SUN EXPOSURE MAY TRIGGER CERTAIN AUTOIMMUNE DISEASES IN WOMEN

More bad news for women. The sun may trigger autoimmune disease.

SUN EXPOSURE MAY TRIGGER CERTAIN AUTOIMMUNE DISEASES IN WOMEN

U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Institute of Environmental Health Sciences (NIEHS)
For Immediate Release: Thursday, July 30, 2009

CONTACT: Robin Mackar, 919-541-0073,

SUN EXPOSURE MAY TRIGGER CERTAIN AUTOIMMUNE DISEASES IN WOMEN

Ultraviolet (UV) radiation from sunlight may be associated with the development of certain autoimmune diseases, particularly in women, according to a study by researchers at the National Institute of Environmental Health Sciences (NIEHS), part of the National Institutes of Health.

"This study found that women who lived in areas with higher levels of UV exposure when they developed an autoimmune muscle disease called myositis were more likely to develop the form known as dermatomyositis, which weakens the muscles and causes distinctive rashes, instead of the form called polymyositis that does not have a rash," said Frederick W. Miller, M.D., Ph.D., chief of the Environmental Autoimmunity Group, Program of Clinical Research, at NIEHS. "Although we have not shown a direct cause and effect link between UV exposure and this particular autoimmune disease, this study confirms the association between UV levels and the frequency of dermatomyositis that we found in a previous investigation," said Miller.

The study, published in the August issue of Arthritis & Rheumatism, is also the first to evaluate and find a possible UV radiation association in autoimmune diseases in women.

According to Miller, women are more likely than men to develop many autoimmune diseases, but the reasons for this have not been clear. "We only found the association between UV exposure and dermatomyositis in women and not in men, and it could be that inherent differences in how women and men respond to UV radiation may play a role in the development of certain autoimmune diseases," said Dr. Miller. Miller also noted that other researchers have shown that female mice develop more skin inflammation after UV light exposure compared to male mice and these effects may be related to the new findings in dermatomyositis.

The study was designed to determine if there was a relationship between the level of UV exposure at the onset of the disease and the type of myositis and autoantibodies that people developed. Dermatomyositis and polymyositis are the two major forms of myositis and both are considered autoimmune diseases, in which the body's immune system attacks muscle or skin and sometimes other tissues. Dermatomyositis is typically accompanied by a distinctive reddish-purple rash on the upper eyelids or over the knuckles and is often made worse with sun exposure.

To conduct the study, the NIEHS researchers collaborated with myositis centers across the country that had seen 380 patients who had been diagnosed with dermatomyositis or polymyositis and determined their autoantibodies. "Patients with autoimmune diseases make a variety of autoantibodies that are unique to different conditions. One autoantibody specifically associated with dermatomyositis is called the anti-Mi-2 autoantibody and we know from our previous research that UV radiation increases levels of the Mi-2 protein that this autoantibody binds to," said Miller.

In addition to finding an association between the level of UV radiation and the proportion of women who developed dermatomyositis compared to polymyositis, the researchers found an association between UV levels and the proportion of women with the anti-Mi-2 autoantibody. "More research is clearly needed to understand the potential links between UV radiation and the development of autoimmune diseases and autoantibodies in women," said Miller.

"While the causes of autoimmune diseases are not known, we suspect from emerging research that they develop after one or more environmental exposures in genetically susceptible people," said NIEHS Director Linda Birnbaum, Ph.D. "This study adds UV radiation to the growing list of environmental exposures possibly important in the development of autoimmune diseases."

The NIEHS supports research to understand the effects of the environment on human health and is part of NIH. For more information on environmental health topics, visit our Web site at .

The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit .
--------------------------
REFERENCE: Love LA, Weinberg CR, McConnaughey DR, Oddis CV, Medsger TA, Reveille JD, Arnett FC, Targoff IN, Miller FW. "Ultraviolet Radiation Intensity Predicts the Relative Distribution of Dermatomyositis and Anti-Mi-2 Autoantibodies in Women." Arthritis & Rheumatism. August, 2009.

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SUN EXPOSURE MAY TRIGGER CERTAIN AUTOIMMUNE DISEASES IN WOMEN

U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Institute of Environmental Health Sciences (NIEHS)
For Immediate Release: Thursday, July 30, 2009

CONTACT: Robin Mackar, 919-541-0073,

SUN EXPOSURE MAY TRIGGER CERTAIN AUTOIMMUNE DISEASES IN WOMEN

Ultraviolet (UV) radiation from sunlight may be associated with the development of certain autoimmune diseases, particularly in women, according to a study by researchers at the National Institute of Environmental Health Sciences (NIEHS), part of the National Institutes of Health.

"This study found that women who lived in areas with higher levels of UV exposure when they developed an autoimmune muscle disease called myositis were more likely to develop the form known as dermatomyositis, which weakens the muscles and causes distinctive rashes, instead of the form called polymyositis that does not have a rash," said Frederick W. Miller, M.D., Ph.D., chief of the Environmental Autoimmunity Group, Program of Clinical Research, at NIEHS. "Although we have not shown a direct cause and effect link between UV exposure and this particular autoimmune disease, this study confirms the association between UV levels and the frequency of dermatomyositis that we found in a previous investigation," said Miller.

The study, published in the August issue of Arthritis & Rheumatism, is also the first to evaluate and find a possible UV radiation association in autoimmune diseases in women.

According to Miller, women are more likely than men to develop many autoimmune diseases, but the reasons for this have not been clear. "We only found the association between UV exposure and dermatomyositis in women and not in men, and it could be that inherent differences in how women and men respond to UV radiation may play a role in the development of certain autoimmune diseases," said Dr. Miller. Miller also noted that other researchers have shown that female mice develop more skin inflammation after UV light exposure compared to male mice and these effects may be related to the new findings in dermatomyositis.

The study was designed to determine if there was a relationship between the level of UV exposure at the onset of the disease and the type of myositis and autoantibodies that people developed. Dermatomyositis and polymyositis are the two major forms of myositis and both are considered autoimmune diseases, in which the body's immune system attacks muscle or skin and sometimes other tissues. Dermatomyositis is typically accompanied by a distinctive reddish-purple rash on the upper eyelids or over the knuckles and is often made worse with sun exposure.

To conduct the study, the NIEHS researchers collaborated with myositis centers across the country that had seen 380 patients who had been diagnosed with dermatomyositis or polymyositis and determined their autoantibodies. "Patients with autoimmune diseases make a variety of autoantibodies that are unique to different conditions. One autoantibody specifically associated with dermatomyositis is called the anti-Mi-2 autoantibody and we know from our previous research that UV radiation increases levels of the Mi-2 protein that this autoantibody binds to," said Miller.

In addition to finding an association between the level of UV radiation and the proportion of women who developed dermatomyositis compared to polymyositis, the researchers found an association between UV levels and the proportion of women with the anti-Mi-2 autoantibody. "More research is clearly needed to understand the potential links between UV radiation and the development of autoimmune diseases and autoantibodies in women," said Miller.

"While the causes of autoimmune diseases are not known, we suspect from emerging research that they develop after one or more environmental exposures in genetically susceptible people," said NIEHS Director Linda Birnbaum, Ph.D. "This study adds UV radiation to the growing list of environmental exposures possibly important in the development of autoimmune diseases."

The NIEHS supports research to understand the effects of the environment on human health and is part of NIH. For more information on environmental health topics, visit our Web site at .

The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit .
--------------------------
REFERENCE: Love LA, Weinberg CR, McConnaughey DR, Oddis CV, Medsger TA, Reveille JD, Arnett FC, Targoff IN, Miller FW. "Ultraviolet Radiation Intensity Predicts the Relative Distribution of Dermatomyositis and Anti-Mi-2 Autoantibodies in Women." Arthritis & Rheumatism. August, 2009.

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SPECIES BARRIER MAY PROTECT MACAQUES FROM CHRONIC WASTING DISEASE

More information on a prion disease. Prions still remain controversial as infectious agents among some researchers.

SPECIES BARRIER MAY PROTECT MACAQUES FROM CHRONIC WASTING DISEASE

U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Institute of Allergy and Infectious Diseases (NIAID)
For Immediate Release: Wednesday, July 29, 2009

MEDIA CONTACT: Ken Pekoc, 406-375-9690,

SPECIES BARRIER MAY PROTECT MACAQUES FROM CHRONIC WASTING DISEASE

Data from an ongoing multi-year study suggest that people who consume deer and elk with chronic wasting disease (CWD) may be protected from infection by an inability of the CWD infectious agent to spread to people. The results to date show that 14 cynomolgus macaques exposed orally or intracerebrally to CWD remain healthy and symptom free after more than six years of observation, though the direct relevance to people is not definitive and remains under study. Cynomolgus macaques often are used as research models of human disease because they are very close genetically to humans and are susceptible to several forms of human brain-damaging disease. Thus, it was decided to see whether exposure to CWD could induce disease in the macaques. The study appears online in the journal Emerging Infectious Diseases.

CWD is a type of brain-damaging disease known as a transmissible spongiform encephalopathy (TSE) or prion disease. CWD primarily affects deer, elk, and moose. Other TSE diseases include mad cow disease, or bovine spongiform encephalopathy (BSE) in cattle, scrapie in sheep, and sporadic Creutzfeldt-Jakob disease (CJD) in humans. Humans are not susceptible to sheep scrapie, but BSE appears to have infected about 200 people, primarily in Europe in the 1990s. Those findings provided the rationale for the present CWD-macaque study, which began in 2003.

"We plan to continue this study for at least several more years because, although the risk to macaques so far appears to be low, we know that these diseases can take more than 10 years to develop," says Bruce Chesebro, M.D., chief of the Laboratory of Persistent Viral Diseases at Rocky Mountain Laboratories (RML) in Hamilton, Mont. RML is part of the National Institute of Allergy and Infectious Diseases (NIAID) of the National Institutes of Health (NIH). The RML group is leading the study with collaborators from the Colorado Division of Wildlife; State University of New York Downstate Medical Center; New York State Institute for Basic Research in Developmental Disabilities; American Red Cross; and the University of Wyoming.

The findings by the RML group support published field studies done by others in regions of Colorado and Wyoming where CWD is endemic. Between 1979 and 2001, there were no significant increases in human TSE diseases despite the likelihood that hunters in those areas were exposed to CWD through contact with infected animal tissue and contaminated hunting tools such as knives and saws. Extensive laboratory data also supports a human species barrier against CWD.

Notably, the RML study also included identical testing in squirrel monkeys, which are genetically less similar to humans than macaques. Of 15 squirrel monkeys exposed orally to CWD, two displayed disease symptoms 69 months after infection. Of 13 squirrel monkeys exposed intracerebrally to CWD, 11 displayed symptoms between 33 and 53 months after infection. In symptomatic animals, the presence of the CWD agent was confirmed in brain, spleen and lymph nodes.

The results in squirrel monkeys were not surprising because a study elsewhere in two squirrel monkeys yielded similar results. The study by the RML group was different, however, in that it tested oral exposure to CWD and also studied eight CWD samples from different areas of the country. The results in squirrel monkeys confirmed that disease progression in that species appears consistent with disease progression in deer and elk, where severe weight loss is nearly always present.

"The fact that the squirrel monkeys, like the deer and elk, suffered severe weight loss suggests that chronic wasting disease might affect a common region of the brain in different species," notes Dr. Chesebro.

NIAID conducts and supports research-at NIH, throughout the United States, and worldwide-to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID Web site at .

The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit .
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REFERENCE: Race B et al. Susceptibilities of nonhuman primates to chronic wasting disease. "Emerging Infectious Diseases." DOI: 10.3201/eid1509.090253.

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Sildenafil Stopped for Pulmonary Hypertension in Sickle Cell

Pulmonary hypertension remains a horrible disease with bad treatment options. This is more bad news....

NHLBI STOPS STUDY OF TREATMENT FOR PULMONARY HYPERTENSION IN PATIENTS WITH SICKLE CELL DISEASE DUE TO SAFETY CONCERNS

U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Heart, Lung, and Blood Institute (NHLBI)
For Immediate Release: Tuesday, July 28, 2009

CONTACT: NHLBI Communications Office, 301-496-4236,

NHLBI STOPS STUDY OF TREATMENT FOR PULMONARY HYPERTENSION IN PATIENTS WITH SICKLE CELL DISEASE DUE TO SAFETY CONCERNS

The National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health has stopped a clinical trial testing a drug treatment for pulmonary hypertension in adults with sickle cell disease nearly one year early due to safety concerns. In an interim review of safety data from 33 participants who completed 16 weeks of treatment, researchers found that, compared to participants on placebo (dummy pill), participants taking sildenafil (Revatio) were significantly more likely to have serious medical problems. The most common problem was episodes of severe pain called sickle cell crises, which resulted in hospitalization. No deaths have been associated with the drug in the clinical trial.

Known as walk-PHaSST, the study was the first multicenter, randomized clinical trial to test the safety and effectiveness of sildenafil for pulmonary hypertension in patients with sickle cell disease, one of the most common genetic blood disorders in the United States. Pulmonary hypertension is a debilitating condition of high blood pressure in the arteries that carry blood to the lungs, which can lead to heart failure and death. Approximately 30 percent of sickle cell disease patients develop pulmonary hypertension, and even mild levels of pulmonary hypertension have been associated with sudden death in people with sickle cell disease.

"The increase in sickle cell medical problems is concern enough for us to stop this clinical trial to protect the safety of our participants," said NHLBI Director Elizabeth G. Nabel, M.D. "We will continue to look into the possible causes of these preliminary results. In the meantime, we encourage patients with sickle cell disease who are taking sildenafil for pulmonary hypertension to talk with their physicians about the potential risks and benefits of the medication and what actions they should consider, including whether to taper off this medication and how to best manage both sickle cell disease and pulmonary hypertension."

Because the medical problems experienced in walk-PHaSST were complications specific to sickle cell disease, "The findings of the walk-PHaSST study should not be applied to other groups of patients with pulmonary hypertension where the drug has been found to be safe and effective," Nabel added.

Researchers are conducting extensive analyses of the study results, which could contribute to recommendations for treating pulmonary hypertension in patients with sickle cell disease. They will prepare reports of their research for publication in peer-reviewed journals.

The NHLBI stopped the study on July 7, 2009, based on the unanimous recommendations of the Pulmonary Complications of Sickle Cell Disease Data and Safety Monitoring Board (DSMB), an independent advisory group that has been monitoring the study since it began. This DSMB is composed of experts in sickle cell disease, lung disease, statistics, and bioethics.

Participants in walk-PHaSST have discussed the preliminary findings of the study with their study clinicians. They have been instructed to taper sildenafil treatment over a period of three to seven days to minimize problems associated with immediate withdrawal from the drug, such as worsening of symptoms of pulmonary hypertension. Researchers will continue to monitor participants and conduct further analyses to assess the findings.

Walk-PHaSST was designed to determine whether sildenafil lessens the symptoms of pulmonary hypertension, such as shortness of breath, by improving heart and lung function, in individuals with sickle cell disease who develop pulmonary hypertension. The primary outcome measure was the results of a six-minute walk test, a standard indicator of a person's heart and lung function. Hence, the name walk-PHaSST reflects the primary test used to assess effectiveness of the treatment ("walk" test) for Pulmonary Hypertension and Sickle Cell Disease with Sildenafil Therapy. Researchers also evaluated the safety of the drug for sickle cell disease patients through reports of adverse effects and laboratory tests.

Sildenafil is approved by the Food and Drug Administration for use in patients with pulmonary hypertension. In general, the drug treats pulmonary hypertension by relaxing the blood vessels in the lungs to allow blood to flow more easily. Since sildenafil is not FDA-approved to treat pulmonary hypertension in patients with sickle cell disease, the walk-PHaSST study was conducted under an investigational new drug application. The FDA was notified of the termination of the study on July 14.

Walk-PHaSST began recruiting participants in July 2007 and enrolled 74 patients over the age of 19 (average age 45). Participants had sickle cell disease and mild to severe pulmonary hypertension. They were randomly assigned to receive sildenafil or placebo for 16 weeks. Participants could also receive other therapies as needed to manage sickle cell and related complications. After completing the study treatment (or placebo), participants could choose to be part of the open-label follow-up phase of the study and continue to be assessed for up to one year. In the open-label study, participants and clinicians knew that sildenafil was being taken. When the study was stopped, 33 participants had completed the clinical trial.

Researchers found that 38 percent of participants taking sildenafil had serious adverse effects -- primarily sickle cell pain crises -- compared to 8 percent of participants in the placebo group.

"Although these preliminary results are disappointing, we expect that the study's results, once fully analyzed, will provide important insights into the role of pulmonary hypertension in sickle cell disease," said Mark Gladwin, M.D., lead investigator of walk-PHaSST and director of the Vascular Medicine Institute at the University of Pittsburgh. Gladwin is also a special volunteer for the NHLBI and was formerly a senior investigator with the Critical Care Medicine Department at the NIH Clinical Center and chief of the NHLBI Pulmonary and Vascular Medicine Branch.

The design of the walk-PHaSST study was based on extensive evidence that sildenafil improves pulmonary hypertension regardless of its cause and on results of a small, open-label, nonrandomized pilot study led by Gladwin while he was at the NIH. The pilot study evaluated 12 sickle cell patients with mild or moderate pulmonary hypertension who were being treated with sildenafil and with hydroxyurea, a drug known to help reduce the numbers of episodes of sickle cell pain crises and acute chest syndrome, as well as hospitalizations and blood transfusions needed. In 2005, Gladwin and his colleagues reported that after about 6 months, sildenafil was well tolerated, decreased pulmonary blood pressure, and increased exercise capacity.

"Walk-PHaSST emphasizes the importance of multi-site, blinded, randomized clinical trials to increase our understanding of both the benefits and the potential risks of specific treatments," noted Jonathan C. Goldsmith, M.D., NHLBI project officer of walk-PHaSST. "As with all clinical studies, patient safety is paramount."

Walk PHaSST was conducted at the following locations:

-- Children's Hospital, Oakland, Calif.
-- University of Colorado, Denver
-- Howard University Hospital, Washington, D.C.
-- University of Illinois at Chicago
-- Johns Hopkins Medical Institutions, Baltimore
-- NIH Clinical Center, Bethesda, Md.
-- Albert Einstein College of Medicine, New York City
-- Columbia University, New York City
-- Children's Hospital, Pittsburgh
-- Imperial College London and Hammersmith Hospital, London, England

Rho Inc. of Chapel Hill, N.C., serves as the data coordinating center. Pfizer provided the treatment drug and placebo for the study.

Sickle cell anemia affects millions of people worldwide. An estimated 70,000 to 100,000 people in the United States have sickle cell disease, primarily African Americans and, to a lesser degree, people whose families come from South or Central America. Patients with this disease have abnormal hemoglobin molecules in their red blood cells. The abnormal molecules deform the red blood cells, causing them to clump together and block blood flow through blood vessels, leading to painful sickle cell crises, organ damage, and anemia. Life-threatening complications include infections, acute chest syndrome, stroke, and pulmonary hypertension. Painful crises are the leading cause of emergency room visits and hospitalizations of people who have sickle cell anemia.

There are currently no established guidelines for treating pulmonary hypertension in patients with sickle cell disease. Pulmonary hypertension can lead to heart failure and death as the heart must work harder to push blood into the lungs. In general, intensive management of sickle cell disease through hydroxyurea, blood transfusions, and/or bone marrow transplantation may be indicated. Other treatment options may include blood-thinning medicines, diuretics, and oxygen therapy.

"As new treatments have evolved over the past several years, sickle cell patients are living longer than in previous decades, presenting new challenges for managing chronic problems and complications such as pulmonary hypertension," noted Susan Shurin, MD, NHLBI deputy director and a hematologist. "The NHLBI continues to maintain a strong commitment to supporting research in adults as well as in children to discover new and better ways to improve quality of life and survival for patients with sickle cell disease."

Further information about this trial (NCT00492531) can be found at . To arrange an interview with an NHLBI spokesperson or Dr. Gladwin, please contact the NHLBI Communications Office at (301) 496-4236 or email . Dr. Gladwin can also be reached at .

Part of the National Institutes of Health, the National Heart, Lung, and Blood Institute (NHLBI) plans, conducts, and supports research related to the causes, prevention, diagnosis, and treatment of heart, blood vessel, lung, and blood diseases; and sleep disorders. The Institute also administers national health education campaigns on women and heart disease, healthy weight for children, and other topics. NHLBI press releases and other materials are available online at .

The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit .
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RESOURCES:

Sickle cell disease .

Pulmonary hypertension

Report of the National Heart, Lung, and Blood Advisory Council Subcommittee Review of the NHLBI Sickle Cell Disease Program, February 29, 2008

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INTENSIVE GLUCOSE CONTROL HALVES COMPLICATIONS OF LONGSTANDING TYPE 1 DIABETES

The NIH is saying that better blood sugar control in diabetes results in fewer health complications. - BRH

U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Embargoed for Release: Monday, July 27, 2009, 4 p.m. EDT

CONTACT:
Mary Harris, Joan Chamberlain, 301-496-3583,

INTENSIVE GLUCOSE CONTROL HALVES COMPLICATIONS OF LONGSTANDING TYPE 1 DIABETES
Study Finds Improved Long-Term Outlook

Near-normal control of glucose beginning as soon as possible after diagnosis would greatly improve the long-term prognosis of type 1 diabetes, concludes a study published in the July 27, 2009, issue of the Archives of Internal Medicine, which updates information about the clinical course of type 1 diabetes. The study also found that the outlook for people with longstanding type 1 diabetes has greatly improved in the past 20 years due to a better understanding of the importance of intensive glucose control as well as advances in insulin formulations, insulin delivery, glucose monitoring, and the treatment of cardiovascular risk factors.

"The demonstration that near-normal glucose control substantially lowers microvascular and cardiovascular complications has heralded a new era of type 1 diabetes care," says lead author David M. Nathan, M.D., of Massachusetts General Hospital. Nathan is also co-chair of the landmark Diabetes Control and Complications Trial (DCCT) and its follow-up study, the Epidemiology of Diabetes Interventions and Complications (EDIC), both funded by the National Institutes of Health. "The remarkable improvement in long-term outcomes achieved with intensive glucose control should encourage clinicians and patients alike to implement intensive therapy as early in the course of type 1 diabetes as possible."

The DCCT, conducted from 1983 to 1989, found that intensive glucose control was superior to conventional control in delaying or preventing the complications of type 1 diabetes. EDIC continues to follow DCCT participants to determine the long-term effects of prior intensive versus conventional blood glucose control.

The authors compared overall rates of eye, kidney, and cardiovascular complications in three groups of people diagnosed with type 1 diabetes an average of 30 years earlier. Two groups consisted of DCCT/EDIC participants--those randomly assigned to intensive glucose control or to conventional control. The third group was a subset of patients in the Pittsburgh Epidemiology of Diabetes Complications (EDC) study, who were matched to DCCT/EDIC participants by age, duration of diabetes, and degree of eye damage. The EDC, also funded by NIH, is a population-based study that has been following residents of Allegheny County, Pa., who were diagnosed with type 1 diabetes from 1950 to 1980.

After 30 years of diabetes, DCCT participants randomly assigned to intensive glucose control had about half the rate of eye damage compared to those assigned to conventional glucose control (21 percent vs. 50 percent). They also had lower rates of kidney damage (9 percent vs. 25 percent) and cardiovascular disease events (9 percent vs. 14 percent) compared to those receiving conventional glucose control. Eye damage ranged from significant damage without vision loss to blindness. Kidney damage ranged from mild kidney disease to kidney failure. Cardiovascular events encompassed heart attack, stroke, angina, and obstruction of the coronary arteries.

The intensively treated DCCT group also had lower complication rates than EDC participants, whose rates were similar to DCCT's conventional control group: eye damage (47 percent), kidney damage (17 percent), and cardiovascular disease events (14 percent).

"Better treatment of blood pressure and cholesterol is also helping to reduce complication rates. The similar event rates in the DCCT conventional control group and the EDC study suggest that the results of the DCCT trial are likely to be generally applicable to those with type 1 diabetes," said Trevor Orchard, M.D., of the University of Pittsburgh, who heads the EDC study.

Not only did intensive glucose control halve the rates of eye and kidney damage, but the rates of vision loss and kidney failure were much lower than had been seen historically. "After 30 years of diabetes, fewer than 1 percent of those receiving intensive glucose control in the DCCT had significantly impaired vision, kidney failure, or needed a limb amputation due to diabetes," noted Saul Genuth, M.D., of Case Western University, who co-chairs the EDIC study. "Tight control is difficult to achieve and maintain, but its benefits have changed the course of diabetes."

The DCCT compared intensive management of blood glucose to conventional control in 1,441 people 13 to 39 years of age with type 1 diabetes. At the time, conventional treatment consisted of one or two insulin injections a day with daily urine or blood glucose testing. Participants randomly assigned to intensive treatment were asked to keep glucose levels as close to normal as possible. That meant trying to keep hemoglobin A1c (A1C) readings at 6 percent or less with at least three insulin injections a day or an insulin pump, guided by frequent self-monitoring of blood glucose. (A1C reflects average blood glucose over the previous two to three months.)

In addition, the rates of eye damage (30 percent) and kidney disease (12 percent) in all DCCT/EDIC participants who had type 1 diabetes for 25 years were also significantly lower than the rates of eye damage (40-53 percent) and kidney disease (35 percent) reported in the medical literature for comparable patients diagnosed in the 1950s to 1970s.

"These data give clinicians a realistic description of the clinical outcomes they can discuss with their patients. When intensive therapy, now the standard of care, is implemented early in the course of diabetes, most patients with type 1 diabetes should be able to avoid the disastrous long-term complications that were so common in the past," said Nathan.

Major improvements in glucose monitoring and insulin delivery introduced in the past decade are now helping patients control their blood glucose more precisely and conveniently and reduce the risk of hypoglycemia. For example, several continuous glucose monitoring devices approved by the Food and Drug Administration give both trend and real-time information on glucose levels. Insulin pump technology is also improving, and researchers have begun testing a system that combines both technologies in patients with newly diagnosed type 1 diabetes.

In the United States, nearly 24 million people have diabetes. In adults, type 1 diabetes accounts for 5 to 10 percent of all diagnosed cases of diabetes. Formerly called juvenile-onset diabetes or insulin-dependent diabetes, type 1 diabetes develops when the body's immune system destroys pancreatic beta cells, the only cells in the body that make the hormone insulin that regulates blood glucose. This form of diabetes usually arises in children and young adults, but it can occur at any age. Management involves keeping blood glucose levels as close to normal as possible with three or more insulin injections a day or treatment with an insulin pump, careful monitoring of glucose, and close attention to diet and exercise.

Type 2 diabetes, or adult-onset diabetes, accounts for about 90 to 95 percent of all diagnosed cases of diabetes in adults. It usually begins as insulin resistance, a disorder in which the cells do not use insulin properly. As the need for insulin rises, the pancreas gradually loses its ability to produce it. Type 2 diabetes is associated with older age, obesity, family history of diabetes, history of gestational diabetes, impaired glucose metabolism, physical inactivity, and race/ethnicity. African Americans, Hispanic/Latino Americans, American Indians, and some Asian Americans and Native Hawaiians or other Pacific Islanders are at particularly high risk for type 2 diabetes and its complications.

The DCCT is registered as NCT00360815, and EDIC is registered as NCT00360893 in . The DCCT/EDIC is funded by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), the National Eye Institute, the National Institute of Neurological Disorders and Stroke, and the General Clinical Research Centers Program, National Center for Research Resources, within the NIH. Genentech contributed to the DCCT/EDIC through a Cooperative Research and Development Agreement with the NIDDK. Lifescan, Roche, Aventis, Eli Lilly, Omnipod, Can-Am, B-D, Animas, Medtronic, Medtronic Minimed, Bayer, and Omron, contributed free or discounted supplies to the DCCT/EDIC. The EDC study is funded by the NIDDK.

NIDDK, part of the NIH, conducts and supports basic and clinical research and research training on some of the most common, severe and disabling conditions affecting Americans. The Institute's research interests include diabetes and other endocrine and metabolic diseases; digestive diseases, nutrition, and obesity; and kidney, urologic and hematologic diseases. For more information, visit .

The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit .

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Blood Pressure Genetic Variants

U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Human Genome Research Institute (NHGRI) <http://www.nhgri.nih.gov/>
Embargoed for Release: Thursday, July 16, 2009, 8:01 p.m. EDT

CONTACT: Raymond MacDougall, 301-402-0911, e-mail: macdougallr@mail.nih.gov

RESEARCHERS UNCOVER GENETIC VARIANTS LINKED TO BLOOD PRESSURE IN AFRICAN-AMERICANS
Findings May Point to New Avenues for Treatment, Prevention

A team led by researchers from the National Institutes of Health (NIH) today reported the discovery of five genetic variants related to blood pressure in African-Americans, findings that may provide new clues to treating and preventing hypertension. The effort marks the first time that a relatively new research approach, called a genome-wide association study, has focused on blood pressure and hypertension in an African-American population.

Hypertension, or chronic high blood pressure, underlies an array of life-threatening conditions, including heart disease, stroke and kidney disease. Diet, physical activity and obesity all contribute to risk of hypertension, but researchers also think genetics plays an important role.

About one-third of U.S. adults suffer from hypertension. The burden is considerably greater in the African-American community, in which the condition affects 39 percent of men and 43 percent of women.

"This work underscores the value of using genomic tools to untangle the complex genetic factors that influence the risk for hypertension and other common diseases," said Eric Green, M.D., Ph.D., scientific director for the National Human Genome Research Institute (NHGRI), part of NIH. "We hope these findings eventually will translate into better ways of helping the millions of African-Americans at risk for hypertension, as well as improved treatment options for other populations."

In addition to NHGRI researchers, scientists from the Coriell Institute for Medical Research in Camden, N.J.; Boston University; and Howard University, in Washington, D.C., collaborated on the study, which was published in the July 17 online issue of PLoS Genetics.

To produce their findings, researchers analyzed DNA samples from 1,017 participants in the Howard University Family Study, a multigenerational study of families from the Washington, D.C., metropolitan area who identified themselves as African-American. Half of the volunteers had hypertension and half did not. To see if there were any genetic differences between the two groups, researchers scanned the volunteers' DNA, or genomes, analyzing more than 800,000 genetic markers called single-nucleotide polymorphisms (SNPs).

The researchers found five genetic variants significantly more often in people with hypertension than in those without the condition. The variants were associated with high systolic blood pressure, but not with diastolic blood pressure or combined systolic/diastolic blood pressure.

Blood pressure is measured in millimeters of mercury (mm Hg), and expressed with two numbers; for example, 120/80 mm Hg. The first number (systolic pressure) is the pressure when the heart beats while pumping blood. The second number (diastolic pressure) is the pressure in large arteries when the heart is at rest between beats.

"This is the first genome-wide association study for hypertension and blood pressure solely focused on a population with majority African ancestry," said the study's senior author, Charles Rotimi, Ph.D., NHGRI senior investigator and director of the trans-NIH Center for Research on Genomics and Global Health (CRGGH). "Although the effect of each individual genetic variant was modest, our findings extend the scope of what is known generally about the genetics of human hypertension."

In a genome-wide association study, researchers identify strategically selected markers of genetic variation. If disease status differs for individuals with certain genetic variants, this indicates that something in that chromosomal neighborhood likely influences the disease. Variants detected using this approach can accurately point to the region of the genome involved, but may not themselves directly influence the trait.

In May, two major international studies used the genome-wide association approach to identify 13 genetic variants associated with blood pressure and hypertension in people with primarily European and South Asian ancestry. While each variant was associated with only a slight increase in blood pressure, that work found that the more variants an individual had, the greater his or her risk of hypertension. Two genes identified by one of those studies were also associated with blood pressure in the new study.

In their pioneering study of African-Americans, Dr. Rotimi and his colleagues found that all of the five genetic variants associated with blood pressure were located in or near genes that code for proteins thought to be biologically important in hypertension and blood pressure. Previous research had implicated two of those genes in blood pressure regulation, and additional analyses by Dr. Rotimi's group revealed that all of the variants are likely involved in biological pathways and networks related to blood pressure and hypertension.

An existing class of anti-hypertension drugs, called calcium channel blockers, already targets one of the genes, CACNA1H. However, the additional genes may point to new avenues for treatment and prevention.

To follow up and expand upon their findings in African-Americans, the researchers scanned DNA from 980 West Africans with and without hypertension. The work confirmed that some of the genetic variants detected in African-Americans were also associated with blood pressure in West Africans. "The Western African population is of particular significance since it is the ancestral population of many African-Americans," said lead author Adebowale Adeyemo, M.D., CRGGH staff scientist.

This study was supported by the NHGRI, CRGGH, and the National Institute of General Medical Sciences, all part of NIH; and by a W.W. Smith Foundation grant to the Coriell Institute. The Howard University General Clinical Research Center carried out the enrollment of study participants.

For more information about hypertension, visit <http://www.nhlbi.nih.gov/health/dci/Diseases/Hbp/HBP_WhatIs.html>.

To learn more about the genome-wide association approach, visit <http://www.genome.gov/20019523>.
NHGRI is one of the 27 institutes and centers at the NIH, an agency of the Department of Health and Human Services. The NHGRI Division of Intramural Research develops and implements technology to understand, diagnose and treat genomic and genetic diseases. Additional information about NHGRI can be found at its Web site, <www.genome.gov>.

The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit <www.nih.gov>.

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What is CS3?

It turns out that CS3 is about Adobe Creative Suite (CS). I came across this when trying to learn more about Adobe Photoshop.

Apparently CS3 stands for Creative Suite Three while CF3 stands for computer form, fit, and function.

Human Connectome Project

National Institute of Neurological Disorders and Stroke (NINDS) National Institute of Mental Health (NIMH)

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For Immediate Release Wednesday, July 15, 2009 E-mail this page Subscribe Contact: Daniel Stimson, NINDS 301-496-5751 Marsh Love, NIMH 301-443-4536 NIH Launches the Human Connectome Project to Unravel the Brain�s Connections The National Institutes of Health Blueprint for Neuroscience Research is launching a $30 million project that will use cutting-edge brain imaging technologies to map the circuitry of the healthy adult human brain. By systematically collecting brain imaging data from hundreds of subjects, the Human Connectome Project (HCP) will yield insight into how brain connections underlie brain function, and will open up new lines of inquiry for human neuroscience. Investigators have been invited to submit detailed proposals to carry out the HCP, which will be funded at up to $6 million per year for five years. The HCP is the first of three Blueprint Grand Challenges, projects that address major questions and issues in neuroscience research. The Blueprint Grand Challenges are intended to promote major leaps in the understanding of brain function, and in approaches for treating brain disorders. The three Blueprint Grand Challenges to be launched in 2009 and 2010 address: The connectivity of the adult, human brain Targeted drug development for neurological diseases The neural basis of chronic pain disorders "The HCP is truly a grand and critical challenge: to map the wiring diagram of the entire, living human brain. Mapping the circuits and linking these circuits to the full spectrum of brain function in health and disease is an old challenge but one that can finally be addressed rigorously by combining powerful, emerging technologies," says Thomas Insel, M.D., director of the National Institute of Mental Health (NIMH), which is part of the NIH Blueprint. Scientists have studied the relationship between the structure and function of the human brain since the 1800s. Some parts of the brain serve basic functions such as movement, sensation, emotion, learning and memory. Others are more important for uniquely human functions such as abstract thinking. The connections between brain regions are important for shaping and coordinating these functions, but scientists know little about how different parts of the human brain connect. "Neuroscientists have only a piecemeal understanding of brain connectivity. If we knew more about the connections within the brain — and especially their susceptibility to change — we would know more about brain dysfunction in aging, mental health disorders, addiction and neurological disease," says Story Landis, Ph.D., director of the National Institute of Neurological Disorders and Stroke (NINDS), also part of the NIH Blueprint. For example, there is evidence that the growth of abnormal brain connections during early life contributes to autism and schizophrenia. Changes in connectivity also appear to occur when neurons degenerate, either as a consequence of normal aging or of diseases such as Alzheimer�s. In addition to brain imaging, the HCP will involve collection of DNA samples, demographic information and behavioral data from the subjects. Together, these data could hint at how brain connectivity is influenced by genetics and the environment, and in turn, how individual differences in brain connectivity relate to individual differences in behavior. Primarily, however, the data will serve as a baseline for future studies. These data will be freely available to the research community. The complexity of the brain and a lack of adequate imaging technology have hampered past research on human brain connectivity. The brain is estimated to contain more than 100 billion neurons that form trillions of connections with each other. Neurons can connect across distant regions of the brain by extending long, slender projections called axons — but the trajectories that axons take within the human brain are almost entirely uncharted. In the HCP, researchers will optimize and combine state-of-the-art brain imaging technologies to probe axonal pathways and other brain connections. In recent years, sophisticated versions of magnetic resonance imaging (MRI) have emerged that are capable of looking beyond the brain�s gross anatomy to find functional connections. Functional MRI (fMRI), for example, uses changes in blood flow and oxygen consumption within the brain as markers for neuronal activity, and can highlight the brain circuits that become active during different behaviors. Three imaging techniques are suggested, but are not required, for carrying out the HCP: High angular resolution diffusion imaging with magnetic resonance (HARDI), which detects the diffusion of water along fibrous tissue, and can be used to visualize axon bundles. Resting state fMRI (R-fMRI), which detects fluctuations in brain activity while a person is at rest, and can be used to look for coordinated networks within the brain. Electrophysiology and magnetoencephalography (MEG) combined with fMRI (E/M fMRI), which adds information about the brain�s electrical activity to the fMRI signal. In this procedure, the person performs a task so that the brain regions associated with that task become active. Since this is the first time that researchers will combine these brain imaging technologies to systematically map the brain�s connections, the HCP will support development of new data models, informatics and analytic tools to help researchers make the most of the data. Funds will be provided for building an on-line platform to disseminate HCP data and tools, and for engaging and educating the research community about how to use these data and tools. "Human connectomics has been gaining momentum in the research community for a few years," says Michael Huerta, Ph.D., associate director of NIMH and the lead NIH contact for the HCP. "The data, the imaging tools and the analytical tools produced through the HCP will play a major role in launching connectomics as a field." The field of neuroscience emerged in the late 19th century, when scientists observed individual brain cells for the first time. Since then, researchers have made breathtaking progress in understanding the anatomy, cell biology, physiology and chemistry of the brain in both health and disease. Yet many fundamental questions remain unanswered, including how brain function translates into mental function and why brain function declines with age. Advances in neuroimaging, genomics, computational neuroscience and engineering have put us on the brink of another great era in neuroscience, when we can expect to make unprecedented discoveries regarding normal brain activity, disorders of the brain and our very sense of self. The NIH Blueprint for Neuroscience Research (www.neuroscienceblueprint.nih.gov) is a cooperative effort among the NIH Office of the Director and the 15 NIH Institutes and Centers that support research on the nervous system. By pooling resources and expertise, the Blueprint supports transformative neuroscience research, and the development of new tools, training opportunities, and other resources to assist neuroscientists. The mission of the NIMH is to transform the understanding and treatment of mental illnesses through basic and clinical research, paving the way for prevention, recovery and cure. For more information, visit the www.nimh.nih.gov. NINDS (www.ninds.nih.gov) is the nation�s primary supporter of biomedical research on the brain and nervous system. The National Institutes of Health (NIH) — The Nation's Medical Research Agency — includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov. Home > News & Events E-mail this page Subscribe to receive future NIH news releases. Image via Wikipedia