By C.-H. Cho, J.-Y. Wang, C. Sakamoto
ISBN-10: 3805573820
ISBN-13: 9783805573825
Over the past decade, significant development has been made in figuring out mobile and molecular mechanisms concerned with gastrointestinal mucosal harm and service. those findings give you the foundation to spot the etiology and pathogenesis of assorted intestine mucosal injury-related illnesses and to increase new healing methods. The book to hand is split into 3 sections: Epithelial restitution, mucosal fix and ulcer therapeutic, and experimental therapeutics. the 1st half highlights the early speedy mucosal restitution, focussing at the roles of extracellular matrix, cytoskeleton, cytokines, Ca2+ signaling, polyamines, and the protein kinase C / DAG pathways. the following part bargains with points of continual mucosal therapeutic, focusing on the jobs of fundamental reaction gene expression, angiogenesis and angiogenic development elements, platelets, and the mechanisms of cellphone renewal after damage in exact situations. The final half explores new healing ways.
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Extra info for Gastrointestinal Mucosal Repair and Experimental Therapeutics (Frontiers of Gastrointestinal Research)
Example text
Am J Physiol 1981;241:6365–6375. Chung RSK, Sum PT, Goldman H, Field M, Silen W: Effects of chelation of calcium on the gastric mucosal barrier. Gastroenterology 1970;59:200–207. Wang JY, Johnson LR: Role of transglutaminase and protein cross-linking in the repair of mucosal stress erosions. Am J Physiol 1992;262:G818–G825. Wang JY, Viar MJ, Johnson LR: Transglutaminase in response to hypertonic NaCl-induced gastric mucosal injury in rats. Gastroenterology 1993;104:65–74. Lorand L, Conrad SM: Transglutaminases.
Although important discoveries have been made over the past decade, many critical issues regarding the role of Ca2ϩ in mucosal restitution remains to be demonstrated. Studies to examine the molecular mechanism responsible for Kϩ channel gene expression, Ca2ϩ channels of intestinal epithelial cells, and Ca2ϩ sensitive proteins and their downstream targets are needed to fully elucidate the biological function of Ca2ϩ signal in the regulation of mucosal restitution. It can be predicted with some confidence that the cellular and molecular analysis of the signal pathways controlled by Ca2ϩ will lead to a better understanding of mechanisms of gastrointestinal epithelial restitution.
The resultant increase in [Ca2ϩ]cyt activates RhoA activity and others that drive the assembly of actin-myosin microfilaments, thereby stimulating cell migration and intestinal epithelial restitution. Although important discoveries have been made over the past decade, many critical issues regarding the role of Ca2ϩ in mucosal restitution remains to be demonstrated. Studies to examine the molecular mechanism responsible for Kϩ channel gene expression, Ca2ϩ channels of intestinal epithelial cells, and Ca2ϩ sensitive proteins and their downstream targets are needed to fully elucidate the biological function of Ca2ϩ signal in the regulation of mucosal restitution.
Gastrointestinal Mucosal Repair and Experimental Therapeutics (Frontiers of Gastrointestinal Research) by C.-H. Cho, J.-Y. Wang, C. Sakamoto
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