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:

Monday, January 23, 2017

Hypertension Opens the Flood Gates to the Gut Microbiota

Should we get around this problem by a young gut bacteria transplant? Ask your doctor how they would do that. How young are we talking about? 1 month? 1 year? 5 years? 15 years?

Restoring gut bacteria to youthful age linked to improved stroke recovery in mice
W. Robert Taylor, Kiyoko Takemiya

There continues to be a rapidly evolving interest in the role of the gut microbiome in cardiovascular disease. It has long been known that the gut microbiome has a fundamentally mutualistic, symbiotic relationship with the human host. However, from earlier observations using mice grown in germ-free environments to more recent advances in identifying unique metabolic products of the gut microbiome,1 the data have led to a compelling story linking cardiovascular disease to the trillions of prokaryotic organisms that live in the human gut.
Article, see p 312
In this issue of Circulation Research, Santisteban et al2 have provided provocative data demonstrating very definitively that, in 2 different animal models of hypertension, there is decreased expression of several tight junction proteins in the gut and a concomitant increase in intestinal permeability. Furthermore, their data show that in the spontaneously hypertensive rat model, the increase in permeability is a result of increased sympathetic nerve activity before the development of hypertension. They therefore conclude that there is a direct, causal link between the sympathetic nerve activity derived from the central nervous system and increased gut permeability (Figure). They further hypothesize that the changes in gut permeability result in hypertension and cause a shift in the types of bacteria that are present in the gut. Finally, they have shown that the changes in sympathetic activity resulting in increased gut permeability are also associated with an increase in inflammatory cells within the intestinal wall thus potentially bringing the contributions of the immune system to hypertension into this pathophysiological mechanism.

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