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الصفحة 1
الصفحة 1
Cell Therapy, Stem Cells and Brain Repair
As our world continues to evolve, the field of regenerative medicine f- lows suit. Although many modern day therapies focus on synthetic and na- ral medicinal treatments for brain repair, many of these treatments and prescriptions lack adequate results or only have the ability to slow the p- gression of neurological disease or injury. Cell therapy, however, remains the most compelling treatment for neurodegenerative diseases, disorders, and injuries, including Parkinson’s disease, Huntington’s disease, traumatic brain injury, and stroke, which is expanded upon in more detail in Chapter 1 by Snyder and colleagues. Cell therapy is also unique in that it is the only therapeutic strategy that strives to replace lost, damaged, or dysfunctional cells with healthy ones.
Cell Signaling in Vascular Inflammation
Although inflammatory disease of the vascular bed of the lung is a major cause of morbidity and mortality in both adult and pediatric age groups, the importance of vascular biology to its understanding, and in developing novel therapeutics, has been overlooked. In Cell Signaling in Vascular Inflammation, leading basic and clinical researchers review the signal transduction mechanisms responsible for lung inflammation, including vascular hyperpermeability, white cell accumulation, and vascular remodeling. The authors cut across disciplines to bring together a broad-based presentation of inflammatory challenge, both in the initial phases of the inflammatory response, as well as in the more prolonged phase of genomic involvement.
Advances in multiple Sclerosis and Experimental Demyelinating Diseases
Challenging Charcot’s hypothesis that inflammatory response is the primary contributor to demyelination, Dr. Rodriguez and colleagues take a fresh, bold look at the causes and possible treatments of MS.Assuming oligodendrocyte injury as a prerequisite to MS, the authors explore viruses, toxins and genetic defects as possible culprits. They present novel methods to interrupt and reverse demyelination. This book examines the correlation between axonal loss and clinical deficits, including the implied role of the CD8+ T cell and perforin. It assesses proteases, specifically, kallikrein 6, which are strongly associated with active demyelination. By directing natural autoantibodies against oligodendrocytes that demonstrate remyelination in animal models, the authors envision clinical trials for remyelination enhancement.
