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.

Wednesday, February 19, 2020

Dynamic Changes and Prognostic Value of Gut Microbiota-Dependent Trimethylamine-N-Oxide in Acute Ischemic Stroke

Useless. NO SOLUTION PROVIDED, that restores the gut microbiota to the proper levels. 

Or maybe you want to determine yourself what needs to be done, but you can't listen to me, I'm not medically trained.

 


Dynamic Changes and Prognostic Value of Gut Microbiota-Dependent Trimethylamine-N-Oxide in Acute Ischemic Stroke

Chuhong Tan1, Huidi Wang1, Xuxuan Gao1, Ruoting Xu1, Xiuli Zeng1, Ziming Cui2, Jiajia Zhu1, Qiheng Wu1, Genghong Xia1, Hongwei Zhou3,4, Yan He3* and Jia Yin1*
  • 1Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China
  • 2Department of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China
  • 3Division of Laboratory Medicine, Microbiome Medicine Center, Zhujiang Hospital, Southern Medical University, Guangzhou, China
  • 4State Key Laboratory of Organ Failure Research, Zhujiang Hospital, Southern Medical University, Guangzhou, China
Background:
Acute ischemic stroke (AIS) is an atherothrombotic disease. Trimethylamine-N-oxide (TMAO), a gut microbiota-dependent metabolite, has been shown to be proatherogenic and prothrombotic. However, the involvement of TMAO in AIS remains unclear. This study aimed to observe the dynamic changes of TMAO in AIS patients and identify the prognostic value of TMAO for major ischemic events and unfavorable functional outcomes.
Methods:
This study included 204 AIS patients and 108 healthy controls. Blood samples for TMAO analyses were drawn at admission, 2 and 7 days of admission. Logistic regression models and receiver operating characteristic curves were established to identify associations between TMAO levels and major ischemic events (ischemic stroke, myocardial infarction, or death from an ischemic vascular event), as well as unfavorable functional outcomes (modified Rankin Scale score ≥3), at 90 days and 12 months.
Results:
TMAO levels showed no significant changes before and within 24 h of AIS treatment (at admission) but decreased significantly thereafter. Elevated log2-transformed baseline TMAO levels were associated with increased risks of 90-day [odds ratio (OR), 2.62; 95% confidence interval (CI), 1.55–4.45; p < 0.001] and 12-month (OR, 3.59; 95% CI, 2.12–6.09; p < 0.001) major ischemic events, as well as 90-day (OR, 2.89; 95% CI, 1.46–5.71; p = 0.002) and 12-month (OR, 2.58; 95% CI, 1.50–4.46; p = 0.001) unfavorable functional outcomes, after adjustments for confounding factors. The areas under curve of baseline TMAO levels for predicting 90-day and 12-month major ischemic events were 0.72 (95% CI, 0.61–0.83; p < 0.001) and 0.76 (95% CI, 0.66–0.85; p < 0.001). Baseline TMAO levels improved the prognostic accuracy of conventional risk factors, National Institutes of Health Stroke Scale (NIHSS) score and N-terminal B-type natriuretic peptide (NT-proBNP) level.
Conclusions:
TMAO levels decreased with time since stroke onset. Elevated TMAO levels at an earlier period portended poor stroke outcomes, broadening the potential clinical utility of TMAO as an independent prognostic marker and therapeutic target.

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