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慢性糖尿病大鼠水平半规管神经的形态计量学分析

Morphometric analysis of horizontal canal nerves of chronically diabetic rats.

作者信息

Myers S F, Tormey M C, Akl S

机构信息

Department of Biology, University of Michigan-Flint 48502-2186, USA.

出版信息

Otolaryngol Head Neck Surg. 1999 Feb;120(2):174-9. doi: 10.1016/S0194-5998(99)70402-X.

Abstract

Horizontal canal nerves of 3-, 6-, 9-, and 12-month-diabetic rats were compared with those of age-matched controls. The myelin sheaths of the horizontal canal nerves in diabetic rats were thinner than those of age-matched controls (mean +/- SD 0.63 +/- 0.04 micron (n = 16) vs. 0.71 +/- 0.05 micron (n = 9); p < 0.0001, one-tailed t test). Regression analysis revealed that myelin sheath thickness did not correlate with severity of diabetes, but myelin thinning did occur as a function of the duration of diabetes (p < 0.05, regression ANOVA). The progression of myelin thinning over time is consistent with the possibility of an accelerated decline in vestibular function with age in diabetic patients. That myelin thinning did not correlate with the severity of diabetes suggests that this thinning is not directly related to the aging effects attributed to nonenzymatic glycosylation of myelin proteins. Multivariate analysis revealed a significant difference between diabetic and control groups when fiber diameter and intrasheath diameter were considered together (p < 0.008, canonical discriminant-function analysis). Diabetic and control groups did not differ significantly in total nerve fiber counts. In the diabetic group, however, nerve fiber counts were higher in animals with higher blood glucose levels (p < 0.02, linear-regression ANOVA; r2 = 0.49). The finding of higher nerve fiber counts in more severely diabetic rats is consistent with an earlier transmission electron microscopic finding of false myelinated nerve fiber profiles in micrographs from more severely diabetic rats. These false profiles are believed to represent phagocytosis-like Schwann cell reactions against their own myelin, triggered by excess myelin glycosylation.

摘要

将3个月、6个月、9个月和12个月糖尿病大鼠的水平半规管神经与年龄匹配的对照组进行比较。糖尿病大鼠水平半规管神经的髓鞘比年龄匹配的对照组更薄(平均值±标准差为0.63±0.04微米(n = 16),而对照组为0.71±0.05微米(n = 9);p < 0.0001,单尾t检验)。回归分析显示,髓鞘厚度与糖尿病严重程度无关,但髓鞘变薄确实是糖尿病病程的函数(p < 0.05,回归方差分析)。髓鞘变薄随时间的进展与糖尿病患者前庭功能随年龄加速下降的可能性一致。髓鞘变薄与糖尿病严重程度无关,这表明这种变薄与髓鞘蛋白非酶糖基化导致的衰老效应没有直接关系。多变量分析显示,当同时考虑纤维直径和鞘内直径时,糖尿病组和对照组之间存在显著差异(p < 0.008,典型判别函数分析)。糖尿病组和对照组的总神经纤维计数没有显著差异。然而,在糖尿病组中,血糖水平较高的动物神经纤维计数更高(p < 0.02,线性回归方差分析;r2 = 0.49)。在糖尿病更严重的大鼠中神经纤维计数更高这一发现与早期透射电子显微镜观察结果一致,即在糖尿病更严重的大鼠的显微照片中发现了假髓鞘化神经纤维轮廓。这些假轮廓被认为代表了雪旺细胞对自身髓鞘的吞噬样反应,由髓鞘糖基化过多引发。

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