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Brain may use clot-busting drug naturally to offer protection against stroke

May 6, 2010 By vani Leave a Comment

Washington, May 6 (ANI): The clot-busting stroke drug tPA (tissue-type plasminogen activator) can act as a neuroprotectant and may form the keystone of an adaptive response to a reduction in blood flow, say scientists from Emory University School of Medicine.

In a new study, the boffins have shown that certain parts of the brains of mice lacking the gene for tPA are more vulnerable to stroke. In addition, tPA can protect neurons in the same part of the brain from the stress of hypoxia (low oxygen).

The results are published online in the Journal of Clinical Investigation.

“tPA is not only a drug, it is a natural protein produced in response to hypoxia,” says senior author Manuel Yepes, MD, associate professor of neurology at Emory University School of Medicine. “If you look at the parts of brain where the gene for tPA is turned on the most, one of these is the hippocampus. It is well known that the hippocampus is especially vulnerable to hypoxia compared with other regions of the brain. We believe there is a reason for this overlap.”

The hippocampus is a structure in the middle of the brain thought to be responsible for memory formation. In mice lacking the gene for tPA, neurons in the hippocampus are more vulnerable to dying after a short simulated stroke lasting 20 minutes, Yepes and his colleagues found. In the laboratory, pre-treatment with tPA protects hippocampal neurons in culture from hypoxia. In contrast, tPA has the opposite effect on neurons from the cortex.

tPA”s protective properties suggest that it may be playing a role in a process called “ischemic preconditioning,” where a less-than-lethal stroke can protect the brain against a later repeat, Yepes says. tPA”s effects on the blood-brain barrier can be seen as a way to get more blood to a deprived part of the brain. (ANI)

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High dietary phosphate intake may increase skin cancer risk

March 24, 2010 By vani Leave a Comment

Washington, March 24 (ANI): A new study by researchers at Emory University School of Medicine has shown that a high intake of phosphates can contribute to tumor growth in skin cancer.

In the study, the researchers applied dimethylbenzanthracene, a carcinogen found in cigarette smoke, to the skins of mice, followed by another chemical that stimulates cell growth.

Feeding these mice a high phosphate diet (1.2 percent by weight) increased skin papilloma number by 50 percent compared with a low phosphate diet (0.2 percent).

Skin papillomas are the initial stage of skin cancer development, which may progress to full carcinoma.

“This is a very well established model for the initiation and progression of cancer, and the effects of many physiological conditions on cancer initiation have been measured this way,” said senior author George Beck, assistant professor of medicine (endocrinology) and a member of the Winship Cancer Institute, Emory University.

The study has been published in the journal Cancer Prevention Research. (ANI)

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Imaging layer of fat around heart may help predict disease

March 16, 2010 By vani Leave a Comment

Washington, Mar 16 (ANI): The layer of fat around the heart can provide extra information compared with standard diagnostic techniques such as coronary artery calcium scoring, say scientists.

The size of the layer of fat around the heart, or imaging epicardial adipose tissue, can be measured by X-ray imaging techniques such as CT or MRI, according to research by cardiologists at Emory University School of Medicine.

“This information may be used as a ”gate keeper”, in that it could help a cardiologist decide whether a patient should go on to have a nuclear stress test,” says Paolo Raggi, MD, professor of medicine (cardiology) and radiology and director of Emory”s cardiac imaging center.

Results from two studies were presented at the American College of Cardiology meeting in Atlanta on Sunday, March 14.

The first study, presented by cardiology fellow Nikolaos Alexopoulos, MD, now at the University of Athens, Greece, shows that patients with a larger volume of epicardial adipose tissue tend to have the types of atherosclerotic plaques cardiologists deem most dangerous: non-calcified plaques.

Calcium tends to build up in atherosclerotic plaques. Even though the heart”s overall coronary calcium burden is a good predictor of heart disease, calcium in an individual plaque doesn”t necessarily mean imminent trouble, Raggi says. Researchers have been learning that non-calcified plaques indicate active buildup in that coronary artery, and studies suggest that the fat around the heart secretes more inflammatory hormones, compared to the fat just under the skin.

“Release of inflammatory factors from epicardial adipose tissue may be promoting an active atherosclerotic process, and this is indicated by the presence of non-calcified plaques,” Raggi says.

Emory researchers examined 214 patients through cardiac CT, and performed coronary artery scoring as well as assessing the patients” epicardial adipose tissue volume and the plaque in their coronary arteries. The epicardial adipose tissue volume was highest in the patients with non-calcified plaques (roughly 60 percent more than those with calcified plaques).

The second study, presented by Emory cardiology fellow Matthew Janik, MD, measured epicardial fat in patients receiving a nuclear stress test. The 382 patients had chest pain but did not have known cardiovascular disease. A nuclear stress test picks up signs of inducible ischemia: deficiencies in blood flow in the heart muscle.

In this, the researchers found that the presence of ischemia correlated more closely with epicardial adipose tissue volume than with the coronary calcium score. (ANI)

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”Mischievous” gut bugs could be making you fat

March 5, 2010 By vani Leave a Comment

Washington, Mar 5 (ANI): You can blame bacteria in your stomach for those unwanted pounds. A new study claims that the bugs, which are found in the digestive tract, boost appetite.

They also appear to cause cholesterol and blood pressure problems and raise the odds of diabetes and liver disease, the study claims.

According to research being published online this week by Science magazine, increased appetite and insulin resistance can be transferred from one mouse to another via intestinal bacteria.

“It has been assumed that the obesity epidemic in the developed world is driven by an increasingly sedentary lifestyle and the abundance of low-cost high-calorie foods,” says senior author Andrew Gewirtz, PhD, associate professor of pathology and laboratory medicine at Emory University School of Medicine. “However, our results suggest that excess caloric consumption is not only a result of undisciplined eating but that intestinal bacteria contribute to changes in appetite and metabolism.”

The first author of the paper is Emory faculty member Matam Vijay-Kumar, PhD, who has been studying a mouse strain with an altered immune system. These mice were engineered to lack a gene, Toll-like receptor 5 (TLR5), which helps cells sense the presence of bacteria. TLR5 recognizes flagellin, the main component of the apparatus (flagella) that many bacteria use to propel themselves.

The study began with Emory researcher Jesse Aitken”s unexpected observation that TLR5-deficient mice are about 20 percent heavier than regular mice and have elevated triglycerides, cholesterol and blood pressure. They also have mildly elevated blood sugar and increased production of insulin, Vijay-Kumar and Gewirtz found. TLR5-deficient mice tended to consume about 10 percent more food than their regular relatives. When their food was restricted they lost weight but still had a decreased response to insulin (i.e. insulin resistance). When fed a high-fat diet, TLR5-deficient mice gained more weight than regular mice and, moreover, developed full-blown diabetes and fatty liver disease. In short, TLR5-deficient mice exhibit “metabolic syndrome,” a cluster of disorders that in humans increases the risk of developing heart disease and diabetes.

Previous research has shown that TLR5 plays a prominent role in controlling bacteria in the intestine. Under certain conditions, many TLR5-deficient mice develop colitis, an inflammatory bowel disease, while the majority of the mice have chronic low-level inflammation.

“The intestine is like a complex community, with good and bad actors,” Gewirtz says. “We can think of TLR5 as being like a neighborhood police officer who can distinguish law-abiding residents from potential trouble makers. Take away TLR5, and the safety of the community deteriorates.”

Treating TLR5-deficient mice with strong antibiotics, enough to kill most of the bacteria in the intestine, reduces their metabolic abnormalities. This led Gewirtz”s team to analyze the composition of the intestinal bacteria of TLR5-deficient mice, collaborating with Ruth Ley at Cornell University.

Ley”s earlier research on mice and humans shows that obesity results in more bacteria of the Firmicutes family and less of the Bacteroidetes, which increases the intestine”s ability to harvest calories from food. In contrast, TLR5-deficient mice had normal proportions of Firmicutes and Bacteroidetes but differed in the bacterial species that comprised these families.

Importantly, Gewirtz and his team found that transfer of the intestinal bacteria from TLR5-deficient mice to regular mice transferred many of the characteristics of metabolic syndrome including increased appetite, obesity, elevated blood sugar, and insulin resistance. (ANI)

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”Mischievous” gut bugs could be making you fat

March 5, 2010 By vani Leave a Comment

Washington, Mar 5 (ANI): You can blame bacteria in your stomach for those unwanted pounds. A new study claims that the bugs, which are found in the digestive tract, boost appetite.

They also appear to cause cholesterol and blood pressure problems and raise the odds of diabetes and liver disease, the study claims.

According to research being published online this week by Science magazine, increased appetite and insulin resistance can be transferred from one mouse to another via intestinal bacteria.

HIV uses several routes to escape immune system pressure

September 19, 2009 By admin Leave a Comment

Washington, September 19 (ANI): Researchers at the Emory Vaccine Center have shown that HIV relies upon a number of strategies rather than use any preferred escape route to escape immune system pressure.

The human immune system has the ability to temporarily overpower HIV in early infection.

Studies conducted in the recent past have shown that most newly infected patients develop neutralizing antibodies. These are blood proteins that glob onto the virus and would allow patients to defend themselves – if they were facing only one target.

However, the problem occurs when HIV mutates, and disguises itself enough to get away from the antibodies. The virus eventually wears down the immune system into exhaustion.

The Emory team’s findings attain significance as they suggest that even if any scientist succeeds in identifying a vaccine component that can stimulate neutralizing antibodies, HIV’s capacity for rapid mutation could still be a confounding factor.

Dr. Cynthia Derdeyn, associate professor of pathology at Emory University School of Medicine, Emory Vaccine Center and Yerkes National Primate Research Center, says that a single type of neutralizing antibody may not be enough to contain HIV.

“These neutralizing antibodies work really well – they hit the virus fast and hard. But so far, every time we look, the virus escapes,” she says.

During the study, the researchers took blood samples from the participants a few weeks after infection occurred, and then later as two participants’ immune responses continued.

They isolated individual viruses over the first two years of HIV infection, and tested how well the patients’ own antibodies could neutralize them.

“In one patient where we had very early samples, there was evidence that neutralizing antibody came up within weeks, and that’s earlier than what was previously thought,” Derdeyn says.

In both patients, some viruses mutated part of their outer proteins so that after the mutation, an enzyme would be likely to attach a sugar molecule to it.

Though the sugar molecule interferes with antibody attack, this tactic, known as the “glycan shield”, was not observed in all cases.

Other viruses mutated the part of the outer protein that the neutralizing antibodies stick to directly. In both patients, many changes in the virus’ genetic code were necessary for escape.

“We need to understand early events in the immune response if we are going to figure out what a potential vaccine should have in it. What we can show is that even in one patient, several escape strategies are going on,” Derdeyn says.

According to her, that means that in order to be immune to HIV infection, someone may need to have several types of neutralizing antibodies ready to go.

Seeing how the virus mutates will allow researchers to choose the best parts to put in a vaccine, she says.

The results are online and scheduled for publication in the September issue of the journal Public Library of Science Pathogens.(ANI)

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Early life nurturing influences social behaviors in adulthood

September 1, 2009 By admin Leave a Comment

Washington, Sept 1 (ANI): A new study, conducted by researchers at the Yerkes National Primate Research Center, Emory University, has shown that early life nurturing impacts later life relationships.

The researchers used prairie voles as a model to understand the neurochemistry of social behavior.

Prairie voles are small, highly social, hamster-sized rodents that often form stable, life-long bonds between mates.

By influencing early social experience in prairie voles, researchers gained insight into what aspects of early social experience drive diversity in adult social behavior.

In the wild, there is striking diversity in how offspring are reared. Some pups are reared by single mothers, some by both parents and some in communal family groups.

For the study, Todd Ahern, a graduate student in the Emory University Neuroscience Program, and Larry Young, PhD, professor of psychiatry and behavioral sciences at the Yerkes Research Center and Emory University School of Medicine, compared pups raised by single mothers (SM) to pups raised by both parents (BP) to determine the effects of these types of early social environments on adult social behavior.

“Our findings demonstrate that SM- and BP-reared animals experienced different levels of care during the neonatal period and that these differences significantly influenced bonding social behaviors in adulthood,” Ahern said.

Young added: “These results suggest naturalistic variation in social rearing conditions can introduce diversity into adult nurturing and attachment behaviors. SM-raised pups were slower to make life-long partnerships, and they showed less interest in nurturing pups in their communal families.

The researchers also found differences in the oxytocin system. Oxytocin is best known for its roles in maternal labor and suckling, but, more recently, it has been tied to prosocial behavior, such as bonding, trust and social awareness.

“Very simply, altering their early social experience influenced adult bonding,” Ahern said.

Further studies will look at the altered oxytocin levels in the brain to determine how these hormonal changes affect relationships.

The study is currently available online in a special edition of Frontiers in Behavioral Neuroscience. (ANI)

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Glucose challenge test accurate, economical for diabetes screening

June 27, 2009 By admin Leave a Comment

Washington, June 26 (ANI): Emory University researchers have found that a test commonly used to help identify women with diabetes during pregnancy may be an accurate, convenient and economical way to screen the general population for unrecognized diabetes and prediabetes.

“Widespread use of the glucose challenge test (GCT) to screen Americans for prediabetes and diabetes could provide a major opportunity to improve the health of more than 40 million people,” said lead study author Lawrence S. Phillips, MD, Emory University School of Medicine Professor of Medicine, Division of Endocrinology.

The researchers screened 1,573 volunteer participants who had never been diagnosed with diabetes.

At a first visit, at different times of the day and without restriction of meals, participants were given a 50-gram glucose drink. Glucose was measured both before the drink (random glucose) and an hour after the drink (GCT glucose).

At a follow-up visit held in the morning after an overnight fast, participants had measurement of hemoglobin A1c (a standard test used to monitor diabetes), and a 75-gram oral glucose tolerance test (OGTT). The OGTT is the “gold standard” for diagnosing diabetes and prediabetes.

After screening, researchers found that 4.6 percent of the participants had previously unrecognized diabetes, and 18.7 percent had prediabetes.

The GCT was the most accurate screening test for these problems, significantly better than the random glucose or A1c tests.

Since the good performance of the GCT was unaffected by the time of day, or times after meals, the GCT could be performed during a routine office visit.

If a patient’s GCT glucose level is low, he/she wouldn’t need to be screened again for another two or three years, but if the GCT glucose level is high, patients would need a confirmatory oral glucose tolerance test.

This approach is similar to screening women for diabetes during pregnancy. GCT screening is almost universal for women in their sixth month of pregnancy.

The GCT provided consistent results for a diverse group of patients – old and young, normal weight and overweight, men and women, with and without a family history of diabetes, etc. The GCT also appeared to be less expensive than other screening strategies.

“Glucose challenge test screening could help improve disease management by permitting early initiation of therapy aimed at preventing or delaying the development of diabetes and its complications,” said Phillips.

The results of the study will be published online and in print in the journal Diabetologia. (ANI)

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Obstructive sleep apnea raises heart disease risk

May 5, 2009 By admin Leave a Comment

Washington, May 5 (ANI): Obstructive sleep apnea, or periodic interruptions in breathing throughout the night, can increase the risk of several forms of heart and vascular disease, researchers have found.

What’s more, the common sleep apnea thickens sufferers’ blood vessels, the study published in the May 1 issue of the American Journal of Respiratory Cell and Molecular Biology claimed.

Emory researchers have found enzyme NADPH oxidase as important for the effects obstructive sleep apnea has on blood vessels in the lung.

Standard treatment for obstructive sleep apnea involves a mechanical application of air pressure. Anything that blunts sleep apnea’s effects on blood vessel physiology could reduce its impact on disease risk, senior author C. Michael Hart, professor of medicine at Emory University School of Medicine and Atlanta Veterans Affairs Medical Center said.

Cyclically depriving mice of oxygen – researchers call this “chronic intermittent hypoxia” — in a way that simulates obstructive sleep apnea gives them pulmonary hypertension. Pulmonary hypertension, which can be life threatening, is a condition in which the right side of the heart has trouble pumping blood because of resistance in the lung’s blood vessels.

Chronic intermittent hypoxia forces the blood vessels in the lung to make more NADPH oxidase, Hart and his colleagues found. Mice that lack NADPH oxidase are immune to hypoxia’s effects.

NADPH oxidase is a helpful enzyme because it is responsible for making superoxide, a reactive free radical that the immune system uses to kill bacteria. But superoxide also interferes with nitric oxide, a signal that allows blood vessels to relax.

Humans with mutations in genes for NADPH oxidase have recurrent bacterial infections because their ability to fight the bacteria is weakened. Therefore, according to Hart, inhibiting the NADPH oxidase enzyme in the entire body may be harmful, and he favors an indirect intervention.

“We think that strategies to lower NADPH oxidase expression induced by hypoxia may be useful in preventing hypoxia-induced pulmonary hypertension,” says Hart. (ANI)

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DNA repair enzymes relocate when cells are under stress

March 29, 2009 By admin Leave a Comment

Washington, Mar 27 (ANI): In times of stress and genetic damage, some DNA repair enzymes can relocate to the part of the cell that needs their help, according to a collaborative team study led by scientists at Emory University School of Medicine.

The study found that the signal that prompts relocation is oxidative stress-an imbalance of cellular metabolism connected with several human diseases.

Dr. Paul Doetsch, professor of Biochemistry, Radiation Oncology, and Hematology and Oncology, says that the finding may lead to new targets for anti-cancer drugs that interfere with DNA repair.

“DNA damage and oxidative stress are very closely related. For example, the way radiation inflicts most of its damage on DNA is through oxidative stress. The more we know about how cells respond to oxidative stress, the more chances there could be to influence those responses for diagnostic or therapeutic purposes,” said Doetsch.

The DNA inside cells already remains under assault by heat, radiation, and oxygen.

And cells have an extensive set of repair enzymes that comb through DNA, continually excising and re-copying damaged segments. Also, mitochondria (cells’ miniature power plants) have their own DNA.

For the study, the researchers genetically modified strains of yeast so that two different DNA repair enzymes would be fluorescent.

They could track the enzymes around the cell when yeast was exposed to hydrogen peroxide, causing oxidative stress, or to other chemicals causing DNA damage.

It was found that one DNA repair enzyme they studied, Ntg1, moves to the nucleus or the mitochondria depending on where DNA damage is concentrated.

On the other hand, a related enzyme, Ntg2, remains in the nucleus under all conditions.

The authors found that the cells apparently direct Ntg1′s relocation by briefly attaching a small protein called SUMO to what needs to be moved around.

SUMO is found in fungi, plants and animals and is already being investigated by several research groups as a possible target for anti-cancer drugs.

The study has been published in the journal Molecular and Cellular Biology. (ANI)

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Diets targeting oxidized cysteine may reduce inflammation and lower disease risk

March 28, 2009 By admin 1 Comment

Washington, March 28 (ANI): Scientists at Emory University School of Medicine say that they have found a direct association between oxidative stress and inflammatory signals in the blood.

The researchers believe that their finding may pave the way for improved strategies for preventing several diseases by including antioxidants in the diet, and for reducing the impact of inflammation in critically ill patients by adding cysteine to intravenous or tube feeding.

Dr. Dean P. Jones, professor of medicine and director of the Clinical Biomarkers Laboratory at Emory University School of Medicine, points out that many normal metabolic functions produce reactive forms of oxygen that can damage cells.

He says that oxidative stress, a disruption of the body’s ability to control reactive forms of oxygen, has been connected with heart disease, diabetes and several neurodegenerative diseases.

However, adds the researcher, scientists are still learning about the best ways to measure and reduce oxidative stress-for example, large-scale clinical trials have shown little benefit in supplementing the diet with antioxidants such as vitamins C and E.

Working in collaboration with his colleague Dr. Thomas R. Ziegler, Jones concentrated on a measure of oxidative stress in the blood: cysteine, an amino acid found in most proteins in the body.

Cysteine can exist in two forms: oxidized and reduced. The higher the level of oxidative stress outside the cell, the more oxidized cysteine there is. Other indicators like glutathione are more important inside cells.

The researchers underscore the fact that several studies have shown that levels of oxidized cysteine in the blood tend to rise as people age. Smoking and alcohol consumption are also linked with higher levels of oxidized cysteine, they add.

Jones and Ziegler have found that critical illness and malnutrition are associated with oxidative stress and oxidized cysteine in the blood.

Their team also included graduate student Smita Iyer and immunologist Mauricio Rojas, who found that a high level of oxidized cysteine drives white blood cells to send out inflammatory messages in the form of the protein IL-1 beta.

During the study, the researchers used a mouse model of sepsis to test the effects of dietary cysteine on reducing inflammation.

They treated the mice with LPS, which mimics the inflammatory effect of bacteria on the human immune system and causes an increase in the level of IL-1 beta.

Upon supplementing the mice’s diets with cysteine, the researchers found IL-1 beta levels to drop, thus blunting the impact of a sepsis-like inflammation.

In a subsequent study of healthy, but overweight adult volunteers with an average age of 62, IL-1 beta levels also rose and fell in association with the amount of dietary cysteine.

“Our research shows a direct mechanistic link between the oxidative stress biomarker (cysteine redox potential) and pro-inflammatory cytokines, which have been linked to multiple age-related and chronic diseases,” says Jones.

“Our group and others have already established that cysteine redox potential is oxidized with aging and with a number of health risk factors. This suggests that one could target cysteine redox potential as a means to decrease chronic proinflammatory signaling as an intervention for age-related diseases and for the acute inflammation of sepsis or lung injury,” he adds.

He revealed that his research team would continue studying the link between cysteine and markers of inflammation in different age groups, in overweight and normal weight individuals, and in critically ill patients requiring intravenous feeding.

The study has been published online in the journal PLoS One.(ANI)

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Exposure to family violence worsens physical, mental health of older women

March 6, 2009 By admin Leave a Comment

Washington, Mar 6 (ANI): Older women exposed to high levels of family violence during lifetimes are likely to have poor health, according to a new study.

In the study involving African American women aged 50 years or older, the researchers found that exposure to family violence, be it intimate partner violence or elder maltreatment, worsens their physical and mental health.

The authors suggest that a holistic approach to caring for older women should include greater awareness by clinicians of current and past violence exposure and the negative effects it may have on the health status of these women.

For the study, the research team from Temple University School of Medicine and Emory University School of Medicine used a survey to assess lifetime family violence levels, including physical violence, emotional, financial, and sexual abuse, neglect, and coercion.

“This study provides further evidence of the enduring harmful effects that family violence can have on both mental and physical health, and in particular it highlights the association between such exposure and the health of older African American women,” said Dr Susan G. Kornstein, Editor-in-Chief of Journal of Women’s Health, and Executive Director of the Virginia Commonwealth University Institute for Women’s Health, Richmond, VA.

The research team included Dr Anuradha Paranjape, MPH, Nancy Sprauve-Holmes, MPH, John Gaughan, PhD, and Nadine Kaslow, PhD, from Temple University School of Medicine (Philadelphia, PA) and Emory University School of Medicine (Atlanta, GA).