多媒体网络应用于人体解剖学教学中的体会

网络教育正以一种势不可挡的趋势伴随着人类发展，其基本特征是集多种媒体功能于一身，将图、文、声、画、视频等诸多信息媒体有机地进行组合、显示共同完成新的教育技术条件下的视听教学。将这种教学理念引入到人体解剖学教学中。充分利用多媒体技术和网络丰富的信息资源，真正实现资源共享，将对医学教学大有裨益。文章主要探讨利用多媒体技术和网络资源改进医学人体解剖学教学的体会。     

高渗液对体外培养星形胶质细胞中水通道蛋白4 mRNA表达的影响

目的　研究体外培养星形胶质细胞高渗状态下水通道蛋白 4 (AQP4 ) m RNA表达的变化特点及其所起的作用。方法　取生后 2 d的新生 Wistar大鼠大脑皮质进行星形胶质细胞纯培养 ,分别用不同渗透压的高渗培养液作用于星形胶质细胞 ,建立星形胶质细胞对高渗反应的实验模型 ;采用原位杂交、乳酸脱氢酶(L DH)活性测定及图像分析等方法 ,研究体外培养星形胶质细胞对高渗液的反应和 AQP4 m RNA的表达规律。结果　 32 0、333和 345 m mol/ L的高渗培养液作用于星形胶质细胞 3、6、12和 2 4 h后 ,L DH活性测定的吸光度 A值在各时间点均显著高于对照组 (P均 <0 .0 5 ) ;原位杂交分析表明 ,AQP4 m RNA表达明显增高 ,与正常组相比有显著意义 ,尤以高渗液作用 12 h时最明显 ,而且与作用时间及渗透压相关。结论　在高渗状态下 ,细胞活性明显下降 ,AQP4 m RNA表达增强。 AQP4可能在高渗性脱水的早期起重要的调节作用。     

脑缺血再灌注后AQP4 mRNA表达及其与BBB通透性改变的关系

近年来的研究发现，水通道蛋白-4(aquaporin-4，AQP4)与脑水肿的发生有着密切关系。但关于脑缺血再灌注(cerebral ischemic reperfusion，CIR)后AQP4mRNA表达变化及其与血脑屏障(blood-brain barrier，BBB)通透性变化是否有关，目前尚未见报道。故我们用CIR大鼠模型，探讨AQP4mRNA表达和BBB通透性改变之间的关系，进一步证明两者与CIR后脑水肿的形成相关。     

留学生系统解剖学教学的体会

为了提高外国留学生解剖学课程的教学效果，根据教学过程的组织、实施等方面进行了探讨。就了解学生的特点、课前准备、讲课方法及提高教师素质等几方面讨论如何提高留学生的教学质量，以供其他基础课及临床课的教师参考。     

大鼠脑出血后血肿周围Ca2+浓度的变化与磷酸化CaMKⅡ表达的实验研究

目的 探讨脑出血后血肿周围脑组织钙离子浓度和磷酸化的钙调蛋白依赖性蛋白激酶Ⅱ（P-aMKⅡ)表达的变化及其相关联系。方法 采用胶原酶注入尾状核建立大鼠脑出血模型，干湿重法测量脑组织含水量，Fura-2／AM荧光法测定血肿周围Ca^2 浓度，免疫组化方法检测P-CaMKⅡ的表达。结果 与正常组相比，脑出血后6h，Ca^2 浓度、脑含水量和P-CaMKⅡ的表达均开始上调，第3天达高峰，此后逐渐回落，持续1周仍高于正常水平；Ca^2 浓度的变化与P-CaMKⅡ的表达强度呈明显正相关。结论 脑出血后细胞内钙超载，导致CaMKⅡ磷酸化作用增强，它们共同参与了出血性脑水肿的损伤过程。     

脑红蛋白在内毒素脑损伤大鼠模型中的表达变化

Objective To investigate the expression of neuroglobin(Ngb) in frontal cortex, cere-brospinal fluid (CSF) and serum in rats with brain injury induced by LPS and to elucidate its significance. Methods Seventy adult Sprague-Dawley rats were randomly divided into LPS (n = 60, with injection of 0.1 mg/kg LPS into cistern) and control (C, n =10, with injection of equal volume of isotonic saline into cistern) groups, with 10 rats in each group. The plasma, CSF as well as frontal cortex from sacrificed rats were collected in LPS group at 3, 6, 12, 24, 48, 72 post injection hour (PIH), with 10 rats at each time point. The protein expression of Ngb was measured by enzyme-linked immunosorbent assay(ELISA) and Western blot. Expression of Ngb in frontal cortex was determined by SP. Water content of frontal cortex was assessed by drying method. The correlation among Ngb contents in serum, CSF, frontal cortex and water con-tent of frontal cortex was analyzed with multiple comparison. Results Ngb expression ( by ELISA) : Ngb expression of frontal cortex, CSF, and serum in LPS group was higher than that in C group at each time point, and it peaked at 48 PBH (35.4±3.9, 22.7±3.1, 14.4±2.8 ng/mL, respectively, P <0.01). Ngb ex-pression ( by Western blot) : Ngb protein with relative molecular mass of 17×103 was observed in each group. Ngb expression detected by Western blot was similar to that detected by ELISA. Brain water content was significantly greater in LPS group than that of C group at 6-72 PIH ( P<0.01) , and it peaked at 48 PBH ( 83.3±1.9) %. Ngb contents in serum, CSF, frontal cortex, and water content of frontal cortex were positively correlated with muhipie comparison (γ=0.631-0.719, P<0.01). Conclusions Up-regu-lation of Ngb expression in brain injury induced by LPS is correlated with duration after challenge of LPS.     

两种脑出血动物模型的AQP4表达与磁共振成像的比较研究

目的比较两种脑出血(ICH)动物模型磁共振成像(MRI)的差异,并对其分子机制进行探讨。方法将胶原酶和自体血注入大鼠尾状核建立脑出血模型,分别于术后6h、12h、1d、2d、3d和7d进行磁共振成像扫描,观察两组脑出血模型血肿体积的大小;运用干湿重法、伊文思蓝(EB)测定法和免疫印迹分别检测两组脑出血模型的脑含水量(BWC)、血脑屏障(BBB)通透性和AQP4的表达变化。结果胶原酶模型组的血肿体积在脑出血后1d达到最大并持续至3d,自体血组的血肿体积在12h达到最大;胶原酶模型组的BWC在1d达到高峰并持续至3d,而自体血组BWC在2d逐渐降低;胶原酶模型组的EB含量在12h达到高峰并持续至2d,而自体血组EB含量在1d逐渐下降;两组模型的AQP4表达量在6h开始升高,1d达到高峰,2d逐渐降低。两组模型比较具有统计学差异(P<0.05)。结论胶原酶对BBB和细胞外基质的破坏以及AQP4的表达变化是两组脑出血模型血肿体积出现差异的重要原因。     

兔脊髓压迫器的研制及其评价

目的建立一种新型、可靠的脊髓压迫动物模型,为探索脊髓受压后的分子机制及临床治疗的研究奠定基础。方法根据兔椎骨及脊柱的形态特点,设计一种新型的兔脊髓压迫器,并用以制作兔脊髓急性压迫模型。运用改良Tarlov法、TTC、HE及Nissl染色验证该模型的可靠性。结果脊髓受压后,兔后肢的肌力减退、行动迟缓;TTC结果显示压迫段及其相邻节段均有不同程度的缺血,压迫后段还存在不同程度的出血及组织坏死;脊髓受压后出现组织水肿,神经元肿胀、核固缩,尼氏体减少甚至消失等病理改变。结论①用自行设计的压迫器制作兔脊髓压迫模型具有方法简便、科学、重复性强等特点;②本实验制作的兔脊髓压迫模型是用于研究脊髓压迫性损伤病理生理机制及临床治疗的理想模型。     

脑红蛋白在内毒素脑损伤大鼠模型中的表达变化

Objective To investigate the expression of neuroglobin(Ngb) in frontal cortex, cere-brospinal fluid (CSF) and serum in rats with brain injury induced by LPS and to elucidate its significance. Methods Seventy adult Sprague-Dawley rats were randomly divided into LPS (n = 60, with injection of 0.1 mg/kg LPS into cistern) and control (C, n =10, with injection of equal volume of isotonic saline into cistern) groups, with 10 rats in each group. The plasma, CSF as well as frontal cortex from sacrificed rats were collected in LPS group at 3, 6, 12, 24, 48, 72 post injection hour (PIH), with 10 rats at each time point. The protein expression of Ngb was measured by enzyme-linked immunosorbent assay(ELISA) and Western blot. Expression of Ngb in frontal cortex was determined by SP. Water content of frontal cortex was assessed by drying method. The correlation among Ngb contents in serum, CSF, frontal cortex and water con-tent of frontal cortex was analyzed with multiple comparison. Results Ngb expression ( by ELISA) : Ngb expression of frontal cortex, CSF, and serum in LPS group was higher than that in C group at each time point, and it peaked at 48 PBH (35.4±3.9, 22.7±3.1, 14.4±2.8 ng/mL, respectively, P <0.01). Ngb ex-pression ( by Western blot) : Ngb protein with relative molecular mass of 17×103 was observed in each group. Ngb expression detected by Western blot was similar to that detected by ELISA. Brain water content was significantly greater in LPS group than that of C group at 6-72 PIH ( P<0.01) , and it peaked at 48 PBH ( 83.3±1.9) %. Ngb contents in serum, CSF, frontal cortex, and water content of frontal cortex were positively correlated with muhipie comparison (γ=0.631-0.719, P<0.01). Conclusions Up-regu-lation of Ngb expression in brain injury induced by LPS is correlated with duration after challenge of LPS.     

大鼠脊髓压迫性损伤后脱髓鞘病变及MBP、Id2的表达变化

目的 分析脊髓压迫性损伤(compressed spinal cord injury,CSCI)后脱髓鞘病变与髓鞘碱性蛋白(myelin basic protein,MBP)、DNA结合抑制物2(inhibitor of DNA binding2,Id2)的表达变化之间的关系,以探讨CSCI脱髓鞘病变机制.方法 采用自行设计的方法制作SD大鼠CSCI模型,通过锇酸染色检测CSCI后1、3、7d有髓神经纤维变化;运用免疫荧光双标和免疫印迹(Westem blot)检测MBP及Id2的表达变化.结果 CSCI后出现脱髓鞘病变,并随着压迫时间延长,髓鞘逐渐发生水肿、变性、崩解;脊髓损伤后MBP表达下调,其表达趋势与脱髓鞘溃变的严重程度一致;CSCI后,Id2广泛分布于白质,随着压迫时间延长,其表达逐渐上调.结论 Id2表达上调,并负向调控MBP基因启动子的活性,使MBP的表达下降,是CSCI后神经纤维脱髓鞘病变的机制之一.