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.

Wednesday, January 25, 2012

Animal Models of Angiogenesis and Lymphangiogenesis

A good explanation of what would need to occur in the brain for our purposes.
http://www.intechopen.com/source/pdfs/26387/InTech-Animal_models_of_angiogenesis_and_lymphangiogenesis.pdf
1. Introduction
Blood and lymphatic vessels are present in all tissues, and play important roles for their function, homeostasis and maintenance. Angiogenesis, the growth of new blood vessels, is therefore highly important during development, but is largely not observed in the adult, except for during the female reproduction cycle and during wound healing. In pathological situations, however, angiogenesis may be turned on, and in this case contribute to the onset and progression of most severe human pathologies characterized by high mortality, including cancer, diabetes, obesity and retinopathies (Carmeliet, 2003) or is insufficiently activated such as in the case of myocardial infarction and stroke (Y Cao et al, 2005). Thus, angiogenesis is one of the largest and fastest evolving areas of research today. Angiogenesis is a highly complicated process, involving many different cell types, and it is therefore highly recommended that researchers use in vivo animal models for their studies.
Accordingly, today there are many in vivo models available.
The aim of this chapter is to give insights into the most commonly used in vivo angiogenesis models in both mice and zebrafish. We will provide detailed descriptions and discussions of the adipose tissue-, tumor-, ischemic hind limb- wound healing- and corneal micropocket angiogenesis models in mice and developmental-, tumor-, hypoxia-induced retinal- and regenerating tail fin angiogenesis models in zebrafish. We will provide a base for comparison between the different assays to quickly identify which model is best suited for a particular research focus.
1.1 Basic mechanisms of angiogenesis
Angiogenesis is a multistep process which is tightly regulated by an intimate balance between pro- and anti-angiogenic factors. Angiogenesis is stimulated by angiogenic factors the most commonly studied being members of the vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), transforming growth factor (TGF) or platelet derived growth factor (PDGF) families in the tissue.

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