Heart attacks are still among the most frequent causes of death in the developed world. The cause of a heart attack is the closure of a coronary artery that supplies blood to the heart, which kills heart muscle cells. Cardiomyocytes, are the heart muscle cells responsible for the contraction of the heart, are not able to regenerate after a heart attack. The massive loss of cells and tissue, and the highly restricted regeneration capacity of the adult heart, lead to an impaired blood supply throughout the body that drastically affects a patient's quality of life. To restore the heart's function after a major heart attack, clinicians require functionally mature cardiomyocytes that perform like the native cells in the adult heart to replace the cells that were killed. The production of such functional cardiomyocytes from well-defined cardiovascular progenitor cells (CPCs) is the focus of the research team led by Prof. Dr. Katja Schenke-Layland from the Fraunhofer Institute for Interfacial Engineering and Biotechnology IGB in Stuttgart and her colleagues, Dr. Ali Nsair of the University of California Los Angeles (UCLA) and Prof. Dr. Robb MacLellan of the University of Washington in Seattle, who have now succeeded in identifying such cells in a mouse model. The work could revolutionize the treatment of heart disease. They identified two markers, the receptors Flt1 (VEGFR1) and Flt4 (VEGFR3), on the surface of CPCs with which these cells can be clearly identified while fully preserving their biological function. This discovery allows scientists to isolate clinically relevant cardiovascular progenitor cells that can be functionally matured. The researchers investigated the cardiovascular progenitor cells using microarray gene expression profiling. These studies show exactly which genes are active at a specific point in time. The resulting data from this analysis were compared to the sequencing data from existing databases of already known as cell markers. Researchers were tried to stimulate the regeneration of heart muscle cells. For this purpose, they inject stem cells or stem cell-derived cardiomyocytes into the heart. The majority of studies found a slight improvement in heart function, in most cases, neither long-term integration nor the differentiation of the cells into heart muscle. (Source: http://www.sciencedaily.com /releases /2012/11/121122112833.htm)
INCB-13739, being developed by Incyte Corp, is a novel, first-in-class 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) inhibitor for the potential treatment of metabolic disorders, including type 2 diabetes mellitus (T2DM) and obesity. INCB-13739 has high selectivity for 11beta-HSD1 over other dehydrogenases and glucocorticoid and mineralocorticoid receptors, with prolonged pharmacodynamic activity and good pharmacokinetic/pharmacodynamic properties. INCB-13739 demonstrated improved hepatic and peripheral insulin sensitivity with a satisfactory reduction in fasting plasma glucose and cholesterol after 28 days of treatment in patients with T2DM, with a dose-dependent weight loss, decrease in triglyceride levels and an improvement in blood pressure. Clinical data demonstrated that INCB-13739 had a better efficacy to tolerability ratio compared with potential competitors. The unique differentiation of INCB-13739 is its effects on both glucose and lipid parameters coupled with its effects on body weight and hypertension
Hyperornithinemia-Hyperammonemia-Homocitrullinuria (HHH) Syndrome was first described in 1969. In affected patients, plasma Ornithine is found to be dramatically elevated. Hyperammonemia is chronically present, but worsens postprandially. The etiology is a deficiency of a mitochondrial carrier protein that normally functions to transport Ornithine into the mitochondria as part of the urea cycle. When transport is defective, Ornithine accumulates in the cytosol and the urea cycle is impaired, resulting in hyperammonemia. The ORNT 1 gene that codes for the transport protein is located on chromosome 13, and several mutations have been identified in affected patients
A retrovirus is a germ whose genes are encoded in RNA as a replacement for of DNA. Although, like further viruses, retroviruses necessitate to use the cellular machinery of the organisms they infect to make copies of themselves, infection by a retrovirus requires an additional step. The retrovirus genome needs to be reverse-transcribed into DNA by an enzyme called reverse-transcriptase before it can be copied in the usual way. Integration is a distinctive and essential process in the HIV infection cycle and thus represents an attractive antiviral drug target
Coffee is thought to have originated in the Ethiopian province of Kaffa and brought out of Africa and the Arab world by the Dutch. It is now consumed worldwide and its popularity is growing. Consumption has increased to more than 2 percent annually in recent years according to the International Coffee Organization. Although commonly consumed for its stimulant effect and social benefits, coffee is now gaining popularity as a disease preventing beverage. The prophylactic effect of drinking coffee on the development of cardiovascular diseases and diabetes mellitus is compelling and irrefutable. Most health benefits appear to be related to imbibing about 4 cups a day. This article briefly summarizes the evidence based benefits associated with coffee drinking.
Testosterone is the predominant sex hormone in men. Hypogonadism usually results in decreased libido, erectile dysfunction, decreased muscle mass and strength, obesity, depressed mood and diminished energy, osteoporosis and decreased sexual hair. However, low testosterone levels are also associated with a spectrum of serious complications. These include hypertension, diabetes mellitus, obesity, metabolic syndrome, dyslipidemia and chronic inflammation. Low testosterone levels have been shown to be an independent risk factor for cardiovascular and all-cause mortality. This study looks at the prevalence of low serum testosterone levels in hypertensive men and briefly reviews its impact on associated cardiovascular risk factors.