Titlebook: Cellular and Molecular Approaches to Regeneration and Repair; Paul A. Lapchak,John H. Zhang Book 2018 Springer International Publishing AG

欺骗手段

FRET

The Combination of Stem Cell Factor (SCF) and Granulocyte-Colony Stimulating Factor (G-CSF) in Repaithis chapter, we have reviewed the biological function of SCF and G-CSF in hematopoiesis, neural plasticity, and neurogenesis, and summarized the preclinical studies illustrating the neurorestorative effects of SCF and G-CSF post-acute stroke.

Enrage

蔑视

META

Stem Cell Transplants in the Aged Stroke Brain: Microenvironment Factorsntly with age both in men and women with incidence rates accelerating above 70 years. Since stroke afflicts mostly the elderly comorbid patients it is highly desirable to test the efficacy of cell therapies in an appropriate animal stroke model. It has been noted that the potential for neurogenesis

狼群

Modulating Endogenous Adult Neural Stem Cells to Improve Regeneration in Stroke Brainesses could be activated in the brain following stroke. However, the spontaneous brain repair process is constrained with limited improvement of neurological outcome. Neurogenesis, oligodendrogenesis, angiogenesis, axonal outgrowth, and synaptogenesis are major brain repair processes during stroke r

FLUSH

Mobilization of Endogenous Neural Stem Cells to Promote Regeneration After Strokete gyrus. Following cerebral insults, they are mobilized from their niches to engage in regeneration and mediate functional recovery. After cerebral ischemia, eNSC generate new neurons in a process called neurogenesis, but also indirectly mediate regeneration via pleiotropic functions including neur

欢呼

饮料

Lipoprotein

Stem Cell-Paved Biobridge: A Merger of Exogenous and Endogenous Stem Cells Toward Regenerative Medic window and risk for hemorrhagic transformation. Stroke is a multiphasic disease with a complex pathology. After the initial insult, a cascade of events occur causing secondary cell death and the expansion of the penumbra. The major contributing factors to this secondary cell death are depletion of