医学教育学硕士研究生教育培养方案的研究

开展医学教育学硕士研究生培养方案的研究工作将有助于培养具有专业知识和能力的医学教育学人才,以进一步促进医学教育学专业化与持续性发展。在教育研究实践中,在人才培养目标的指导下,围绕着学生思想政治素质、科学研究能力、理论实践知识学习应用方面建立了较为完善的理论课程体系;并对研究生培养中的实践课程进行了合理设计,对效果的评价方式做了科学合理的规划。通过研究,使医学教育学硕士研究生的培养工作有章可循,对教育培养工作质量提升起到促进作用。     

维兰特罗/乌美溴铵联合罗氟司特对COPD患者肺功能和mMRC评分的影响

目的研究维兰特罗/乌美溴铵联合罗氟司特对慢性阻塞性肺病(COPD)患者肺功能和改良英国医学研究组理事会呼吸困难指数(mMRC) 评分的影响。方法COPD患者120例随机分为观察组以及对照组各60例,均采用维兰特罗/乌美溴铵进行治疗,观察组在此基础上联合采用罗氟司特进行治疗,比较两组治疗效果、肺功能、mMRC评分、免疫功能及不良反应。结果观察组治疗总有效率高于对照组(P＜0.05);治疗后两组用力呼气量(FEV)、第1秒用力呼气量(FEV1)、第1秒用力呼气量占用力肺活量百分率(FEV1%)升高,且观察组高于对照组(P＜0.05);观察组mMRC评分低于对照组(P＜0.05);治疗后两组CD3＋、CD4＋、CD8＋、CD4＋/CD8＋水平显著升高,且观察组高于对照组(P＜0.05)。结论维兰特罗/乌美溴铵联合罗氟司特治疗COPD患者其肺功能以及mMRC评分显著改善,建议临床推广。     

基底核区高血压脑出血不同治疗方式预后的比较

目的:比较基底核区高血压脑出血不同治疗方式的预后。方法:回顾性分析基底核区脑出血患者132例,根据治疗方式分为手术组94例(外侧裂-岛叶入路亚组42例和颞中回入路亚组52例)和保守组38例,随访6月,采用格拉斯哥预后评分(GOS)评估疗效。结果:保守组死亡率55.26%,手术组死亡率26.60%(外侧裂-岛叶入路亚组为23.81%,颞中回入路亚组为28.85%),与保守组比较差异有统计学意义(P=0.025,P=0.030)。手术组中GOS 5分0例,4分33例(35.11%),3分22例(23.40%),2分14例(14.89%),1分25例(26.60%);保守组中GOS 5分0例,4分5例(13.16%),3分5例(13.16%),2分7例(18.42%),1分21例(55.26%);2组4分比例差异有统计学意义(P=0.011)。结论:高血压脑出血患者手术治疗死亡率低,术后神经功能恢复好。     

医学生终身学习能力与培养模式研究

医学生终身学习能力培养,是提升医学生学习成绩的重要工作,也是医科高校人才培养工作的重要项目。立足医学生入学后在思想观念、价值观念、心理状态和职业认知等方面的新变化,以及医学生终身学习能力培养新要求,建立包括培养理念、学习观念、学习方法和重要途径等要素在内的系统性、应用性医学生终身学习能力培养模式,不仅是提高大学生人才培养质量的重要措施,更是对创新型人才储备、学习型社会建设和区域医学教育均衡发展有重要应用价值。     

Caspase-3、Bcl-2在甲状腺功能减退症大鼠心肌组织中的表达及与甲状腺功能关系的研究

目的观察甲状腺功能减退症大鼠心肌损伤时Caspase-3和Bcl-2在心肌细胞中的表达,探讨甲减心肌损伤的发生机制以及与甲状腺功能的关系。方法用丙基硫氧嘧啶(PTU)连续灌胃制作甲状腺功能减退症大鼠模型。分别动态观察对照组、甲减组和干预组(给予左甲状腺素钠和停止给予PTU进行干预治疗)大鼠的心肌病理改变及损伤情况,并同时应用免疫组化技术及末端脱氧核苷酸转移酶介导的缺口末端标记法检测Caspase-3和Bcl-2在心肌细胞中的表达及心肌细胞凋亡情况。结果甲减大鼠出现心肌细胞凋亡,并且随着病程进展凋亡逐渐加重,并与甲状腺功能密切相关。干预组心肌细胞凋亡均较甲减组减轻。结论甲减时心肌损伤与心肌细胞凋亡密切相关,即心肌细胞凋亡可引起甲减心肌损伤,甲状腺激素参与调控细胞凋亡。     

重症急性胰腺炎继发胰周感染的手术时机探讨

重症急性胰腺炎(SAP)病死率高达30%～60%[1].约半数以上的死亡原因与感染有关[2].重视SAP后期胰周感染的防治.选择恰当的手术时机和方法,是提高SAP治愈率的重要环节.现将我院26例SAP继发胰周感染手术治疗的经验和体会报道如下.     

移动通信基站电磁辐射对周边环境影响的评价分析

目的了解移动通信基站电磁辐射对周边环境的影响,为制定安全防护措施提供依据。方法采用职业卫生学调查和电磁辐射测试,依据电磁辐射环境标准,对基站的安全防护距离进行综合评价。结果全球移动通讯系统900（GSM900）基站的垂直防护距离为4．2m,水平防护距离为25．1m,时分同步码分多址（TD-SCDMA）基站的垂直防护距离为2．3m,水平防护距离为13．8m;随着距离的增加电磁辐射强度而迅速衰减。结论利用安全防护距离来保护敏感点免受过量电磁辐射是有效的。     

曲尼司特对环孢素A诱导的人肾小管上皮细胞向间充质转变的抑制作用

目的 研究曲尼司特(Tran)对环孢素A(CsA)诱导的人肾小管上皮细胞(HK-2)向间充质转变的影响,并探讨该药抗纤维化的机制.方法 所有用于实验的HK-2细胞株均为8～12代细胞,分为4组:(1)空白对照组,收获细胞,不做任何处理;(2)CsA组,加入4.2μmol/LCsA;(3)CsA+Tran组,预先加入100μmol/L Tran,作用2 h后再加入4.2 μmol/L CsA;(4)Tran组,仅加入100μmol/L Tran.72 h后于共聚焦显微镜下观察各组细胞形态学变化;用免疫荧光法以及免疫印迹法检测各组钙黏蛋白(E-cadherin)、平滑肌肌动蛋白α(α-SMA)和骨桥蛋白(OPN)的表达.结果 HK-2细胞在正常情况下表现为典型的"鹅卵石"样形态,细胞圆钝,且与邻近的细胞连接较为紧密;空白对照组和Tran组细胞表现为典型的HK-2细胞形态;CsA组细胞变狭长,甚至向周边伸出"伪足"样改变,细胞间连接较为稀疏;CsA+Tran组的细胞形态学改变有明显改善.CsA组细胞E-cadherin荧光表达强度明显弱于对照组,α-SMA、OPN荧光表达强于对照组;CsA+Tran组细胞E-cadherin荧光表达强于CsA组,α-SMA、OPN荧光表达弱于CsA组.免疫印迹检查中,CsA组细胞E-cadherin 的表达明显低于对照组,而α-SMA、OPN的表达明显高于对照组,CsA+Tran组细胞E-cadherin的表达高于CsA组,而α-SMA、OPN的表达低于CsA组.结论 曲尼司特能抑制CsA诱导的HK-2细胞由肾小管上皮向间充质细胞转化的过程,其机制可能与抑制OPN的表达有关.

Abstract：

Objective To study the effect of tranilast on cyclosporine A (CsA)-induced epithelial-to-mesenchymal transition in human renal tubular epithelial cells, and investigate the mechanism of its antifibrotic effect. Methods Cultured HK-2 cells were divided into four groups: (1)In the control group, cells were treated without any medicine; (2) The cell were treated with CsA (4. 2μmol/L) for 72 h; (3) The cells were treated with a combination of CsA (4. 2 μmol/L) and tranilast (100μmol/L); (4) The cells were treated with tranilast (100 μmol/L) alone for 72 h.Morphological changes of the cells were assessed by phase-contrast microscopy. The immunofluorescence and Western blotting were adopted to detect the expression of E-cadherin, α-SMA and OPN mRNA and proteins respectively. Results Tranilast could markedly ameliorate the morphological changes of HK-2 cells stimulated by CsA. The irmmunofluorescence staining revealed the expression of E-cadherin was markedly decreased in HK-2 cells stimulated with CsA for 72 as compared with the control group, while the expression of α-SMA and OPN was significantly higher in CsA group than the control group. The expression of E-cadherin in the CsA + Tranilast group was higher than the CsA group, while the expression of α-SMA and OPN in the CsA + Tranilast group was lower than the CsA group. Western blotting showed that protein expression level of E-cadherin in CsA group was dramatically lower than that in the control group (P＜0. 05), while that of α-SMA and OPN in CsA group was significantly higher than in the control group (P＜0.05). The protein expression level of E-cadherin in HK-2 cells in the CsA + Tranilast group was markedly higher than in the CsA group (P＜0.05), and that of α-SMA and OPN in CsA + Tranilast group was significantly lower than in the CsA group (P＜0. 05). Conclusion Tranilast can block the CsA-induced epithelialto-mesenchymal transition in HK-2 cells probably by suppressing the expression of OPN.     

曲尼司特对环孢素A诱导的人肾小管上皮细胞向间充质转变的抑制作用

Objective To study the effect of tranilast on cyclosporine A (CsA)-induced epithelial-to-mesenchymal transition in human renal tubular epithelial cells, and investigate the mechanism of its antifibrotic effect. Methods Cultured HK-2 cells were divided into four groups: (1)In the control group, cells were treated without any medicine; (2) The cell were treated with CsA (4. 2μmol/L) for 72 h; (3) The cells were treated with a combination of CsA (4. 2 μmol/L) and tranilast (100μmol/L); (4) The cells were treated with tranilast (100 μmol/L) alone for 72 h.Morphological changes of the cells were assessed by phase-contrast microscopy. The immunofluorescence and Western blotting were adopted to detect the expression of E-cadherin, α-SMA and OPN mRNA and proteins respectively. Results Tranilast could markedly ameliorate the morphological changes of HK-2 cells stimulated by CsA. The irmmunofluorescence staining revealed the expression of E-cadherin was markedly decreased in HK-2 cells stimulated with CsA for 72 as compared with the control group, while the expression of α-SMA and OPN was significantly higher in CsA group than the control group. The expression of E-cadherin in the CsA + Tranilast group was higher than the CsA group, while the expression of α-SMA and OPN in the CsA + Tranilast group was lower than the CsA group. Western blotting showed that protein expression level of E-cadherin in CsA group was dramatically lower than that in the control group (P＜0. 05), while that of α-SMA and OPN in CsA group was significantly higher than in the control group (P＜0.05). The protein expression level of E-cadherin in HK-2 cells in the CsA + Tranilast group was markedly higher than in the CsA group (P＜0.05), and that of α-SMA and OPN in CsA + Tranilast group was significantly lower than in the CsA group (P＜0. 05). Conclusion Tranilast can block the CsA-induced epithelialto-mesenchymal transition in HK-2 cells probably by suppressing the expression of OPN.