Pharmacologic management of brain edema
ABSTRACT Cerebral edema is an intrinsic response to a variety of structural and metabolic insults. It is a major contributing factor in the development of intracranial hypertension and brain herniation, underscoring the need for early identification through an integration of clinical and neuroimaging findings, followed by timely institution of measures to reduce brain edema and intracranial hypertension. The management of cerebral edema requires a comprehensive approach in which pharmacologic treatments play a central role. These include glucocorticoids, hyperosmolar agents, diuretics, and sedative-anesthetic agents. Basic, translational, and clinical studies are needed to further unravel mechanisms underlying brain edema, with the goal of identifying new treatment strategies. Promising targets include modulators of endothelial cell tight junction proteins and of aquaporin channel expression within the blood-brain barrier.
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- "tem, respiratory apparatus, central nervous system, skin play important roles   . Papadopoulos MC reported that AQP4- mediated transcellular water movement was crucial in the resolution and formation of vasogenic brain edema  . Sidhaye overexpressed AQP5 in airway epithelial cells and found that altered AQP5 expression modulates paracellular permeability . "
ABSTRACT: AQP3 is a water/glycerol transporter expressed at the basolateral membrane of colonic epithelial cells. Although AQPs are expressed in the gastrointestinal tract, their effect on intestinal barrier has not been clear. Here, we showed that knockdown of AQP3 caused a dramatic, dose-dependent increase in E. coli C25 translocation, with the reduction of TEER and increasing LY permeability. Western blots revealed that expression of Claudin-1 and Occludin were significantly decreased in the AQP3 knockdown group, demonstrating that this treatment enhances paracellular permeability via an opening of the tight junction complex. These data not only describe the correlation between transcellular and paracellular pathways in human intestines, but also show that targeted knockdown of AQP3 might impair the intestinal barrier integrity.FEBS letters 09/2011; 585(19):3113-9. DOI:10.1016/j.febslet.2011.08.045 · 3.34 Impact Factor
Conference Paper: Input collapse of CMOS logic gates with a series-connected MOSFET chain[Show abstract] [Hide abstract]
ABSTRACT: We propose a generic series-connected MOSFET chain model (SMCM) extending the PDSMM, to describe the peculiar DC characteristics of a series MOSFET chain. Initial state propagation delays (ISPD) are defined as propagation delays due to initial states of intermediate nodes of a series-connected MOSFET chain. Two extreme and important ISPD, called as fast ISPD and slow ISPD, are introduced. The effect of input patterns of CMOS logic gates on propagation delays in the two ISPD is discussed. Finally, an efficient mapping algorithm for every possible input pattern to an equal input ramp is introduced.Solid-State and Integrated Circuits Technology, 2004. Proceedings. 7th International Conference on; 11/2004