Children, Males and Blacks at Increased Risk For Food Allergies
A new NIH-funded study estimates that 2.5 percent
of the U.S. population has food allergies. Food allergy rates were found to be higher for children, non-Hispanic blacks and males, according to the researchers.
|A new NIH-funded study estimates that 2.5 percent of the U.S. population has food allergies.
The research, which appears in the October issue of the Journal of Allergy and Clinical
Immunology, is the first to use a nationally representative
sample as well as specific
immunoglobulin E (IgE) or antibody levels to quantify allergic sensitization to common
foods, including peanuts,
milk, eggs and shrimp. The hallmark of food allergy is production of IgE antibodies to a specific food protein. Once IgE antibody is made, further exposure to the food triggers an allergic response.
“This study is very comprehensive in its scope,” said Dr. Darryl Zeldin of NIEHS, senior author on the paper. “It is the first study to use specific
blood serum levels and look at food allergies
across the whole life spectrum, from young children aged 1 to 5, to adults 60 and older. This research has helped us identify some high risk populations for food allergies.”
NIH Scientists Discover How Dengue Virus
NIH researchers discovered a key step in how the dengue virus infects a cell. They found out how the dengue virus releases itself from the protective membrane that shields it as it penetrates
deep inside the cell. The discovery allows researchers to study the invasion process in the laboratory and provides a means to test potential treatments for the virus. Dr. Leonid V. Chernomordik
of NICHD and colleagues published their findings online Oct. 7 in PLoS Pathogens.
Transmitted by mosquitoes, dengue infects up to 100 million people each year; 22,000 people—most of them children—die from dengue annually,
according to the World Health Organization.
To infect a cell, the virus binds to the cell membrane.
The cell membrane engulfs the virus, enveloping it in a pouch-like structure known as an endosome. To begin the infection process, the virus delivers its hereditary material into the cytosol, the fluid interior of the cell, where it begins reproducing
itself. To do so, however, it must first release itself from the endosome. The virus does this by fusing its membrane with the endosomal membrane.
When the two membranes come together, they form a pore through which the virus’s genetic material is released.
Study Details Structure of Potential Target for HIV and Cancer Drugs
In a technical tour de force, structural biologists funded by NIH have determined the three-dimensional
structure of a molecule involved in HIV infection and in many forms of cancer. The high-resolution structure sheds light on how the molecule
functions and could point to ways to control its activity, potentially locking out HIV and stalling cancer’s spread. The findings appeared in the Oct. 7 advance online issue of Science. The NIH Common Fund and the Protein Structure Initiative funded the study.
The molecule, CXCR4, is part of a large family of proteins called G-protein coupled receptors (GPCRs). These molecules span the cell’s membrane
and transmit signals from the external environment to the cell’s interior. GPCRs help control practically every bodily process, including cell growth, hormone secretion and light perception.
Nearly half of all drugs on the market target these receptors.
Gene Variations that Alter Key Enzyme Linked To Prostate Cancer
Researchers at NIH have found that variations in a gene for an enzyme involved in cell energy metabolism
appear to increase the risk for prostate cancer.
The genetic variations all impair the enzyme phosphodiesterase
11A (PDE11A), which helps regulate a cell’s responses to hormones and other signals. Previous studies by NIH researchers have linked genetic variations that inactivate PDE11A with increased susceptibility to testicular cancer and adrenal tumors.
Scientists found that a group of men with prostate cancer were nearly four times more likely to have variations affecting the activity of PDE11A than did men who did not have prostate cancer.
“Our study indicates that PDE11A one day may have a place in genetic screening for predisposition to prostate cancer,” said senior author Dr. Constantine
Stratakis of NICHD. The findings were published
online in the Journal of Clinical Endocrinology and Metabolism.—