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Cryptosporidium infection impairs growth and muscular protein synthesis in suckling rats.隐孢子虫感染会损害乳鼠的生长和肌肉蛋白质合成。
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Health sequelae of human cryptosporidiosis in immunocompetent patients.免疫功能正常患者感染人隐孢子虫病后的健康后遗症。
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Visceral hyperalgesia and intestinal dysmotility in a mouse model of postinfective gut dysfunction.感染后肠道功能障碍小鼠模型中的内脏痛觉过敏和肠道运动障碍
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Evidence for the absence of an intestinal adaptive mechanism to compensate for C. parvum-induced amino acid malabsorption in suckling rats.关于乳鼠中不存在肠道适应性机制以补偿微小隐孢子虫诱导的氨基酸吸收不良的证据。
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Long-lasting anticryptosporidial activity of nitazoxanide in an immunosuppressed rat model.硝唑尼特在免疫抑制大鼠模型中的持久抗隐孢子虫活性。
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Intestinal peptide transporter PepT1 is over-expressed during acute cryptosporidiosis in suckling rats as a result of both malnutrition and experimental parasite infection.由于营养不良和实验性寄生虫感染,肠道肽转运体PepT1在乳鼠急性隐孢子虫病期间过度表达。
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短暂的新生儿隐孢子虫感染引发免疫功能正常大鼠空肠对扩张的长期超敏反应。

Transient neonatal Cryptosporidium parvum infection triggers long-term jejunal hypersensitivity to distension in immunocompetent rats.

作者信息

Marion Rachel, Baishanbo Asiya, Gargala Gilles, François Arnaud, Ducrotté Philippe, Duclos Celia, Fioramonti Jean, Ballet Jean Jacques, Favennec Loïc

机构信息

Laboratoire de Parasitologie and ADEN UPRES EA-3234, CHU Charles-Nicolle, 1, rue de Germont, 76031 Rouen, France.

出版信息

Infect Immun. 2006 Jul;74(7):4387-9. doi: 10.1128/IAI.02055-05.

DOI:10.1128/IAI.02055-05
PMID:16790818
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1489692/
Abstract

In 5-day-old immunocompetent Sprague-Dawley rats infected with either 10(2) or 10(5) Cryptosporidium parvum oocysts, transient infection resulted 120 days later in increased cardiovascular depressor response to jejunal distension and jejunal myeloperoxidase activity (P < 0.05). Nitazoxanide treatment normalized jejunal sensitivity (P < 0.001) but not myeloperoxidase levels (P > 0.05). Data warrant further evaluation of the role of early cryptosporidiosis in the development of chronic inflammatory gut conditions.

摘要

在感染了10²或10⁵个微小隐孢子虫卵囊的5日龄免疫功能正常的斯普拉格-道利大鼠中,120天后短暂感染导致对空肠扩张的心血管降压反应增强以及空肠髓过氧化物酶活性增加(P < 0.05)。硝唑尼特治疗使空肠敏感性恢复正常(P < 0.001),但髓过氧化物酶水平未恢复正常(P > 0.05)。这些数据值得进一步评估早期隐孢子虫病在慢性炎症性肠道疾病发展中的作用。