Stopping blood clots, saving lives.

ucsdhealthsciences:

Greg Maynard, MD, clinical professor of medicine in the Division of Hospital Medicine at UC San Diego and director of the UC San Diego Center for Innovation and Improvement Science is this month’s UC Health Innovator. 

Greg Maynard is on the front lines of quality improvement. His target: stopping blood clots, a common, potentially fatal — and often preventable — problem.

Maynard is a hospitalist, a physician who specializes in caring for patients in the hospital.

When Maynard joined UC San Diego in 2003, he was one of its four hospitalists. Now there are nearly 40, and Maynard has become a national leader in the growing field. He is senior vice president of the Society for Hospital Medicine’s Center for Healthcare Innovation and Improvement. He and other UC hospitalists played a key role in the society winning the 2011 John M. Eisenberg Patient Safety and Quality Award for national efforts to increase patient safety, including reducing blood clots.

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Enzyme Offers New Therapeutic Target for Cancer Drugs

ucsdhealthsciences:

Researchers at the University of California, San Diego School of Medicine have uncovered a new signal transduction pathway specifically devoted to the regulation of alternative RNA splicing, a process that allows a single gene to produce or code multiple types of protein variants. The discovery, published in the June 27, 2012 issue of Molecular Cell, suggests the new pathway might be a fruitful target for new cancer drugs.

Signal transduction in the cell involves kinases and phosphatases, enzymes that transfer or remove phosphates in protein molecules in a cascade or pathway. SRPK kinases, first described by Xiang-Dong Fu, PhD, professor of cellular and molecular medicine at UC San Diego in 1994, are involved in controlling the activities of splicing regulators in mammalian cells.

Prior studies have implicated SRPK1 in cancer and other human diseases.  For example, it has been shown that SRPK1 plays a critical role in regulating the function of Vascular Endothelial Growth Factor or VEGF, which stimulates blood vessel growth in cancer. SRPK1 has been found to be dysregulated in a number of cancers, from kidney and breast to lung and pancreatic.

Conversely, studies suggest the absence of SRPK1 may be problematic as well, at least in terms of controlling some specific cancer phenotypes. Reduced SRPK1, for example, has been linked to drug resistance, a major problem in chemotherapy of cancer.

In their new paper, Fu and colleagues place SRPK1 in a major signal transduction pathway in the cell. “The kinase sits right in the middle of the PI3K-Akt pathway to specifically relay the growth signal to regulate alternative splicing in the nucleus,” said Fu. “It’s a new signaling branch that has previously escaped detection.”

As such, the SRPK offers a new target for disease intervention and treatment, researchers say. “It’s a good target because of its central role and because it can be manipulated with compounds that suppress its activity, which appears quite effective in suppressing blood vessel formation in cancer,” Fu said.

(via timmyxcabbage)

Source: ucsdhealthsciences

ucsdhealthsciences: A stained cross-sectional slide, magnified 10 times, of human epidermal and dermal skin layers, both normal. Protein May Be Key to Psoriasis and Wound Care Psoriasis is an autoimmune disorder in which skin cells proliferate out of control. For some hard-to-heal wounds, the problem is just the opposite: Restorative skin cells don’t grow well or fast enough. In a paper published in the June 21, 2012 issue of Immunity, researchers at the University of California, San Diego School of Medicine describe a molecule that may lead to new treatments for both problems. An international team of scientists led by principal investigator Richard L. Gallo, MD, PhD, professor of medicine and chief of UC San Diego’s Division of Dermatology, analyzed skin biopsies of patients with and without psoriasis, as well as the skin of mice with psoriasis and with wounds on their backs. They discovered that a molecule called regenerating islet-derived protein 3-alpha (REG3A) is highly expressed in skin cells during psoriasis and wound-healing, but not under normal skin conditions. In tests on mice, researchers found that inhibiting REG3A slowed wound-healing but cleared up psoriasis, which is commonly characterized by patches of inflammation and white, scaly skin. More here
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ucsdhealthsciences:

A stained cross-sectional slide, magnified 10 times, of human epidermal and dermal skin layers, both normal.

Protein May Be Key to Psoriasis and Wound Care

Psoriasis is an autoimmune disorder in which skin cells proliferate out of control. For some hard-to-heal wounds, the problem is just the opposite: Restorative skin cells don’t grow well or fast enough. In a paper published in the June 21, 2012 issue of Immunity, researchers at the University of California, San Diego School of Medicine describe a molecule that may lead to new treatments for both problems.

An international team of scientists led by principal investigator Richard L. Gallo, MD, PhD, professor of medicine and chief of UC San Diego’s Division of Dermatology, analyzed skin biopsies of patients with and without psoriasis, as well as the skin of mice with psoriasis and with wounds on their backs. They discovered that a molecule called regenerating islet-derived protein 3-alpha (REG3A) is highly expressed in skin cells during psoriasis and wound-healing, but not under normal skin conditions.

In tests on mice, researchers found that inhibiting REG3A slowed wound-healing but cleared up psoriasis, which is commonly characterized by patches of inflammation and white, scaly skin.

More here