Atlanta, Gorgia - August 13, 2010
Isolating cells from a patient’s blood or bone marrow that nourish blood vessels may be a safer and less arduous route to treatment of cardiovascular disease than obtaining rare stem cells, according to research from Emory University School of Medicine.

Young-sup Yoon, MD, Ph.D Emory University School of Medicine Photo: stemyoon.org

In recent clinical trials, doctors in several countries have tested the ability of a patient’s bone marrow cells to repair damage, such as heart attacks and peripheral artery disease, created by problems of blood flow.

“The focus has been on stem cells, but it looks like the main beneficial effects come from transplanted cells’ ability to support the growth of nearby blood vessels,” says senior author Young-sup Yoon, MD, PhD, associate professor of medicine (cardiology) at Emory University School of Medicine. “Based on this idea, we wanted to identify a population of cells enriched with the capacity to regenerate blood vessels.”

The blood vessel repairing properties of selected cells from human blood were described in the Aug. 10 issue of the Journal of the American College of Cardiology, with a related paper on cells derived from mouse bone marrow published online July 15 by the journal Circulation Research.

The first author of the JACC paper is postdoctoral fellow Sung-Whan Kim, PhD. The first author of the Circulation Research paper is Hyongbum Kim, MD, PhD, now an assistant professor in Korea.

Yoon’s team focused on the molecule CD31, also known as platelet endothelial cell adhesion molecule-1 or PECAM-1, because of its presence on endothelial cells - the cells that form the inner lining of blood vessels. In experiments with donated blood from human volunteers or mouse bone marrow cells, the researchers showed that cells with CD31 on their surfaces secrete hormones that support the growth of blood vessels.

About a third of the cells in the blood or bone marrow have CD31 on their surfaces, including some differentiated immune cells. In culture, sorted cells displaying CD31 can form tubular structures mimicking the growth of blood vessels in the body.

“We can show that after transplantation, some CD31 positive cells do become endothelial cells, but their main effect is more to support other cells than to become the building blocks,” Yoon says.

The researchers used antibodies against CD31 to sort human blood or mouse bone marrow cells into two groups: cells with CD31 and those without. They then tested these cells’ ability to spur blood vessel regrowth in mice whose hind legs had a blocked blood supply.

In the project described in Circulation Research, after two weeks more than 80 percent of the mouse hind legs transplanted with CD31 positive bone marrow cells survived, while less than 15 percent of the legs transplanted with CD31 negative cells survived. In laser Doppler images, the mice with CD31 positive cells injected into their legs had greatly enhanced blood flow and an increased number of capillaries.

Yoon says harvesting CD31 positive cells may have several advantages compared to previous methods of treating cardiovascular disease. The cells can be prepared without the need to grow them in a dish for several days, and it may not be necessary to take large volumes of blood or bone marrow from the patient - an advantage with respect to safety. In addition, cells from mice used to simulate atherosclerosis (mutant for a gene that helps clear fat from the blood and given a high fat diet) do not seem to lose their repair potential.

“Based on the insights gained from preclinical and clinical studies from several investigators, we view the use of CD31 positive cells as a second generation cardiovascular cell therapy that could be a novel option for the treatment of peripheral artery disease,” Yoon says.

He adds that CD31 positive cells may have potential for treating other conditions, including heart attack, heart failure and diabetic neuropathy, which his team is investigating in animal models.

The research was supported by the National Institutes of Health, the Department of Defense and the Korean Ministry of Education, Science and Technology.

Learn more about Emory’s health sciences: http://emoryhealthblog.com

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KYUNGBUK KOREA , July 21, 2010
Capsaicin, the stuff that gives chili peppers their kick, may cause weight loss and fight fat buildup by triggering certain beneficial protein changes in the body, according to a new study on the topic. The report, which could lead to new treatments for obesity, appears in ACS’ monthly Journal of Proteome Research.

Chili peppers contain an ingredient that may cause weight loss and fight fat.

Jong Won Yun and colleagues point out that obesity is a major public health threat worldwide, linked to diabetes, high blood pressure, heart disease, and other health problems. Laboratory studies have hinted that capsaicin may help fight obesity by decreasing calorie intake, shrinking fat tissue, and lowering fat levels in the blood. Nobody, however, knows exactly how capsaicin might trigger such beneficial effects.

In an effort to find out, the scientists fed high-fat diets with or without capsaicin to lab rats used to study obesity. The capsaicin-treated rats lost 8 percent of their body weight and showed changes in levels of at least 20 key proteins found in fat. The altered proteins work to break down fats. “These changes provide valuable new molecular insights into the mechanism of the antiobesity effects of capsaicin,” the scientists say.

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CINCINNATI - Scientists at Cincinnati Children’s Hospital Medical Center have discovered that a diet with high levels of fructose - levels equivalent to that in high fructose corn syrup - and of trans fats not only increases obesity, but also leads to significant fatty liver disease with scar tissue.

The study’s main author Rohit Kohli, M.D., gastroenterologist at Cincinnati Children’s Hospital Medical Center Photo: cincinnatichildrens.org

Moreover, the researchers conducted the study in a new mouse model of obesity and liver disease that so closely models human disease they will now be able to test therapies to determine their effectiveness, according to Rohit Kohli, M.D., a gastroenterologist at Cincinnati Children’s Hospital Medical Center and the study’s main author.

“Fructose consumption accounts for approximately 10.2 percent of calories in the average diet in the United States and has been linked to many health problems, including obesity, cardiovascular disease and liver disease,” says Dr. Kohli. “We’ve developed a mouse model that is very close to human disease, allowing us to better understand the process involved in the development and progression of obesity-related fatty liver disease.”

The study also includes preliminary data on a simple blood test for a biomarker that differentiates the stages of disease in this model. Physicians currently monitor the progression of fatty liver disease by taking liver biopsies, which are invasive procedures.

The study, which was conducted with scientists from the Metabolic Disease Institute at the University of Cincinnati, is published online in the journal Hepatology.

The study was conducted in mice, some of which were fed a normal diet of rodent chow and some a 16 week diet of high fructose enriched drinking water and trans fat solids. Their liver tissue was then analyzed for fat content, scar tissue formation (fibrosis), and the biological mechanism of damage. This was done by measuring reactive oxygen stress, inflammatory cell type and plasma levels of oxidative stress markers, which are known to play important roles in the development of obesity related liver disease and its progression to end stage liver disease.

The investigators found that mice fed the normal calorie chow diet remained lean and did not have fatty liver disease. Mice fed high calorie diets (trans fat alone or a combination of trans fat and high fructose) became obese and had fatty liver disease. “Interestingly, it was only the group fed the combination of trans fat and high fructose which developed the advanced fatty liver disease which had fibrosis,” says Dr. Kohli. “This same group also had increased oxidative stress in the liver, increased inflammatory cells, and increased levels of plasma oxidative stress markers.”

Dr. Kohli hopes to further investigate the mechanism of liver injury caused by high fructose enriched drinking water and study a therapeutic intervention of antioxidant supplementation. Antioxidants are natural defenses against oxidative stress and may reverse or protect against advanced liver damage, according to Dr. Kohli.

The investigators also would like to use this model to better understand human fatty liver disease and perform clinical trials using novel therapeutic and monitoring tools.

“Our data suggest that supplementation with pharmaceuticals agents should be tested on our new model to establish whether one is able to reverse or protect against progressive liver scarring and damage,” says Dr. Kohli.

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WASHINGTON, May 21, 2010
Sexual activity declines in the year after heart attack for patients who don’t get instructions from their doctors about when it’s safe to resume sex, researchers reported at the American Heart Association’s 11th Scientific Forum on Quality of Care and Outcomes Research in Cardiovascular Disease and Stroke.

Stacy Tessler Lindau, M.D. Lead author of the study and associate professor of obstetrics/ gynecology and medicine- geriatrics at the University of Chicago Photo: sshvs.org

In a study of 1,184 male and 576 female acute heart attack patients, nearly half the men and about a third of women reported receiving discharge instructions on resuming sexual activity. Even fewer - less than 40 percent of men and less than 20 percent of women - talked about sex with their physicians in the year following their heart attack.

One year after heart attack, more than two thirds of the men reported some sexual activity, and about 40 percent of the women reported sexual activity. Men were 1.3 times and women 1.4 times more likely to report a loss of sexual activity after one year if they didn’t receive information on when to resume sexual activity.

“Sexuality is an important part of life throughout life, and most heart attack patients are sexually active” said Stacy Tessler Lindau, M.D., lead author of the study and associate professor of obstetrics/gynecology and medicine geriatrics at the University of Chicago. “For the most part, physicians just aren’t discussing this topic with their patients after a heart attack.”

Most participants were assessed at one month and again at one year following their heart attack regarding level of sexual activity both before and after heart attack. Researchers set up gender separate models to predict the frequency of sexual activity at one year following a heart attack in those who were sexually active prior to or since their heart attack. Male participants (average age 59 years) were more likely to be married than women participants (average age 61 years) and were more likely to be sexually active prior to the heart attack. Even after adjusting for these differences, patients who had been given instructions about resuming sexual activity at hospital discharge were more likely to engage in such activity over the following year.

The study was part of TRIUMPH (Translational Research Investigating Underlying Disparities in Recovery from Acute Myocardial Infarction: Patients’ Health Status). Participants were asked questions about their sexual activity prior to and after having a heart attack.

“As survival after a heart attack continues to improve, it is important to begin studying the outcomes of patients who survive; their symptoms, function and quality of life,” said John A. Spertus, M.D., M.P.H., Clinical Director of Outcomes Research at Saint Luke’s Mid America Heart Institute/UMKC and Principal Investigator of the TRIUMPH Study. “To date, few studies have examined whether patients who survive a heart attack resume sexual activity.”

“Little is known about what happens to patients’ sexuality and sexual function after a heart attack, particularly for women” Lindau said. “While most hospitals have a regimented process of presenting discharge information to patients after heart attack, the question of when it’s safe to resume sexual activity after heart attack is not always addressed.”

Even when it’s discussed, the researchers aren’t sure what’s being said. “We don’t yet know the content or value of the instructions patients are receiving,” she said

The consensus among physicians is that it’s safe to resume sexual activity after a heart attack once the patient feels better and is capable of performing moderate exercise.

“The likelihood of dying during sexual intercourse, even among people who have had a heart attack, is really small,” Lindau said.

Some physicians are reluctant to discuss sex with patients who are older, aren’t married or belong to a conservative religious group, she said. “But in the case of sexuality, stereotypes don’t work. Older patients may not be married but still have an intimate romantic partner.”

Physicians need to bring up the subject, even if it’s not part of a routine discharge check list, because “not raising the question of sexuality leaves the door closed.”

Noting their data are preliminary, Lindau said further study is required to determine what information the patients were given by their physicians, what patients need to know, and how to tailor information for patients so that they will feel free to ask questions and to seek help.

“Often physicians are focused on saving lives, and sexual health may not be valued as much as medications and other treatments to prevent further progression of their coronary disease,” she said. “Doctors need to be proactive and help patients recover their whole lives after heart attack. Physicians need to assess a patient’s sexual history to ensure all aspects of a patient’s physical and emotional well-being are addressed. This is an essential part of healthcare.”

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EAST LANSING, Mich. - MAY 18, 2010
Cholesterol crystals, known to be a catalyst for heart attacks and strokes, also cause cells to send out danger signals that can lead to the inflammation and hardening of arteries, according to a Michigan State University cardiologist.

George Abela, chief of the cardiology division in MSU’s College of Human Medicine. of Medicine Photos:news.msu.edu

The protruding elements seen in the different slides are cholesterol crystals. Those elements are arising from within the artery wall, causing tearing and damage to the artery. The colors have been added for enhancement and imagery.

The discovery by George Abela, chief of the cardiology division in MSU’s College of Human Medicine, and a team of researchers provides new insights into how arteries harden - a process called atherosclerosis - and gives hope for new and early treatments of cardiovascular disease.

The findings are published in the most recent edition of the journal Nature.

Past research has shown that as cholesterol builds up along the wall of an artery, it crystallizes from a liquid to a solid state and expands, said Abela, who has been studying cholesterol crystals for nearly a decade. As the crystals expand, they can disrupt plaque and cause clotting, leading to cardiac attacks. That research also was recently highlighted recently in the Journal of Clinical Lipidology.

In a new discovery, Abela and the team - while looking at causes of inflammation during atherosclerosis in mice - found that the once cholesterol crystals form in the arterial wall, they activate a biomarker called NLRP3 that induces inflammation.

“What we have found now, at the cellular level, is that the crystals are an early cause rather than a late consequence of inflammation,” Abela said.

The discovery could lead to new treatments for heart disease.

“Since cholesterol crystals form very early in the process of heart disease, with great potential to aggravate atherosclerosis, we can target them early on,” Abela said. “We can target new therapies by reducing cholesterol crystal deposits early on or use an inhibitor to block the inflammatory biomarker.”

Abela added that the biomarker activated by the crystals could be a better indicator of potential cardiovascular disease than others, such as serum cholesterol, or the amount of cholesterol found in the bloodstream.

“Now we treat atherosclerosis on the systematic level; with this discovery we can also treat it the cellular level,” he said.

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BUFFALO, N.Y. - MAY 3, 2010
Obesity, a condition linked to heart disease and diabetes, now appears to be associated with another health problem, but one that affects men only - low testosterone levels.

Sandeep Dhindsa, MD is an endocrinology specialist in the UB Department of Medicine of Medicine Photo:diabetes- endocrinologycenterofwny.com

Results of a study published online ahead of print in the journal Diabetes Care, conducted by University at Buffalo endocrinologists, showed that 40 percent of obese participants involved in the Hypogonadism in Males (HIM) study had lower than normal testosterone readings.

The percentage rose to 50 percent among obese men with diabetes. Results also revealed that as body mass index (BMI) - a relationship of weight to height - increased, testosterone levels fell.

“The effect of diabetes on lowering testosterone levels was similar to that of a weight gain of approximately 20 pounds,” says Sandeep Dhindsa, MD, an endocrinology specialist in the UB Department of Medicine and first author on the study.

“In view of the fact that almost one-third of the U.S. is obese, these observations have profound pathophysiological, clinical, epidemiological and public health implications.”

This is the largest analysis of the association between obesity and low testosterone, and the first to compare prevalence of low testosterone with obesity and diabetes separately and together. The study shows that obesity and diabetes may exert independent influences on testosterone concentrations.

“We published a report in 2004 on the high prevalence of low testosterone levels in men with type 2 diabetes, and multiple studies all over the world have confirmed the association of low testosterone with diabetes,” Dhindsa notes.

“The Endocrine Society now recommends that all men with type 2 diabetes should have their testosterone levels measured. Our new study shows that obese men also have a very high prevalence of low testosterone levels, so physicians should consider screening obese non diabetic men, as well, for low testosterone.”

The HIM study was funded by Solvay Pharmaceuticals Inc., and was conducted from November 2003 to February 2004 in 95 primary care practices throughout the U.S. The study involved 2,165 men 45 years or older who provided blood samples for analysis of testosterone concentrations.

UB researchers excluded participants from the full study who had no BMI data or were on certain drugs that can affect testosterone levels, providing a study population of 1,849 men - 398 with diabetes and 1,451 non diabetics.

“With the rising prevalence of obesity in the U.S. and the rest of the world,” says Paresh Dandona, MD, head of the Division of Endocrinology, Diabetes and Metabolism at UB and Kaleida Health, and senior author of the study, “it is imperative that the prevalence of low testosterone levels in obese men be defined. In addition, the magnitude of the contribution of obesity to subnormal testosterone needs to be quantified.

“We hypothesized that obese men are more likely to have low testosterone than non-obese men, and that we would find more low testosterone levels in men with diabetes than in men without diabetes, both obese and non obese.”

Results confirmed these hypotheses, showing a 40 percent higher prevalence of low testosterone in obese men compared to the non obese participants. Men with diabetes, whether obese or not, showed lower levels of testosterone than non diabetic men across all weight categories. Testosterone levels decreased significantly in both diabetic and non diabetic men as BMI increased.

“In view of the increasing prevalence of obesity, even in younger populations, it would be important to conduct a similar study in the men at the prime of their reproductive years,” he says.

UB endocrinologists published a study in Diabetes Care in 2008 showing that more than 50 percent of men between 18 and 35 years old with type 2 diabetes had lower than normal testosterone levels.

“In view of the high rates of subnormal testosterone in patients with obesity or diabetes, testosterone concentrations should be measured regularly in these populations, especially when these conditions occur together,” says Dandona.

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New research in the FASEB Journal shows that high levels of phosphate in sodas and processed foods accelerate the aging process in mice and contribute to age associated complicationssuch as chronic kidney disease.

Here’s another reason to kick the soda habit. New research published online in the FASEB Journal (http://www.fasebj.org) shows that high levels of phosphates may add more “pop” to sodas and processed foods than once thought. That’s because researchers found that the high levels of phosphates accelerate signs of aging. High phosphate levels may also increase the prevalence and severity of age-related complications, such as chronic kidney disease and cardiovascular calcification, and can also induce severe muscle and skin atrophy.

Mohammed Shawkat Razzaque, PhD,MB Department of Medicine Infection and Immunity, Harvard School of Dental Medicine Photo:hsdm.harvard.edu

“Humans need a healthy diet and keeping the balance of phosphate in the diet may be important for a healthy life and longevity,” said M. Shawkat Razzaque, M.D., Ph.D., from the Department of Medicine, Infection and Immunity at the Harvard School of Dental Medicine. “Avoid phosphate toxicity and enjoy a healthy life.”

To make this discovery, Razzaque and colleague examined the effects of high phosphate levels in three groups of mice. The first group of mice was missing a gene (klotho), which when absent, causes mice to have toxic levels of phosphate in their bodies. These mice lived 8 to 15 weeks. The second group of mice was missing the klotho gene and a second gene (NaPi2a), which when absent at the same time, substantially lowered the amount of phosphate in their bodies. These mice lived to 20 weeks. The third group of mice was like the second group (missing both the klotho and NaPi2a genes), except they were fed a high phosphate diet. All of these mice died by 15 weeks, like those in the first group. This suggests that phosphate has toxic effects in mice, and may have a similar effect in other mammals, including humans.

“Soda is the caffeine delivery vehicle of choice for millions of people worldwide, but comes with phosphorous as a passenger” said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal. “This research suggests that our phosphorous balance influences the aging process, so don’t tip it.”

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In a large study in Japan, women who reported eating more foods containing the B-vitamins folate and B-6 were less likely to die from stroke and heart disease.
Japanese men reporting diets high in these B vitamins were less likely to die of heart failure.

Eating more foods containing the B vitamins folate and B-6 lowers the risk of death from stroke and heart disease for women and may reduce the risk of heart failure in men, according to Japanese research reported in Stroke: Journal of the American Heart Association.

Hiroyasu Iso M.D. professor of public health at Osaka University Photo:Osaka University

“Japanese people need more dietary intake of folate and vitamin B-6, which may lead to the prevention of heart disease,” said Hiroyasu Iso, M.D., professor of public health at Osaka University.

The findings on the value of B vitamins were consistent with studies in Europe and North America, although the dietary consumption of vitamin B-6 is generally lower in Japan than in the United States.

Researchers analyzed data from 23,119 men and 35,611 women (ages 40-79) who completed food frequency questionnaires as part of the large Japan Collaborative Cohort (JACC) Study. During a median 14 years of follow up, 986 died from stroke, 424 from heart disease and 2,087 from all diseases related to the cardiovascular system.

Investigators divided participants into five groups based on their intake of folate, vitamin B-6 and vitamin B-12. Comparing those with the diets lowest and highest for each nutrient, they found that higher consumption of folate and vitamin B-6 was associated with significantly fewer deaths from heart failure in men, and significantly fewer deaths from stroke, heart disease and total cardiovascular diseases in women. Vitamin B-12 intake was not associated with reduced mortality risk.

The protective effects of folate and vitamin B-6 didn’t change when researchers adjusted for the presence of cardiovascular risk factors, nor when they eliminated supplement users from the analysis. Folate and vitamin B-6 may help guard against cardiovascular disease by lowering homocysteine levels, the investigators said. Homocysteine is an amino acid in the blood that’s affected by diet and heredity. Folic acid and other B vitamins help break down homocysteine in the body.

A direct causal link hasn’t been established, but evidence has shown that too much homocysteine may damage the inner lining of arteries and promote the formation of blood clots.

Sources of folate include vegetables and fruits, whole or enriched grains, fortified cereals, beans and legumes. Sources of vitamin B-6 include vegetables, fish, liver, meats, whole grains and fortified cereals.

Co authors include: Renzhe Cui, M.D.; Chigusa Date, M.D.; Shogo Kikuchi, M.D.; Akiko Tamakoshi, M.D.; and the JACC study group. Press Release:American Heart Association.

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Johns Hopkins researchers discover pathway in mice for resveratrol’s apparent protective effect Researchers at Johns Hopkins say they have discovered the way in which red wine consumption may protect the brain from damage following a stroke.

Sylvain Dore, Ph.D. - professor of anesthesiology and critical care medicine and pharmacology and molecular sciences at the Johns Hopkins University School of Medicine

Two hours after feeding mice a single modest dose of resveratrol, a compound found in the skins and seeds of red grapes, the scientists induced an ischemic stroke by essentially cutting off blood supply to the animals’ brains. They found that the animals that had preventively ingested the resveratrol suffered significantly less brain damage than the ones that had not been given the compound.

Sylvain Dore, Ph.D., an associate professor of anesthesiology and critical care medicine and pharmacology and molecular sciences at the Johns Hopkins University School of Medicine, says his study suggests that resveratrol increases levels of an enzyme (heme oxygenase) already known to shield nerve cells in the brain from damage. When the stroke hits, the brain is ready to protect itself because of elevated enzyme levels. In mice that lacked the enzyme, the study found, resveratrol had no significant protective effect and their brain cells died after a stroke.

“Our study adds to evidence that resveratrol can potentially build brain resistance to ischemic stroke,” says Dore, the leader of the study, which appears online in the journal Experimental Neurology.

Dore cautions against taking resveratrol supplements, available alongside vitamins and minerals and on websites touting its benefits, because it is unclear whether such supplements could do harm or good. He has not tested resveratrol in clinical trials. And while resveratrol is found in red grapes, it’s the alcohol in the wine that may be needed to concentrate the amounts of the beneficial compound. Dore also cautions that drinking alcohol carries risks along with potential benefits.

He also notes that even if further research affirms the benefits of red wine, no one yet knows how much would be optimal to protect the brain, or even what kind of red wine might be best, because not all types contain the same amount of resveratrol. More research is needed, he says.

Dore says his research suggests that the amount needed could end up being quite small because the suspected beneficial mechanism is indirect. “Resveratrol itself may not be shielding brain cells from free radical damage directly, but instead, resveratrol, and its metabolites, may be prompting the cells to defend themselves,” he suggests.

“It’s not likely that brain cells can have high enough local levels of resveratrol to be protective,” he says. The resveratrol is needed to jump-start this protective enzymatic system that is already present within the cells. “Even a small amount may be sufficient,” Dore says.

Dore says his ongoing research also suggests some therapeutic benefits to giving resveratrol to mice after a stroke to limit further neuronal damage.

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University of Utah Hospital only the second center in the country to implant new device. After receiving only the fourth U.S. implant of a new generation, Utah made ventricular assist (VAD ) device, an Idaho man with heart failure is looking forward to resuming an active life following an operation on March 17 at University of Utah Hospital.

Craig H. Selzman, MD - Surgical Director of Heart Transplant and Cardiac Mechanical Assist University of Utah Health Care photo: University of Utah

Douglas Wiley, Kuna, Idaho, received the Levacor™ VAD as part of national clinical trial under way at the University and is anxious to give his new VAD a real world tryout. “I can’t wait to get back on my motorcycle,” the 44 year old says.

The clinical trial, which is evaluating how well the new VAD serves as a bridge for people awaiting a heart transplant, is one of several leading edge treatment options the University’s cardiovascular program offers for people suffering from heart disease, according to Craig H. Selzman, M.D., the Utah principal investigator in the trial and a cardiothoracic surgeon with University of Utah Health Care.

“This new generation VAD represents a potentially important step in giving patients such as Mr. Wiley the chance to regain their strength and vitality while they wait for a heart transplant,” Selzman said. “The University of Utah has a long and proud history in the development and use of implanted blood pumps, and with the Levacor™ clinical trial we are expanding our commitment to help those with this devastating disease.”

As an academic medical system, University of Utah Health Care offers the full range of options for people with heart disease - medical treatment, transplantation, and vanguard technologies and trials such as new VADs and even stem cell transplants to help damaged hearts heal themselves.

The Levacor™ VAD was initially developed at and spun off from the University of Utah and is being commercialized by WorldHeart Corporation, a Salt Lake City based company. Unlike other VADs, this one uses a fully magnetically suspended rotor to help pump blood, allowing it to operate without bearings or other moving parts that wear out and can damage blood. Potentially, the Levacor™ VAD could last years longer than other blood pumps.

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KINGSTON, R.I.

URI pharmacy researcher finds beneficial compounds in pure maple syrup
Most are disease fighting anti-oxidants

Before you dig in to your next stack of French toast or waffles, you might want to pour on pure maple syrup.

That’s because University of Rhode Island researcher Navindra Seeram, who specializes in medicinal plant research, has found more than 20 compounds in maple syrup from Canada that have been linked to human health, 13 of which are newly discovered in maple syrup. In addition, eight of the compounds have been found in the Acer (maple) family for the first time.

The URI assistant professor of biomedical and pharmaceutical sciences in URI’s College of Pharmacy presented his findings Sunday, March 21 at the American Chemical Society’s Annual Meeting in San Francisco. The project was made possible by Conseil pour le développement de l’agriculture du Québec (CDAQ), with funding provided by Agriculture and Agri-Food Canada’s Advancing Canadian Agriculture and Agri-Food (ACAAF) program.

Several of these anti-oxidant compounds newly identified in maple syrup are also reported to have anti-cancer, anti-bacterial and anti-diabetic properties.

Prior to the study, the Federation of Quebec Maple Syrup Producers already knew that its product was full of naturally occurring minerals such as zinc, thiamine and calcium. But it enlisted Seeram to research the presence of plant anti-oxidants. The Federation awarded Seeram a two-year, $115,000 grant with the help of the CDAQ and Agriculture and Agri-Food Canada. His research continues to determine if the compounds exist in beneficial quantities.

Serge Beaulieu, president of the Federation of Quebec Maple Syrup Producers, said Seeram’s lab is but one in an expanding multi-national network of research facilities dedicated to the study of maple products from Canada.

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(Yale University)
A new method of growing arteries could lead to a “biological bypass”-or a non-invasive way to treat coronary artery disease, Yale School of Medicine researchers report with their colleagues in the April issue of Journal of Clinical Investigation.

Michael Simons,MD - chief of the Section of Cardiology at Yale School of Medicine photo: yalemedicalgroup.org

Coronary arteries can become blocked with plaque, leading to a decrease in the supply of blood and oxygen to the heart. Over time this blockage can lead to debilitating chest pain or heart attack. Severe blockages in multiple major vessels may require coronary artery bypass graft surgery, a major invasive surgery.

“Successfully growing new arteries could provide a biological option for patients facing bypass surgery,” said lead author of the study Michael Simons, M.D., chief of the Section of Cardiology at Yale School of Medicine.

In the past, researchers used growth factors-proteins that stimulate the growth of cells-to grow new arteries, but this method was unsuccessful. Simons and his team studied mice and zebrafish to see if they could simulate arterial formation by switching on and off two signaling pathways-ERK1/2 and P13K.

“We found that there is a cross-talk between the two signaling pathways. One half of the signaling pathway inhibits the other. When we inhibit this mechanism, we are able to grow arteries,” said Simons. “Instead of using growth factors, we stopped the inhibitor mechanism by using a drug that targets a particular enzyme called P13-kinase inhibitor.”

“Because we’ve located this inhibitory pathway, it opens the possibility of developing a new class of medication to grow new arteries,” Simons added. “The next step is to test this finding in a human clinical trial.”

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Cholesterol’s link to heart disease gets clearer - and more complicated
By considering molecular level events on a broader scale, researchers now have a clearer, if more complicated, picture of how one class of immune cells goes wrong when loaded with cholesterol. The findings reported in the February 3rd issue of Cell Metabolism, a Cell Press publication, show that, when it comes to the development of atherosclerosis and heart disease, it’s not about any one bad actor - it’s about a network gone awry.

The new findings also highlight a pretty remarkable thing, Heinecke says: “Despite 30 years of study, we still don’t know how cholesterol causes heart disease.” But, with the new findings, scientists are getting closer.

Earlier studies had shown that heart disease is about more than just high LDL (”bad”) cholesterol. Cells known as macrophages also play a critical role. Macrophages are part of the innate immune system that typically gobble up pathogens and clear away dead cells. But they also take up and degrade cholesterol derivatives. When they get overloaded with those lipoproteins, they take on a foamy appearance under the microscope to become what scientists aptly refer to as foam cells. Those foam cells are the ones that seem to have critical importance in the development of atherosclerosis.

People had typically thought about this problem in terms of linear pathways, Heinecke explained. In essence, macrophages end up with too much cholesterol going in and not enough coming out. The macrophages get overwhelmed and trapped in the artery wall, and somehow plaques form as a result.

But the new results show that it isn’t really about simple paths in and out; rather, there is an integrated network of macrophage proteins involved. When that network gets disrupted, as it does when too much cholesterol comes in, atherosclerosis forms. “It’s definitely a different way to think about what is going on,” Heinecke says.

Heinecke’s group applied sophisticated technologies and statistical tools to get a global view of what happens to macrophage proteins when they turn into foam cells. Their analysis revealed what they call a macrophage sterol responsive network (MSRN), including proteins already known to work together. Most of them are also found in one place, within microvesicles outside the macrophage cells.

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New research findings from a team at the Providence Heart + Lung Institute at St. Paul’s Hospital and the University of British Columbia (UBC) may lead to new treatment options for abdominal aortic aneurysms (AAA) - a potentially fatal disease that currently has no pharmacological treatments.

“Dr. David Granville University of British Columbia and St. Paul’s Hospital photo: UBC

An aortic aneurysm is a bulging of the aorta, the largest blood vessel in the body. If the aneurysm ruptures, it causes rapid blood loss and a high risk of death. About 75 per cent of all aortic aneurysms occur in the part of the aorta that is located in the abdomen, which supplies blood to the lower limbs.

Published in today’s American Journal of Pathology, a study led by Dr. David Granville, a researcher with UBC and the Providence Heart + Lung Institute, reveals a novel therapeutic target for AAA that could have a major impact on the treatment of this disease.

Using experimental models of AAA, Dr. Granville and his team identified a protein degrading enzyme called Granzyme B that is abundant in aneurysms. To determine whether Granzyme B was contributing to aneurysms, the enzyme was genetically knocked out.

“When we removed Granzyme B, we found that it not only slowed the progression of aneurysms, but also markedly improved survival,” says Dr. Granville. “This suggests that drugs designed specifically to target Granzyme B could be an effective means of treating aneurysms.”

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Universite de Montreal research team developing leptin based pill to control hunger. A Universite de Montreal research team is developing a pill composed of leptin, the protein that tells our brain to stop eating. “Mice deprived of leptin will not stop eating. They become so big they have trouble moving around,” says Moise Bendayan, a pathology professor at the Universite de Montreal Faculty of Medicine who has studied the leptin protein extensively.

“Dr Moise Bendayan Universite de Montreal Faculty of Medicine photo: Universite de Montreal

Leptin regulates appetite in mammals and its levels decrease when fasting and rise during meals. It has been proven to be an appetite suppressant when administered intravenously to pathologically obese people.

Postdoctoral student Philippe Cammisotto is leading the charge for a leptin based, appetite suppressing pill with Dr. Bendayan and Emile Levy, a professor from the Department of Nutrition. “Taken orally, such a pill would provide obese people with the sensation of being full. They would eat less and in turn lose weight,” says Dr. Cammisotto.

“We hope to start animal testing in 2010,” says Bendayan. “The molecule is easy to synthesize and the protocol is ready.”

After decades of building his reputation in fundamental research, Bendayan is happy to collaborate on something more tangible. “Obesity is a big problem in our society, no pun intended,” says Bendayan. “To develop medication to combat obesity would be a great way for our laboratory to contribute to public health.”

>>>>>Read the full Press Release in our HeartVigor.com News Pages.