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.

Showing posts with label phospholipids. Show all posts
Showing posts with label phospholipids. Show all posts

Thursday, February 23, 2017

High OxPL-apoB levels linked to recurrent stroke, first major coronary events

Has your doctor done ANYTHING AT ALL to prevent your next stroke? Like a diet for stroke prevention? Or maybe some of these risk reduction ideas?
 Like maybe a 307%  stroke risk reduction from these 11 possibilities?

http://www.healio.com/cardiology/stroke/news/online/%7B0f8b210a-b89c-46c9-9646-f00bb420d76e%7D/high-oxpl-apob-levels-linked-to-recurrent-stroke-first-major-coronary-events
Elevated oxidized phospholipids on apolipoprotein B-100 levels are an indicator of recurrent stroke and first major coronary events in patients who had prior stroke or transient ischemic attack, according to recently published data.
“Although ischemic heart disease and ischemic stroke have commonalities in risk factors and underlying disease mechanisms, the strength of the association varies according to individual risk factors,” Young Sup Byun, MD, from the division of cardiovascular diseases at the University of California, San Diego, and colleagues wrote. “Novel biomarkers and therapeutic targets would be useful to predict new or recurrent stroke and identify high-risk individuals for preventive measures.”
The SPARCL trial was designed to assess the predictive value of oxidized phospholipids on apolipoprotein B-100 (OxPL-apoB) levels, the efficacy of atorvastatin therapy and their relationship to recurrent stroke or first major CV event, the researchers wrote. The study evaluated whether patients who had prior cerebrovascular events and high levels of OxPL-apoB, but no prior CAD, are at elevated recurrent stroke risk and CAD events after high-dose statin therapy.
At baseline, the SPARCL trial measured levels of OxPL-apoB in 4,385 patients with stroke or TIA and in 3,106 patients at 5 years after randomization to placebo or 80 mg atorvastatin.
The primary endpoint was the time from randomization to second nonfatal or fatal stroke. Secondary endpoints included first major coronary events and any CV event.
Patients with recurrent stroke had higher median OxPL-apoB levels at baseline than patients without (15.5 nmol/L vs. 11.6 nmol/L; P < .0001).
After multivariable adjustment, elevated OxPL-apoB at baseline predicted recurrent stroke (HR = 4.3; P < .0001), first major coronary events (HR = 4; P < .0001) and any CV event (HR = 4.4; P < .0001). There was no difference by treatment in comparison for any endpoint, shown as a nonsignificant interaction test, according to the researchers.
There was a significant improvement in net reclassification improvement, integrated discrimination improvement and area under the receiver-operating characteristic curve (AUC) when OxPL-apoB was added to the models, with change in AUC of 0.0505 (P < .0001) for recurrent stroke, 0.0409 (P < .0001) for first major coronary event and 0.0791 (P < .0001) for any CV event.

Steven K. Feske
“A major proportion of ischemic stroke results directly from atherosclerosis in large arteries or indirectly from coronary atherosclerotic disease,” Steven K. Feske, MD, from the neurology department at Brigham and Women’s Hospital, wrote in a related editorial. “These new findings suggest that from these discoveries, patients at risk will likely see the benefit of more effective prevention of stroke as well as the atherosclerotic heart and peripheral vascular disease.” – by Dav

Tuesday, December 17, 2013

Dietary Strategy to Repair Plasma Membrane After Brain Trauma Implications for Plasticity and Cognition

Will your hospital use this to set up human clinical trials? Or are they going to do nothing?
Remember, while your neurons are dying due to inaction by your doctors, thats ok because you can't practice medicine on your own.
http://nnr.sagepub.com/content/28/1/75.abstract?etoc
  1. Aiguo Wu, PhD1
  2. Zhe Ying1
  3. Fernando Gomez-Pinilla, PhD1,2
  1. 1University of California at Los Angeles, Los Angeles, CA, USA
  2. 2UCLA Brain Injury Research Center, Los Angeles, CA, USA
  1. Fernando Gomez-Pinilla, Department of Integrative Biology and Physiology, 621 Charles E. Young Drive, Los Angeles, CA 90095, USA. Email: fgomezpi@ucla.edu

Abstract

Background. Damage to the plasma membrane is a prevalent but often neglected aspect of traumatic brain injury (TBI), which can impair neuronal signaling and hamper neurological recovery. Objective. This study was performed to assess a new noninvasive intervention to counteract peroxidative damage to the phospholipids in the membrane using the powerful action of foods. Although dietary docosahexaenoic acid (C22:6n-3; DHA) provides protection against TBI, the pervasive effects of TBI that cause phospholipid damage, including to DHA, raises concerns about how to preserve DHA in the brain for optimal functional recovery. Methods. Rats were maintained on curcumin and/or DHA-enriched diets for 2 weeks postinjury, and their brains were subjected to analyses. Results. Fluid percussion injury reduced DHA levels as well as levels of enzymes involved in the metabolism of DHA such as FADS2 and 17β-HSD4 and elevated levels of markers of lipid peroxidation such as 4-hydroxy-2-nonenal (4-HNE) and 4-hydroxy-2-hexenal (4-HHE). These effects were counteracted by DHA or curcumin, whereas the combination of curcumin and DHA had an enhanced effect on DHA and 4-HNE. The combination of curcumin and DHA was also efficient in counteracting reductions in the plasticity markers, brain-derived neurotrophic factor and its receptor p-trkB, and learning ability, which had been lessened after TBI. Conclusions. Curcumin complements the action of DHA on TBI pathology, and this property appears to be a viable strategy to counteract neuronal dysfunction after TBI and complement the application of rehabilitative interventions to foster functional recovery.