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.

Sunday, March 22, 2020

Genes associated with inflammation may serve as biomarkers for the diagnosis of coronary artery disease and ischaemic stroke

Once you know you have these genes, WHAT IS THE EXACT PREVENTION PROTOCOL THAT WILL PREVENT BAD THINGS HAPPENING?

Genes associated with inflammation may serve as biomarkers for the diagnosis of coronary artery disease and ischaemic stroke

Lipids in Health and DiseaseZheng PF, Liao FJ, Yin RX, et al. | March 17, 2020

In the present study, the researchers sought to identify genes and pathways involved in coronary artery disease (CAD) and ischaemic stroke (IS) and related mechanisms. Two array CAD datasets of (GSE66360 and GSE97320) and an array IS dataset (GSE22255) have been downloaded. Using the limma package, differentially expressed genes (DEGs) were identified. In total, 20 common DEGs (all upregulated) were identified between the CAD/IS and control groups. The top 5 high degree genes, including Jun proto-oncogene (JUN, degree = 9), C-X-C motif chemokine ligand 8 (CXCL8, degree = 9), tumour necrosis factor (TNF, degree = 9), suppressor of cytokine signalling 3 (SOCS3, degree = 8) and TNF alpha induced protein 3 (TNFAIP3, degree = 8) were noted following MCODE analysis. Findings suggested that the inflammation-related CXCL8, TNF, SOCS3 and TNFAIP3 can serve as biomarkers for CAD or IS diagnosis. Possible mechanisms can include Toll-like receptor, TNF, NF-kappa B, cytokine-cytokine receptor interactions and the NOD-like receptor signalling pathways.

Read the full article on Lipids in Health and Disease


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