Injury
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Traumatic brain injury (TBI) is a major cause of death and disability in both children and the elderly. Mortality from TBI is said account for 1-2% of all deaths. One-third to one-half of all traumatic deaths is due to head injury. Of those who survive, the majority is left with significant disabilities, including 3% who remain in a vegetative state and only approximately 30% who make a good recovery. Microarray studies and other genomic techniques facilitate the discovery of new targets for the treatment of diseases, which aids in drug development, immunotherapeutics and gene therapy. Gene expression profiling or microarray analysis enables the measurement of thousands of genes in a single RNA sample. ⋯ In this study, we will review the current understanding of the genetic susceptibility of TBI with microarrays. Our results highlight the importance of genes that control the response of the brain to injury as well as the suitability of microarrays for identifying specific targets for further study.
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To compare lung and liver injury and laboratory results in haemorrhagic shock and sepsis models treated with combinations of lactated Ringer's solution (LR), 7.5% hypertonic saline (HTS), hydroxyethyl starch (HES), and pentoxifylline (PTX). ⋯ HTS-PTX was superior to HES, LR-PTX, and LR for treating shock and sepsis, and LR-PTX and HES gave better results than LR therapy alone.
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Activity of the epithelial sodium channels (ENaCs) in the lung tissue plays a critical role on sodium/fluid homeostasis and the lung fluid clearance. The serum- and glucocorticoid-inducible kinase-1 (SGK1), one of the critical regulation proteins of ENaC, is activated by insulin and growth factors possibly through 3-phosphoinositide-dependent kinase PDK1 or/and phosphatidylinositol 3-kinase (PI3K). However, it is uncertain whether insulin shows its stimulatory action on ENaC by activation of SGK1 in lipopolysaccharide (LPS)-induced acute lung injury (ALI) condition. ⋯ Furthermore, α-ENaC was up-regulated by insulin treatment. Simultaneously, injection with LPS significantly reduced α-ENaC expression. These findings demonstrated that insulin up-regulates ENaC in vivo possibly resulting from activation of SGK1.
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The purpose of this study is to investigate the effects of dexamethasone on repair of a critical size defect of the mandible in male Sprague-Dawley rats. ⋯ In a model of bone healing of a mandible defect, dexamethasone-treated rats exhibited impaired osteogenic differentiation and maturation due to the inhibition of COX-2, osteogenic gene, RUNX2 and collagen protein expression, which resulted in delayed bone repair. Although perioperative short-term therapy did not exhibit long-term effects on wound healing of the maxillofacial bone, the application of glucocorticoids should be cautiously considered in the clinic.