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, January 18, 2018

Amlexanox inhibits cerebral ischemia-induced delayed astrocytic high-mobility group box 1 release and subsequent brain damage

Whom the fuck is going do something about this? Followup studies? Translational interventions? Never mind, NOTHING WILL OCCUR.
3 earlier studies back to Nov. 2012 gives you an idea of the incompetency out there in stroke. And it doesn't need to be delivered in minutes or hours to do some good. If I wasn't such a calm and nice person I would have exploded by now. 
http://europepmc.org/abstract/med/29330155
High-mobility group box 1 (HMGB1) is increased in the cerebrospinal fluid (CSF) and serum during the early- and late-phases of brain ischemia and is known to contribute to brain damage. However, detailed characterization underlying cell type-specific HMGB1 release and pathophysiological roles of extracellularly released HMGB1 in ischemic brain remain unclear. Here, we examined cell type-specific HMGB1 release and therapeutic potential of amlexanox, an inhibitor of non-classical release, and an anti-HMGB1 antibody against ischemic brain damage. HMGB1 depletion from neuronal nuclei was observed within 3 h after transient middle cerebral artery occlusion (tMCAO), whereas the intracerebroventricular (i.c.v.) pretreatment with amlexanox blocked HMGB1 release from neurons, resulting in HMGB1 redistribution in the nuclei and cytoplasm. HMGB1 was selectively released from astrocytes 27 h after tMCAO and this HMGB1 release was blocked by the late-treatment of amlexanox (i.c.v.) 24 h after tMCAO. Proximity extension assay revealed that HMGB1 level was elevated in the CSF at 3 and 27 h after tMCAO. This late-treatment of amlexanox significantly protected the brain from ischemic damage, but its pretreatment 30 min before tMCAO failed to show any protection. The late-treatment (i.c.v.) of anti-HMGB1 antibody 24 h after tMCAO also ameliorated ischemic brain damage 48 h after tMCAO. Thus, the inhibition of brain damage by late-treatment of amlexanox or anti-HMGB1 antibody indicates that late HMGB1 release plays a role in the maintenance of stroke-induced brain damage, and the inhibition of this release would be a novel therapeutic target for protection of ischemic brain damage.

No comments:

Post a Comment