Although the ADAPT (The Alzheimer`s Disease Anti-inflammatory Prevention Trial) trial was stopped early, recent results suggest that NSAIDs can help people with early stages of AD but that prolonged treatment is necessary to see benefit.

Researchers from the University of Zurich, in collaboration with colleagues from the ETH Zurich and University of Bern investigated what impact immune system challenges (similar to having a severe viral infection) would have on the development of AD in mice. Results showed that a single infection before birth (during late gestation) was enough to induce long-term neurological changes and significant memory problems at old age.

These mice had a persistent increase in inflammatory cytokines, increased levels of amyloid precursor protein (APP), and altered cellular localization of Tau. If this immune system challenge was repeated during adulthood the effect was strongly exacerbated, resulting in changes similar to those seen for pathological aging.

Dr Irene Knuesel who led this research explained, “The AD-like changes within the brain of these mice occurred without an increase in amyloid β (Aβ). However, in mice genetically modified to produce the human version of Aβ, the viral-like challenge drastically increased the amount of Aβ at precisely the sites of inflammation-induced APP deposits. Based on the similarity between these APP/AƒÒ aggregates in mice and those found in human AD, it seems likely that chronic inflammation due to infection could be an early event in the development of AD.

Source: Science Daily

ScienceDaily (July 2, 2012) — Growing evidence suggests that Parkinson’s disease (PD) often starts with non-motor symptoms that precede diagnosis by several years. In the first study to examine patterns in the quality of life of Parkinson’ disease patients prior to diagnosis, researchers have documented declines in physical and mental health, pain, and emotional health beginning several years before the onset of the disease and continuing thereafter.

Their results are reported in the latest issue of Journal of Parkinson’s Disease.

"We observed a decline in physical function in PD patients relative to their healthy counterparts beginning three years prior to diagnosis in men and seven and a half years prior to diagnosis in women," says lead investigator Natalia Palacios, PhD, Department of Nutrition, Harvard School of Public Health. "The decline continues at a rate that is five to seven times faster than the average yearly decline caused by normal aging in individuals without the disease."

The study included 51,350 male health professionals enrolled in the Health Professionals Follow Up Study (HPFS) and 121,701 female registered nurses enrolled in the Nurses’ Health Study (NHS). In both ongoing studies, participants fill out biannual questionnaires about a variety of lifestyle characteristics and document the occurrence of major chronic disease. In the NHS study, questionnaires measured health-related quality of life in eight areas: physical functioning, role limitations due to physical problems, role limitations due to emotional problems, vitality, bodily pain, social functioning, mental health, and general health perceptions. In the HPFS, only physical functioning was assessed.

Researchers identified 454 men and 414 women with PD in the two cohorts. At 7.5 years prior to diagnosis, physical function among PD cases, in both men and women, was comparable to that in the overall cohort. A decline began approximately 3 years prior to diagnosis in men and approximately 7.5 years prior to diagnosis in women. Physical function continued to decline thereafter at a rate of 1.43 and 2.35 points per year in men and women, respectively. In comparison, the average yearly decline in individuals without PD was 0.23 in men and 0.42 in women. Other measures of quality of life, available only in women, declined in a similar pattern.

Dr. Palacios notes that a strength of the study is the availability of prospective data on both PD patients and a healthy comparison group, and the ability to chart the deterioration in functioning and quality of life over the whole study follow-up, which included many years prior to diagnosis.

"This result provides support to the notion that the pathological process leading to PD may start several years before PD diagnosis," says Dr. Palacios. "Our hope is that, with future research, biological markers of the disease process may be recognizable in this preclinical phase."

Source: Science Daily