Molecular & Cell Biology

Overeating in mice triggers a molecule once considered to be only involved in detecting and fighting viruses to also destroy normal metabolism, leading to insulin resistance and setting the stage for diabetes. The new study, led by researchers at the Harvard School of Public Health (HSPH), specifically links together the immune system and metabolism, a pairing increasingly suspected in diseases that include — in addition to diabetes — heart disease, fatty liver, cancer, and stroke. Understanding how to regulate the molecule through targeted drugs or nutrients could eventually change the way these diseases are prevented and treated in humans. The study will publish in the February 5, 2010, issue of Cell.

Health & Medicine

Researchers at the National Institutes of Health have identified DNA variants in mothers and fetuses that appear to increase the risk for preterm labor and delivery. The DNA variants were in genes involved in the regulation of inflammation and of the extracellular matrix, the mesh-like material that holds cells within tissues.

Biology

In a finding that overturns conventional wisdom, scientists are reporting the first discovery of the female sex hormone progesterone in a plant. Until now, scientists thought that only animals could make progesterone. A steroid hormone secreted by the ovaries, progesterone prepares the uterus for pregnancy and maintains pregnancy. A synthetic version, progestin, is used in birth control pills and other medications. The discovery is reported in the American Chemical Society's Journal of Natural Products, a monthly publication.

Molecular & Cell Biology

Nuclear pore complexes are best known as the communication channels that regulate the passage of all molecules to and from a cell's nucleus. Researchers at the Salk Institute for Biological Studies, however, have shown that some of the pores' constituent proteins, called nucleoporins, pull double duty as transcription factors regulating the activity of genes active during early development.




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