A novel breakthrough advance in fighting low-density lipoprotein (LDL) or "bad" cholesterol in the body has been announced by investigators from the University of Leicester and University of California Los Angeles (UCLA). The universities have filed two patents in order to develop targeted medications designed to lower levels of LDL. LDL is frequently associated to medical conditions, such as stroke, heart disease and clogged arteries. Cells in the liver generate an LDL receptor that attaches to "bad" cholesterol and eliminates it from the blood, thus reducing cholesterol levels. Although, the goal of these receptors can sometimes be obstructed. According to the researchers, an enzyme called IDOL plays a vital and specific role in the ability of the receptor to attach with LDL. Targeting IDOL with medications would help the receptors to lower cholesterol levels in humans.
The US Food and Drug Administration (FDA) announced on Wednesday that it has approved the first generic version of the world's top-selling medicine, the cholesterol-lowering drug Lipitor (atorvastatin), currently marketed by Pfizer Inc. Ranbaxy Laboratories Limited, India's largest pharmaceutical company, has gained FDA approval to make generic atorvastatin calcium tablets in 10 milligram, 20 mg, 40 mg, and 80 mg strengths. The tablets will be made by Ohm Laboratories in New Brunswick, New Jersey, says the FDA. A statement from Raxbaxy says Ranbaxy Pharmaceuticals Inc, a wholly owned subsidiary of Ranbaxy Laboratories Ltd, will be marketing the generic atorvastatin in the US. Janet Woodcock, director of the FDA's Center for Drug Evaluation and Research, told the press the agency was "working very hard" to ensure patients get generic drugs as fast as the law will permit: "This medication is widely used by people who must manage their high cholesterol over time, so it is important to have affordable treatment options, " said Woodcock.
Scientists from the University of Leicester and the University of California Los Angeles (UCLA) have announced a major advance towards developing drugs to tackle dangerous, or 'bad', cholesterol in the body. They have filed two patents for developing targeted drugs that would act as a catalyst for lowering levels of 'bad' cholesterol. Two research papers published by the academics enhance the understanding of the regulation of low-density lipoprotein (LDL) or "bad" cholesterol. LDL, the so-called "bad" cholesterol, is often linked to medical problems like heart disease, stroke and clogged arteries. In the body, cells in the liver produce an LDL receptor that binds LDL and removes it from the blood, thereby lowering cholesterol levels. The scientists have characterised an enzyme called IDOL that plays a key role in regulating the amount of LDL receptor available to bind with 'bad' cholesterol.
Collaborative research from Perelman School of Medicine at the University of Pennsylvania has shown that psoriasis patients have an increased risk of heart attack, stroke and cardiovascular death, especially if the psoriasis is moderate to severe. Now, Penn researchers have discovered the potential underlying mechanism by which the inflammatory skin disease impacts cardiovascular health. In two new studies presented at the 2011 American Heart Association Scientific Sessions, Penn researchers show that the systemic inflammatory impact of psoriasis may alter both the makeup of cholesterol particles and numbers, as well as impair the function of high density lipoprotein (HDL), the "good" cholesterol. "Anecdotally, many researchers have observed that HDL levels may be lower in states of inflammation, such as rheumatoid arthritis, psoriasis and even obesity, " said lead study author Nehal Mehta, MD, MSCE, director of Inflammatory Risk in Preventive Cardiology at Penn.
By changing the behavior of certain cells within human blood vessels, Cornell University researchers have discovered important clues as to the underlying causes of atherosclerosis - a discovery researchers hope can lead to more targeted drug therapies for the prevention of the disease. "One of the things we wanted to do was understand how aging is linked to atherosclerosis, and how the mechanism of vessel stiffening plays into this link, " said Cynthia Reinhart-King, Cornell professor of biomedical engineering and lead author of "Age-Related Intimal Stiffening Enhances Endothelial Permeability and Leukocyte Transmigration, " published online in the journal Science Translational Medicine. The researchers showed that by changing the behavior of endothelial cells in hardened vessels, without making the vessels any less stiff, they could reduce the effects of aging on vessel health.