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.

Thursday, October 15, 2015

A molecular switch to stop inflammation

This is incredibly fucking important.  If our researchers and stroke leadership don't immediately use this to figure out how to reduce the inflammation in our arteries they should be shot. That was my measured opinion, don't follow me.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=157329&CultureCode=en
Our immune system is vital to us and can sometimes overreact causing chronic illnesses, such as for instance rheumatism and allergy. Now, researchers from Umeå University and University of Gothenburg have identified a molecular switch – MYSM1 – that can suppress such an overreaction and avoid inflammation. The study is published in the prestigious journal Immunity.
“The discovery of MYSM1 is a major milestone in our understanding of how our immune system works, and how its response could be controlled in order to prevent inflammatory diseases such as sepsis,” says Nelson O. Gekara, research leader at MIMS, Molecular Infection Medicine Sweden at Umeå University.
Our innate immune system is activated when our body needs to protect itself against pathogens, for instance bacteria and viruses, as well as for tissue healing. In some people, the immune system overreacts which can cause chronic inflammatory diseases and result in tumour development. The innate immune system is activated by receptors that recognise certain molecular patterns found on microbes or dead cells. These receptors are called pattern-recognition receptors (PRRs).
“Most infectious or inflammatory situations are associated with the simultaneous or sequential activation of multiple PRR pathways. Therefore, it is essential to avert a disproportionate self-destructive immune response in a synchronised fashion once activated. How this is accomplished has been unclear,” says Nelson O. Gekara.
Nelson O. Gekara’s at Umeå University and his doctoral student Swarup Panda are now closing in on a solution. For years, they have been searching for possible genes required for the regulation of the immune system. Together with Professor Jonas A Nilsson at Sahlgrenska Cancer Center at the University of Gothenburg, the Umeå researchers have now identified MYSM1 – a molecule in the cell core (nucleus) of resting cells. For the first time, the researchers are now able to show that during infection or inflammation MYSM1 accumulates outside of the nucleus, in the cytoplasm where it disrupts the function of signalling molecules involved in activation of PRR pathways, thereby terminating inflammation.
MYSM1 can be said to act like a molecular switch that can turn off several inflammatory pathways. Therefore lack of MYSM1 in animal results in unrestrained activation of the innate immune system, leading to inflammatory diseases” says Nelson O. Gekara.
His research team is now screening for small molecule compounds that are able to modulate the MYSM1 molecule activity. The hope is to find new therapeutics against infections and other inflammatory diseases.
http://www.cell.com/immunity/abstract/S1074-7613%2815%2900395-7

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