A STROKE WILL KILL YOU

 Hello class, to give everyone a little background strokes are categorized into two different types: ischemic and hemorrhage.  Ischemic strokes are caused by either a thrombosis or an embolism.  Hemorrhage strokes are either intracranial or intracerebral.  And if you are wondering what kind of stroke you can look forward to dying from and at what percent, then I am glad to inform you that you are probably going to die of a ischemic stroke at betting line of ~80%.   The public access paper only talks about ischemic strokes, and I will try to summarize it for you: INFLAMMATION IS BAD FOR THE BRAIN.  If that is a good enough explanation for you, by all means stop reading, if you crave more info you can read on.  Other then food and oxygen the brain really hates help from the body.  In the case of a stroke, the body sends leukocytes in the form of neutrophils followed by lymphocytes to the brain.  Both leukocytes have deleterious roles and also tissue-damaging properties within the brain leading to permanent brain damage.  These inflammatory cells also release cytotoxic agents inducing more cell damage as well as disruptions in the blood brain barrier.  Studies have found that inhibition of neutrophil infiltration will significantly reduce the infarct volume within the brain.  Other studies have found that inhibition of certain adhesion molecules: selectins, immunoglobulins and integrins show higher recovery of rates for brain tissue following brain ischemia.  Also interesting is the relation between diabetes and stroke due to TNF-alpha.  While it has been shown that stroke is exacerbated in diabetic rats, TNF-A is a double-edged sword in stroke.  Studies have shown that TNF-A appears to be involved in two different pathways due to the signaling of the TNF-A receptor 1 (TNFR1).  TNFR1 is thought to have a bifurcation in its signaling pathway which leads to cell life or death.  One route leads to the Fasassociated death domain (FADD) and apoptosis.  The other route TNFR1 to TNFR associating factor 2 may lead to anti-inflammatory and anti-apoptotic function, i.e. ischemic tolerance.