Coffee and Tea May Contribute to a Healthy Liver

 — Surprise! Your morning cup of tea or coffee may be doing more than just perking you up before work.

An international team of researchers led by Duke-NUS Graduate Medical School (Duke-NUS) and the Duke University School of Medicine suggest that increased caffeine intake may reduce fatty liver in people with non-alcoholic fatty liver disease (NAFLD).

Worldwide, 70 percent of people diagnosed with diabetes and obesity have NAFLD, the major cause of fatty liver not due to excessive alcohol consumption. It is estimated that 30 percent of adults in the United States have this condition, and its prevalence is rising in Singapore. There are no effective treatments for NAFLD except diet and exercise.

Using cell culture and mouse models, the study authors -- led by Paul Yen, M.D., associate professor and research fellow, and Rohit Sinha, Ph.D of the Duke-NUS Graduate Medical School's Cardiovascular and Metabolic Disorders Program in Singapore -- observed that caffeine stimulates the metabolization of lipids stored in liver cells and decreased the fatty liver of mice that were fed a high-fat diet. These findings suggest that consuming the equivalent caffeine intake of four cups of coffee or tea a day may be beneficial in preventing and protecting against the progression of NAFLD in humans.

The findings will be published in the September issue of the journal Hepatology.

"This is the first detailed study of the mechanism for caffeine action on lipids in liver and the results are very interesting," Yen said. "Coffee and tea are so commonly consumed and the notion that they may be therapeutic, especially since they have a reputation for being "bad" for health, is especially enlightening."

The team said this research could lead to the development of caffeine-like drugs that do not have the usual side effects related to caffeine, but retain its therapeutic effects on the liver. It could serve as a starting point for studies on the full benefits of caffeine and related therapeutics in humans.

In addition to Yen and Sinha, collaborators included Christopher Newgard, PhD, director of the Sarah W. Stedman Nutrition and Metabolism Center at Duke University School of Medicine, where the metabolomics analysis of the data was conducted.

The study was supported by funding from Singapore's Agency for Science, Technology, and Research; the Ministry of Health; and the Ministry of Education.

How to Stop Bleeding in the ER Caused by Warfarin

 — Prothrombin complex concentrates (PCCs) are faster and more effective than fresh frozen plasma at reversing hemorrhage caused by the anti-coagulant warfarin, despite plasma being the most commonly used therapy. A literature review published last month in Annals of Emergency Medicinesuggests that physicians in the United States should join those around the world in following recommendations of multiple specialty organizations to use PCCs as the first line of defense in this common and life-threatening emergency ("Rapid Reversal of Warfarin-Associated Hemorrhage in the Emergency Department by Prothrombin Complex Concentrates").

"The typical remedies for hemorrhage caused by warfarin are slow and unpredictable," said author Kenneth Frumkin, PhD, MD of the Naval Medical Center in Portsmouth, Va. "By contrast, prothrombin complex concentrates reverse warfarin anticoagulation in minutes rather than hours. Its relative underuse in the U.S. compared to other countries seems to derive from lack of familiarity and infrequent availability."

PCCs (products made from pooled human plasma) were initially developed to treat hemophilia. They can be infused rapidly and generally reverse anticoagulation three to five times faster than fresh frozen plasma, which must be thawed. Recombinant Activated Factor VII (Factor rVIIa), while approved in the United States only for surgery or bleeding in hemophiliacs, has been used to reverse warfarin-associated bleeding. Factor rVIIa works faster than fresh frozen plasma, but carries more risk and costs much more.

"The April 2013 approval by the Food and Drug Administration of a form of PCC specifically intended for warfarin reversal should expand the use of these life-saving products," said Dr. Frumkin.

The views expressed by Dr. Frumkin are his own, and do not necessarily reflect the official policy or position of the Department of the Navy, Department of Defense, or the United States Government.

                             courtesy:science daily

Ileus: causes 
MD SPUGERS:
Mesenteric ischemia
Drugs (see below)
Surgical (post-op)
Peritonitis/ Pancreatitis (sentinnel loop)
Unresolved mechanical obstruction (eg mass, intussusception, blockage)
Gram negative sepsis
Electrolyte imbalance (eg hypokalemia)
Retroperitoneal bleed or hematoma
Spinal or pelvic fracture
Drugs are Aluminum hydroxide, Ba++, Ca carbonate, opiates, TCA, verapamil

MNEMONIC FOR ABDOMINAL PAIN:MEDICAL CAUSES
"ABDOMENAL PANE" [abdominal pain]:
Acute rheumatic fever
Blood [purpura, a/c hemolytic crisis]
DKA
cOllagen vascular disease
Migraine [abdominal migraine]
Epilepsy [abdominal epilepsy]
Nephron [uremia]
Abdominal angina
Lead
Porphyria
Arsenic
NSAID's
Enteric fever

Calcium Linked to Increased Risk of Heart Disease and Death in Patients With Kidney Disease

 — Kidney patients who take calcium supplements to lower their phosphorus levels may be at a 22 per cent higher risk of death than those who take other non-calcium based treatments, according to a new study by Women's College Hospital's Dr. Sophie Jamal.

---

The study, published today in theLancet, calls into question the long-time practice of prescribing calcium to lower phosphate levels in patients with chronic kidney disease. The researchers suggest some of the calcium is absorbed into the blood stream and may expedite hardening of the arteries, leading to a higher risk of heart disease and even death. Cardiovascular disease is a leading cause of death for people with chronic kidney disease.

"Doctors commonly prescribe calcium supplements to prevent elevated phosphate levels, which can damage the body, but a growing number of studies have shown calcium supplements may actually increase the risk of heart disease," explains Dr. Sophie Jamal, a physician at Women's College Hospital and an associate professor of medicine at the University of Toronto. "Our study validates these claims and, for the first time, shows the long-term consequences of taking calcium supplements can be dangerous for patients with kidney disease."

As part of their analysis, researchers reviewed 11 randomized, controlled studies that included more than 4,600 patients. The researchers assessed the risk of heart disease, including heart attack, stroke, and hardening of the arteries, along with death among individuals prescribed the medication containing calcium and those prescribed the medication without calcium. They found:

• A 22% reduction in death among patients who took non-calcium based treatments sevelamer and lanthanum.
• Less artery calcification (hardening) in patients who did not take calcium supplements.

"Some researchers and physicians have been saying for years that kidney disease patients need to get off calcium, now we think our review shows there is much more solid evidence to argue for that change to clinical practice," the study's senior author Ross Tsuyuki from the University of Alberta's faculty of medicine and dentistry.

In the meantime, given the study's findings, the researchers suggest non-calcium containing treatments be used as a first line of treatment to lower phosphate for patients with chronic kidney disease.

"The findings of our study provides the best evidence as to what doctors should be prescribing their patients, but further research is necessary to help us understand how exactly calcium increases the risk of death, if non calcium-based treatments reduce the risk of death, and whether certain types of treatments may be more effective and beneficial than others," says Dr. Jamal.

                                      courtesy:science daily

THE SOUNDS OF SUCCESS..............

Successful Restoration of Hearing and Balance

 — The sounds of success are ringing at Kansas State University through a research project that has potential to treat human deafness and loss of balance

Philine Wangemann, university distinguished professor of anatomy and physiology in the College of Veterinary Medicine, and her international team have published the results of their study in the July issue of the journal PLOS Genetics.

"When the SLC26A4 gene is mutated, it leads to a loss of pendrin expression, which causes swelling of the inner ear and loss of hearing and balance," Wangemann said. "In my research, I have been interested in how the inner ear functions. We worked on the idea that if you keep one domino in the chain standing, then the others would continue to stand and function normally. In other words, if we could restore the proper expression of pendrin in the endolymphatic sac and thereby prevent swelling of the sac, this may prevent swelling of other parts of the inner ear and rescue hearing and balance."

More than 28 million people in the United States suffer some form of hearing loss. Wangemann said mutation of SLC26A4is one of the most common forms of hereditary hearing loss in children, not only in the U.S. and Europe, but also in China, Japan and Korea, which makes this research very significant on a global scale.

The foundation of Wangemann's study is that this human disease is largely recapitulated in a mutant mouse model. SLC26A4 is normally found in the cochlea and vestibular organs of the inner ear as well as in the endolymphatic sac, which is a non-sensory part of the inner ear. When the mutant mice lack SLC26A4 expression, their inner ears swell during embryonic development. This leads to failure of the cochlea and the vestibular organs, resulting in deafness and loss of balance. The multitude of sites where SLC26A4 is located made the goal to restore function look futile, unless some sites were more important than others.

"We generated a new mutant mouse that expresses SLC26A4 in the endolymphatic sac, but not in the cochlea or the vestibular organs of the inner ear," Wangemann said. "Fantastically, this mouse did not develop the detrimental swelling of the inner ear and even more exciting, the mouse developed normal hearing and balance."

That restoration of hearing and balance lasted for the duration of the testing period, which suggests that the restoration is permanent.

"Our study provides the proof-of-concept that a therapy aimed at repairing the endolymphatic sac during embryonic development is sufficient to restore a lifetime of normal hearing and balance," Wangemann said.

While these findings are made in a mouse model, Wangemann said that eventually the idea is to develop a pharmacological treatment for human patients, but much more research will be necessary, such as to understand how fluid secretion and absorption is supported and how the balance of secretion and absorption is maintained to prevent the detrimental swelling.

Wangemann's study was supported by the College of Veterinary Medicine at Kansas State University and by grants from the National Institutes of Health, the National Institutes on Deafness and Other Communication Disorders, the Kansas IDeA Network of Biomedical Research Excellence and other sources.

Her team includes researchers from Kansas State University, the National Institutes on Deafness and Other Communication Disorders, Georges-Pompidou European Hospital and Sorbonne University Paris Cite in France, and the University of Utah.

                                  courtesy:science daily

NEW PLAN OF ATTACK AGAINST CANCER..........

New Plan of Attack in Cancer Fight: Two-Drug Combination, Under Certain Circumstances, Can Eliminate Disease

— New research conducted by Harvard scientists is laying out a road map to one of the holy grails of modern medicine: a cure for cancer.

As described in a paper recently published in eLife, Martin Nowak, a professor of mathematics and of biology and director of the Program for Evolutionary Dynamics, and co-author Ivana Bozic, a postdoctoral fellow in mathematics, show that, under certain conditions, using two drugs in a "targeted therapy" -- a treatment approach designed to interrupt cancer's ability to grow and spread -- could effectively cure nearly all cancers.

Though the research is not a cure for cancer, Nowak said it does offer hope to researchers and patients alike.

"In some sense this is like the mathematics that allows us to calculate how to send a rocket to the moon, but it doesn't tell you how to build a rocket that goes to the moon," Nowak said. "What we found is that if you have a single point mutation in the genome that can give rise to resistance to both drugs at the same time, the game is over. We need to have combinations such that there is zero overlap between the drugs."

Importantly, Nowak said, for the two-drug combination to work, both drugs must be given together -- an idea that runs counter to the way many clinicians treat cancer today.

"We actually have to work against the status quo somewhat," he said. "But we can show in our model that if you don't give the drugs simultaneously, it guarantees treatment failure."

In earlier studies, Nowak and colleagues showed the importance of using multiple drugs. Though temporarily effective, single-drug targeted therapy will fail, the researchers revealed, because the disease eventually develops resistance to the treatment.

To determine if a two-drug combination would work, Nowak and Bozic turned to an expansive data set supplied by clinicians at New York's Memorial Sloan-Kettering Cancer Center that showed how patients respond to single-drug therapy. With data in hand, they were able to create computer models of how multidrug treatments would work. Using that model, they then treated a series of "virtual patients" to determine how the disease would react to the multidrug therapy.

"For a single-drug therapy, we know there are between 10 and 100 places in the genome that, if mutated, can give rise to resistance," Nowak explained. "So the first parameter we use when we make our calculations is that the first drug can be defeated by those possible mutations. The second drug can also be defeated by 10 to 100 mutations.

"If any of those mutations are the same, then it's a disaster," he continued. "If there's even a single mutation that can defeat both drugs, that is usually good enough for the cancer -- it will become resistant, and treatment will fail. What this means is we have to develop drugs such that the cancer needs to make two independent steps -- if we can do that, we have a good chance to contain it."

How good a chance?

"You would expect to cure most patients with a two-drug combination," Bozic said. "In patients with a particularly large disease burden you might want to use a three-drug combination, but you would cure most with two drugs."

The trick now, Nowak and Bozic said, is to develop those drugs.

To avoid developing drugs that are not vulnerable to the same mutation, Bozic said, pharmaceutical companies have explored a number of strategies, including using different drugs to target different pathways in cancer's development.

"There are pharmaceutical companies here in Cambridge that are working to develop these drugs," Nowak said. "There may soon be as many as 100 therapies, which means there will be as many as 10,000 possible combinations, so we should have a good repertoire to choose from.

"I think we can be confident that, within 50 years, many cancer deaths will be prevented," Nowak added. "One hundred years ago, many people died from bacterial infections, and now they would be cured. Today, many people die from cancer, and we can't help them, but I think once we have these targeted therapies, we will be able to help many people -- maybe not everyone -- but many people."
                                                courtesy:science daily

Molecule Drives Aggressive Breast Cancer

 — Recent studies by researchers at Thomas Jefferson University's Kimmel Cancer Center have shown a gene known to coordinate initial development of the eye (EYA1) is a powerful breast tumor promoter in mice. The gene EYA1 was also shown to be overexpressed in a genetic breast cancer subtype called luminal B.

The scientists found that excess activity of this gene -- EYA1 -- also enhances development of breast cancer stem cells that promote resistance to cancer therapy, recurrence, and poor survival.

Because EYA1 is an enzyme, the scientists are now working to identify a natural compound that could shut down EYA1 activity, says Richard Pestell, M.D., Ph.D., Director of Kimmel Cancer Center.

"It was known that EYA1 is over-expressed in some breast cancers, but no one knew what that meant," he says. "Our studies have shown the enzyme drives luminal B breast tumor growth in animals and the enzyme activity is required for tumor growth."

In a mouse model of aggressive breast cancer, the research team targeted a single amino acid on the EYA1 phosphatase activity. They found that inactivating the phosphatase activity of EYA1 stopped aggressive human tumors from growing.

"We are excited about the potential of drug treatment, because it is much easier to develop a drug that targets a phosphatase enzyme like EYA1, than it is to target a gene directly," he says.

Tracing how EYA1 leads to poor outcomes

The study, which was published in the May 1 issue of Cancer Research, examined 2,154 breast cancer samples for the presence of EYA1. The researchers then linked those findings to patient outcomes. They found a direct relationship between increased level of EYA1 and cyclin D1 to poor survival.

They then chose one form of breast cancer -- luminal B -- and traced the bimolecular pathway of how EYA1 with cyclin D1 increases cancer aggressiveness. Luminal B breast cancer, one of five different breast cancer subtypes, is a hormone receptor-positive form that accounts for about 20 percent of human breast cancer. It is more aggressive than luminal A tumors, a hormone receptor-positive cancer that is the most common form of breast cancer.

Their work delineated a string of genes and proteins that are affected by EYA1, and they also discovered that EYA1 pushes an increase in formation of mammospheres, which are a measure of breast cancer stem cells.

"Within every breast cancer are breast cancer stem cells, which give rise to anti-cancer therapy resistance, recurrence and metastases," Dr. Pestell says. "We demonstrated in laboratory experiments that EYA1 expression increase the number of mammospheres and other markers of breast cancer stem cells."

"As the EYA1 phosphatase activity drove breast cancer stem cell expansion, this activity may contribute to worse survival," he says.

AMAZING!!!!!!!! ISN'T IT??!!!

Babies Can Read Each Other’s Moods, Study Finds

 — Although it may seem difficult for adults to understand what an infant is feeling, a new study from Brigham Young University finds that it's so easy a baby could do it.

Psychology professor Ross Flom's study, published in the academic journalInfancy, shows that infants can recognize each other's emotions by five months of age. This study comes on the heels of other significant research by Flom on infants' ability to understand the moods of dogs, monkeys and classical music.

Research shows that babies can understand each others emotional signals at five months of age. These baby boys are cousins - the one on the left is four months old and the one on the right is five months. (Credit: Image courtesy of Brigham Young University)

"Newborns can't verbalize to their mom or dad that they are hungry or tired, so the first way they communicate is through affect or emotion," says Flom. "Thus it is not surprising that in early development, infants learn to discriminate changes in affect."

Infants can match emotion in adults at seven months and familiar adults at six months. In order to test infant's perception of their peer's emotions, Flom and his team of researchers tested a baby's ability to match emotional infant vocalizations with a paired infant facial expression.

"We found that 5 month old infants can match their peer's positive and negative vocalizations with the appropriate facial expression," says Flom. "This is the first study to show a matching ability with an infant this young. They are exposed to affect in a peer's voice and face which is likely more familiar to them because it's how they themselves convey or communicate positive and negative emotions."

In the study, infants were seated in front of two monitors. One of the monitors displayed video of a happy, smiling baby while the other monitor displayed video of a second sad, frowning baby. When audio was played of a third happy baby, the infant participating in the study looked longer to the video of the baby with positive facial expressions. The infant also was able to match negative vocalizations with video of the sad frowning baby. The audio recordings were from a third baby and not in sync with the lip movements of the babies in either video.

"These findings add to our understanding of early infant development by reiterating the fact that babies are highly sensitive to and comprehend some level of emotion," says Flom. "Babies learn more in their first 2 1/2 years of life than they do the rest of their lifespan, making it critical to examine how and what young infants learn and how this helps them learn other things."

Flom co-authored the study of 40 infants from Utah and Florida with Professor Lorraine Bahrick from Florida International University.

Flom's next step in studying infant perception is to run the experiments with a twist: test whether babies could do this at even younger ages if instead they were watching and hearing clips of themselves.

Brain's 'Garbage Truck' May Hold Key to Treating Alzheimer's and Other Disorders

 — In a perspective piece appearing today in the journal Science, researchers at University of Rochester Medical Center (URMC) point to a newly discovered system by which the brain removes waste as a potentially powerful new tool to treat neurological disorders like Alzheimer's disease. In fact, scientists believe that some of these conditions may arise when the system is not doing its job properly.

"Essentially all neurodegenerative diseases are associated with the accumulation of cellular waste products," said Maiken Nedergaard, M.D., D.M.Sc., co-director of the URMC Center for Translational Neuromedicine and author of the article. "Understanding and ultimately discovering how to modulate the brain's system for removing toxic waste could point to new ways to treat these diseases."

Scientists point to a newly discovered system by which the brain removes waste as a potentially powerful new tool to treat neurological disorders like Alzheimer's disease. In fact, scientists believe that some of these conditions may arise when the system is not doing its job properly. (Credit: © James Steidl / Fotolia)

The body defends the brain like a fortress and rings it with a complex system of gateways that control which molecules can enter and exit. While this "blood-brain barrier" was first described in the late 1800s, scientists are only now just beginning to understand the dynamics of how these mechanisms function. In fact, the complex network of waste removal, which researchers have dubbed the glymphatic system, was only first disclosed by URMC scientists last August in the journal Science Translational Medicine.

The removal of waste is an essential biological function and the lymphatic system -- a circulatory network of organs and vessels -- performs this task in most of the body. However, the lymphatic system does not extend to the brain and, consequently, researchers have never fully understood what the brain does its own waste. Some scientists have even speculated that these byproducts of cellular function where somehow being "recycled" by the brain's cells.

One of the reasons why the glymphatic system had long eluded comprehension is that it cannot be detected in samples of brain tissue. The key to discovering and understanding the system was the advent of a new imaging technology called two-photon microscopy which enables scientists to peer deep within the living brain. Using this technology on mice, whose brains are remarkably similar to humans, Nedergaard and her colleagues were able to observe and document what amounts to an extensive, and heretofore unknown, plumbing system responsible for flushing waste from throughout the brain.

The brain is surrounded by a membrane called the arachnoid and bathed in cerebral spinal fluid (CSF). CSF flows into the interior of the brain through the same pathways as the arteries that carry blood. This parallel system is akin to a donut shaped pipe within a pipe, with the inner ring carrying blood and the outer ring carrying CSF. The CSF is draw into brain tissue via a system of conduits that are controlled by a type support cells in the brain known as glia, in this case astrocytes. The term glymphatic was coined by combining the words glia and lymphatic.

The CSF is flushed through the brain tissue at a high speed sweeping excess proteins and other waste along with it. The fluid and waste are exchanged with a similar system that parallels veins which carries the waste out of the brain and down the spine where it is eventually transferred to the lymphatic system and from there to the liver, where it is ultimately broken down.

While the discovery of the glymphatic system solved a mystery that had long baffled the scientific community, understanding how the brain removes waste -- both effectively and what happens when this system breaks down -- has significant implications for the treatment of neurological disorders.

One of the hallmarks of Alzheimer's disease is the accumulation in the brain of the protein beta amyloid. In fact, over time these proteins amass with such density that they can be observed as plaques on scans of the brain. Understanding what role the glymphatic system plays in the brain's inability to break down and remove beta amyloid could point the way to new treatments. Specifically, whether certainly key 'players' in the glymphatic system, such as astrocytes, can be manipulated to ramp up the removal of waste.

"The idea that 'dirty brain' diseases like Alzheimer may result from a slowing down of the glymphatic system as we age is a completely new way to think about neurological disorders," said Nedergaard. "It also presents us with a new set of targets to potentially increase the efficiency of glymphatic clearance and, ultimately, change the course of these conditions."

                                                     courtesy:science daily

ECG: left vs. right bundle block
"WiLLiaMMaRRoW":
W pattern in V1-V2 and M pattern in V3-V6 is Left bundle block.
M pattern in V1-V2 and W in V3-V6 is Right bundle block.
Note: consider bundle branch blocks when QRS complex is wide.

Spleen: dimensions, weight, surface anatomy
"1,3,5,7,9,11":
Spleen dimensions are 1 inch x 3 inches x 5 inches.
Weight is 7 ounces.
It underlies ribs 9 through 11.

Depressed ST-segment: causes
DEPRESSED ST:
Drooping valve (MVP)
Enlargement of LV with strain
Potassium loss (hypokalemia)
Reciprocal ST- depression (in I/W AMI)
Embolism in lungs (pulmonary embolism)
Subendocardial ischemia
Subendocardial infarct
Encephalon haemorrhage (intracranial haemorrhage)
Dilated cardiomyopathy
Shock
Toxicity of digitalis, quinidine

mnemonic

Median nerve: hand muscles innervated
"The LOAF muscles":
Lumbricals 1 and 2
Opponens pollicis
Abductor pollicis brevis
Flexor pollicis brevis
Alternatively: LLOAF, with 2 L's, to recall there's 2 lumbricals.
To remember that these are the Median nerve muscles, think "Meat LOAF".

mnemonic

Spleen: dimensions, weight, surface anatomy
"1,3,5,7,9,11":
Spleen dimensions are 1 inch x 3 inches x 5 inches.
Weight is 7 ounces.
It underlies ribs 9 through 11.

New Molecular-Level Understanding of the Brain's Recovery After Stroke

 — A specific MicroRNA, a short set of RNA (ribonuclease) sequences, naturally packaged into minute (50 nanometers) lipid containers called exosomes, are released by stem cells after a stroke and contribute to better neurological recovery according to a new animal study by Henry Ford Hospital researchers.

---

The important role of a specific microRNA transferred from stem cells to brain cells via the exosomes to enhance functional recovery after a stroke was shown in lab rats. This study provides fundamental new insight into how stem cells affect injured tissue and also offers hope for developing novel treatments for stroke and neurological diseases, the leading cause of long-term disability in adult humans.

The study is being published in the journal Stem Cells.

Although most stroke victims recover some ability to voluntarily use their hands and other body parts, nearly half are left with weakness on one side of their body, while a substantial number are permanently disabled.

Currently no treatment exists for improving or restoring this lost motor function in stroke patients, mainly because of mysteries about how the brain and nerves repair themselves.

"This study may have solved one of those mysteries by showing how certain stem cells play a role in the brain's ability to heal itself to differing degrees after stroke or other trauma," says study author Michael Chopp, Ph.D., scientific director of the Henry Ford Neuroscience Institute and vice chairman of the department of Neurology at Henry Ford Hospital.

The researchers noted that Henry Ford's Institutional Animal Care and Use Committee approved all the experimental procedures used in the new study.

The experiment began by isolating mesenchymal stem cells (MSCs) from the bone marrow of lab rats. These MSCs are then genetically altered to release exosomes that contain specific microRNA molecules. The MSCs then become "factories" producing exosomes containing specific microRNAs. These microRNAs act as master switches that regulate biological function.

The new study showed for the first time that a specific microRNA, miR-133b, carried by these exosomes contributes to functional recovery after a stroke.

The researchers genetically raised or lowered the amount of miR-133b in MSCs and, respectively, treated the rats. When these MSCs are injected into the bloodstream 24 hours after stroke, they enter the brain and release their exosomes. When the exosomes were enriched with the miR-133b, they amplified neurological recovery, and when the exosomes were deprived of the miR-133b, the neurological recovery was substantially reduced.

Stroke was induced under anesthesia by inserting a nylon thread up the carotid artery to occlude a major artery in the brain, the middle cerebral artery. MSCs were then injected 24 hours after the induction of stroke in these animals and neurological recovery was measured.

As a measure on neurological recovery, rats were given two types of behavioral tests to measure the normal function of their front legs and paws -- a "foot-fault test," to see how well they could walk on an unevenly spaced grid; and an "adhesive removal test" to measure how long it took them to remove a piece of tape stuck to their front paws.

Researchers then separated the disabled rats into several groups and injected each group with a specific dosage of saline, MSCs and MSCs with increased or decreased miR-133b, respectively. The two behavioral tests were again given to the rats three, seven and 14 days after treatment.

The data demonstrated that the enriched miR-133b exosome package greatly promoted neurological recovery and enhanced axonal plasticity, an aspect of brain rewiring, and the diminished miR-133b exosome package failed to enhance neurological recovery

While the research team was careful to note that this was an animal study, its findings offer hope for new ways to address the single biggest concern of stroke victims as well as those with neural injury such as traumatic brain injury and spinal cord damage -- regaining neurological function for a better quality of life.

                                              courtesy-science daily

Sugar Overload Can Damage Heart

 — Too much sugar can set people down a pathway to heart failure, according to a study led by researchers at The University of Texas Health Science Center at Houston (UTHealth).

A single small molecule, the glucose metabolite glucose 6-phosphate (G6P), causes stress to the heart that changes the muscle proteins and induces poor pump function leading to heart failure, according to the study, which was published in the May 21 issue of theJournal of the American Heart Association. G6P can accumulate from eating too much starch and/or sugar.

Heart failure kills 5 million Americans a year, according to the Centers for Disease Control. The one-year survival rate after diagnosis is 50 percent and there are 550,000 new patients in the United States diagnosed with heart failure each year.

"Treatment is difficult. Physicians can give diuretics to control the fluid, and beta-blockers and ACE inhibitors to lower the stress on the heart and allow it to pump more economically," said Heinrich Taegtmeyer, M.D., D.Phil., principal investigator and professor of cardiology at the UTHealth Medical School. "But we still have these terrible statistics and no new treatment for the past 20 years."

Taegtmeyer performed preclinical trials in animal models, as well as tests on tissue taken from patients at the Texas Heart Institute who had a piece of the heart muscle removed in order to implant a left ventricle assist device by O.H. "Bud" Frazier, M.D., and his team. Both led to the discovery of the damage caused by G6P.

"When the heart muscle is already stressed from high blood pressure or other diseases, and then takes in too much glucose, it adds insult to injury," Taegtmeyer said.

The study has opened doors to possible new treatments. Two drugs, rapamycin (an immunosuppressant) and metformin (a diabetes medication) disrupt signaling of G6P and improved cardiac power in small animal studies.

"These drugs have a potential for treatment and this has now cleared a path to future studies with patients," Taegtmeyer said.

The study was supported in part by grants from the National Institutes of Health (R01 HL061483, TL1RR024147, R21 HL102627 and R01 HL08972).

                                                  courtesy-science daily

MNEMONIC

Deep tendon reflexes: root supply
"1,2,3,4,5,6,7,8":
S1-2: ankle
L3-4: knee
C5-6: biceps, supinator
C7-8: triceps

MNEMONIC

Carpal tunnel syndrome causes:
MEDIAN TRAP:
Myxoedema
Edema premenstrually
Diabetes
Idiopathic
Agromegaly
Neoplasm
Trauma
Rheumatoid arthritis
Amyloidosis
Pregnancy
 Mnemonic fits nicely since median nerve is trapped.

MEDICINE IN KITCHEN.........

Ginger Compounds May Be Effective in Treating Asthma Symptoms, Study Suggests

May 19, 2013 — Gourmands and foodies everywhere have long recognized ginger as a great way to add a little peppery zing to both sweet and savory dishes; now, a study from researchers at Columbia University shows purified components of the spicy root also may have properties that help asthma patients breathe more easily.

The results of the study will be presented at the ATS 2013 International Conference.

Asthma is characterized by bronchoconstriction, a tightening of the bronchial tubes that carry air into and out of the lungs. Bronchodilating medications called beta-agonists (β-agonists) are among the most common types of asthma medications and work by relaxing the airway smooth muscle (ASM) tissues. This study looked at whether specific components of ginger could help enhance the relaxing effects of bronchodilators.

"Asthma has become more prevalent in recent years, but despite an improved understanding of what causes asthma and how it develops, during the past 40 years few new treatment agents have been approved for targeting asthma symptoms," said lead author Elizabeth Townsend, PhD, post-doctoral research fellow in the Columbia University Department of Anesthesiology. "In our study, we demonstrated that purified components of ginger can work synergistically with β-agonists to relax ASM."

To conduct their study, the researchers took human ASM tissue samples and caused the samples to contract by exposing them to acetylcholine, a neurotransmitting compound that causes bronchoconstriction. Next, the researchers mixed the β-agonist isoproterenol with three separate components of ginger: 6-gingerol, 8-gingerol or 6-shogaol. Contracted tissue samples were exposed to each of these three mixtures as well as unadulterated isoproterenol and the relaxation responses were recorded and compared.

At the conclusion of their study, the researchers found that tissues treated with the combination of purified ginger components and isoproterenol exhibited significantly greater relaxation than those treated only with isoproterenol; of the three ginger components, 6-shogaol appeared most effective in increasing the relaxing effects of the β-agonist.

Once they were able to demonstrate that the ginger components enhanced the relaxing effects of the β-agonist, they turned their attention to learning why. First, the researchers wanted to determine if the ginger components might work by affecting an enzyme called phosphodiesterase4D (PDE4D). Previous studies have shown that PDE4D, which is found in the lungs, inhibits processes that otherwise help relax ASM and lessen inflammation. Using a technique called fluorescent polarization, they found that all three components significantly inhibited PDE4D.

Next, the study looked at F-actin filaments, a protein structure which previous studies have shown plays a role in the constriction of ASM, and found that 6-shogaol was effective in speedily dissolving these filaments.

"Taken together, these data show that ginger constituents 6-gingerol, 8-gingerol and 6-shogaol act synergistically with the β-agonist in relaxing ASM, indicating that these compounds may provide additional relief of asthma symptoms when used in combination with β-agonists," Dr. Townsend noted."By understanding the mechanisms by which these ginger compounds affect the airway, we can explore the use of these therapeutics in alleviating asthma symptoms."

Dr. Townsend and her colleague, Dr. Charles Emala, hope future studies will enable them to gain a better understanding of the cellular mechanisms that facilitate ASM relaxation and to determine whether aerosol delivery of these purified constituents of ginger may have therapeutic benefit in asthma and other bronchoconstrictive diseases.

                                        courtesy:science daily
.

mnemonic

Brachial plexus: numbers of each section
It is the same backwards and forwards:
5-3-2-3-5:
5 Rami
3 Trunks
2 Divisions
3 Cords
5 Terminal nerves

mnemonic

Brachial plexus: branches of posterior cord
STAR:
Subscapular [upper and lower]
Thoracodorsal
Axillary
Radial

HERE IS ANOTHER REASON TO ADOPT HEALTHIER LYFSTYLE............

Healthy Lifestyle Choices Mean Fewer Memory Complaints

 — Research has shown that healthy behaviors are associated with a lower risk of Alzheimer's disease and dementia, but less is known about the potential link between positive lifestyle choices and milder memory complaints, especially those that occur earlier in life and could be the first indicators of later problems.

To examine the impact of these lifestyle choices on memory throughout adult life, UCLA researchers and the Gallup organization collaborated on a nationwide poll of more than 18,500 individuals between the ages of 18 and 99. Respondents were surveyed about both their memory and their health behaviors, including whether they smoked, how much they exercised and how healthy their diet was.

As the researchers expected, healthy eating, not smoking and exercising regularly were related to better self-perceived memory abilities for most adult groups. Reports of memory problems also increased with age. However, there were a few surprises.

Older adults (age 60-99) were more likely to report engaging in healthy behaviors than middle-aged (40-59) and younger adults (18-39), a finding that runs counter to the stereotype that aging is a time of dependence and decline. In addition, a higher-than-expected percentage of younger adults complained about their memory.

"These findings reinforce the importance of educating young and middle-aged individuals to take greater responsibility for their health -- including memory -- by practicing positive lifestyle behaviors earlier in life," said the study's first author, Dr. Gary Small, director of the UCLA Longevity Center and a professor of psychiatry and biobehavioral sciences at the Semel Institute for Neuroscience and Human Behavior at UCLA who holds the Parlow-Solomon Chair on Aging.

Published in the June issue of International Psychogeriatrics, the study may also provide a baseline for the future study of memory complaints in a wide range of adult age groups.

For the survey, Gallup pollsters conducted land-line and cell phone interviews with 18,552 adults in the U.S. The inclusion of cell phone-only households and Spanish-language interviews helped capture a representative 90 percent of the U.S. population, the researchers said.

"We found that the more healthy lifestyle behaviors were practiced, the less likely one was to complain about memory issues," said senior author Fernando Torres-Gil, a professor at UCLA's Luskin School of Public Affairs and associate director of the UCLA Longevity Center.

In particular, the study found that respondents across all age groups who engaged in just one healthy behavior were 21 percent less likely to report memory problems than those who didn't engage in any healthy behaviors. Those with two positive behaviors were 45 percent less likely to report problems, those with three were 75 percent less likely, and those with more than three were 111 percent less likely.

Interestingly, the poll found that healthy behaviors were more common among older adults than the other two age groups. Seventy percent of older adults engaged in at least one healthy behavior, compared with 61 percent of middle-aged individuals and 58 percent of younger respondents.

In addition, only 12 percent of older adults smoked, compared with 25 percent of young adults and 24 percent of middle-aged adults, and a higher percentage of older adults reported eating healthy the day before being interviewed (80 percent) and eating five or more daily servings of fruits and vegetables during the previous week (64 percent).

According to the researchers, older adults may participate in more healthy behaviors because they feel the consequences of unhealthy living and take the advice of their doctors to adopt healthier lifestyles. Or there simply could be fewer older adults with bad habits, since they may not live as long.

While 26 percent of older adults and 22 percent of middle-aged respondents reported memory issues, it was surprising to find that 14 percent of the younger group complained about their memory too, the researchers said.

"Memory issues were to be expected in the middle-aged and older groups, but not in younger people," Small said. "A better understanding and recognition of mild memory symptoms earlier in life may have the potential to help all ages."

Small said that, generally, memory issues in younger people may be different from those that plague older generations. Stress may play more of a role. He also noted that the ubiquity of technology -- including the Internet, texting and wireless devices that can result in constant multi-tasking, especially with younger people -- may impact attention span, making it harder to focus and remember.

Small noted that further study and polling may help tease out such memory-complaint differences. Either way, he said, the survey reinforces the importance, for all ages, of adopting a healthy lifestyle to help limit and forestall age-related cognitive decline and neurodegeneration.

                                    courtesy:science daily

NEW ANTIDEPRESSANT WITHOUT SIDE EFFECTS..............

Ketamine Cousin Rapidly Lifts Depression Without Side Effects, Study Suggests

 — GLYX-13, a molecular cousin to ketamine, induces similar antidepressant results without the street drug side effects, reported a study funded by the National Institute of Mental Health (NIMH) that was published last month inNeuropsychopharmacology.

Major depression affects about 10 percent of the adult population and is the second leading cause of disability in U.S. adults, according to the World Health Organization. Despite the availability of several different classes of antidepressant drugs such as selective serotonin reuptake inhibitors (SSRIs), 30 to 40 percent of adults are unresponsive to these medications. Moreover, SSRIs typically take weeks to work, which increases the risk for suicide.

Enter NMDA (N-methyl-D-aspartate) receptor modulators. In the 1970s, researchers linked the receptors to learning and memory. Biotech and pharmaceutical companies in the 1980s attempted to apply chemical blockers to these receptors as a means to prevent stroke. But blocking these receptors led to the opposite effect -- --the rise of cardiovascular disease. Research in the field dampened until a glutamate receptor antagonist already approved for anesthesia, and known on the streets as "Special K," ketamine, made headlines in the early 2000s. Human clinical studies demonstrated that ketamine can ward off major and bipolar depressive symptoms within 2 hours of administration and last for several days. Ketamine is fraught with serious side effects including excessive sleepiness, hallucinations, and substance abuse behavior.

"Ketamine lit the field back up," said Joseph Moskal, Ph.D., a molecular neurobiologist at Northwestern University and senior study author. "Our drug, GLYX-13, is very different. It does not block the receptor ion channel, which may account for why it doesn't have the same side effects."

Moskal's journey with GLYX-13 came about from his earlier days as a Senior Staff Fellow in NIMH's Intramural Research Program. While at NIMH, he created specific molecules, monoclonal antibodies, to use as new probes to understand pathways of learning and memory. Some of the antibodies he created were for NMDA receptors. When he moved to Northwestern University, Moskal converted the antibodies to small protein molecules. Composed of only four amino acids, GLYX-13 is one of these molecules.

Previous electrophysiological and conditioning studies had suggested that GLYX-13, unlike ketamine, enhanced memory and learning in rats, particularly in the brain's memory hub or hippocampus. GLYX-13 also produced analgesic effects. Using several rat behavioral and molecular experiments, Moskal's research team tested four compounds: GLYX-13, an inactive, "scrambled" version of GLYX-13 that had its amino acids rearranged, ketamine, and the SSRI fluoxetine.

Results of the Study

GLYX-13 and ketamine produced rapid acting (1 hour) and long-lasting (24 hour) antidepressant-like effects in the rats. Fluoxetine, an SSRI that typically takes from 2-4 weeks to show efficacy in humans, did not produce a rapid antidepressant effect in this study. As expected, the scrambled GLYX-13 showed no antidepressant-like effects at all. The researchers observed none of the aforementioned side effects of ketamine in the GLYX-13-treated rats.

Protein studies indicated an increase in the hippocampus of the NMDA receptor NR2B and a receptor for the chemical messenger glutamate called AMPA. Electrophysiology studies in this brain region showed that GLYX-13 and ketamine promoted long-lasting signal transmission in neurons, known as long-term potentiation/synaptic plasticity. This phenomenon is essential in learning and memory. The researchers propose how GLYX-13 works: GLYX-13 triggers NR2B receptor activation that leads to intracellular calcium influx and the expression of AMPA, which then is responsible for increased communication between neurons.

These results are consistent with data from a recent Phase 2 clinical trial, in which a single administration of GLYX-13 produced statistically significant reductions in depression scores in patients who had failed treatment with current antidepressants. The reductions were evident within 24 hours and persisted for an average of 7 days. After a single dose of GLYX-13, the drug's antidepressant efficacy nearly doubled that seen with most conventional antidepressants after 4-6 weeks of dosing. GLYX-13 was well tolerated and it did not produce any of the schizophrenia-like effects associated with other NMDA receptor modulating agents.

Significance

NMDA receptors need a molecule each of the amino acid chemical messengers glutamate and glycine to become activated. Moskal speculates that GLYX-13 either directly binds to the glycine site on the NMDA receptor or indirectly modulates how glycine works with the receptor. Resulting activation of more NMDA and AMPA receptors leads to an increase in memory, learning -- and antidepressant effects. By contrast, ketamine only blocks the NMDA receptor, but also increases the activity of the AMPA receptor. Knowledge of these mechanisms could lead to the development of more effective antidepressants.

What's Next

GLYX-13 is now being tested in a Phase 2 repeated dose antidepressant trial, where Moskal and his colleagues at Naurex, Inc., a biotechnology company he founded, hope to find in humans the optimal dosing for the drug. They also want to see if this molecule, and others like it, regulate other NMDA receptor subtypes -- there are over 20 of them -- and whether it will work on other disorders, such as schizophrenia, attention-deficit hyperactivity disorder, and autism.

"One could call NMDA modulators such as GLYX-13 'comeback kids,'" said Moskal. "A toolkit that I developed in 1983 is now setting the stage in 2013 for the development of possible new therapeutics that may provide individuals suffering from depression with a valuable new treatment option."
                                                  courtesy:science daily

Probiotics Prevent Diarrhea Related to Antibiotic Use, Review Shows

 — Probiotic supplements have the potential to prevent diarrhea caused by antibiotics, according to a new Cochrane systematic review. The authors studied Clostridium difficile (C. difficile) infections in patients taking antibiotics and found symptoms of diarrhea were substantially reduced when patients were also treated with probiotics.

Antibiotics disturb the beneficial bacteria that live in the gut and allow other harmful bacteria like C. difficile to take hold. Although some people infected with C. difficile show no symptoms, others suffer diarrhea or colitis. The so-called "good bacteria" or yeast in probiotic foods and supplements may offer a safe, low-cost way to help prevent C. difficile-associated diarrhea (CDAD). This finding is important because CDAD is expensive to treat.

CDAD cases were reported in 23 trials involving 4,213 adults and children. Probiotics taken in conjunction with antibiotics reduced the number of people who suffered diarrhea by 64%. Only 2% of participants who took probiotics had CDAD compared to nearly 6% of those who took placebo. In 26 trials reporting on adverse events, there were fewer adverse events in the group taking probiotics.

"In the short-term, taking probiotics in conjunction with antibiotics appears to be a safe and effective way of preventing diarrhea associated with Clostridium difficile infection," said lead researcher Bradley Johnston of The Hospital for Sick Children Research Institute in Toronto, Canada. "The introduction of some probiotic regimens as adjuncts to antibiotics could have an immediate impact on patient outcomes, especially in outbreak settings. However, we still need to establish the probiotic strains and doses that provide the best results, and determine the safety of probiotics in immunocompromised patients."

Although taking probiotics in combination with antibiotics helped to prevent CDAD, it did not reduce the number of people who were infected with C. difficile. "We think it's possible that probiotics act to prevent the symptoms of C. difficile infection rather than to prevent the infection itself," said Johnston. "This possibility needs to be investigated further in future trials, which should help us to understand more about how probiotics work."
                                                    courtesy:science daily

Hormone Levels May Provide Key to Understanding Psychological Disorders in Women

 — Women at a particular stage in their monthly menstrual cycle may be more vulnerable to some of the psychological side-effects associated with stressful experiences, according to a study from UCL.

The results suggest a monthly window of opportunity that could potentially be targeted in efforts to prevent common mental health problems developing in women. The research is the first to show a potential link between psychological vulnerability and the timing of a biological cycle, in this case ovulation.

A common symptom of mood and anxiety problems is the tendency to experience repetitive and unwanted thoughts. These 'intrusive thoughts' often occur in the days and weeks after a stressful experience.

In this study, the researchers examined whether the effects of a stressful event are linked to different stages of the menstrual cycle. The participants were 41 women aged between 18 and 35 who had regular menstrual cycles and were not using the pill as a form of contraception. Each woman watched a 14-minute stressful film containing death or injury and provided a saliva sample so that hormone levels could be assessed. They were then asked to record instances of unwanted thoughts about the video over the following days.

"We found that women in the 'early luteal' phase, which falls roughly 16 to 20 days after the start of their period, had more than three times as many intrusive thoughts as those who watched the video in other phases of their menstrual cycle," explains author Dr Sunjeev Kamboj, Lecturer in UCL's Department of Clinical, Educational and Health Psychology. "This indicates that there is actually a fairly narrow window within the menstrual cycle when women may be particularly vulnerable to experiencing distressing symptoms after a stressful event."

The findings could have important implications for mental health problems and their treatment in women who have suffered trauma.

"Asking women who have experienced a traumatic event about the time since their last period might help identify those at greatest risk of developing recurring symptoms similar to those seen in psychological disorders such as depression and post-traumatic stress disorder (PTSD)," said Dr Kamboj.

"This work might have identified a useful line of enquiry for doctors, helping them to identify potentially vulnerable women who could be offered preventative therapies," continued Dr Kamboj.

"However, this is only a first step. Although we found large effects in healthy women after they experienced a relatively mild stressful event, we now need to see if the same pattern is found in women who have experienced a real traumatic event. We also need further research to investigate how using the contraceptive pill affects this whole process."

                                       courtesy:science daily

STUDIES ON TO DEFEAT HIV.............

Promising Strategy to Help Vaccines Outsmart HIV

 — A new discovery at Oregon Health & Science University highlights an ingenious method to ensure the body effectively reacts when infected with the highly evasive HIV virus that causes AIDS. The same team of researchers has been utilizing this unique approach to develop its own HIV vaccine candidate, which has so far shown promising results in animal studies.

This latest research finding will be published in the May 24, 2013, edition of the journal Science.

"A major challenge in developing an effective HIV vaccine is figuring out how to target this evasive virus," said Dr. Louis Picker, M.D., associate director of the OHSU Vaccine and Gene Therapy Institute, where the work was conducted.

CD8+ "cytotoxic" T cells are an important component of the immune system and are particularly important for pathogens, like HIV, that easily evade antibodies. They serve as sentries within the body that detect and destroy virus-infected cells, accomplishing this function by recognizing short viral peptides on the surface of infected cells. T-cells are designed to be quite frugal in the number of different viral peptides they recognize, typically responding to just a handful of such peptides. This is a problem for control of HIV, which is able to able change its peptides and thus escape T cells responses that do not target the relatively few functionally critical peptides that can't change without debilitating the virus. In the vast majority of HIV infections, the few viral peptides recognized by T cells are not the vulnerable ones, and the virus escapes.

Therefore, the strategy that Dr. Picker and his colleagues adopted was to try to develop a vaccine to increase the number of viral peptides that T cells would recognize, reasoning that increasing this "recognition breadth" would allow T cells to more effectively respond to HIV.

The researchers found that cytomegalovirus or CMV, a common virus already carried by a large percentage of the population, may hold the key. Their studies in the non-human primate model of HIV, called SIV, found that a modified version of CMV engineered to express SIV proteins generates SIV-specific T cells that recognize three-fold as many SIV peptides as T cell generated by conventional vaccines and SIV itself. Moreover, these responses were entirely different from conventional responses, such that even viruses that had previously escaped natural responses would still be vulnerable. In effect, the hunters of the body were provided with a much better targeting system to help them find and destroy an elusive enemy.

Picker and his colleagues believe an HIV vaccine equipped with a modified CMV vector might be able to both prevent infection (prophylactic vaccine) and effectively battle the virus even if applied post-infection in individuals with infections suppressed by anti-retroviral therapy. Moving forward, the research team hopes to utilize this new information to create customized CMV vectors with a broad ability to identify several components of HIV and then incorporate this component into an effective vaccine.

"We hope we can begin clinical trials in human patients within a few years," explained Dr. Picker. "This new information gives us a much clearer roadmap for effectively targeting the disease which to this point has found ways to evade the human immune system."

National Institutes of Health (P01 AI094417, RO1 AI060392, RO1 AI059457, P51 OD 011092 and contract #HHSN261200800001E), the Bill & Melinda Gates Foundation and the International AIDS Vaccine Initiative funded this research.

OHSU and paper authors Drs. Picker, Hansen, Früh and Nelson have a significant financial interest in TomegaVax, Inc., a company that may have a commercial interest in the results of this research and technology. The potential individual and institutional conflicts of interest have been reviewed and managed by OHSU.
                           courtesy:science daily

PROVNG D OLDEST SAYING WRONG-"AADAKKE BARLILLA ANDRE ANGALA DONKU".........

How Playing Surfaces Affect Athletic Performance, Injury Potential

 — A group of University of Rhode Island students have been jumping up and down for weeks on a variety of playing surfaces in a study to evaluate how each affects athletic performance and injury potential.

Disa Hatfield, URI assistant professor of kinesiology, said little is known about whether athletes perform better or are more susceptible to injury on the various surfaces.

"People make decisions all the time that amount to spending thousands of dollars to buy artificial turf or to plant one kind of grass or another, but those decisions are based mostly on cost," Hatfield said. "We think this study will answer a lot of important questions, especially about injury risk."

Hatfield and her students are testing four surfaces -- a hard metal plate, artificial turf like that used in many National Football League stadiums, and grass planted on either a sandy loam soil or on peat soil.

The surfaces are being tested using 42 volunteer subjects who are asked to jump in five different ways to measure the height of each jump, the power they produce, and their landing pattern. According to Hatfield, jumping height and power directly correlate to athletic performance.

The volunteers are also filmed so the researchers can examine the angles of their legs, knees and ankles as they land to analyze injury risk.

"We expect performance to be a little better on the artificial turf, but we may also get more ankle and knee movements on the landing because of the harder impact," she said.

Hatfield said that many people, especially women, experience knee valgus -- their knees cave inward upon landing -- which is associated with a high risk of anterior cruciate ligament (ACL) injury.

"When we see knee valgus to a certain degree, that's a serious risk factor for injury," she said.

The study is particularly timely because of increasing concern, especially in the NFL, about the high prevalence of injuries on artificial turf.

"The problem is that maintaining artificial turf is much cheaper and easier than maintaining live grass. The cost factor is much less," she said. "But I'm hoping that we'll be able to show a decreased injury risk on natural surfaces, which have a higher capacity to absorb impacts."

While the professional athletic venues may be one driver of the research, Hatfield believes her data will be equally useful to recreational venues where the majority of amateur and recreational athletes exercise and compete.

"Most of those venues aren't going to be investing in an artificial surface, but they will want to know what we learn about the differences between soil types," Hatfield said. "There is some speculation that because sand is denser and doesn't bend as much, injury potential will be higher, but there is no research yet to verify that."

Hatfield will spend the summer and fall analyzing the data that is being collected this spring, and she hopes to have results to report at the end of the year.

Her research was funded in part by the New England Regional Turfgrass Foundation and with guidance from turfgrass scientists W. Michael Sullivan at URI and Jason Henderson at the University of Connecticut.

                                 courtesy:science daily

First Drug to Significantly Improve Heart Failure Mortality in Over a Decade

 — Coenzyme Q10 decreases all cause mortality by half, according to the results of a multicentre randomised double blind trial presented today at Heart Failure 2013 congress. It is the first drug to improve heart failure mortality in over a decade and should be added to standard treatment, according to lead author Professor Svend Aage Mortensen (Copenhagen, Denmark).

Heart Failure 2013 is being held from 25-28 May in Lisbon, Portugal. It is the main annual meeting of the Heart Failure Association of the European Society of Cardiology (1).

Coenzyme Q10 (CoQ10) occurs naturally in the body and is essential to survival. CoQ10 works as an electron carrier in the mitochondria, the powerhouse of the cells, to produce energy and is also a powerful antioxidant. It is the only antioxidant that humans synthesise in the body.

CoQ10 levels are decreased in the heart muscle of patients with heart failure, with the deficiency becoming more pronounced as heart failure severity worsens. Statins are used to treat many patients with heart failure because they block the synthesis of cholesterol, but these drugs also block the synthesis of CoQ10, which further decreases levels in the body.

Double blind controlled trials have shown that CoQ10 improves symptoms, functional capacity and quality of life in patients with heart failure with no side effects. But until now, no trials have been statistically powered to address effects on survival.

The Q-SYMBIO study (2) randomised 420 patients with severe heart failure (New York Heart Association (NYHA) Class III or IV) to CoQ10 or placebo and followed them for 2 years. The primary endpoint was time to first major adverse cardiovascular event (MACE) which included unplanned hospitalisation due to worsening of heart failure, cardiovascular death, urgent cardiac transplantation and mechanical circulatory support. Participating centres were in Denmark, Sweden, Austria, Slovakia, Poland, Hungary, India, Malaysia and Australia.

CoQ10 halved the risk of MACE, with 29 (14%) patients in the CoQ10 group reaching the primary endpoint compared to 55 (25%) patients in the placebo group (hazard ratio=2; p=0.003). CoQ10 also halved the risk of dying from all causes, which occurred in 18 (9%) patients in the CoQ10 group compared to 36 (17%) patients in the placebo group (hazard ratio=2.1; p=0.01).

CoQ10 treated patients had significantly lower cardiovascular mortality (p=0,02) and lower occurrence of hospitalisations for heart failure (p=0.05). There were fewer adverse events in the CoQ10 group compared to the placebo group (p=0.073).

Professor Mortensen said: "CoQ10 is the first medication to improve survival in chronic heart failure since ACE inhibitors and beta blockers more than a decade ago and should be added to standard heart failure therapy."

He added: "Other heart failure medications block rather than enhance cellular processes and may have side effects. Supplementation with CoQ10, which is a natural and safe substance, corrects a deficiency in the body and blocks the vicious metabolic cycle in chronic heart failure called the energy starved heart."

CoQ10 is present in food, including red meat, plants and fish, but levels are insufficient to impact on heart failure. CoQ10 is also sold over the counter as a food supplement but Professor Mortensen said: "Food supplements can influence the effect of other medications including anticoagulants and patients should seek advice from their doctor before taking them."

Patients with ischaemic heart disease who use statins could also benefit from CoQ10 supplementation. Professor Mortensen said: "We have no controlled trials demonstrating that statin therapy plus CoQ10 improves mortality more than statins alone. But statins reduce CoQ10, and circulating CoQ10 prevents the oxidation of LDL effectively, so I think ischaemic patients should supplement statin therapy with CoQ10."

                            courtesy:science daily

A NEW RAY OF HOPE TO GRANDPARENTS..........

Drug Reverses Alzheimer's Disease Deficits in Mice

 — An anti-cancer drug reverses memory deficits in an Alzheimer's disease mouse model, University of Pittsburgh Graduate School of Public Health researchers confirm in the journalScience.

In new research, scientists confirm that an anti-cancer drug reverses memory deficits in an Alzheimer's disease mouse model. (Credit: © fergregory / Fotolia)

The research, funded by the National Institutes of Health's National Institute on Aging and Alzheimer's Association, reviewed previously published findings on the drug bexarotene, approved by the U.S. Food and Drug Administration for use in cutaneous T cell lymphoma. The Pitt Public Health researchers were able to verify that the drug does significantly improve cognitive deficits in mice expressing gene mutations linked to human Alzheimer's disease, but could not confirm the effect on amyloid plaques.

"We believe these findings make a solid case for continued exploration of bexarotene as a therapeutic treatment for Alzheimer's disease," said senior author Rada Koldamova, M.D., Ph.D., associate professor in Pitt Public Health's Department of Environmental and Occupational Health.

Dr. Koldamova and her colleagues were studying mice expressing human Apolipoprotein E4 (APOE4), the only established genetic risk factor for late-onset Alzheimer's disease, or APOE3, which is known not to increase the risk for Alzheimer's disease, when a Case Western Reserve University study was published last year stating that bexarotene improved memory and rapidly cleared amyloid plaques from the brains of Alzheimer's model mice expressing mouse Apolipoprotein E (APOE). Amyloid plaques consist of toxic protein fragments called amyloid beta that seem to damage neurons in the brain and are believed to cause the associated memory deficits of Alzheimer's disease and, eventually, death.

Bexarotene is a compound chemically related to vitamin A that activates Retinoic X Receptors (RXR) found everywhere in the body, including neurons and other brain cells. Once activated, the receptors bind to DNA and regulate the expression of genes that control a variety of biological processes. Increased levels of APOE are one consequence of RXR activation by bexarotene. The Pitt researchers began studying similar compounds a decade ago.

"We were already set up to repeat the Case Western Reserve University study to see if we could independently arrive at the same findings," said co-author Iliya Lefterov, M.D., Ph.D., associate professor in Pitt Public Health's Department of Environmental and Occupational Health. "While we were able to verify that the mice quickly regained their lost cognitive skills and confirmed the decrease in amyloid beta peptides in the interstitial fluid that surrounds brain cells, we did not find any evidence that the drug cleared the plaques from their brains."

The Pitt researchers postulate that the drug works through a different biological process, perhaps by reducing soluble oligomers which, like the plaques, are composed of the toxic amyloid beta protein fragments. However, the oligomers are composed of smaller amounts of amyloid beta and, unlike the plaques, are still able to "move."

"We did find a significant decrease in soluble oligomers," said Dr. Koldamova. "It is possible that the oligomers are more dangerous than the plaques in people with Alzheimer's disease. It also is possible that the improvement of cognitive skills in mice treated with bexarotene is unrelated to amyloid beta and the drug works through a completely different, unknown mechanism."

In the Pitt experiments, mice with the Alzheimer's gene mutations expressing human APOE3 or APOE4 were able to perform as well in cognitive tests as their non-Alzheimer's counterparts 10 days after beginning treatment with bexarotene. These tests included a spatial test using cues to find a hidden platform in a water maze and a long-term memory test of the mouse's ability to discriminate two familiar objects following introduction of a third, novel object.

Bexarotene treatment did not affect the weight or general behavior of the mice. The drug was equally effective in male and female mice.

                                      courtesy:science daily