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.

Friday, April 22, 2011

Injection to limit heart attacks and stroke damages

I like the prevention of inflammatory damage from the stroke, maybe some researchers are finally getting the idea that a lot more interventions need to be available during the acute phase, and not just tPA.

http://news.bioscholar.com/2011/04/simple-jab-could-limit-heart-attacks-and-stroke-damages.html

The damages from heart attacks and stroke could be radically reduced by a simple injection, according to a new study.

Researchers at the University of Leicester are developing a simple injection to limit the devastating consequences of heart attacks and strokes.

Described by the lead researcher as “a fascinating new achievement”, work has already begun to translate the research into novel clinical therapies.

Prof Wilhelm Schwaeble of the Department of Infection, Immunity and Inflammation at the University of Leicester and collaborators identified an enzyme, Mannan Binding Lectin-Associated Serine Protease-2 (MASP-2) that is found in blood and is a key component of the lectin pathway of complement activation, a component of the innate immune system.

The lectin pathway is responsible for the potentially devastating inflammatory tissue response that can occur when any bodily tissue or organ is reconnected to blood supply following ischaemia – a temporary loss of that blood supply and the oxygen that it carries.

This excessive inflammatory response is, in part, responsible for the morbidity and mortality associated with myocardial infarction (heart attack) and cerebrovascular accidents (CVAs or strokes). Moreover, the work succeeded in finding a way to neutralise this enzyme by raising a therapeutic antibody against it.

A single antibody injection in animals has been shown to be sufficient to disrupt the molecular process that leads to tissue and organ destruction following ischaemic events, resulting in significantly less damage and markedly improved outcomes.

“This is a fascinating new achievement in the search for novel treatments to significantly reduce the tissue damage and impaired organ function that occur following ischaemia in widespread and serious conditions such as heart attacks and strokes,” said Schwaeble.

“This new potential therapy was also shown in animals to significantly improve outcomes of transplant surgery and may be applicable to any surgical procedure where tissue viability is at risk due to temporary interruption of blood flow.

“The main focus of our work was to identify a key molecular mechanism responsible for the overshooting inflammatory response that can cause substantial destruction to tissues and organs following their temporary loss of blood supply, a pathophysiological phenomenon called ischaemia/reperfusion injury,” said Schwaeble.

“Limiting this inflammatory response in oxygen-deprived tissues could dramatically improve outcomes and survival in patients suffering heart attacks or strokes,” he added.

The study has been published in the Early Online Edition of the Proceedings of the National Academy of Sciences.

So who is going to follow up with phase trials? And how long after the stroke will it still be useful? We have to push this kind of stuff to make it much better for those who follow us down this path. Contact the NINDS to see if this is one of the research trials they are working on.

No comments:

Post a Comment