Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Saturday, February 4, 2017

Targeting nitric oxide to treat aneurysm

Since nitric oxide is pretty good for you you'll have to have your doctor get the protocol for administering it.

76 posts on nitric oxide for blood pressure and anti-inflammation.

http://science.sciencemag.org/content/355/6324/491.3?utm_campaign=ec_sci_2017-02-02&et_rid=17139052&et_cid=1140907
Science  03 Feb 2017:
Vol. 355, Issue 6324, pp. 491-492
DOI: 10.1126/science.355.6324.491-c
Could nitric oxide inhibitors help prevent cardiac aneurysm?
PHOTO: SUSUMU NISHINAGA/SCIENCE SOURCE
Aneurysms are the abnormal enlargement of arteries and can lead to death if the artery wall bursts. Oller et al. studied patients with Marfan syndrome, an inherited genetic condition in which individuals are prone to cardiac aneurysms. They discovered lower levels of ADAMTS1 in the heart tissue of Marfan syndrome patients compared with that of organ transplant donors. Genetic inactivation of ADAMTS1 in mice resulted in a Marfan syndrome-like disease, which included low blood pressure, aortic dilation, and aneurysm development. These effects were driven by enhanced activity of nitric oxide, and treatment with a nitric oxide inhibitor reduced blood vessel size and reversed the clinical signs of aneurysm formation.
Nat. Med. 10.1038/nm.4266 (2017).

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