Health Highlights – March 11th, 2010

March 11, 2010 | by

Health Highlights is a biweekly summary of particularly interesting articles from credible sources of health and medical information that we follow & read. For a complete list of recommeded sources, see our links page.

Health Highlights

New Approach to Immune Cell Analysis Seen as First Step to Better Distinguish Health and Disease

March 9, 2010 | by

Investigators have developed a new mathematical approach to analyze molecular data derived from complex mixtures of immune cells. This approach, when combined with well-established techniques, readily identifies changes in small samples of human whole blood, and has the potential to distinguish between health and disease states.

Led by Mark Davis, Ph.D., and Atul Butte, M.D., Ph.D., of Stanford University, Calif., the team of investigators received support from the National Institute of Allergy and Infectious Diseases (NIAID), as well as the National Heart, Lung, and Blood Institute and the National Cancer Institute, all part of the National Institutes of Health. Details about their work appear online at Nature Methods.

“Defining the status of the human immune system in health and disease is a major goal of human immunology research,” says NIAID Director Anthony S. Fauci, M.D. “A method allowing clinicians to accurately and quickly characterize the many different immune cells in human blood would be a valuable research and diagnostic tool.”

Over the past 15 years, the technology for gene expression microarrays, which allow investigators to identify and measure relative amounts of many different genes in parallel, has advanced tremendously. Today researchers can measure nearly every gene in the human genome using very small amounts of blood. However, blood contains numerous types of immune cells, such as lymphocytes, basophils and monocytes, and when microarray analysis is performed on this mixture, the interpretation of the results becomes problematic.

Scientists Find New Form of Prion Disease that Damages Brain Arteries

March 9, 2010 | by

National Institutes of Health (NIH) scientists investigating how prion diseases destroy the brain have observed a new form of the disease in mice that does not cause the sponge-like brain deterioration typically seen in prion diseases. Instead, it resembles a form of human Alzheimer’s disease, cerebral amyloid angiopathy, that damages brain arteries.

NIH Newsbot Note: Cerebral amyloid angiopathy (CAA) is a neurological condition in which amyloid protein builds up on the walls of the arteries in the brain. The condition increases an individual’s risk of stroke, brain hemorrhage or dementia. There is no known effective treatment.
Cerebral amyloid angiopathy

The study results, reported by NIH scientists at the National Institute of Allergy and Infectious Diseases (NIAID), are similar to findings from two newly reported human cases of the prion disease Gerstmann-Straussler-Scheinker syndrome (GSS). This finding represents a new mechanism of prion disease brain damage, according to study author Bruce Chesebro, M.D., chief of the Laboratory of Persistent Viral Diseases at NIAID’s Rocky Mountain Laboratories.

Prion diseases, also known as transmissible spongiform encephalopathies, primarily damage the brain. Prion diseases include mad cow disease or bovine spongiform encephalopathy in cattle; scrapie in sheep; sporadic Creutzfeldt-Jakob disease (CJD), variant CJD and GSS in humans; and chronic wasting disease in deer, elk and moose.

The role of a specific cell anchor for prion protein is at the crux of the NIAID study. Normal prion protein uses a specific molecule, glycophosphoinositol (GPI), to fasten to host cells in the brain and other organs. In their study, the NIAID scientists genetically removed the GPI anchor from study mice, preventing the prion protein from fastening to cells and thereby enabling it to diffuse freely in the fluid outside the cells.

The scientists then exposed those mice to infectious scrapie and observed them for up to 500 days to see if they became sick. The researchers documented signs typical of prion disease including weight loss, lack of grooming, gait abnormalities and inactivity. But when they examined the brain tissue, they did not observe the sponge-like holes in and around nerve cells typical of prion disease. Instead, the brains contained large accumulations of prion protein plaques trapped outside blood vessels in a disease process known as cerebral amyloid angiopathy, which damages arteries, veins and capillaries in the brain. In addition, the normal pathway by which fluid drains from the brain appeared to be blocked.

Their study, Dr. Chesebro says, indicates that prion diseases can be divided into two groups:

  • those with plaques that destroy brain blood vessels
  • those without plaques that lead to the sponge-like damage to nerve cells

Dr. Chesebro says the presence or absence of the prion protein anchor appears to determine which form of disease develops.

The new mouse model used in the study and the two new human GSS cases, which also lack the usual prion protein cell anchor, are the first to show that in prion diseases, the plaque-associated damage to blood vessels can occur without the sponge-like damage to the brain. If scientists can find an inhibitor for the new form of prion disease, they might be able to use the same inhibitor to treat similar types of damage in Alzheimer’s disease, Dr. Chesebro says.

Source: NIH News

Food Allergy-Related Disorder Linked to Master Allergy Gene

March 8, 2010 | by

Scientists have identified a region of a human chromosome that is associated with eosinophilic esophagitis (EoE), a recently recognized allergic disease. People with EoE frequently have difficulty eating or may be allergic to one or more foods. This study further suggests that a suspected so-called master allergy gene may play a role in the development of this rare but debilitating disorder.

EoE is characterized by inflammation and accumulation of a specific type of immune cell, called an eosinophil, in the esophagus. Symptoms of EoE vary with age: In young children a major symptom is spitting up food, while in older children and adults, the condition may cause food to become stuck in the esophagus. These symptoms may improve when a person with EoE is restricted to a liquid formula diet that contains no protein allergens or is placed on a diet that lacks six highly allergenic foods (milk, soy, eggs, wheat, peanut and seafood). EoE is not the same as more common food allergies, which also have serious consequences. Little is known about what causes EoE, but the disease runs in families suggesting that specific genes may be involved.

Investigators led by Marc Rothenberg, M.D., Ph.D., at Cincinnati Children’s Medical Center Hospital, and supported by the National Institute of Allergy and Infectious Diseases and the National Institute of Diabetes and Digestive and Kidney Diseases, both part of the National Institutes of Health, performed a genome-wide association analysis in children with EoE and healthy children. This type of study detects markers of genetic variation across the entire human genome and allows researchers to zero in on a region of a chromosome to identify genes that influence health and the development of disease.

The National Health Observances Toolkit

March 3, 2010 | by

Health observances are special days, weeks or months designated by government, health organizations and medical professionals devoted to promoting specific health topics. For 2010, there are over 175 national health observances!

National Health Observances