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Inflammation may help you fight off invading microbes, but it can also kill you, leading to insufficient blood flow and even organ failure. A new study shows that some cancer drugs may be able to quell the excessive inflammation that occurs in conditions such as sepsis, which is responsible for more than 250,000 deaths in the United States each year.

The conclusion is that the high-fat diet triggered chronic inflammation, which in turn triggered an autoimmune response in the mice's central nervous systems. Normally this response protects the brain from invaders like bacteria, but a high-saturated fat diet knocks the process off track, resulting in damage to synapses in the brain - specifically in the hippocampus. Since the hippocampus is a brain area central to memory and learning, the eventual outcome is impaired brain function. In short, the high-fat diet caused brain damage.

Over a million people in the United States have some form of Inflammatory Bowel Disease or IBD. It can be caused by intestinal bacteria, environment or genetics. One thing is for sure, the lining of the intestines don't work correctly because the cells have been disturbed by one of these things. A common finding in Crohn's and IBD is that a molecule called TNF is elevated, and starts the inflammation process. Researchers still don't know what signals the TNF to go up, but maybe they can turn it off with another molecule.

The researchers, Eicke Latz at the University of Bonn and colleagues, followed up on the parents' hypothesis and found that in mice, cyclodextrin indeed blocked plaque formation, melted away plaques that had already formed in arteries, reduced atherosclerosis-associated inflammation, and revved up cholesterol metabolism-even in rodents fed cholesterol-rich diets. In petri dish-based tests, the researchers found that the drug seemed to have the same effects on human cells and plaques.

The activity of some of our genes varies with the seasons throughout the year. The discovery comes from an analysis of blood samples from more than 16,000 people in both hemispheres. The most striking pattern was that 147 genes involved in the immune system made it more reactive or "pro-inflammatory" during winter or rainy seasons, probably to battle the onslaught of cold and flu viruses

Existing mouse models of lethal Ebola virus infection do not reproduce hallmark symptoms of Ebola hemorrhagic fever, neither delayed blood coagulation and disseminated intravascular coagulation, nor death from shock, thus restricting pathogenesis studies to non-human primates. Here we show that mice from the Collaborative Cross exhibit distinct disease phenotypes following mouse-adapted Ebola virus infection. Phenotypes range from complete resistance to lethal disease to severe hemorrhagic fever characterized by prolonged coagulation times and 100% mortality. Inflammatory signaling was associated with vascular permeability and endothelial activation, and resistance to lethal infection arose by induction of lymphocyte differentiation and cellular adhesion, likely mediated by the susceptibility allele Tek. These data indicate that genetic background determines susceptibility to Ebola hemorrhagic fever.

A cornerstone of modern biomedical research is the use of mouse models to explore basic pathophysiological mechanisms, evaluate new therapeutic approaches, and make go or no-go decisions to carry new drug candidates forward into clinical trials. Systematic studies evaluating how well murine models mimic human inflammatory diseases are nonexistent. Here, we show that, although acute inflammatory stresses from different etiologies result in highly similar genomic responses in humans, the responses in corresponding mouse models correlate poorly with the human conditions and also, one another.

In our view, and that of organizations such as the American Society of Clinical Oncology, the World Cancer Research Fund International, and the American Cancer Society, obesity-related cancers will arguably be the most urgent issue in the cancer field in the next decade.

Some 20 percent of cancer-related deaths in the U.S. can be attributed to obesity, making it the number-one preventable cause of cancer death in the country. But with myriad metabolic and inflammatory changes associated with obesity, determining the mechanisms that underlie the obesity-cancer link has proven challenging.