在五年制临床医学专业系统解剖学理论课教学中采用PBL教学法,学期结束后收集学生的反馈评价表进行分析.结果表明,PBL教学法得到了大多数学生的认可,对于培养学生的自学能力、实践能力及交流合作能力具有积极影响,取得了比较好的课堂效果和教学效果,可以作为教学方法的补充应用于五年制临床医疗专业的系统解剖学教学中.

Pentylenetetrazole (PTZ), a γ-aminobutyric acid (GABA(A)) receptor antagonist, has been used extensively to induce seizures in animal models of epilepsy. The aim of the present study was to investigate the effects of PTZ on hippocampal astrocytes. Cells were incubated with 10, 20, or 40 mM PTZ for 24h and viability and apoptosis were examined using an MTT assay and Hoechst staining. The high concentration of PTZ (20 and 40 mM) resulted in a significant decrease in viability (MTT: 83.6 ± 7.8% and 69.3 ± 4.2%, respectively) (P<0.01), whereas the lower concentration of PTZ (10mM) did not induce cell apoptosis or reduce viability. When cells were treated with 10mM PTZ for 0, 0.5, 2, 4, 8, 12, or 24h, the level of brain-derived neurotrophic factor (BDNF), both protein and mRNA, was significantly reduced at 2 to 12h of culture (P<0.01), with maximal reduction detected at 8h; expression was restored to near control levels after 24h. Collectively, our results suggest that astrocytes may participate in epilepsy through a marked, but transient decrease in BDNF expression.

目的 观察糖尿病不同时期视网膜突触后致密物蛋白质95(PSD95)的蛋白表达水平以及视网膜突触超微结构的变化.方法 雄性3月龄SD大鼠56只,随机分为模型组和对照组,分别腹腔内注射链脲佐菌素(STZ)和0.1mol/L枸橼酸-枸橼酸钠缓冲液,于4、8、12周取眼球,入4％多聚甲醛后固定2h,冷冻切片厚20μm,采用免疫组织化学检测PSD95蛋白表达的变化,显微镜观察视网膜全层并摄片,图像分析;透射电镜观察视网膜突触并摄片.结果 PSD95蛋白表达在糖尿病第8周时开始升高,至12周时升高具有显著意义;视网膜内丛状层的突触结构中的突触间隙增大,突触后致密物厚度变薄,突触活性区长度变长.结论 PSD95的蛋白表达水平以及视网膜突触超微结构的改变可能与糖尿病视网膜病变的发展有关.

目的:探讨核因子-κB(NF-κB)在糖尿病(DM)性阴茎勃起功能障碍(ED)中的作用.方法:注射链脲佐菌素建立糖尿病大鼠模型,分别在注射8周和12周后观察阴茎勃起次数、取大鼠阴茎和脊髓第2～4骶椎节段,免疫印迹法检测阴茎核因子-κB(NF-κB)蛋白量的变化,ABC免疫组织化学方法检测脊髓第2～4骶髓节段NF-κB的分布和表达.结果:糖尿病大鼠的阴茎勃起次数明显低于对照组,并随病程延长降低;免疫印迹法结果显示,糖尿病组阴茎NF-κB蛋白量明显升高,12周糖尿病组与8周糖尿病组比较升高明显;NF-κB在脊髓主要分布于脊髓前角的大型运动神经元,12周糖尿病组分别与对照组和8周糖尿病组比较核转移率升高.结论:糖尿病大鼠阴茎NF-κB蛋白量的升高、脊髓第2～4骶髓节段前角NF-κB表达的升高及活性的增强可能参与了糖尿病性ED的形成.

Objective:The purpose of this study is to observe the changes of expressions of N-methyl-D-aspartate receptor (NMDAR) subunits NR1,NR2A and NR2B gene in diabetic rat retina. Methods:Diabetes mellitus (DM) was induced by intraperitoneal injection of streptozotocin in Sprague-Dawley rats. After 4,8,and 16 weeks,the eyeballs were removed for examination. Expression of NR1,NR2A,NR2B in rat retina was examined by in situ hybridization and immunohistochemistory. The staining results were analyzed by RS IMAGE software. Results:In DM group,the expression of NR1,NR2A,NR2B in rat retina was significantly increased in comparison with that in the control group. Conclusion:The upper expression of NR1,NR2A,NR2B in streptozotocin-induced diabetic rat retina is one of the reasons of diabetic retinopathy.

Objective To investigate lipopolysaccharide (LPS) induced acute cerebral inflammatory damage and the therapeutic effect of ginkgolide B (BN52021). Methods Thirty Sprague-Dawley rats were randomly divided into 3 groups ( n = 10 for each group): Control group, Model group and Treatment group (treated with BN52021). LPS were injected into the fourth ventricle of rat to make a neuroinflammatory murine model. Morris water maze was used to detect the learning and memory ability of rats; changes of synapse number and subcellular ultrastructures were observed under a transmission electron microscope; OX-42 positive microglia in the brain was detected by immunohistochemical method. Results The average escape latency in the Treatment group were significantly shortened than that in the Model group; and the percentage of swimming distance traveled in platform quadrant accounting for total distance increased markedly. The rough endoplasmic reticulum and polyribosomes in the Treatment group were more than that in the Model group, but the number of synapses seemed to have no obvious change. The number of OX-42 positive microglia in the Treatment group decreased markedly than that in the Model group, and the grey density of OX-42-positive cells increased significantly. Conclusion LPS can induce inflammatory damages to the brain, but the damage could be antagonized by BN52021. Platelet activating factor receptor antagonist may offer an effective therapy for neurodegeneration diseases.

目的:探讨血小板活化因子受体拮抗剂银杏内脂B(BN52021)抑制细菌脂多糖诱导的脑内炎症反应的神经保护作用.方法: SD大鼠随机分为对照组,模型组和治疗组.Morris水迷宫检测学习和记忆功能,免疫组织化学法检测脑内GFAP阳性星形胶质细胞、OX-42阳性小胶质细胞在颞叶皮质、海马及基底核中的表达.结果:脂多糖(LPS)第4脑室注射使模型动物学习和记忆功能减退,模型组GFAP阳性星形胶质细胞和OX-42阳性小胶质细胞在颞叶皮质、海马及基底核中细胞数量明显增加.BN52021治疗后,对照组和治疗组水迷宫逃避潜伏期、平台象限游泳距离百分比与模型组均有显著性差异;GFAP阳性星形胶质细胞和OX-42阳性小胶质细胞在颞叶皮质、海马及基底核中细胞数量明显减少和阳性染色灰度上升.结论:血小板活化因子受体拮抗剂可抑制LPS诱导的脑内神经炎症,对阿尔茨海默病和艾滋病相关痴呆等以中枢炎症为病理特征的神经退行性变均有治疗作用.

目的:为临床骨延长术及运动医学提供理论依据.方法:选用新西兰幼兔在股骨远端骺软骨两侧安装外固定支架和力传感器并施加不同张力,观察组织细胞形态变化.另用幼兔新鲜离体股骨,作力学性质测试.结果:4 周后张应力使兔股骨增长,骺软骨厚度增加,增殖层和肥大层细胞增生,粗面内质网和毛细血管增生.离体兔股骨随牵张力的增大或间隙时间的增加塑性变形亦增大.结论:在体以较小的张应力能使骺软骨细胞活性增强,实现肢体增长而不影响其强度.延长维持张应力的时间可以增大肢体的生长量.