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:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Thursday, February 20, 2014

Damage to dead cell disposal system may increase heart disease

Is your doctor willing to look into this to see about preventing your next stroke or heart attack?
http://scopeblog.stanford.edu/2014/02/20/damage-to-dead-cell-disposal-system-may-increase-heart-disease/
efferocytosis (from efferre, Latin for 'to take to the grave', 'to bury')
Conducting studies in mice with atherosclerosis, the researchers showed that loss of a candidate gene at this locus leads to impaired “efferocytosis” - from the Latin for “take to the grave” – the process by which dead or necrotic cells are removed. Literally, the burying of dead cells. Mice with this genetic variation showed an increase in buildup of these dead cells, further advancing their atherosclerosis as opposed to those that did not have the genetic variation.

In other words, a commonly inherited genetic variant, which is found in 20 percent of the population, contributes to the development of coronary artery disease (also known as coronary atherosclerosis) by stimulating the accumulation of necrotic debris within the evolving plaque. Coronary atherosclerosis is the process by which plaque builds up in the wall of heart vessels, eventually leading to chest pain and potentially lethal heart attacks. Leeper explained it to me further:

    If you were born with genetic variation at the 9p21 locus, your risk of heart disease is elevated, though we haven’t understood why. This research gets at that hidden risk. You can be a non-smoker, be thin, have low blood pressure, and still be at risk for a heart attack if you were born with this variant. This work may help explain that inherited risk factor, and more importantly help develop a new therapy to prevent the heritable component of cardiovascular disease. 


Rest at link. 
Conducting studies in mice with atherosclerosis, the researchers showed that loss of a candidate gene at this locus leads to impaired “efferocytosis” - from the Latin for “take to the grave” – the process by which dead or necrotic cells are removed. Literally, the burying of dead cells. Mice with this genetic variation showed an increase in buildup of these dead cells, further advancing their atherosclerosis as opposed to those that did not have the genetic variation.
In other words, a commonly inherited genetic variant, which is found in 20 percent of the population, contributes to the development of coronary artery disease (also known as coronary atherosclerosis) by stimulating the accumulation of necrotic debris within the evolving plaque. Coronary atherosclerosis is the process by which plaque builds up in the wall of heart vessels, eventually leading to chest pain and potentially lethal heart attacks. Leeper explained it to me further:
If you were born with genetic variation at the 9p21 locus, your risk of heart disease is elevated, though we haven’t understood why. This research gets at that hidden risk. You can be a non-smoker, be thin, have low blood pressure, and still be at risk for a heart attack if you were born with this variant. This work may help explain that inherited risk factor, and more importantly help develop a new therapy to prevent the heritable component of cardiovascular disease.
- See more at: http://scopeblog.stanford.edu/2014/02/20/damage-to-dead-cell-disposal-system-may-increase-heart-disease/#sthash.Xn1bC5ua.dpuf
efferocytosis

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