Deans' stroke musings: Effects of High-mobility Group Box1 on cerebral angiogenesis and neurogenesis after intracerebral hemorrhage

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.

Friday, November 9, 2012

Effects of High-mobility Group Box1 on cerebral angiogenesis and neurogenesis after intracerebral hemorrhage

This is great, more proof of neural cell migration. Ask your doctor for a protocol to take advantage of this.
http://www.sciencedirect.com/science/article/pii/S0306452212010780

Abstract

Neural stem cells, which reside mainly in the subventricular and subgranular zones of the hippocampus, can regenerate new neuroblasts after various brain insults. Aided by vascular remodeling, these new neuroblasts migrate long distances to injured brain regions. Studies have suggested that high-mobility group box1 (HMGB1), a nonhistone nuclear DNA-binding protein, may stimulate such remodeling in the late phase of some types of brain injury, but it is unclear whether this is true for intracerebral hemorrhage (ICH). Here we used a rat model of collagenase-induced ICH to determine whether HMGB1 can promote neurogenesis and angiogenesis in the late phase of injury. Daily administration of ethyl pyruvate, which inhibited HMGB1 expression, reduced recovery of neurological function, decreased VEGF and NGF levels in the ipsilateral striatum, and decreased the numbers of BrdU- and DCX-positive cells around the hematoma. These findings suggest that HMGB1 may promote angiogenesis and neurogenesis in the late phase of ICH.