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, September 30, 2013

Cannabinoid receptor signaling in progenitor/stem cell proliferation and differentiation

So ask your doctor what cannabinoids have to do with stem cell creation in your brain. Do not take 'I don't know' for an answer,  if it can help your recovery demand to know how you can get cannabinoids.  I would go to Italy or Spain to help my recovery. Why doesn't your doctor know anything?
http://www.sciencedirect.com/science/article/pii/S0163782713000544
  • a Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, IUIN, CIBERNED and IRYCIS, 28040 Madrid, Spain
  • b Department of Biomedical Sciences, University of Teramo, 64100 Teramo, Italy
  • c European Center for Brain Research (CERC)/Santa Lucia Foundation, 00143 Rome, Italy
  • d Department of Experimental Medicine & Surgery, Tor Vergata University of Rome, 00133 Rome, Italy
  • e Center of Integrated Research, Campus Bio-Medico University of Rome, 00128 Rome, Italy

Abstract

Cannabinoids, the active components of cannabis (Cannabis sativa) extracts, have attracted the attention of human civilizations for centuries, much earlier than the discovery and characterization of their substrate of action, the endocannabinoid system (ECS). The latter is an ensemble of endogenous lipids, their receptors [in particular type-1 (CB1) and type-2 (CB2) cannabinoid receptors] and metabolic enzymes. Cannabinoid signaling regulates cell proliferation, differentiation and survival, with different outcomes depending on the molecular targets and cellular context involved. Cannabinoid receptors are expressed and functional from the very early developmental stages, when they regulate embryonic and trophoblast stem cell survival and differentiation, and thus may affect the formation of manifold adult specialized tissues derived from the three different germ layers (ectoderm, mesoderm and endoderm). In the ectoderm-derived nervous system, both CB1 and CB2 receptors are present in neural progenitor/stem cells and control their self-renewal, proliferation and differentiation. CB1 and CB2 show opposite patterns of expression, the former increasing and the latter decreasing along neuronal differentiation. Recently, endocannabinoid (eCB) signaling has also been shown to regulate proliferation and differentiation of mesoderm-derived hematopoietic and mesenchymal stem cells, with a key role in determining the formation of several cell types in peripheral tissues, including blood cells, adipocytes, osteoblasts/osteoclasts and epithelial cells. Here, we will review these new findings, which unveil the involvement of eCB signaling in the regulation of progenitor/stem cell fate in the nervous system and in the periphery. The developmental regulation of cannabinoid receptor expression and cellular/subcellular localization, together with their role in progenitor/stem cell biology, may have important implications in human health and disease.

Abbreviations

  • 2-AG, 2-arachidonoylglycerol;
  • AEA, N-arachidonoylethanolamine;
  • BDNF, brain derived neurotrophic factor;
  • CBD, cannabidiol;
  • CBG, cannabigerol;
  • CFU-GEMM, colony-forming unit: granulocyte, erythrocyte, macrophage, megakaryocyte;
  • CREB, cAMP response element-binding protein;
  • CSF, colony-stimulating factors;
  • DAGL, diacylglycerol lipase;
  • ECB, endocannabinoid;
  • ERK, extracellular-signaling regulated protein kinase;
  • ES, embryonic stem;
  • ECS, endocannabinoid system;
  • FAAH, fatty acid amide hydrolase;
  • FGF, fibroblast growth factor;
  • GAD, glutamate decarboxylase;
  • GSK3β, glycogen synthase kina;
  • ICM, inner cell mass;
  • HSC, hematopoietic stem cells;
  • HPC, hematopoietic progenitor cells;
  • L1-CAM, L1-cell adhesion molecule;
  • MAGL, monoacylglycerol lipase;
  • mGluR, metabotropic glutamate receptors;
  • mTORC1, mammalian target of rapamycin complex 1;
  • NCAM, neural cell adhesion molecule;
  • NGF, nerve growth factor;
  • NP, neural progenitor/stem cell;
  • OEA, N-oleoylethanolamine;
  • PEA, N-palmitoylethanolamine;
  • PI3K, phosphoinositol 3-kinase;
  • PKA, protein kinase-A;
  • PPARγ, peroxisome proliferator activated receptors;
  • RANKL, receptor activator of nuclear factor kappa-B ligand;
  • SVZ, subventricular zone;
  • THC, Δ9-tetrahydrocannabinol;
  • vGlut, vesicular glutamate transporter;
  • VZ, ventricular zone

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