关节镜制备膝关节软骨缺损的动物模型

目的:经微创手术制备膝关节软骨缺损动物模型,减少因手术创伤造成对实验结果的影响。方法:关节镜下对9只山羊(9膝)进行关节面钻孔术,造成软骨缺损模型,对其缺损位置进行准确定位。结果:9只山羊(9膝)均在关节镜下顺利进行了关节软骨缺损模型的建立,并进行了缺损部位的定位。结论:对比开放性手术,经关节镜制备关节缺损模型是一种对实验干预最少的微创方法,有助于减少手术本身造成的实验误差。     

血立停胶囊对早孕大鼠RU486药流后子宫收缩的实验研究

目的:研究血立停胶囊对早孕大鼠Ru486药物流产后对子宫平滑肌收缩频率、收缩幅度及活动力变化的影响,旨在探讨血立停胶囊治疗药物流产后出血的作用机制。方法:选择妊娠Wistar大鼠,随机分为6组,即对照组,米非司酮组,大剂量血立停组,小剂量血立停组,催产素组,止血敏组。于妊娠第7天,开始相应处理,妊娠第14天分别监测以下指标后处死:在体子宫平滑肌收缩力,收缩幅度、收缩频率。结果:大剂量血立停可明显增强大鼠在体子宫平滑肌活动力、提高子宫平滑肌收缩频率、收缩幅度,与对照组比较差异有显著性(p<0.05)。结论:血立停胶囊可增强大鼠子宫平滑肌兴奋性,从而起到对药物流产后阴道出血的治疗作用。     

贵州龙洞和万家洞内部分环境因子与动物群落结构的相关性

分别在2005年的10月和2006年的2月赴遵义龙洞和万家洞对肉眼见到的软体动物、节肢动物和脊索动物进行了观察和采集,在龙洞共获标本454号,隶属3门6纲13目20科29种或类群;在万家洞共获标本1726号,隶属3门7纲11目18科22种或类群。根据两洞内各光带中动物种类和数量组成不同,将其划分为6个动物群落,经群落多样性分析,物种丰富度、群落多样性、最大多样性、均匀度、优势度和相似性指数最高的分别是群落A(3.1932)、C(2.0788)、A(2.8332)、B(0.7828)、E(0.3789)和B-E(1.7854)。此外还研究了部分环境因子与群落多样性的相关性。结果显示,土壤中有机质的含量与群落多样性指数呈极显著正相关,相关系数为0.828(双尾显著性检验≤0.05);空气中CO2的含量与物种数、物种丰富度指数、群落多样性指数、群落最大多样性指数和群落优势度指数都成不显著负相关,相关系数分别为-0.160、-0.263、-0.072、-0.117和-0.031。由此证明土壤有机质的含量和空气中CO2的含量是影响洞穴动物群落变化的重要因子。     

猪骨骼肌磷酸葡萄糖异构酶的提纯及性质研究

本文报道猪骨骼肌磷酸葡萄糖异构酶（ＧＰＩ．ＥＣ ５．３．１．９）的提纯及其性质。设计了四步提纯法（稀盐溶液抽提、有机溶媒沉淀、透析、葡聚糖Ｇ－１００柱层析），对猪的五种不同解剖部位的骨骼风进行了ＧＰＩ的提纯。结果均得到聚丙烯酰胺凝胶电泳（ＰＡＧＥ）图谱为一条带的产品。提纯效果以猪股二头肌为例：提纯１０．６８倍、活力回收３２．３７％，比活力１．６×１０５单位。对提纯酶性质的研究表明；猪肌提纯的ＧＰＩ由三个亚基组成。分子量约为１２０Ｋｄ，等电点为 ６． ６，最适ｐＨ８．５，最适温度 ３５℃，米氏常数：６．０２ｍｍｏｌ／Ｌ，活化能为３２３７８．４焦耳／Ｋ，ｍｏｌ。免疫电泳实验证实猪肌提纯酶具抗原性。其免疫血清与自牛、兔、鸡、鱼的骨骼肌用同法提纯的ＧＰＩ有交叉免疫反应。免疫血清且对原酶液有抑制作用。猪肌ＧＰＩ与其它数种动物肌肉之ＧＰＩ的ＰＡＧＥ行为、混合电泳行为，等电聚焦行为、氨基酸组成等各方面基本相同，可以认为这是猪肌ＧＰＩ与其它数种动物肌肉的ＧＰＩ为同源蛋白质的佐证。     

Estimation in independent observer line transect surveys for clustered populations

This paper introduces a framework for animal abundance estimation in independent observer line transect surveys of clustered populations. The framework generalizes an approach given in Chen (1999, Environmental and Ecological Statistics 6, in press) to accommodate heterogeneity in detection caused by cluster size and other covariates. Both parametric and nonparametric estimators for the local effective search widths, given the covariates, can be derived from the framework. A nonparametric estimator based on conditional kernel density estimation is proposed and studied owing to its flexibility in modeling the detection functions. A real data set on harbor porpoise in the North Sea is analyzed.     

Classic toxin-induced animal models of Parkinson’s disease: 6-OHDA and MPTP

Neurological disorders in humans can be modeled in animals using standardized procedures that recreate specific pathogenic events and their behavioral outcomes. The development of animal models of Parkinsons disease (PD) is important to test new neuroprotective agents and strategies. Such animal models of PD have to mimic, at least partially, a Parkinson-like pathology and should reproduce specific features of the human disease. PD is characterized by massive degeneration of dopaminergic neurons in the substantia nigra, the loss of striatal dopaminergic fibers and a dramatic reduction of the striatal dopamine levels. The formation of cytoplasmic inclusion bodies (Lewy bodies) in surviving dopaminergic neurons represents the most important neuropathological feature of PD. Furthermore, the massive striatal dopamine deficiency causes easily detectable motor deficits in PD patients, including bradykinesia, rigidity, and resting tremor, which are the cardinal symptoms of PD. Over the years, a broad variety of experimental models of PD were developed and applied in diverse species. This review focuses on the two most common classical toxin-induced PD models, the 6-hydroxy-dopamine (6-OHDA model) and the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model. Both neurotoxins selectively and rapidly destroy catecholaminergic neurons, whereas in humans the PD pathogenesis follows a progressive course over decades. This discrepancy reflects one important and principal point of weakness related to most animal models. This review discusses the most important properties of 6-OHDA and MPTP, their modes of administration, and critically examines advantages and limitations of selected animal models. The new genetic and environmental toxin models of PD (e.g. rotenone, paraquat, maneb) are discussed elsewhere in this special issue.This work was supported by grants from the Deutsche Forschungsgemeinschaft.     

Interferon-gamma deficiency reveals that 129Sv mice are inherently more susceptible to Anaplasma phagocytophilum than C57BL/6 mice

Immunocompetent mice 129Sv (129) and C57BL/6 (B6) mice are similarly susceptible to Anaplasma phagocytophilum. We now show that 129 mice lacking interferon-gamma (IFN-gamma) develop more severe infection with A. phagocytophilum than IFN-gamma deficient B6 mice. These data demonstrate that there is an inherent increased susceptibility of 129 mice, compared with B6 mice, to A. phagocytophilum that can only be discerned in the absence of IFN-gamma.     

Impaired host defense to infection and Toll-like receptor 2-independent killing of Borrelia burgdorferi clinical isolates in TLR2-deficient C3H/HeJ mice

To investigate the role of Toll-like receptor 2 (TLR2)-mediated signaling in host innate defense and development of Lyme disease, the pathogenicity of Borrelia burgdorferi sensu stricto clinical isolates representing two distinct genotypes (RST1 and RST3A) was assessed in TLR2(-/-) C3H/HeJ mice. All TLR2(-/-) mice infected with a B. burgdorferi RST1 isolate developed severe arthritis. The numbers of spirochetes in heart, joint and ear biopsy specimens were significantly higher in TLR2(-/-) mice than in wild-type mice similarly infected as determined by real-time quantitative polymerase chain reaction. Interestingly, despite the higher spirochete levels in heart tissues, milder carditis was observed in TLR2(-/-) than in wild-type mice infected with this RST1 isolate (P=0.02). By contrast, no positive cultures were obtained from any of the blood and tissue specimens from TLR2(-/-) mice inoculated with two RST3A clinical isolates. The data suggest that there is impaired host innate defense against infection and TLR2-independent killing of B. burgdorferi clinical isolates in TLR2-deficient C3H/HeJ mice.     

Power-law versus exponential distributions of animal group sizes

There has been some confusion concerning the animal group size: an exponential distribution was deduced by maximizing the entropy; lognormal distributions were practically used; as power-law decay with exponent 3/2 was proposed in physical analogy to aerosol condensation. Here I show that the animal group-size distribution follows a power-law decay with exponent 1, and is truncated at a cut-off size which is the expected size of the groups an arbitrary individual engages in. An elementary model of animal aggregation based on binary splitting and coalescing on contingent encounter is presented. The model predicted size distribution holds for various data from pelagic fishes and mammalian herbivores in the wild.