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What Is Cystitis? What Causes Cystitis?
Cystitis refers to inflammation of the lining of the bladder. It usually occurs when the normally sterile urethra and bladder (lower urinary tract) are infected by bacteria and become irritated and inflamed. Cystitis is fairly common and can affect both men and women and people of all ages. However, it is more common in women.
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Parent Consent For Storage And Use Of Newborn DNA Should Be Required
In response to the press release and position paper released Tuesday by the American College of Medical Genetics-the 2007 recipient of a $4 million, five-year federal grant to serve as the National Coordinating Center (NCC) for the Regional Genetics and Newborn Screening Collaborative Groups-the Citizens" Council on Health Care (CCHC) released the following statement from CCHC"s president, Twila Brase:
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Poniard Rally To Continue: Strong Efficacy And Safety Data From Picoplatin
Poniard announced positive Phase II data from its two trials in CRC and CRPC with picoplatin this morning, including efficacy that was comparable to the current standard of care, with a significantly improved safety profile. We believe that these data provide further evidence of picoplatin"s favorable efficacy and safety profile in two more large oncology markets, in addition to SCLC, and position picoplatin as a platform treatment that can provide solutions in multiple oncology settings. We believe that given these data from CRC and CRPC, in addition to the anticipated Phase III SPEAR data in SCLC, will attract the interest of multiple players and we expect that Poniard will be able to at least secure a large pharma partnership sometime this summer, unless a company like Sanofi (SNY Not Rated), Takeda (TKD Not rated), or Bristol-Myers Squibb (BMY Not Rated) decide to step in and acquire the whole company, for rights to both the IV and oral version of picoplatin.
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Yale Researchers Suggests Gene Inhibition May Help Normalize Type 2 Diabetes

In research that could lead to new approaches for the treatment of type 2 diabetes, a Yale School of Medicine team has found that suppressing a liver enzyme that induces glucose production helped diminish the symptoms of the disease in a rat model - reducing blood glucose concentrations, decreasing rates of glucose production in the liver, and improving insulin sensitivity. Decreasing expression of the gene, Sirtuin 1, also lowered total cholesterol levels. The research appears in the June 15-19 Online Early Edition of the Proceedings of the National Academy of Sciences. Type 2 diabetes is characterized by high blood glucose concentrations and insulin resistance, which play a major factor in causing the disease. In the U.S., rates of type 2 diabetes have doubled since 1990, and the Centers for Disease Control calls the disease an epidemic. Formerly known as "adult-onset diabetes," the disorder is increasingly diagnosed in children. The Yale researchers put the rats on a four-week diet of fructose and high-fat meals to create a metabolic condition that mimics type 2 diabetes. At the same time, they inhibited expression of the Sirtiun 1 gene through injection of an antisense oligonucleotide (short fragments of nucleic acid that inactivate gene expression) specifically targeted to that gene. "Blood glucose levels in the rats came down close to normal, as did their ability to regulate blood glucose levels with insulin," said first author Derek Erion, a graduate student in cellular and molecular physiology at Yale. The authors believe the falling plasma cholesterol levels that also resulted may be attributed to increased cholesterol uptake and export from the liver, due to suppression of key enzymes involved in cholesterol metabolism. Senior author Gerald Shulman, MD, said the results indicate that inhibiting Sirtuin 1 in the liver may be an attractive approach for the treatment of type 2 diabetes. "With this disorder, diet and exercise only get you so far," he said. "Many patients may need drug intervention to avoid suffering the debilitating effects of type 2 diabetes." Shulman is the George R. Cowgill Professor of Physiological Chemistry, Medicine and Cellular and Molecular Physiology at Yale and a Howard Hughes Medical Institute Investigator. Other authors include: Shin Yonemitsu, Yoshio Nagai and Matthew P. Gillum of the Yale School of Medicine and Howard Hughes Medical Institute; Jennifer J. Hsiao, Takanori Iwasaki, Romana Stark, Dirk Weismann, Varman T. Samuel, Tamas. L. Horvath and Qian Gao of Yale School of Medicine; Xing Xian Yu, Susan F. Murray, Sanjay Bhanot and Brett P. Monia of Isis Pharmaceuticals in Carlsbad, CA. The work above was funded in part by the Yale Clinical and Translational Science Award (CTSA) grant from the National Center for Research Res at the National Institutes of Health. Yale University


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