Deans' stroke musings: Neutrophil Extracellular Traps (Nets) Formation After Traumatic Brain Injury

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 31, 2013

Neutrophil Extracellular Traps (Nets) Formation After Traumatic Brain Injury

Sounds like another hyperacute research possibility.
http://journals.lww.com/ccmjournal/Abstract/2012/12001/201___Neutrophil_Extracellular_Traps__Nets_.168.aspx

Abstract

Introduction: Brain inflammation significantly contributes to the progression of tissue damage after traumatic brain injury (TBI). Neutrophil recruitment has been shown to increase over the first 24 hours after experimental TBI. There is evidence that upon activation, neutrophils release DNA fibers decorated with antimicrobial proteins forming neutrophil extracellular traps (NETs). NET formation, when excessive, may also lead to tissue injury. The role of NETs in traumatic brain injury has not been investigated.

Hypothesis: NETs release by activated neutrophils may contribute to tissue damage and edema formation after TBI.

Methods: We used a controlled cortical impact (CCI) as a model for traumatic brain injury (TBI) in anesthetized adult Sprague-Dawley rats and divided in sham,12, 24, and 72 hours groups (n =5 each group) After TBI rats were euthanized at 12, 24 and 72 hours, brains were removed, examined by histology and assayed for histones, MPO and NE activity

Results: Significant increase in neutrophil accumulation, MPO and NE activity was demonstrated in the traumatized area at 12, 24 and even 72 hours after TBI when compared with non-traumatized area and sham animals.

Conclusions: We provide evidence for the formation of neutrophil extracellular traps (NETs), in areas of tissue injury, suggesting their potential link with brain tissue damage.