tailieunhanh - Báo cáo y học: "Dynamic simulation of red blood cell metabolism and its application to the analysis of a pathological condition"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: Dynamic simulation of red blood cell metabolism and its application to the analysis of a pathological condition | Theoretical Biology and Medical Modelling BioMed Central Research Open Access Dynamic simulation of red blood cell metabolism and its application to the analysis of a pathological condition Yoichi Nakayama Ayako Kinoshita and Masaru Tomita Address Institute for Advanced Biosciences Keio University Tsuruoka 997-0017 Japan Email Yoichi Nakayama - ynakayam@ Ayako Kinoshita - ayakosan@ Masaru Tomita - mt@ Corresponding author Published 09 May 2005 Received 19 November 2004 Theoretical Biology and Medical Modelling 2005 2 18 doi 1742-4682-2-18 Accepted 09 May 2005 This article is available from http content 2 1 18 2005 Nakayama et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Cell simulation which aims to predict the complex and dynamic behavior of living cells is becoming a valuable tool. In silico models of human red blood cell RBC metabolism have been developed by several laboratories. An RBC model using the E-Cell simulation system has been developed. This prototype model consists of three major metabolic pathways namely the glycolytic pathway the pentose phosphate pathway and the nucleotide metabolic pathway. Like the previous model by Joshi and Palsson it also models physical effects such as osmotic balance. This model was used here to reconstruct the pathology arising from hereditary glucose-6-phosphate dehydrogenase G6PD deficiency which is the most common deficiency in human RBC. Results Since the prototype model could not reproduce the state of G6PD deficiency the model was modified to include a pathway for de novo glutathione synthesis and a glutathione disulfide GSSG export system. The de novo glutathione GSH synthesis pathway