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, April 14, 2016

Abstract TP264: ST2 Signaling is Essential in Restricting Acute Ischemic Brain Injury

I don't understand so ask your doctor what use this will be for you. More studies needed so ask your doctor to update the stroke strategy and talk to the stroke leadership to followup this research.
http://stroke.ahajournals.org/content/47/Suppl_1/ATP264.short
  1. Jun Chen
+ Author Affiliations
  1. Univ of Pittsburgh, Pittsburgh, PA

Abstract

Background and Purpose: ST2, a member of the interleukin 1 receptor family, and its ligand interleukin 33 (IL-33) play critical roles in immune regulation and inflammatory responses. The engagement of ST2 has been shown to reduce myocardial infarction and preserve heart function. Recent study documented an increase in blood ST2 expression after stroke. The exact roles of ST2 in the ischemic brain injury, however, are not explored.
Methods: C57/BL6 wild type and ST2 knockout mice were subjected to 60-minute transient cerebral ischemia (tMCAO). The expression of ST2 and IL-33 in the ischemic brain was measured at different time points after tMCAO using RT-PCR. Brain infarct was quantified using TTC staining and MAP2 immunostaing. Neurobehavioral tests were performed up to 14 days after tMCAO. Differences of immune cell components in blood, spleen, bone marrow and brain between wild type and ST2 knockout mice were assessed by flow cytometry analysis. For experiments with ST2 activation, IL-33 was injected intraperitoneally(i.p.) or intracerebroventricularly (i.c.v.) into wide type mice right after the induction of tMCAO.
Results: In wild type mice, the mRNA expression of ST2 in the ischemic brainexhibited a delayed elevation 7d after tMCAO, while the mRNA expression of IL-33 was transiently increased 1d after tMCAO. The deficiency of ST2 resulted in enlarged infarct volume 3d after tMCAO and aggravated neurological deficits lasted out to 14d. The worsened stroke outcome was accompanied by dramatic changes in the number of Th1, Th2 and regulatory T cells in the spleen, bone marrow and brain. Further study showed that either i.p. or i.c.v. injection of IL-33 at the time of reperfusion attenuated the severity of brain infarct in wide type mice, suggesting that both systemic and central activation of ST2 could protect against acute ischemic brain injury.
Conclusions: ST2/IL-33 signaling plays an essential role in restricting acute ischemic brain injury. Such protective effect of ST2/IL-33 involves both immune regulation in the peripheral immune system and a direct protection within the central nervous system. Our study may provide a new therapeutic target for stroke treatment.

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