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, June 14, 2024

Delayed plasma kallikrein inhibition fosters post-stroke recovery by reducing thrombo-inflammation.

 From this earlier research, did your doctors and hospital get adequately powered research going to test this out properly? NO? So MASSIVE INCOMPETENCE?

Delayed plasma kallikrein inhibition fosters post-stroke recovery by reducing thrombo-inflammation.

Steffen Haupeltshofer  1 , Stine Mencl  2 , Rebecca D Szepanowski  2 , Christina Hansmann  2 , Ana I Casas  2   3 , Hanna Abberger  4   5   6 , Wiebke Hansen  4 , Alina Blusch  7 , Cornelius Deuschl  8 , Michael Forsting  8 , Dirk M Hermann  2   9 , Friederike Langhauser #  2 , Christoph Kleinschnitz #  2
Affiliations

Abstract

Activation of the kallikrein-kinin system promotes vascular leakage, inflammation, and neurodegeneration in ischemic stroke. Inhibition of plasma kallikrein (PK) - a key component of the KKS - in the acute phase of ischemic stroke has been reported to reduce thrombosis, inflammation, and damage to the blood-brain barrier. (So where is the written protocol on this located and did it get delivered to every stroke hospital in the world? Obviously not since there is NO stroke leadership that gets things accomplished!) However, the role of PK during the recovery phase after cerebral ischemia is unknown. To this end, we evaluated the effect of subacute PK inhibition starting from day 3(What do we do on days 0-2?) on the recovery process after transient middle artery occlusion (tMCAO). Our study demonstrated a protective effect of PK inhibition by reducing infarct volume and improving functional outcome at day 7 after tMCAO. In addition, we observed reduced thrombus formation in cerebral microvessels, fewer infiltrated immune cells, and an improvement in blood-brain barrier integrity. This protective effect was facilitated by promoting tight junction reintegration, reducing detrimental matrix metalloproteinases, and upregulating regenerative angiogenic markers. Our findings suggest that PK inhibition in the subacute phase might be a promising approach to accelerate the post-stroke recovery process.

Keywords: Blood-brain barrier; Extravasation; Inflammation; Ischemic stroke; Kallikrein-kinin system; Plasma kallikrein; Recovery; Subacute; Thrombo-inflammation; Thrombosis.

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