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.

Thursday, January 24, 2019

Multiple biomarkers covering distinct pathways for predicting outcomes after ischemic stroke

Fuck, fuck, fuck you lazy idiots.  10 million survivors a year don't want predictions they want solutions. Have you never talked to any stroke survivors?  My god, the lack of professionalism in the stroke world is appalling. They are not even trying to solve stroke.

 

Multiple biomarkers covering distinct pathways for predicting outcomes after ischemic stroke


Chongke Zhong, Zhengbao Zhu, Aili Wang, Tan Xu, Xiaoqing Bu, Hao Peng, Jingyuan Yang, Liyuan Han, Jing Chen, Tian Xu, Yanbo Peng, Jinchao Wang, Qunwei Li, Zhong Ju, Deqin Geng, Jiang He, Yonghong Zhang
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Abstract

Objective To study the prognostic significance of multiple novel biomarkers in combination after ischemic stroke.
Methods We derived data from the China Antihypertensive Trial in Acute Ischemic Stroke, and 12 informative biomarkers were measured. The primary outcome was the combination of death and major disability (modified Rankin Scale score ≥3) at 3 months after ischemic stroke, and secondary outcomes included major disability, death, and vascular events.
Results In 3,405 participants, 866 participants (25.4%) experienced major disability or died within 3 months. In multivariable analyses, elevated high-sensitive C-reactive protein, complement C3, matrix metalloproteinase-9, hepatocyte growth factor, and antiphosphatidylserine antibodies were individually associated with the primary outcome. Participants with a larger number of elevated biomarkers had increased risk of all study outcomes. The adjusted odds ratios (95% confidence intervals) of participants with 5 elevated biomarkers were 3.88 (2.05–7.36) for the primary outcome, 2.81 (1.49–5.33) for major disability, 5.67 (1.09–29.52) for death, and 4.00 (1.22–13.14) for vascular events, compared to those with no elevated biomarkers. Simultaneously adding these 5 biomarkers to the basic model with traditional risk factors led to substantial reclassification for the combined outcome (net reclassification improvement 28.5%, p < 0.001; integrated discrimination improvement 2.2%, p < 0.001) and vascular events (net reclassification improvement 37.0%, p = 0.001; integrated discrimination improvement 0.8%, p = 0.001).
Conclusion We observed a clear gradient relationship between the numbers of elevated novel biomarkers and risk of major disability, mortality, and vascular events. Incorporation of a combination of multiple biomarkers observed substantially improved the risk stratification for adverse outcomes in ischemic stroke patients.

Glossary

aCL=
anticardiolipin antibodies;
aPS=
antiphosphatidylserine antibodies;
BP=
blood pressure;
CATIS=
China Antihypertensive Trial in Acute Ischemic Stroke;
CI=
confidence interval;
eGFR=
estimated glomerular filtration rate;
HGF=
hepatocyte growth factor;
hsCRP=
high-sensitive C-reactive protein;
IDI=
integrated discrimination improvement;
IgG=
immunoglobulin G;
IL-6=
interleukin-6;
Lp-PLA2=
lipoprotein-associated phospholipase A2;
MMP-9=
matrix metalloproteinase-9;
mRS=
modified Rankin Scale;
NIHSS=
NIH Stroke Scale;
NRI=
net reclassification improvement;
NT-proBNP=
N-terminal pro-brain natriuretic peptide;
OR=
odds ratio;
RF=
rheumatoid factor

Footnotes

  • * These authors contributed equally to this work.
  • Go to Neurology.org/N for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article.
  • Editorial page 157
  • Received April 30, 2018.
  • Accepted in final form September 12, 2018.
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