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.

Monday, August 25, 2014

Modeling Immunity and Inflammation in Stroke Can Mice Be Trusted?

Sounds like a researcher problem to solve.
http://stroke.ahajournals.org/content/45/9/e177.extract?etoc
  1. Ulrich Dirnagl, MD
+ Author Affiliations
  1. From the Departments of Neurology and Experimental Neurology Charité, Center for Stroke Research Berlin, Charité, ExcellenceCluster NeuroCure–Universitätsmedizin Berlin, Berlin, Germany; German Center for Neurodegenerative Diseases (DZNE), Partner Site, Berlin, Germany; and German Center for Cardiovascular Diseases (DZHK), Partner Site, Berlin, Germany.
  1. Correspondence to Ulrich Dirnagl, MD, Center for Stroke Research Berlin, Charité Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany. E-mail ulrich.dirnagl@charite.de
Key Words:

Introduction

Sixty-five million years have passed since mouse and man shared a common ancestor. The principles of evolution, as well as the scientific literature, suggest that there are many similarities between both mammal species but also significant differences. Humans are definitely no 75 kg mice,1 but is it true that “the mouse model has been totally misleading for at least three major killers—sepsis, burns, and trauma,” as the New York Times concluded after the publication of a study by Seok et al?2 By looking at transcriptional responses of blood cells, this study found “that, although acute inflammatory stresses from different etiologies result in highly similar genomic responses in humans, the responses in corresponding mouse models correlate poorly with the human conditions and also, one another.”
The results of the Seok et al2 study are by no means surprising or new,3 but they nevertheless carry an important message for experimental stroke research. The authors used male mice of the C57 BL/6J strain, which is exquisitely resistant to sepsis: more than one million-fold doses of endotoxin are required to cause shock in this mouse strain. The mice are inbred and raised under specific pathogen-free conditions, so at the time of the study, the 8-week-old mice had a naive and immature immune system.
In contrast, rodents are as sensitive to focal cerebral ischemia as humans. The evolution of the infarct and surrounding penumbra has similar temporal and histopathologic dynamics, and the time windows for thrombolysis after embolic stroke are practically …

No comments:

Post a Comment