N,O-羧甲基壳聚糖对小白鼠精子畸形的影响

目的:观察能明显促进禽类等动物的生长发育,改善肉质的新型饲料添加剂N,O-羧甲基壳聚糖对昆明种小白鼠精子畸形的影响,分析其应用在畜牧生产中的安全性。方法:实验于2005-06-22/2005-08-06于南京农业大学动物医学院药理组实验室完成。挑选体质量25～28g的小鼠50只,以随机数字表法分为生理盐水组、环磷酰胺组、N,O-羧甲基壳聚糖(南京龙源天然多酚合成厂提供,商品名为毕罗喜,质量浓度为105g/kg)2,4,8g/kg剂量组,每组10只。N,O-羧甲基壳聚糖2,4,8g/kg剂量组分别给予相应剂量的N,O-羧甲基壳聚糖,溶于1mL生理盐水,2,4g/kg剂量1次灌服,8g/kg剂量分2次灌服,每次间隔约3h;生理盐水组给予生理盐水1mL;环磷酰胺组给予环磷酰胺0.04g/kg,溶于1mL生理盐水。给药前禁食10h,不禁水。连续灌胃5d,给药后30d麻醉下处死,取两侧附睾按Wyrobek方法涂片,观察小白鼠精子畸形状况。评估标准参照农业部兽药评审委员会办公室编写的兽药试验技术规范汇编(2001年)。评估内容参照沈建忠主编的动物毒理学(中国农业出版社,2002年),包括各种畸形的精子形态:不定形、胖头、香蕉头、无钩、双头(多头)和双尾(多尾)等,及其分类计数。每组随机选取5只小鼠,计算总畸形率。精子畸形率(%)=畸形精子总数/检查精子总数×100。结果:最终25只小鼠进入结果分析,每组5只。①环磷酰胺组的精子畸形率远高于生理盐水组和N,O-羧甲基壳聚糖2,4,8g/kg剂量组(6.10%,2.48%,2.46%,2.64%,2.78%,P<0.01);N,O-羧甲基壳聚糖2,4,8g/kg剂量组与生理盐水组比较,差异无显著性意义(P>0.05),且各剂量组之间差异也没有显著性意义(P>0.05)。②各组精子畸形主要表现为头部或尾部异常。以无定形和胖头居多,占35.48%(292/823)和29.28%(241/823);其次是无钩形及香焦形多见,占19.68%(162/823)和13.49%(111/823);偶尔可见双头双尾形,只占2.07%。结论:N,O-羧甲基壳聚糖精子畸形试验结果呈阴性,说明其对雄性生殖细胞没有明显的遗传毒性。     

放松训练配合理疗对高正常血压患者血压的影响

目的　随着人们对高血压病的深入研究 ,越来越认识到血压增高对人体的危害。血压越高 ,持续时间越长 ,心、脑、肾等脏器损害出现的时间越早 ,程度越重。因此 ,早期发现和治疗高血压病日渐重要。本文通过对住院疗养的高正常血压患者 30例 ,经放松训练、松脂粉矿泉浸浴、高压电子的非药物治疗后 ,患者收缩压及舒张压均有下降 ,(P<0 .0 1)。为预防高血压病的发生 ,控制血压水平提供一条简便、易行的治疗方法。     

三种方法治疗颈源性头痛的疗效比较

目的:观察比较仅行手法治疗、仅行双侧星状神经节半导体激光照射及综合治疗方法对颈源性头痛的疗效。方法:选择2002-05/2005-03在解放军总医院门诊的颈源性头痛患者58例。各组患者在年龄、性别、病程及疼痛评分方面均差异不显著。随机分为3组:①手法治疗组19例,按压痛点轻重程度行颈椎定点伸引手法,每隔四五天一次,一般两三次。②激光照射组18例,行双侧星状神经节半导体激光照射,1次/d,单侧9min(一侧一侧的照射),5次为1个疗程,所有患者均仅治疗1个疗程。③综合治疗组21例,先用激光照射5次,再用手法治疗。根据目测类比评分法(0分表示无痛,10分表示难以忍受的最剧烈的疼痛)进行疼痛评价。对3组患者进行治疗前、治疗后及治疗后1个月的疼痛评分。结果:58例患者均进入结果分析。①治疗后即刻进行比较:综合治疗组比手法治疗组、激光照射组显著降低(0.83±0.07,2.74±0.14,2.93±0.19,t=17.88,15.55,P<0.05)。②治疗1个月后进行比较:综合治疗组比手法治疗组、激光照射组显著降低(0.91±0.10,3.18±0.16,3.85±0.18,t=21.91,227.16,P<0.05)。结论:综合治疗组比仅行手法治疗、仅行双侧星状神经节半导体激光照射组有效。     

先天性输尿管异常疾病的超声诊断

本文报告121例先天性输尿管异常疾病的超声诊断结果，经与手术和病理结果对比其病因诊断符合率92．6％。结果表明，超声能为临床诊治该类疾病提供可靠的依据，其中对某些疾病，超声检查具有明显的优越性和独特的诊断价值。     

ATP binding cassette G8 T400K polymorphism may affect the risk of gallstone disease among Chinese males

BACKGROUND: Supersaturation of bile with cholesterol is a primary step in the formation of cholesterol gallstones. ATP binding cassette (ABC) G5 and G8 play an important role in regulating sterol absorption and secretion. To investigate a possible association between transporter gene polymorphism and gallstone formation, we examined five common polymorphisms in the ABCG5 (Q604E) and ABCG8 (D19H, Y54C, T400K, A632V) genes in patients with gallstone disease (GS). METHODS: Study subjects included 287 patients with GS and 219 gallstone free controls (GSF). Polymorphisms were determined using PCR-RFLP analysis or the Taqman MGB assay. Plasma and biliary lipid levels were measured. RESULTS: 2 SNPs of ABCG8 gene (Y54C and T400K) showed strong linkage disequilibrium (D'=0.824, r2=0.579). Male carriers of the less frequent K allele of ABCG8 T400K had a 2.31-fold elevated risk [95% confidence interval (CI) 1.12 approximately 4.76, P=0.023] for gallstone disease compared to male with the common genotype after the adjustment for age, body mass index. Males with the K allele had lower plasma triglyceride (P=0.044) and biliary phospholipid (P=0.035) levels than TT homozygotes. No such association was found in female or other 4 SNPs. CONCLUSIONS: These findings indicate that the T400K polymorphism in ABCG8 may be associated with the incidence of gallstone disease in males.     

Cyclooxygenase‐2 in epilepsy

Epilepsy is one of the more prevalent neurologic disorders in the world, affecting approximately 50 million people of different ages and backgrounds. Epileptic seizures propagating through both lobes of the forebrain can have permanent debilitating effects on a patient's cognitive and somatosensory brain functions. Epilepsy, defined by the sporadic occurrence of spontaneous recurrent seizures (SRS), is often accompanied by inflammation of the brain. Pronounced increases in the expression of key inflammatory mediators (e.g., interleukin ‐1β [IL‐1β], tumor necrosis factor alpha [TNFα], cyclooxygenase‐2 [COX‐2], and C‐X‐C motif chemokine 10 [CXCL10]) after seizures may cause secondary damage in the brain and increase the likelihood of repetitive seizures. The COX‐2 enzyme is induced rapidly during seizures. The increased level of COX‐2 in specific areas of the epileptic brain can help to identify regions of seizure‐induced brain inflammation. A good deal of effort has been expended to determine whether COX‐2 inhibition might be neuroprotective and represent an adjunct therapeutic strategy along with antiepileptic drugs used to treat epilepsy. However, the effectiveness of COX‐2 inhibitors on epilepsy animal models appears to depend on the timing of administration. With all of the effort placed on making use of COX‐2 inhibitors as therapeutic agents for the treatment of epilepsy, inflammation, and neurodegenerative diseases there has yet to be a selective and potent COX‐2 inhibitor that has shown a clear therapeutic outcome with acceptable side effects.     

Region‐specific impairments in striatal synaptic transmission and impaired instrumental learning in a mouse model of Angelman syndrome

Angelman syndrome (AS) is a neurodevelopmental disorder characterized by mental retardation and impaired speech. Because patients with this disorder often exhibit motor tremor and stereotypical behaviors, which are associated with basal ganglia pathology, we hypothesized that AS is accompanied by abnormal functioning of the striatum, the input nucleus of the basal ganglia. Using mutant mice with maternal deficiency of AS E6‐AP ubiquitin protein ligase Ube3a (Ube3a^m?/p+), we assessed the effects of Ube3a deficiency on instrumental conditioning, a striatum‐dependent task. We used whole‐cell patch‐clamp recording to measure glutamatergic transmission in the dorsomedial striatum (DMS) and dorsolateral striatum (DLS). Ube3a^m?/p+ mice were severely impaired in initial acquisition of lever pressing. Whereas the lever pressing of wild‐type controls was reduced by outcome devaluation and instrumental contingency reversal, the performance of Ube3a^m?/p+ mice were more habitual, impervious to changes in outcome value and action–outcome contingency. In the DMS, but not the DLS, Ube3a^m?/p+ mice showed reduced amplitude and frequency of miniature excitatory postsynaptic currents. These results show for the first time a selective deficit in instrumental conditioning in the Ube3a deficient mouse model, and suggest a specific impairment in glutmatergic transmission in the associative corticostriatal circuit in AS.     

Nesfatin-1 Decreases Excitability of Dopaminergic Neurons in the Substantia Nigra

Nesfatin-1, a newly discovered satiety molecule which reduces feeding behavior, has been recognized as a unique regulatory neuropeptide with its multiple roles, both central and peripheral. However, whether it had neuronal modulation effect on dopaminergic neurons is largely unknown. In the present study, using whole-cell patch clamp under current-clamp mode, we investigate the effects of nesfatin-1 on the electrical activity of rat nigral dopaminergic neurons. Nesfatin-1 could produce a resting membrane potential hyperpolarization on the majority of dopaminergic neurons tested. The spike frequency decreased by 23.13?±?5.93 and 43.20?±?5.56 % in 5-nM and 10-nM nesfatin-1 groups, respectively. These effects persisted in the presence of ionotropic glutamate and GABA receptor antagonists. Our study suggests that nesfatin-1 postsynaptically inhibits the electrical activity of nigral dopaminergic neurons.