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, June 6, 2013

Cezanne Paints Inflammation by Regulating Ubiquitination

Your doctor can translate and give you a stroke protocol to stop inflammation during the hyperacute phase. And if you believe that, there is a Brooklyn bridge for sale.
The short version here;
 http://circres.ahajournals.org/content/112/12/1526.extract.html?etoc
Hypoxia–reoxygenation can induce inflammation by activating nuclear factor (NF)-κB. In endothelial cells, this process is critical for the pathogenesis of many chronic inflammatory conditions, such as atherosclerosis and autoimmune disease. Recent publication from Evans’s laboratory shows the critical role of deubiquitinating enzyme Cezanne, regulating its extent of NF-κB activation and expression of inflammatory genes.1 In particular, they showed that the inhibition of polyubiquitination of TNF receptor associated factor (TRAF) 6 is a specific anti-inflammatory mechanism by Cezanne. In this editorial, we briefly review the TRAF6-mediated NF-κB signaling and other posttranslational modifications that play a key role in modulating endothelial cell inflammation.
Article, see p 1583
NF-κB transcription factor complexes consist of a heterodimer of p65 (RelA) and p50 or p52.2 In most nonstimulated cells, p65-containing NF-κB complexes are kept in an inactive cytoplasmic form, bound to one family of inhibitor proteins, the inhibitory κBs (IκBs). Two IκB kinases, IKKα and IKKβ, target phosphorylation of IκB after hypoxia–reoxygenation, cytokine, or ultraviolet stress stimulation. Phosphorylation of IκBs promotes their ubiquitination and degradation by the proteasome, which releases the p65 complex, allowing it to translocate to the nucleus.3 An ubiquitin E2 conjugating enzyme of the ubiquitin-conjugating enzyme (Ubc)4/5 family and the SCF-βTrCP E3 ligase (Skp1-Cul1-F-box ligase containing the F-box beta protein βTrCP) execute ubiquitination of IκB. Once IκB is phosphorylated, p-transducin repeat containing protein 1 (βTrCP1) and βTrCP2 associate with phosphorylated IκB.4,5 The polyubiquitinated IκB is selectively degraded by the 26S proteasome, and then mature p52 and
Full story here;
http://circres.ahajournals.org/content/112/12/1526.full

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