近年来,人体解剖学学科每年均有高学历青年人加入教师队伍.由于目前存在发表论文和申请课题的压力,多数研究生学位课题选择分子层面的研究内容,与解剖学教学内容吻合度较低.这直接导致了新教师在任教之初,往往存在解剖学理论知识、操作技能薄弱,缺乏教学经验,育人意识及能力欠缺,课堂难以驾驭等等问题,甚或产生迷茫、无处着手、不知所措等畏难情绪.如何能尽快进入教师角色、胜任教师工作,是每个初为人师的新教师必须面对的问题.

临床医学不断发展,大量诊疗方法不断更新以及各种现代化的教学手段层出不穷,在教学内容和教学方式等诸多方面对人体解剖学的教学提出严峻挑战.文章就解剖学课程特点,结合教学过程中的体会,在如何激发学生学习热情和兴趣以及充分调动教师积极性、提高教学水平等方面提出建议和设想,以探索更适应时代发展的解剖学教学方法.

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.

Objective To study of the hypoxic tolerance effect of compound rhodiola mixure in Mice.Methods The effects of compound rhodiola mixure on hypoxia tolerance in mice were measured through three kinds of experiments: the closed normobaric hypoxia mice ex periment,NaNO2poisoning-hypoxia experiment and acute cerebral ischemic-hypoxico experiment.Forty mice were used in each experi ment,and mice were randomly divided 4 groups: bland control group;low dose group,middle dose group and high dose group,and com pared the average survival time of each group.Results Compared with blank control group,three dose of compound rhodiola mixure could obviously improve the survival time of mice with the closed normobaric hypoxia and NaNO2 poisoning-hypoxia experiment(P 0.05 orP0.01).Low dose of compound rhodiola mixure could not obviously improve the survival time of mice with acute cerebral isch emic(P0.05);but middle and high dose groups could obviously improve the survival time of mice with acute cerebral ischemic(P 0.05).Conclusion Compound rhodiola mixure can effectively improve the ability of hypoxia tolerance of mice.

Objective To investigate the neurotoxicity of β-amyloid protein (Aβ) in vivo and its effects on rats' learning and memory ability. Methods The aggregated Aβ(25-35) was injected bilaterally into entorbi- hal cortex(EC) of rats. Control rats were injected with saline water. All rats were subjected to Y-maze task at 7 d and 8d after operation. After behavioral testing, the rats were sacrificed. The neurpathological changes of EC were examined by Nissl staining, HE staining and Congo Red staining. Results The cumulative number of electric shocks in acquisition test and retention test of the saline group was 19.17±5.58 and 10.56±1.72 31 respectively. The corresponding number in Aβ-treated rats was 31.13±6.98 and 18.47±4.64, and significantly increased compared with control group (P<0.05). A Congo Red-positive deposit of aggregated material was found at Aβ injection site accompanied by neurons loss and gliacyte reaction. The damaged area of Aβ-treated rats was significandy greater than that of control rats and was negatively correlated with the learning ability (r=-0.241, P < 0.05). Conclusion Bilateral injection of aggregated Aβ into EC induces behavioral deficits and amyloid pathology similar to those observed in early phases of AD. These results show definite neurotoxicity of Aβ in vivo. Therefore, injection of Aβ into EC constitutes a promising animal model for investigating selective aspects of AD and for screening drug candidates designed against Aβ pathology.

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.

BACKGROUND: As a result of immature brain of children and their imperfect blood brain barrier, improper clinical treatment would affect growth and development of children. It is fully important to perform further investigation on immature brain injury induced neurodegeneration.OBJECTIVE: To observe the ultramicrostructure of neurons in homolateral parietal cortex and hippocampus in newborn 7-day SD rat with contusion of parietal cortex.DESIGN: Completely randomized controlled trial.SETTING: Laboratories of Nerve Morphology and Cytobiology, Medical College of Shanghai Jiaotong University; Electron Microscope Room of Institute for Physiology, Chinese Academy of Science.MATERIALS: The experiment was performed in Teaching and Research Section of Anatomy, Laboratories of Nerve Morphology and Cytobiology ofShanghai Second Medical University (Medical College of Shanghai Jiaotong University; Electron Microscope Room of Institute for Physiology of Chinese Academy of Science from October 2002 to June 2003. A total of 19newborn 7-day SD rats were randomly divided into experimental group, operation control group and normal control group with 15, 2 and 2 in each group respectively.METHODS: In experimental group, free-fall device for brain injury was used for establishing model of contusion of parietal cortex in newborn 7-day SD rat. Anesthesia and scalp incision were conducted, without using free-fall device in operation control group. But above procedures were not carried out in normal control group. The changes of ultramicrostructure were observed under transmission electron microscope after routine treatment of electron microscopic samples.MAIN OUTCOME MEASURES: Ultramicrostructure of neurons in homolateral parietal cortex and hippocampus.RESULTS: All the 19 rats entered results analysis. ① There were two sorts of morphological changes in neurons in experimental group. One was evident swelling of dendrites and bodies of neurons, accompanied with the changes of organelles. In the early stage, expansion of endoplasmic reticulum cisterna could be observed and mitochondria became compact and concentrated. Then, vacuolization of endoplasmic reticulum, progressive swelling and vacuolization of mitochondria, dissociation of polysomes from rough endoplasmic reticulum and scattering of them in cytoplasm could be seen. Changes of nucleolus presented after significant changes of cytoplasm. Nuclear chromatin clustered together under karyotheca and arranged as clockface, which were some masses with irregular contours gathering to the center. Axons were almost normal. The other was concentration of cytoplasm and nucleolus with vacuolizations of unequal size in cytoplasm. ②There was no abnormal change in neurons in homolateral parietal cortex and hippocampus both in operation control group and normal control group.CONCLUSION: Swelling of brain cell and concentration of cytoplasm and nucleolus after brain injury play important roles in brain injury-induced neurodegeneration of immature rats.

Objective To present a new neurovascular island flap for fingertip reconstruction. Methods Based on the transverse palmar branch of the digital artery, this flap was designed on the volar side of a digit and reversed to repair the fingertip defects. Results 12 fingers in 11 patients were reconstructed using this flap. Of them, 11 flaps survived and one necrosed. The contour of the reconstructed fingers looked well. Conclusion This new neurovascular island flap provides excellent padding and sensation for fingertip reconstruction. The technique is simple.;

目的:从形态学角度探讨新生鼠脑外伤后神经元变性的机理.方法:建立新生7 d大鼠顶叶皮质脑挫伤动物模型,在脑外伤后2 h、6 h、24 h对同侧顶叶皮质和海马神经细胞进行电镜观察.结果:神经元有两类改变:(1)神经元树突和胞体呈巨大膨胀.早期内质网池扩大,线粒体致密和浓缩;此后内质网空泡化,线粒体进行性肿胀和空泡化,多聚核糖体从粗面内质网上解离,并散在于胞浆.核的改变出现于胞浆改变明显之后.核染色质由簇状集聚于核膜下呈钟面排列到向中央积聚成轮廓不规则的团块.轴突基本正常.(2)胞浆和胞核均浓缩,胞浆中有大小不等的空泡.结论:内源性兴奋毒对未成熟脑创伤性神经元变性起十分重要的作用.

目的:研究隔-下托投射定位关系.材料与方法:1%WGA-HRP与10%HRP混合液用微量注射器注射入大鼠背侧下托,存活36 h,取材.海马切片用H2O2-DAB显色确定注射点位置,隔区切片用TMB显色显示逆行标记神经元.结果:HRP逆行标记细胞主要出现于同侧内侧隔核(MS)和斜带核(NDBV),Bregma点0.70 mm～0.48mm的平面上达到高峰.对侧MS和NDBV仅见少量逆行标记神经元.结论:下托接受同侧MS-NDBV大量神经元投射,其中背海马下托前部与MS-NDBV的中部存在明显定位关系.

目的:探讨外源性谷氨酸对新生鼠脑细胞的兴奋毒性作用.方法:新生7天SD大鼠,背部皮下注射单钠谷氨酸(MSG)2 mg/g,在2 h、6～8 h、24～28 h分别光镜和电镜观察脑细胞的形态改变.结果:光镜下,2 h未见明显异常,此后可见多处脑细胞肿胀,进而细胞固缩.电镜着重观察海马神经元,变化-为神经元胞体和树突巨大膨胀,伴随着内质网膜的空泡化及线粒体由最早期的浓缩到巨大膨胀,轴突基本正常,核染色质由簇状集聚于核膜下呈钟面排列到向中央积聚成轮廓不规则的团块;变化二为胞浆和胞核均浓缩,胞奖中有大小不等的空泡.结论:外源性谷氨酸能引起未成熟脑细胞的死亡,为某些食品添加剂对儿童脑细胞的影响的相关研究提供一定的形态学基础.

采用盐酸和胶原酶消化动脉外膜的技术,对正常的脑动脉、蛛网膜下腔出血后痉挛的脑动脉及经前列腺素F2α(prostaglandin F2α,PGFZa)处理的脑动脉平滑肌细胞构筑进行研究.结果显示:正常平滑肌细胞是梭形的,沿着血管长轴环行分布,细胞间通过突起相连,肌细胞外膜面通常是光滑的;痉挛的脑动脉和经PGF2α处理的脑动脉平滑肌外膜面均出现非常相似的膜皱折和卷曲,肌间隙增宽.透射电镜显示急性痉挛管壁病理变化轻微;迟发性痉挛出现明显病理性超微结构改变.实验结果提示急性脑血管痉挛是由平滑肌收缩引起,病理变化轻微;迟发性脑血管痉挛是血管持久收缩伴病理性超微结构改变.

本工作报道了血管内照射(650nm,5mW,cw)对家兔尾核、下丘脑DA和NE的影响,发现DA在尾核和下丘脑中均有下降现象,但均P＞0.05.在大鼠光照"扶突"穴中亦发现DA在脑干和尾核中,亦有下降倾向,NE有脑干和尾核中则有上升倾向.5-HT则均下降,但亦均未达显著性差异,(P＞0.05).另发现在人体血管内照射时,血液中NO.含量随照射次数增加而递减倾向.这些变化作者认为与光照的光化学反应引发的神经体液性调控有关.在本工作中还发现光照后神经未梢中的线粒体有肿胀现象.