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本文引用的文献

1
Simultaneous measurement and imaging of intracellular Ca(2+) and H(+) transport in isolated rabbit gastric glands.在分离的兔胃腺中同时测量和成像细胞内钙离子(Ca(2+))和氢离子(H(+))转运
J Physiol. 2001 Dec 15;537(Pt 3):735-45. doi: 10.1111/j.1469-7793.2001.00735.x.
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Pathogenesis of rotavirus diarrhea.轮状病毒腹泻的发病机制。
Microbes Infect. 2001 Nov;3(13):1145-56. doi: 10.1016/s1286-4579(01)01475-7.
3
Evidence of amiloride-sensitive fluid absorption in rat descending colonic crypts from fluorescence recovery of FITC-labelled dextran after photobleaching.光漂白后FITC标记葡聚糖荧光恢复显示大鼠降结肠隐窝中存在氨氯地平敏感的液体吸收证据。
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4
Cloning of a new aquaporin (AQP10) abundantly expressed in duodenum and jejunum.一种在十二指肠和空肠中大量表达的新型水通道蛋白(AQP10)的克隆。
Biochem Biophys Res Commun. 2001 Oct 5;287(4):814-9. doi: 10.1006/bbrc.2001.5661.
5
Microbes and microbial toxins: paradigms for microbial-mucosal interactions. VIII. Pathological consequences of rotavirus infection and its enterotoxin.微生物与微生物毒素:微生物 - 黏膜相互作用的范例。VIII. 轮状病毒感染及其肠毒素的病理后果。
Am J Physiol Gastrointest Liver Physiol. 2001 Aug;281(2):G303-10. doi: 10.1152/ajpgi.2001.281.2.G303.
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Pathogenesis of rotavirus gastroenteritis.轮状病毒胃肠炎的发病机制。
Novartis Found Symp. 2001;238:82-96; discussion 96-100. doi: 10.1002/0470846534.ch6.
7
Gastroenteritis viruses: an overview.肠胃炎病毒:概述
Novartis Found Symp. 2001;238:5-19; discussion 19-25. doi: 10.1002/0470846534.ch2.
8
Early events of rotavirus infection: the search for the receptor(s).轮状病毒感染的早期事件:寻找受体
Novartis Found Symp. 2001;238:47-60; discussion 60-3. doi: 10.1002/0470846534.ch4.
9
Group C rotavirus NSP4 induces diarrhea in neonatal mice.C组轮状病毒NSP4可诱导新生小鼠腹泻。
Arch Virol. 2001;146(4):801-6. doi: 10.1007/s007050170148.
10
A lack of consistent amino acid substitutions in NSP4 between rotaviruses derived from diarrheal and asymptomatically-infected kittens.源自腹泻和无症状感染小猫的轮状病毒之间,NSP4中缺乏一致的氨基酸替换。
Microbiol Immunol. 2001;45(2):173-7. doi: 10.1111/j.1348-0421.2001.tb01277.x.

I, 2. 肠道与病毒性腹泻相关的生理学和病理生理学。

I, 2. Physiology and pathophysiology of the gut in relation to viral diarrhea.

作者信息

Michelangeli Fabián, Ruiz Marie Christine

机构信息

Laboratorio de Fisiología Gastrointestinal, Centro de Biofísica y Bioquímica, Instituto Venezolano de Investigaciones Científicas (IVIC) Caracas, Venezuela.

出版信息

Perspect Med Virol. 2003;9:23-50. doi: 10.1016/S0168-7069(03)09003-7. Epub 2004 Sep 14.

DOI:10.1016/S0168-7069(03)09003-7
PMID:32308248
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7157931/
Abstract

Many advances have been made in the understanding of intestinal electrolyte transport from the molecular to the whole-tissue level. This chapter discusses the molecular mechanisms of intestinal epithelial ion transport processes, as well as the intra- and extracellular factors involved in their regulation, as a framework for the understanding of virus-induced gastroenteritis. Based on the present knowledge of the effects of rotavirus (RV) infection on the physiology of the intestine at different levels of organization, a working model for the pathogenesis of RV diarrhea is presented in the chapter. The understanding of the pathogenic processes of viral diarrheas may serve as the basis for a rational approach in the design of novel therapeutic strategies and the search for new antiviral drugs.

摘要

在从分子水平到全组织水平理解肠道电解质转运方面已经取得了许多进展。本章讨论肠道上皮离子转运过程的分子机制,以及参与其调节的细胞内和细胞外因素,作为理解病毒感染性胃肠炎的框架。基于目前对轮状病毒(RV)感染在不同组织水平对肠道生理学影响的认识,本章提出了RV腹泻发病机制的工作模型。对病毒性腹泻致病过程的理解可为设计新型治疗策略和寻找新抗病毒药物的合理方法提供依据。