Download Acrodermatitis Enteropathica: A Clinician's Guide by Pooya Khan Mohammad Beigi, Emanual Maverakis PDF

By Pooya Khan Mohammad Beigi, Emanual Maverakis

This new textual content presents perception and therapies for the coated affliction, together with dozens of top quality photos, illustrations, and medical tables. subject matters coated contain the background of the affliction, different types of the disease, molecular research, epidemiology, results on physique platforms, illness signs, and therapy. Acrodermatitis Enteropathica is a unprecedented sickness of zinc metabolism that happens in a single of 2 varieties: inborn and purchased. If untreated, the affliction is deadly and affected contributors may possibly die inside quite a few years, yet seeing that there's no treatment for the , it's severe that physicians are conscious of the signs with regards to AE and the best remedies on hand for sufferers. A complete consultant to Acrodermatitis Enteropathica is the one ebook of its sort to provide perception into this infrequent ailment. Written by means of and for dermatologists, pediatric experts, and ObGYN’s, this booklet comprises one of many biggest medical learn reports performed on Acrodermatitis Enteropathica during the last decade.​

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Extra resources for Acrodermatitis Enteropathica: A Clinician's Guide

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20 Chapter 2. Epidemiology and Etiology As the ZIP1 is located beneath the intestinal microvilli in differentiated cells but is not present in the apical membrane, it can only affect zinc absorption indirectly. The indirect effect of the ZIP1 protein in zinc absorption is demonstrated by the 20 % reduction in zinc uptake in cells that have had their ZIP1 gene knocked-out. It has been observed that zinc uptake is doubled in cells where the ZIP1 gene is overexpressed [59]. Additionally, there have been other studies in which these results have been duplicated: overexpression of ZIP1 in PC-3 prostate cells [83].

Theoretically, the best ZIP and ZNT candidates for inherited forms of zinc deficiency comparable to AE would be those abundantly present in absorptive enterocytes. According to mouse and various rodent models, a short list of candidate genes can be inferred, which include SLC30A1, SLC30A2, SLC30A4, SLC30A5, SLC30A6, SLC30A7, SLC39A4, and SLC39A5 [76]. In addition, the sole member of GufA subfamily of ZIP family, SLC39A11, is also abundantly expressed in murine digestive system, and notably in the stomach, ileum, and caecum [77, 78], which do not constitute the primary intestinal sites of zinc homeostasis, but could have an important role in intestinal zinc absorption.

J Nutr. 2001;131(1):46–52. 80. McMahon RJ, Cousins RJ. Regulation of the zinc transporter ZnT-1 by dietary zinc. Proc Natl Acad Sci. 1998;95(9):4841–6. 81. Hambidge KM, et al. Changes in zinc absorption during development. J Pediatr. 2006;149(5 Suppl):S64–8. 82. Zemann N, et al. Differentiation-and polarization-dependent zinc tolerance in Caco-2 cells. Eur J Nutr. 2011;50(5):379–86. 83. Franklin R, et al. Human ZIP1 is a major zinc uptake transporter for the accumulation of zinc in prostate cells.

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