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:

Thursday, January 5, 2017

Serum Carnosine Dipeptidase 1 and Ubiquitin C – Terminal Hydrolase L1 as Markers of Brain Damage in Patients After Carotid Endarterectomy

If you are getting a carotid endarterectomy you'll have to ask your doctor how this brain damage is going to be prevented.
Marek Ilzecki, Joanna Ilzecka, Stanislaw Przywara, Aneta Grabarska, Piotr Terlecki, Andrzej Stepulak, Shawn Dave, Tomasz Zubilewicz.

Introduction: Carotid endarterectomy (CEA) is the recommended surgical procedure in the prevention of ischemic stroke. However, this procedure may lead to vascular neurological complications. The aim of the study was to measure serum carnosine dipeptidase 1 (CNDP1) and ubiquitin C – terminal hydrolase L1 (UCHL1) as markers of brain damage in patients that underwent CEA due to high-grade internal carotid artery stenosis.
Material and Methods: This study included 25 patients. Blood samples were taken from the antecubital vein at three different intervals (within a 24 hour period prior to CEA, 12 hours following surgery, and 48 hours after surgery). Serum CNDP1 and UCHL1 levels were measured by a commercially available enzyme-linked immunosorbent assay (ELISA).
Results: The study showed that serum CNDP1 and UCHL1 levels were significantly decreased 12 hours after CEA when compared to the level before the surgery. Furthermore, these enzymes levels were normalized 48 hours after CEA.
Conclusion: Data from our study showed that CEA significantly affects serum CNDP1 and UCHL1 levels. Moreover, these enzyme levels seems to reflect a brain ischemia resulting from severe internal carotid artery stenosis in patients undergoing CEA.

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