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Gewirtz's team, including researchers at Emory, Cornell University and the University of Colorado at Boulder, became intrigued by the relationship between gut bugs and weight when they noticed that lab mice lacking a certain protein had more of the bugs than other animals and were about 15% heavier. These mice also had a higher level of inflammation, which the authors explain in their paper published online Thursday in Science Express is what may account for the extra weight. Inflammatory signaling can promote a condition called metabolic syndrome, which causes weight gain, high blood pressure and high cholesterol levels...
...fatter mice in Gewirtz's study had been bred to lack a protein known as toll-like receptor 5 (TLR5), which most intestinal cells sprout on their surface. Its job is to recognize and bind to the whiplike flagella that bacteria use to move around. TLR5 acts as a traffic cop for controlling the mass of pathogens living in the intestine; without it, the normally harmless gut bacteria tend to overflourish and expand in number. (See and listen to an audio slideshow about obesity rehab...
...then they are less likely to take up glucose and process it effectively. Such a desensitization to insulin and glucose then leads to the symptoms of metabolic syndrome, such as weight gain, high cholesterol and triglyceride levels and elevated blood pressure - which were all present in the TLR5-deficient mice. (See the top 10 medical breakthroughs...
...team of scientists from the U.S., Indonesia and Japan, led by virologist Yoshihiro Kawaoka at the University of Wisconsin - Madison, combined a strain of the deadly H5N1 avian virus with strains of H3N2 human seasonal flu, creating 254 new, mutated viruses. By injecting them in lab mice, researchers found that some of the hybrid viruses were both deadly (like bird flu) and transmissible (like seasonal human flu) - the kind of genetically mutated superflu viruses that experts have been warning about for decades. (See how to prevent illness...
...PNAS study undermines that hope. The key difference in this study was the presence of a single gene from the H3N2 human virus: the PB2 protein, which gave the hybrid viruses the ability to spread easily among the lab mice. Scientists think the protein may allow hybrid viruses to grow more efficiently in the lower temperatures of the upper respiratory tract, from which the virus can more easily spread to others. (The H5N1 virus tends to infect the lower respiratory tract in humans, where it can't easily get out and spread...