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.

Wednesday, September 27, 2017

Immune cell-related proteins may speed healing after stroke

I don't know why people even bother to write hopeful articles like this. We have NO stroke leadership and NO stroke strategy that will do ANY followup to get this into translation science.
Now if we could just get some followup on this which LEADERS would accomplish. But we have none.  Ask your stroke hospital president whom the LEADERS are in stroke and what they are doing that makes them LEADERS. 
https://www.nih.gov/news-events/nih-research-matters/immune-cell-related-proteins-may-speed-healing-after-stroke

At a Glance

  • Two proteins associated with immune cells may play critical roles in helping the brain to heal after a stroke.
  • Additional studies are needed to find out whether these proteins could be used for treating stroke. 
Microscopic image of brain cell culture Brain nerve cells (green) and astrocytes (red), a type of support cell, in a rat cell culture after exposure to a mixture from red blood cells. The researchers used this as a model for the damage caused to the brain by intracerebral hemorrhagic stroke.Aronowski lab, University of Texas Health Science Center, Houston
Intracerebral hemorrhages are a form of stroke caused by ruptured blood vessels. The leaked blood causes swelling and increased pressure in the skull, which damage cells and tissues in the brain. Over time, additional damage may be caused by the buildup of toxic levels of blood products and infiltrating immune cells. Symptoms of a hemorrhagic stroke can include sudden weakness; paralysis or numbness of the face, arms, or legs; trouble speaking or understanding speech; and trouble seeing.
Decades of research suggest that neutrophils are some of the earliest immune cells to respond to a hemorrhage, and that they may have both harmful and healing effects in the brain. A team led by Dr. Jaroslaw Aronowski at the University of Texas Health Science Center at Houston set out to find out what role neutrophils may play in healing after hemorrhagic stroke. The study was funded by NIH’s National Institute of Neurological Disorders and Stroke (NINDS). Results appeared on September 19, 2017, in Nature Communications.
The team first measured interleukin-27 (IL-27), a protein that controls the activity of various immune cells, in the brain and blood of mice after a brain hemorrhage. They detected elevated IL-27 levels within an hour after hemorrhage. Levels peaked at 24 hours and remained high for 3 days. Further experiments suggested that brain cells called microglia produced IL-27 in response to the presence of red blood cells.
The team found that, once released, the IL-27 molecules appeared to travel to the bones of the mice and infiltrate the marrow, where neutrophils are born. When the researchers extracted neutrophils from the bones and treated them with IL-27, the chemical raised the activity of genes associated with healing. IL-27 may thus shift the role of neutrophils from harming to helping with recovery.
The researchers injected IL-27 into mice after a hemorrhage. Days after the stroke, the treated mice were better than untreated mice at walking, limb stretching, and navigating holes in a floor. The brains of the mice treated with IL-27 also showed less damage. They had less swelling around the hemorrhages and lower levels of two compounds that are toxic at high levels, iron and the blood protein hemoglobin. In contrast, injections of a compound that blocked natural IL-27 activity slowed recovery.
One notable gene for which IL-27 raised the level of activity in neutrophils was the gene for lactoferrin, a protein that neutralizes toxic iron. The team tested lactoferrin’s effect on stroke recovery. They injected mice and rats with lactoferrin 30 minutes after a brain hemorrhage. The treated animals recovered faster and had less brain damage than animals given placebos. Giving mice lactoferrin 24 hours after a stroke was also effective.
“Intracerebral hemorrhage is a damaging and often fatal form of stroke for which there are no effective medicines,” Aronowski says. “Our results are a hopeful first step towards developing a treatment for this devastating form of stroke.”

Related Links

References: Neutrophil polarization by IL-27 as a therapeutic target for intracerebral hemorrhage. Zhao X, Ting SM, Liu CH, Sun G, Kruzel M, Roy-O'Reilly M, Aronowski J. Nat Commun. 2017 Sep 19;8(1):602. doi: 10.1038/s41467-017-00770-7. PMID: 28928459.
Funding: NIH’s National Institute of Neurological Diseases and Stroke (NINDS).


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