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, March 20, 2013

Saneron and Henry Ford Health: Cell Therapy Combo Aids Stroke

This might be difficult for your doctor to acquire the day you have a stroke so you better tell your doctor to stock up.
http://www.newswise.com/articles/saneron-and-henry-ford-health-cell-therapy-combo-aids-stroke
Researchers at the Henry Ford Health System (Detroit, MI) and colleagues at Saneron CCEL Therapeutics, Inc. of Tampa, Florida, have found that when human umbilical cord blood cells (HUCBCs) were transplanted into test rats modeled with stroke, the addition of Simvastatin to the HUCBCs significantly increased the therapeutic benefit of the HUCBCs.
The study was published in a recent issue of Neuroscience (227:223-231)
According to N. Kuzmin-Nichols, Saneron president and COO, the combination treatment, delivered 24 hours after the test animals were subjected to simulated stroke, showed an interactive effect in improving neurological outcome. When compared with monotherapy, the combination therapy increased densities of key blood vessels, arteries, and smooth muscle cells in vascular walls.
“HUCBCs are a source for blood stem cells, endothelial cell precursors, mensenchymal cell progenitors, and other multipotent and pluripotent stem cells,” said Kuzmin-Nichols. “They offer a promising therapy for stroke. However, when HUCBCs are used alone, and injected via a vascular route for brain repair, success has been limited.”
Because the drug Simvastatin has been demonstrated to be a neurorestorative and neuroprotective agent in ischemic brain injury, the research team hypothesized that the combination of therapeutic doses of Simvastatin and HUCBCs would increase the expression of Angiopoietin-1(Ang-1, a protein with important roles in vascular development and blood vessel growth) and its receptor Tie2 (a cell-surface receptor that binds with Ang-1). Both Ang-1 and Tie2 promote vascular stabilization and artery growth and could enhance blood vessel remodeling (angiogenesis) after stroke, said the researchers.
According to the researchers, HUCBCs contain a “ready supply” of neurotrophic and angiogenic factors that induce neurogenesis (neural cell repair) and angiogenesis (blood vessel growth), both of which are critical to promoting neurological recovery post stroke. While transplanted HUCBCs have been found to selectively migrate to the injured brain, past and recent research has discovered that few transplanted HUCBCs express neural cell characteristics, and few find their way to the ischemic region of the brain.
“Our study using subtherapeutic monotherapy doses did not show significant improvement in either vasculogenesis or functional outcome,” said Dr. Jieli Chen of Henry Ford Hospital and the study corresponding author. “However, the combination of HUCBCs and Simvastatin did show an interactive effect with a significant improvement in neurological outcome. The combination also amplified endogenous angiogenesis and arteriogenesis, and enhanced vascular remodeling.”
Their in vitro experiments showed that combination treatment and Ang-1 significantly increased capillary-like tube formation and arterial cell migration while anti-Ang-1 significantly reduced combination treatment-induced tube formation and artery cell migration.
Dr. Chen noted that combination treatment likely increases the signaling between the brain vasculature and parenchymal cells that facilitate the migration of HUCBCs into the injured cerebral tissue. This signaling may be attributed to the increased expression of stromal derived factor (SDF-1) in brain vascular and parenchymal cells and its receptor (CXCR4) in HUCBCs.
The researchers concluded that their findings “indicate that the combination of sub-therapeutic doses of Simvastatin and HUCBCs increases Ang1/Tie2 and thereby enhances vascular remodeling that contribute to improved functional outcome after stroke.”
“Our results in this preclincial study support further exploration of the use of combination therapies - such as those combining Simvastatin and HUCBCs - for stroke treatment,” said Kuzmin-Nichols.
Funding for the study came from grants from the National Institute on Aging, RO1 AG031811,National Institute of Neurological Disorder and Stroke, PO1 NS23393 and 1R41NS064708, and from the American Heart Association, grant 09GRNT2300151.

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