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.

Tuesday, August 13, 2013

Changes of hypoxia-inducible factor-1 signaling and the effect of cilostazol in chronic cerebral ischemia*

I have no idea what this is useful for but I'm quite positive your doctor won't either. So call up your stroke association and ask for a detailed analysis and the translational work they are doing to get it into a stroke protocol. At least that's what a great stroke association would do.
http://www.sjzsyj.org:8080/Jweb_sjzs/CN/article/downloadArticleFile.do?attachType=PDF&id=651
Research Highlights
(1) Hypoxia-inducible factor-1 under hypoxia is a hot topic in the field of neural regeneration re-search. Under hypoxia and ischemia/reperfusion, heme oxygenase-1 is upregulated by hypox-ia-inducible factor-1. The available research mainly focuses on the role of hypoxia-inducible factor-1 and heme oxygenase-1 following acute cerebral ischemia and hypoxia, while very few studies have examined changes in the hypoxia-inducible factor-1/heme oxygenase-1 signaling pathway.
(2) This is the first report showing that the hypoxia-inducible factor-1/heme oxygenase-1 signaling pathway is activated and sustained following chronic cerebral ischemia.
(3) Hypoxia-inducible factor-1 and heme oxygenase-1 expression was downregulated by cilostazol in rats subjected to chronic cerebral ischemia. Our findings are the first to show that cilostazol pro-tects against apoptosis in the fontal cortex of chronic cerebral ischemic rats. Cilostazol can provide protection against vascular cognitive impairment through its anti-apoptotic effect.
Abstract
Hypoxia-inducible factor-1 and its specific target gene heme oxygenase-1, are involved in acute cerebral ischemia. However, very few studies have examined in detail the changes in the hypox-ia-inducible factor-1/heme oxygenase-1 signaling pathway in chronic cerebral ischemia. In this study, a rat model of chronic cerebral ischemia was established by permanent bilateral common carotid artery occlusion, and these rats were treated with intragastric cilostazol (30 mg/kg) for 9 weeks. Morris water maze results showed that cognitive impairment gradually worsened as the cerebral ischemia proceeded. Immunohistochemistry, semi-quantitative PCR and western blot analysis showed that hypoxia-inducible factor-1α and heme oxygenase-1 expression levels in-creased after chronic cerebral ischemia, with hypoxia-inducible factor-1α expression peaking at 3 weeks and heme oxygenase-1 expression peaking at 6 weeks. These results suggest that the elevated levels of hypoxia-inducible factor-1α may upregulate heme oxygenase-1 expression fol-lowing chronic cerebral ischemia and that the hypoxia-inducible factor-1/heme oxygenase-1 sig-naling pathway is involved in the development of cognitive impairment induced by chronic cerebral ischemia. Cilostazol treatment alleviated the cognitive impairment in rats with chronic cerebral is-chemia, decreased hypoxia-inducible factor-1α and heme oxygenase-1 expression levels, and re-duced apoptosis in the frontal cortex. These findings demonstrate that cilostazol can protect against cognitive impairment induced by chronic cerebral ischemic injury through an anti-apoptotic mecha-nism.

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