秦岭川金丝猴长时间携带死婴行为

本文首次报道了一例秦岭川金丝猴死婴被其母亲和近亲未成年雌猴长时间携带行为。携带者的行为除正常婴猴中常见的检视、嗅吻、理毛行为外,还有嘴叼和手抓携带行为,后者是正常婴猴携带行为中未曾见到过的。对于树栖生活为主的川金丝猴,与正常婴猴相比,死婴的携带更加困难,母亲对死婴的行为方式在一定程度上体现了对婴猴的母爱和照料能力。本文对死婴携带行为发生的原因及其意义进行了初步探讨。     

成年太行山猕猴肩关节变量的研究

本项研究对成年太行山猕猴桃肩并节变量进行了测量和统计,作了异速生长分析,并对太行山猕猴、滇南猕猴、川西猕猴、湘鄂猕猴肩并关节变量进行了比较和聚类分析,与上述３个亚种相比,太行山猕猴较短的肩胛骨,较小的锁肱指数,较大的三角肌止点指数和较小的摆荡指数,表明太行山猕猴肩关节形态结构更适应于地面上的活动,说明其在地面上活动较多,在树上活动较少。     

成年太行山猕猴(Macaca mulatta tcheliensis)肩关节变量的研究

本项研究对成年太行山猕猴肩关节变量进行了测量和统计,作了异速生长分析,并对太行山猕猴(M.mulatta tcheliensis)、滇南猕猴(M.mulatta mulatta)、川西猕猴(M.mulatta lasiotis)、湘鄂猕猴(M.mulatta littoralis)肩关节变量进行了比较和聚类分析。与上述3个亚种相比,太行山猕猴较短的肩胛骨、较小的锁肱指数、较大的三角肌止点指数和较小的摆荡指数,表明太行山猕猴肩关节形态结构更适应于地面上的活动,说明其在地面上活动较多,在树上活动较少。     

促进人工饲养实验猕猴心理康乐

目的促进实验猕猴心理康乐,既能减少动物异常行为的发生、获得可靠的科学数据,同时也是实现这一珍贵非人灵长类实验动物福利的重要内容。实验猕猴社会化集群、环境优化、婴猴饲养方式是影响动物心理康乐几个较大的因素,本文对其研究进展进行了综述,对推进我国灵长类实验动物福利具有积极作用。     

人工哺育期腹泻婴猴奇异变形杆菌的分离与鉴定

目的对一株人工哺育期引发恒河猴婴猴腹泻的奇异变形杆菌进行了鉴定,为实验猕猴疾病检测、鉴别诊断提供参考依据。方法通过培养特性、菌落形态、染色、生化试验和血清学诊断鉴别等检查,对分离菌株进行初步鉴定,同时,对分离菌株进行致病性试验及药敏试验。结果通过表型生物学特性鉴定,并结合血清学诊断鉴别方法,确证该分离菌株为奇异变形杆菌,应用药敏试验筛选出了高度敏感的抗菌药,控制了该病的继续发生,致病性试验证明,该分离菌株对小白鼠有高致病性。结论分离到的奇异变形杆菌是导致本次婴猴腹泻死亡的病原菌,该菌为条件致病菌,对实验猕猴和研究人员均有潜在的危害,尽管该菌不是国家标准要求排除的病原菌,但该菌引发的传染病将对动物实验造成严重影响,故应引起高度重视。     

海南南湾猕猴种群增长的研究

对海南南湾猕猴１９６５～１９９４年间的种群动态和雌性猴生命表的研究表明,该种群年均增长率为９．７％,１９８７年后种群增长率和繁殖率有所下降,猴群中非成年猴比例已不足５０％。半驯化雌性猴的逐年存活率到１７岁仍达０．５８,通过对存活曲线和寿命期望曲线的分析,南湾雌猴寿命可达３３～３８岁。婴猴死亡率较低、成年猴死亡率较高,存活曲线属Ⅰ形即凸形。研究表明静态生命表编制方法不适于灵长类,在建立标准化存活曲线时应考虑种群综合死亡系数。猕猴通过存活率、繁殖率、群体结构变化等社群调节机制达到种群平衡。对南湾猕猴近年内每年可捕捉利用１００～１５０只左右,１０岁以上的猴应占５０％以上,在不影响种群遗传多样性水平上,可适当多捕一些成年雄猴。     

成年太行山猕猴肱骨与锁骨的初步研究

本项研究对成年太行山猕猴的肱骨（３３例）及锁骨（２９例）进行了全面测量及观察,计算了５项指数。对太行山猕猴、滇南猕猴、川西猕猴、湘鄂猕猴的肱骨、锁骨和桡骨有关测量指标及指数进行聚类分析,分析结果表明：与其他３个猕猴亚种相比,太行山猕猴肱骨与锁骨的形态结构更适应于地面上的活动,说明其在地上活动较多,在树上活动较少。     

现生太行山猕猴与猕猴化石骨指数的比较

为探讨现生太行山猕猴与猕猴化石骨指数的差异,对太行山猕猴与广西崇左早更新世猕猴化石的肢间指数(Intermembral index,IM)、臂指数(Brachial index,BI)、股指数(Crural index,CI)和股骨粗壮指数(Robusticity index,RI)等指数进行比较。结果表明,猕猴化石IM值(96)高于太行山猕猴,BI值(94.5)和CI值(88.5)均低于太行山猕猴,推测该猕猴化石在早更新世时期可能地栖生活,适合于陆地四足行走,同时也验证了太行山猕猴主要为半树栖生活。结合对猕猴化石伴生哺乳动物习性的分析,推测广西崇左早更新世的气候温暖潮湿并有一定的水域,植被以森林和灌木为主,有局部的草地或草坡,其自然环境非常适宜高等灵长类生息繁衍。     

太行山猕猴颅骨的形态学及多变量研究

对２１例成年太行山猕猴颅骨的主要形态特征进行了描述和测量,并进行了初步的统计学分析。结果表明,成年太行山猕猴颅骨在耳点间宽（Ｘ１３）、上面宽（Ｘ１９）、左眶宽（Ｘ２７）、右眶宽（Ｘ２８）、两眶宽（Ｘ３７）等变量间存在显的性别差异。与湘鄂、闽粤猕猴颅骨有关变量相比,有显的不同。３个猕猴种群的聚类分析结果显示,湘鄂、闽粤猕猴种群间的生物学距离相对较近,而太行山猕猴与前二种种群间的距离均较远。太行山     

亚洲疣猴与猕猴牙齿的比较

为了研究亚洲疣猴牙齿形态与功能适应性之间的关系,建立异速生长公式比较分析生活于同一大陆的猕猴。主成份分析用来分析来自异速生长公式的残差。结果表明:疣猴出乎意料地展示了比猕猴更小的门齿。导致此结果的可能原因是:疣猴与猕猴之间的食物差异性。但是,这种差异小于亚-非大陆种类。也就是说,在过去的500万年左右的时间里,生活于同一大陆的疣猴和猕猴已经产生了一些对环境和食性的趋同性。当每一个疣猴属分别与猕猴进行比较时,它们之间的差异性揭示了地理分布的差异。金丝猴(Rhinopithecus)和长尾叶猴(Semnopithecus)具有比其他疣猴发达的臼齿。欧氏距离的结果说明疣猴和猕猴牙齿的差异性揭示了它们在系统发育方面的关系。     

Role for dopamine in malonate-induced damage in vivo in striatum and in vitro in mesencephalic cultures

Defects in mitochondrial energy metabolism have been implicated in the pathology of several neurodegenerative disorders. In addition, the reactive metabolites generated from the metabolism and oxidation of the neurotransmitter dopamine (DA) are thought to contribute to the damage to neurons of the basal ganglia. We have previously demonstrated that infusions of the metabolic inhibitor malonate into the striata of mice or rats produce degeneration of DA nerve terminals. In the present studies, we demonstrate that an intrastriatal infusion of malonate induces a substantial increase in DA efflux in awake, behaving mice as measured by in vivo microdialysis. Furthermore, pretreatment of mice with tetrabenazine (TBZ) or the TBZ analogue Ro 4-1284 (Ro-4), compounds that reversibly inhibit the vesicular storage of DA, attenuates the malonate-induced DA efflux as well as the damage to DA nerve terminals. Consistent with these findings, the damage to both DA and GABA neurons in mesencephalic cultures by malonate exposure was attenuated by pretreatment with TBZ or Ro-4. Treatment with these compounds did not affect the formation of free radicals or the inhibition of oxidative phosphorylation resulting from malonate exposure alone. Our data suggest that DA plays an important role in the neurotoxicity produced by malonate. These findings provide direct evidence that inhibition of succinate dehydrogenase causes an increase in extracellular DA levels and indicate that bioenergetic defects may contribute to the pathogenesis of chronic neurodegenerative diseases through a mechanism involving DA.     

Scurvy in capybaras bred in captivity in Argentine

In order to determine if the absence of vitamin C in the diet of capybaras (Hydrochoerus hydrochaeris) causes scurvy, a group of seven young individuals were fed food pellets without ascorbic acid, while another group of eight individuals received the same food with 1 g of ascorbic acid per animal per day. Animals in the first group developed signs of scurvy-like gingivitis, breaking of the incisors and death of one animal. Clinical signs appeared between 25 and 104 days from the beginning of the trial in all individuals. Growth rates of individuals deprived of vitamin C was considerably less than those observed in the control group. Deficiency of ascorbic acid had a severe effect on reproduction of another population of captive capybaras. We found that the decrease in ascorbic acid content in the diet affected pregnancy, especially during the first stages. The results obtained suggest that it is necessary to supply a suitable quantity of vitamin C in the diet of this species in captivity.     

Changes in lactate dehydrogenase activity in chicken tissues in hyperthyreosis in ontogenesis

The lactate dehydrogenase activity in reactions of lactate oxidation and synthesis was studied in subfractions of the chicken brain, heart and liver at the embryonal, early postembryonal and adult stages of development after thyroxine administration. It has been shown that during embryogenesis thyroxine predominantly enhanced the rate of lactate oxidation in the mitochondrial tissues. A marked increase in the lactate synthesis was found in cytoplasm of the adult chicken tissues. Specificity of enzyme activity alterations was detected in the chicken brain during ontogenesis after thyroxine administration.     

SSTR5 ablation in islet results in alterations in glucose homeostasis in mice

Somatostatin (SST) peptide is a potent inhibitor of insulin secretion and its effect is mediated via somatostatin receptor 5 (SSTR5) in the endocrine pancreas. To investigate the consequences of gene ablation of SSTR5 in the mouse pancreas, we have generated a mouse model in which the SSTR5 gene was specifically knocked down in the pancreatic beta cells (betaSSTR5Kd) using the Cre-lox system. Immunohistochemistry analysis showed that SSTR5 gene expression was absent in beta cells at three months of age. At the time of gene ablation, betaSSTR5Kd mice demonstrated glucose intolerance with lack of insulin response and significantly reduced serum insulin levels. Insulin tolerance test demonstrated a significant increase of insulin clearance in vivo at the same age. In vitro studies demonstrated an absence of response to SST-28 stimulation in the betaSSTR5Kd mouse islet, which was associated with a significantly reduced SST expression level in betaSSTR5Kd mice pancreata. In addition, betaSSTR5Kd mice had significantly reduced serum glucose levels and increased serum insulin levels at 12 months of age. Glucose tolerance test at an older age also indicated a persistently higher insulin level in betaSSTR5Kd mice. Further studies of betaSSTR5Kd mice had revealed elevated serum C-peptide levels at both 3 and 12 months of age, suggesting that these mice are capable of producing and releasing insulin to the periphery. These results support the hypothesis that SSTR5 plays a pivotal role in the regulation of insulin secretion in the mouse pancreas.