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Vol. LXIII, No. 14
July 08, 2011

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NIH Researchers Slow Immune Attack on Ovaries in Mice

In a study of mice, researchers have slowed an immune system attack on the ovaries. The mice developed a disorder resembling primary ovarian insufficiency (POI), a menopause-like condition that affects women under the age of 40, sometimes years or even decades before normal menopause. The study was conducted by scientists at NIH and the University of California, San Francisco.

Some cases of POI appear to result from an autoimmune response—an immune system attack on the body’s own tissues. In their mouse study, the researchers nearly halted the immune assault. They believe they were able to do this by teaching the animals’ immune systems to recognize that the ovarian protein is a part of the body’s own tissues.

The study results may one day lead to a way to identify women with a high probability for developing autoimmune POI early, perhaps in time to explore fertility-sparing options such as frozen embryo storage or freezing unfertilized eggs. POI affects about 1 percent of women under the age of 40 in the United States, according to the authors.

The findings appeared online in Endocrinology.

Difficulty Estimating Quantity Linked to Math Learning Disability

Researchers funded by NIH have discovered that the innate ability to estimate quantities is impaired in children who have a math learning disability.
Researchers funded by NIH have discovered that the innate ability to estimate quantities is impaired in children who have a math learning disability.

Researchers funded by NIH have discovered that the innate ability to estimate quantities is impaired in children who have a math learning disability. The study was published in Child Development.

The link between difficulty estimating quantities and math difficulties was seen only in children who had a math learning disability and not in those who did poorly in math but were not considered to be learning disabled.

“The findings suggest that students may struggle with math for very different reasons,” said Dr. Kathy Mann Koepke, director of the Mathematics and Science Cognition and Learning program at NICHD, which funded the study. “Research to identify these reasons may lead to new ways of identifying those at risk and developing the means to help them.”

Math learning disability is also referred to as dyscalculia.

NIH Researchers Identify New Marker to Predict Progressive Kidney Failure, Death

A high level of a hormone that regulates phosphate is associated with an increased risk of kidney failure and death among chronic kidney disease (CKD) patients, according to a recent study led by researchers at the University of Miami and funded by the National Institute of Diabetes and Digestive and Kidney Diseases. Results appeared in the June 15 issue of the Journal of the American Medical Association.

In a previous study of patients beginning hemodialysis for treatment of kidney failure, individuals with elevated blood levels of the hormone fibroblast growth factor 23 (FGF23) were found to be at nearly 6 times greater risk of death compared to those with lower levels. However, the hormone had not been tested in the much larger population of patients with less advanced CKD. Researchers now report that patients with earlier stage kidney disease and high FGF23 are at nearly 2 times higher risk of kidney failure if their baseline estimated glomerular filtration rate (eGFR) is 45 milliliters or higher, while all CKD patients are at 3 times higher risk of death compared to patients with lower levels of the hormone. The eGFR is a measure of kidney function.

Senior study author Dr. Myles Wolf at the University of Miami believes this discovery could lead to earlier diagnosis and treatment of phosphate problems. Treatment typically consists of dietary phosphate restriction and phosphate binders—medications that work like a sponge to soak up phosphate in the gut.

Key Step Identified in Legionnaire’s Disease Infection Process

NIH researchers have uncovered a key step in the biochemical sequence the bacterium that causes Legionnaire’s disease uses to reproduce inside the cells it infects.

The bacterium is known to activate a cell protein to help it hide from the cell’s defenses while it reproduces. In the current study, the researchers have discovered how the bacterium switches off the protein so that its offspring can leave the cell and begin the infection process anew. The finding may one day lead to new ways to treat Legionnaire’s disease and diseases caused by related bacteria. The study was published online in Science Express.

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