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乙型流感病毒诱发瑞氏综合征小鼠模型中肝脏和脑部的变化序列。

The sequence of changes in liver and brain in the influenza B virus mouse model of Reye's syndrome.

作者信息

Blisard K S, Davis L E

机构信息

Research Service, Veterans Administration Medical Center, Albuquerque, NM.

出版信息

J Neuropathol Exp Neurol. 1990 Sep;49(5):498-508. doi: 10.1097/00005072-199009000-00005.

Abstract

The time course of morphologic changes in the influenza B mouse model of Reye's syndrome is described and compared to the clinical, virologic, and biochemical changes. Following an intravenous inoculation of a lethal dose of an egg adapted strain of influenza B/Lee/40 virus, mice first showed clinical signs of lethargy and ruffled fur at 12 hours (h) post inoculation (pi). The earliest morphologic changes in the liver occurred at 12 h pi, and consisted of a slight increase in fat and loss of glycogen in hepatocytes. Over the next 36 h, the accumulation of microvesicular fat increased, and mitochondrial abnormalities such as pleomorphism and loss of dense bodies developed. There was no increase in peroxisomes. In the brain, focal cerebral edema was detected as early at 6-12 h pi. The edema, manifested as swelling of astrocytic foot processes, increased in severity with time. Endothelial cells were not abnormal. Myelin sheath splitting rarely was observed. Since changes occurred simultaneously in the liver and in the brain, we suggest that influenza B virus caused a simultaneous primary insult to both organs.

摘要

描述了乙型流感病毒感染小鼠诱发瑞氏综合征的形态学变化的时间进程,并与临床、病毒学及生化变化进行了比较。给小鼠静脉接种致死剂量的鸡胚适应株乙型流感病毒B/Lee/40后,小鼠在接种后12小时(h)首次出现嗜睡和被毛蓬乱的临床症状。肝脏最早的形态学变化出现在接种后12小时,表现为肝细胞内脂肪略有增加和糖原丢失。在接下来的36小时内,微泡脂肪的积累增加,线粒体出现异常,如多形性和致密小体丢失。过氧化物酶体没有增加。在大脑中,早在接种后6 - 12小时就检测到局灶性脑水肿。水肿表现为星形胶质细胞足突肿胀,随时间推移严重程度增加。内皮细胞无异常。很少观察到髓鞘分裂。由于肝脏和大脑同时出现变化,我们认为乙型流感病毒对这两个器官同时造成了原发性损伤。

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