Body

The vomeronasal organ (VNO) is an odor detection system that mediates many pheromone-sensitive behaviors. Vomeronasal sensory neurons (VSNs), located in the VNO, are the initial site of interaction with odors and pheromones. How an individual VSN transduces chemical signals into electrical signals, however, has been a mystery.

Researchers led by specialists at the Johns Hopkins Wilmer Eye Institute have found that injecting a corticosteroid, triamcinolone, directly into the eye may slow the progression of proliferative diabetic retinopathy, a complication of diabetes that frequently leads to blindness.

Authors of the study caution, however, that because use of steroids in the eye may increase the risk of glaucoma and cataract, laser photocoagulation remains the treatment of choice until further development of drugs that may reproduce the good effects of steroids, without the damage.

Spinal cord disorders like spina bifida arise during early development when future spinal cord cells growing in a flat layer fail to roll up into a tube. In the Dec. 6 issue of Nature Cell Biology, researchers from the Johns Hopkins University School of Medicine team with colleagues at the University of California, Berkeley to report a never-before known link between protein transport and mouse spinal cord development, a discovery that opens new doors for research on all spinal defects.

Some of these common human gene variants are already known to be risk factors for diabetes mellitus. The pathomechanisms of diabetes have intrigued physicians and been the subject of much debate for many decades. These new research results may contribute to a better understanding of the clinical picture of diabetes and its pathogenesis – and could lead to new approaches in early diagnosis and therapy. The findings have been published in the current online issue of the renowned journal Nature Genetics.

Using disinfectants could cause bacteria to become resistant to antibiotics as well as the disinfectant itself, according to research published in the January issue of Microbiology. The findings could have important implications for how the spread of infection is managed in hospital settings.

STANFORD, Calif. — Like a child awaiting the arrival of Christmas, embryonic stem cells exist in a state of permanent anticipation. They must balance the ability to quickly become more specialized cell types with the cellular chaos that could occur should they act too early (stop shaking those presents, kids!).

La Jolla, CA—In order to preserve our DNA, cells have developed an intricate system for monitoring and repairing DNA damage. Yet precisely how the initial damage signal is converted into a repair response remains unclear. Researchers at the Salk Institute for Biological Studies have now solved a crucial piece of the complex puzzle.

Famous for its antioxidant properties and role in tissue repair, vitamin C is touted as beneficial for illnesses ranging from the common cold to cancer and perhaps even for slowing the aging process. Now, a study published online on December 24th by Cell Press in the journal Cell Stem Cell uncovers an unexpected new role for this natural compound: facilitating the generation of embryonic-like stem cells from adult cells.

A new study establishes a molecular link that bridges two rare inherited disorders and explains why these diseases result in genetic instability. The research, published by Cell Press in the December 24th issue of the journal Molecular Cell, may lead to a better understanding of the complex mechanisms that enable cells to repair damaged DNA.

Earlier this year, researchers showed that they could cut the lives of disease-carrying mosquitoes in half by infecting them with a bacterium they took from fruit flies. Now, a new report in the December 24th issue of Cell, a Cell Press publication, suggests that their strategy might do one better: The Wolbachia bacteria also makes the mosquitoes more resistant to infection by viruses that are a growing threat to humans, including those responsible for dengue fever and Chikungunya.

UCLA scientists have identified a molecular switch that prevents Huntington's disease from developing in mice. Published in the Dec. 24 edition of the journal Neuron, the discovery suggests a new approach to treating the genetic disorder, which ultimately leads to death in as little as 10 years.

Cancer progression is commonly thought of as a process involving the growth of a primary tumor followed by metastasis, in which cancer cells leave the primary tumor and spread to distant organs. A new study by researchers at Memorial Sloan-Kettering Cancer Center shows that circulating tumor cells – cancer cells that break away from a primary tumor and disseminate to other areas of the body – can also return to and grow in their tumor of origin, a newly discovered process called "self-seeding."

In Huntington's disease, a mutated protein in the body becomes toxic to brain cells. Recent studies have demonstrated that a small region adjacent to the mutated segment plays a major role in the toxicity. Two new studies supported by the National Institutes of Health show that very slight changes to this region can eliminate signs of Huntington's disease in mice.

Researchers do not fully understand why the protein (called mutant huntingtin) is toxic, but one clue is that it accumulates in ordered clumps of fibrils, perhaps clogging up the cells' internal machinery.

STANFORD, Calif. — Genomic switches can predispose an individual to one set of autoimmune disorders but protect the same person against another set of them, scientists at Stanford University School of Medicine have found.

"Maybe we should stop considering all autoimmune diseases in one lumped category," said Atul Butte, MD, PhD, assistant professor of pediatrics and of biomedical informatics and director of the Center for Pediatric Bioinformatics at Lucile Packard Children's Hospital. "It looks as if there may be at least two different kinds."

Researchers have uncovered the complete genetic make-up of the cavity-causing bacterium Bifidobacterium dentium Bd1, revealing the genetic adaptations that allow this microorganism to live and cause decay in the human oral cavity. The study, led by Marco Ventura's Probiogenomics laboratory at the University of Parma, and Prof. Douwe van Sinderen and Dr Paul O'Toole of the Alimentary Pharmabiotic Centre at University College Cork, is published December 24 in the open-access journal PLoS Genetics.