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E Requirements for the Degree Master of Science in Computer Science by Sree Vidya Peri Fall 2011 iii Copyright 2011 by Sree Vidya Peri All Rights Reserved iv DEDICATION This thesis is dedicated to my parents and husband, who always support and encourage me with their love. v It is not because things are difficult that we do not dare, it is because we do not dare that things are difficult. Seneca vi ABSTRACT OF THE THESIS An AJAX-based Communication among User.
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11-β-hydroxysteroid dehydrogenase type-2 (11β-OHSD2) is the enzyme that converts cortisol into its receptor-inactive congener cortisone.
Given that fetal exposure to excessive amounts of glucocorticoids leads to intrauterine growth retardation, it has been hypothesized that the physiological significance of this placental 11 beta-HSD barrier is to protect the fetus from adverse effects of maternal glucocorticoids.
Function. The protein encoded by this gene is a microsomal enzyme that catalyzes the conversion of the stress hormone cortisol to the inactive metabolite cortisone. In addition, the encoded protein can catalyze the reverse reaction, the conversion of cortisone to cortisol.
11beta-Hydroxysteroid dehydrogenase type 1 (11beta-HSD1) enzyme catalyzes interconversion of inactive cortisone to active cortisol. 11beta-HSD1 expression is higher in liver than in adipose tissue in obese patient., suggesting that this enzyme might have a pathogenic role in obesity and related metabolic disorders.
HSD-11βs are partly responsible for intracellular metabolism that determine the operation of glucocorticoids within cells. Glucocorticoids impact the brain development and ultimately the function of the central nervous system.
Introduction: 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) is an intracellular enzyme that catalyses conversion of cortisone into cortisol; correspondingly, 11β-HSD1 inhibitors inhibit this conversion.
The 11 beta-hydroxysteroid dehydrogenase type 2 (11 PHSD2) enzyme inactivates 11 betahydroxy steroids in sodium-transporting epithelia such as the kidney, thus protecting the non-selective mineralocorticoid receptor (MR) from occupation by cortisol in humans.
The renal 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) enzyme inactivates 11-hydroxy steroids in the kidney, thus protecting the nonselective mineralocorticoid receptor (MR) from occupation by glucocorticoids.
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