Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Monday, November 7, 2011

Identification Of Gene Critical For Cell Responses To Oxygen Deprivation May Have Implications For Heart Disease, Stroke And Cancer

http://www.medicalnewstoday.com/releases/237129.php
Scientists at the Gladstone Institutes have identified a protein that kick-starts the response to low levels of oxygen, suggesting new lines of research relevant to a variety of potentially fatal disorders associated with diminished oxygen supply, including cancer, heart disease, stroke and other neurological conditions that affect millions of people worldwide.

In a paper published in Molecular Cell, the laboratory of Gladstone Associate Investigator Katerina Akassoglou, PhD, maps out the chain of events that take place during hypoxia. Hypoxia is a condition that can occur in people with diseases such as heart disease and stroke. It deprives tissues and organs of an adequate oxygen supply.

"This discovery provides a novel understanding of the steps by which cells normally respond to hypoxia, a fundamental biological process that is implicated in many medical conditions," said Dr. Akassoglou, whose research at Gladstone - a leading and independent biomedical-research organization - investigates the mechanisms of inflammation and tissue repair in the brain.

The paper details how Dr. Akassoglou's lab discovered the previously unknown biological function of a protein called p75NTR. When activated by hypoxia, p75NTR sets off the cascading series of events that results in increased blood-vessel production to replenish oxygen levels during disease.

Previous research had indicated that hypoxia triggers the activation of a protein called HIF1-alpha - an activation that ultimately leads to more blood vessels and an ensuing improvement in oxygen flow. There has been much interest among researchers in modifying levels of the HIF1-alpha protein to spur blood-vessel production in individuals with hypoxic conditions. But Dr. Akassoglou decided to take a different approach in her research.

By monitoring the responses of mice under hypoxic conditions, Dr. Akassoglou found that hypoxia first activated the p75NTR protein, which then activated HIF1-alpha and set everything in motion.

"What was most striking to us was what happened when we removed the gene that makes p75NTR," said Natacha Le Moan, PhD, a Gladstone postdoctoral fellow and the first author of the paper. "By effectively silencing p75NTR, the mice's response to hypoxia was impaired and blood-vessel production decreased."

"Now that we've shown that p75NTR spurs the activation of HIF1-alpha and the production of blood vessels during hypoxia, we can move forward with exploring potential therapies," said Dr. Akassoglou, who is also an associate professor of neurology at the University of California, San Francisco, with which Gladstone is affiliated. In addition, Dr. Akassoglou is also an associate adjunct professor of pharmacology at the University of California, San Diego.

"Dr. Akassoglou's trailblazing discovery could enable the development of pharmaceutical therapies for conditions that are caused or exacerbated by reduced oxygen levels," added Lennart Mucke, MD, who directs neurological research at Gladstone. "This is important news for those who suffer from hypoxia-related illnesses such as heart disease, stroke and certain types of cancer."

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