目的:亚甲基四氢叶酸还原酶基因C677T或A1298C位点多态性是否与出血性脑卒中相关存在争议.文章以此评估亚甲基四氢叶酸还原酶基因C677T或A1298C位点多态性与出血性脑卒中的相关性.方法:检索PubMed、Embase、Web of Science、中国知网、万方数据、维普和中国生物医学服务系统(SinoMed)数据库中的相关文献.由2名人员筛选,提取信息和评价文献质量.建立5种遗传模型:等位基因模型(Tvs.C和Cvs.A)、显性模型[(CT+TT)vs.CC和(AC+CC)vs.AA]、隐性模型[TT vs.(CC+CT)和CC vs.(AA+AC)]、共显性杂合子模型(CT vs.CC和AC vs.AA)及共显性纯合子模型(TT vs.CC和CC vs.AA).利用RevMan 5.4和Stata 14软件,Cochrane'Q检验和I2值评估异质性,合并OR值和95％CI做为效应及指标,亚组分析探索异质性来源,敏感性分析评估结论稳定性,漏斗图、Begg及Egger检验和剪补法评估发表偏倚.结果:纳入24篇高质量观察性研究文献,其中病例对照研究23篇,横断面研究1篇.①亚甲基四氢叶酸还原酶基因C677T位点多态性与出血性脑卒中存在相关性,5 种遗传模型均有显著性意义[Tvs.C:OR=1.39,95％CI:1.18-1.64;(CT+TT)vs.CC:OR=1.46,95％CI:1.18-1.80;TT vs.(CC+CT):OR=1.54,95％CI:1.20-1.96;CT vs.CC:OR=1.31,95％CI:1.08-1.58;TT vs.CC:OR=1.78,95％CI:1.31-2.43].亚组分析提示在亚洲人群中亚甲基四氢叶酸还原酶基因C677T与出血性脑卒中存在相关性,而欧洲和非洲则无,随着年龄的增大,其OR值越大,在控制病例组和对照组混杂因素(年龄和性别)的研究中,合并效应量提示相关性有显著性意义;综合各项假阳性结果报告率,推测假阳性可能性较小.②亚甲基四氢叶酸还原酶基因A1288C位点多态性与出血性脑卒中相关性无显著性意义[Cvs.A:OR=1.16,95％CI:0.98-1.37;(CC+AC)vs.AA:OR=1.19,95％CI:0.96-1.48;CC vs.(AC+AA):OR=1.27,95％CI:0.86-1.88;AC vs.AA:OR=1.04,95％CI:0.71-1.51;CC vs.AA:OR=1.37,95％CI:0.90-2.06];上述位点的亚组分析所得阳性结果,经假阳性结果报告率检验后,结论并不可靠.结论:亚甲基四氢叶酸还原酶基因C677T位点多态性与出血性脑卒中相关,携带突变T等位基因是出血性脑卒中的重要危险因素,尤其是在亚洲人群中,且年龄越大,风险越大.亚甲基四氢叶酸还原酶基因A1298C位点多态性与出血性脑卒中无明显关联.

背景:脑老化后神经细胞凋亡增多,其机制不明确.近年研究表明,褪黑素可调节多种凋亡因子的表达,丰富环境作为一种治疗阿尔茨海默病的有效方案已投入临床使用,然而二者合用是否有更好的疗效及其各自的作用机制目前尚不清楚.目的:探讨丰富环境与褪黑素联合干预对SAMP8小鼠学习记忆功能及脑神经细胞凋亡的影响.方法:选用3月龄雄性SAMP8小鼠24只,利用随机数字表法分成4组:对照组、丰富环境组、褪黑素组和联合处理组,每组6只.对照组和褪黑素组小鼠饲养于标准环境,丰富环境组和联合组饲养于丰富环境,直至小鼠满4月龄;满4月龄次日,褪黑素组、联合处理组小鼠开始皮下注射褪黑素8 mg/(kg·d),对照组、丰富环境组皮下注射等量生理盐水,共30 d.给药结束后继续饲养于原环境至11月龄,采用筑巢实验和Morris水迷宫实验评估小鼠学习记忆能力;行为学实验结束后,采用NeuN免疫荧光/TUNEL双标染色及尼氏染色观察海马CA1区细胞凋亡情况,采用Western blot法检测海马中凋亡相关蛋白Caspase-3、Bax、Bcl-2、P53的表达.结果 与结论:①与对照组相比,其他3组小鼠的筑巢实验得分、Morris水迷宫跨平台次数、海马CA1区NeuN免疫反应性、尼氏染色阳性细胞数量、海马中Bcl-2蛋白表达显著增加(P<0.05),联合处理组上述指标值显著多于丰富环境组、褪黑素组(P<0.05);②苏木精-伊红染色显示,与对照组相比,其他3组小鼠海马CA1区神经细胞形态和排列较佳;③与对照组相比,其他3组小鼠的Morris水迷宫逃避潜伏期、海马CA1区免疫荧光/TUNEL双阳性细胞数量及Caspase-3、Bax、P53蛋白表达水平显著降低(P<0.05),联合处理组上述指标值显著低于丰富环境组、褪黑素组(P<0.05);④结果表明,丰富环境和褪黑素对SAMP8小鼠的学习记忆功能、脑神经细胞凋亡具有改善作用,其机制可能与调控小鼠海马神经细胞P53/P21通路来减少细胞凋亡有关;且将丰富环境和褪黑素联合应用的疗效很可能高于单方案治疗.

背景:脑老化可导致学习记忆功能减退,其机制并不明确.近年研究发现,人参皂苷Rg1可提高阿尔茨海默病模型小鼠的学习记忆能力,其机制可能与其改善突触后密度蛋白95的表达相关.目的:探讨人参皂苷Rg1能否通过脑源性神经营养因子/TrkB信号通路改善D-半乳糖诱导衰老小鼠的学习记忆功能与海马区突触后密度蛋白95的表达.方法:取50只雄性昆仑种小鼠,采用随机数字表法分为5组,每组10只:A组不进行任何处理;B组皮下注射D-半乳糖溶液300 mg/(kg·d)建立脑老化模型;C组造模1 h后每天灌胃给予盐酸多奈哌齐;D组造模1 h后每天灌胃给予人参皂苷Rg1;E组造模1 h后每天灌胃给予人参皂苷Rg1,并且腹腔注射选择性TrkB阻断剂ANA-12(每2 d一次).持续给药6周后,进行学习记忆能力(旷场实验、新物体识别实验、Morris水迷宫实验)测试、脑组织形态学观察及小鼠海马区突触后密度蛋白95、脑源性神经营养因子的蛋白表达检测.结果 与结论:①行为学结果显示:B组小鼠学习记忆能力低于A组(P<0.05);C、D组小鼠学习记忆能力高于B组(P<0.05);D组小鼠学习记忆能力低于C组(P<0.05);E组小鼠学习记忆能力低于D组(P<0.05);②苏木精-伊红、Nissl染色显示,与A组相比,B组小鼠海马CA1区正常神经元数量减少,尼氏体表达明显减少;与B组相比,C、D组正常神经元数量增多,尼氏小体颗粒明显增加;与D组相比,E组正常神经元数量减少,尼氏小体颗粒明显减少;③Western blot检测显示,与A组相比,B组脑源性神经营养因子、突触后密度蛋白95的蛋白表达降低(P<0.05);与B组相比,C、D组脑源性神经营养因子、突触后密度蛋白95的蛋白表达升高(P<0.05);D组小鼠海马脑源性神经营养因子、突触后密度蛋白95的蛋白表达低于C组(P<0.05);与D组相比,E组突触后密度蛋白95的蛋白表达降低(P<0.05),脑源性神经营养因子蛋白表达无明显变化(P>0.05);④结果表明,人参皂苷Rg1可改善D-半乳糖诱导的脑老化小鼠神经元损伤与学习记忆能力,并促进海马中突触后密度蛋白95的表达,而脑源性神经营养因/TrkB信号通路可能为其调控机制之一.

为提高教学质量、提升学生学习 自主性,在系统解剖学运动系统开展以职业为导向的PBL教学.结果显示,本次教学有效地将理论知识与职业技能相结合,使学为主体、教为主导,在提高学习效果、学习 自主能力和分析解决问题能力等方面有很大帮助,培养学生的职业道德精神,为系统解剖学教学改革提供参考.

Objective:To explore the effects and possible mechanisms of melatonin combined with enriched environment on the learning and memory ability of senescence-accelerated mouse prone 8(SAMP8).Methods:Forty-eight SAMP8 male mice aged 4 months were randomly divided into model group, enriched environment group, melatonin group and melatonin combined with enriched environment group (combined intervention group) by random number table method, with 12 mice in each group. Mice in the melatonin group and combined intervention group were subcutaneously injected with melatonin at a dose of 8 mg·kg -1·d -1, and the mice in the model group and the enriched environment group were given the same amount of normal saline instead.The mice in model group and melatonin group were raised in a standard environment, and the mice in enriched environment group and combined intervention group were raised in an enriched environment.The intervention lasted 28 days. The aging degree of mice was scored before and 28 days after the intervention. Morris water maze test was used to detect the learning and memory ability of mice. Nissl staining and TUNEL staining were used to observe the Nissl staining positive cells and apoptotic cells in the CA1 area of hippocampus.ELISA was used to detect the levels of interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in the hippocampus of mice. Western blot was used to detect the levels of amyloid β-protein (Aβ) 1-42, microtubule-associated protein tau (tau) phosphorylated at threonine (Thr) 205 (Tau pT205), Toll-like receptor 4 (TLR4), and nuclear factor-κB (NF-κB) p65 protein in the hippocampus of mice. qRT-PCR was used to detect the levels of TLR4, NF-κB p65 mRNA in the hippocampus of mice. SPSS 22. 0 statistical software was used for repeated measure ANOVA, one-way ANOVA and LSD test. Results:(1) Aging score: after intervention, the aging scores of mice in the four groups were significantly different ( F=120.601, P<0.01). The aging scores of mice in the enriched environment group, melatonin group, and combined intervention group were lower than those in the model group (all P<0.05), while the aging score of mice in the combined intervention group was significantly lower than those in the enriched environment group and melatonin group (both P<0.05). (2) The results of the location navigation experiment showed that the time × group interaction effect of the escape latencies of mice in the four groups were significant ( F=30.524, P<0.001). From the 2nd to 4th day, the escape latencies of mice in the enriched environment group, melatonin group and combined intervention group were all lower than that in the model group (all P<0.05). The results of the space exploration experiment showed that the residence time in the target quadrant and the number of platform crossings of mice in the four groups were significantly different ( F=291.328, 113.482, both P<0.01). The residence time in the target quadrant ((29.45±1.70)s, (32.44±1.55)s, (37.48±0.84) s) and the number of platform crossings ((6.44±0.61) times, (7.16±0.70) times, (12.60±1.23) times) of mice in the enriched environment group, melatonin group and combined intervention group were higher than those in the model group ((15.07±1.28) s, (4.10±0.61) times), while the residence time in the target quadrant and the number of platform crossings of mice in the enriched environment group and the melatonin group were significantly lower than those in the combined intervention group (all P<0.05). (3) Nissl and TUNEL staining showed that the number of Nissl positive neurons in the hippocampal CA1 region of mice in the four groups were significantly different ( F=809.264, P<0.01), and the number of apoptotic cells in the hippocampal CA1 region were also significantly different ( F=1 060.583, P<0.01). The number of Nissl stained positive neurons in the hippocampal CA1 region of mice in the combined intervention group was more than those in the model group, enriched environment group, and melatonin group (all P<0.05), and the number of apoptotic cells were less than those in the model group, enriched environment group, and melatonin group (all P<0.05). (4) The results of ELISA assay showed that there were significantly different in the levels of IL-1β, IL-6 and TNF-α in the hippocampus of mice in the four groups ( F=152.887, 63.506, 432.026, all P<0.01). The contents of IL-1β, IL-6 and TNF-α in the hippocampus of mice in the enriched environment group, melatonin group, and combined intervention group were lower than those in the model group(all P<0.05). Among them, the contents of IL-1β, IL-6 and TNF-α in the hippocampus of mice in the enriched environment group and melatonin group were significantly higher than those in the combined intervention group (all P<0.05). (5) Western blot analysis showed that there were significantly different in the protein expression levels of Aβ1~42, tau pT205, TLR4, NF-κB p65 in the hippocampus of mice in the four groups ( F=122.349, 98.934, 201.635, 116.553, all P<0.01). The protein expression levels of Aβ1-42, tau pT205, TLR4, and NF-κB p65 in the hippocampus of mice in the enriched environment group, melatonin group, and combined intervention group were lower than those in the model group.Among them, the protein expression levels of Aβ1-42, tau pT205, TLR4, NF-κB p65 in the hippocampus of mice in the enriched environment group and melatonin group were significantly higher than those in the combined intervention group (all P<0.05). (6) qRT-PCR showed that the mRNA expression levels of TLR4 and NF-κB p65 in the hippocampus of mice in the four groups were significantly different ( F=42.913, 102.446, both P<0.01). The mRNA expression levels of TLR4 ((0.63±0.05), (0.55±0.04), (0.42±0.03)) and NF-κB p65 ((0.98±0.06), (0.82±0.04), (0.72±0.04)) in the hippocampus of mice in the enriched environment group, melatonin group and combined intervention group were lower than those in the model group ((0.74±0.07), (1.20±0.05)) (all P<0.05). Among them, the mRNA expression levels of TLR4 and NF-κB p65 in the hippocampus of mice in the enriched environment group and melatonin group were significantly higher than those in the combined intervention group (all P<0.05). Conclusion:Melatonin combined with enriched environment can improve the learning and memory ability and neuroinflammatory response of SAMP8 mice, and its mechanism may be related with the down-regulation of TLR4/NF-κB p65 signaling pathway.

目的 探讨山楂果提取物(HFE)提高高温环境下机体热耐受性及热休克蛋白70(HSP70)表达量对血压、血脂影响;为研制针对高温作业工人补充液体的HFE添加提供支持.方法 成年KM小鼠、SD大鼠各40只分别随机分为4个高温跑台组,其中3个组分别补充高、中、低剂量HFE,1个组为对照组,小、大鼠每组10只;实验期30d.热暴露环境的湿球黑球温度(WBGT)指数为(36±1)℃,每只鼠上、下午各跑台30 min用以模拟重体力作业.采用人与动物体表面积法将人的HEF参考摄入量换算为鼠的灌胃剂量,高、中和低剂量小鼠分别为120、60、30 mg/d,大鼠分别为600、300、150 mg/d.于实验结束后,进行各组小鼠的高温游泳力竭实验和致死实验、并记录其时间;于实验开始和实验结束时,测量各组大鼠鼠尾收缩压(SBP)和舒张压(DBP);实验结束后,测定各组大鼠的血脂水平,并在每组大鼠中随机抽取3只测定肝组织HSP 70表达量.结果 高、中剂量HFE组小鼠高温游泳力竭时间和致死时间长于对照组和低剂量HFE组(均P<0.05).高、中、低剂量HFE组大鼠肝组织HSP70表达量均高于对照组(均P<0.05),且高、中剂量HFE组大鼠HSP70表达量高于低剂量组(均P<0.05);热暴露30d后各组大鼠BP均有升高(均P<0.001),高剂量HFE组SBP升高值、以及高、中剂量HFE组DBP升高值均低于其它各组(均P<0.05);高剂量HFE组的TG低于、HDL-C高于HE组和低剂量组(均P<0.05),且该组TC、LDL-C低于其它各组(均P<0.05).结论 小鼠补充山楂提取物120 mg/d,能明显提高其对高温环境的热耐受性;大鼠补充山楂提取物600 mg/d,能通过提升HSP70表达量,降低热暴露大鼠的血压升高幅度和血脂水平.

为了探讨miR-148a及己糖激酶2(hexokinase 2,HK2)基因对人乳腺癌细胞糖酵解代谢途径的影响和可能机制,利用实时荧光定量PCR(real-time fluorescent quantitative PCR,qRT-PCR)检测多种乳腺癌细胞系中miR-148a的表达量,从中筛选miR-148a表达量相对较低的乳腺癌细胞系作为研究对象.再通过观察miR-148a表达量的变化对乳腺癌细胞葡萄糖摄取量、乳酸生成量和细胞增殖指标的影响,以探究miR-148a对乳腺癌细胞糖代谢能力的影响.随后,通过TargetScan在线数据库预测miR-148a和HK2基因的靶向关系,再通过双荧光素酶报告实验、Western免疫印迹以及基因回复实验进行验证,以进一步明确miR-148a和HK2在乳腺癌细胞的糖酵解代谢途径中的作用机制.通过qRT-PCR发现miR-148a在多种乳腺癌细胞系表达降低,尤其是在乳腺癌细胞系MDA-MB231中表达量显著降低(P<0.0001).过表达miR-148a使MDA-MB231细胞的葡萄糖摄取量、乳酸生成量、细胞增殖指标均显著下降(P<0.01);而抑制miR-148a表达使MDA-MB231细胞葡萄糖摄取量、乳酸生成量、细胞增殖指标均显著上升(P<0.01).通过TargetScan在线数据库预测得出,miR-148a与HK2基因3′非编码区(3′-untranslated region,3′-UTR)具有部分结合位点;而双荧光素酶报告实验发现miR-148a与野生型HK2基因的3′-UTR荧光素酶报告载体结合,不与突变型HK2基因的3′-UTR结合.Western免疫印迹检测结果表明,过表达miR-148a使MDA-MB231细胞中HK2蛋白表达量显著下降(P<0.0001),而抑制miR-148a表达则促进HK2蛋白表达量显著上升(P<0.05).基因回复实验显示,过表达HK2基因使MDA-MB231乳腺癌细胞的葡萄糖摄取量、乳酸生成量、细胞增殖指标显著上升(P<0.01);将过表达miR-148a载体与过表达HK2载体共转染MDA-MB231细胞,miR-148a逆转了HK2所致的葡萄糖摄取量增加和乳酸生成量上升,并抑制细胞增殖.因此,研究提示,miR-148a可通过靶向抑制HK2基因表达而抑制乳腺癌细胞MDA-MB231糖酵解代谢和细胞增殖.

目的 探讨经计算机断层扫描技术(CT)及磁共振成像(MRI)对下咽癌患者颈淋巴结转移诊断中的价值.方法 下咽癌患者103例,以患者颈部CT、MRI和病理结果为对照,分析CT、MRI对下咽癌颈淋巴结转移的诊断价值.结果 病理结果显示,103例下咽癌患者中,68例发生颈淋巴结转移,转移淋巴结146个,淋巴结总转移率为65.7％;CT结果显示,转移患者颈部淋巴结直径、短长径比值、数目明显高于无转移患者(P<0.05);MRI结果显示,下咽癌颈转移淋巴结与周围软组织边界、淋巴结边缘、增强后表现均低于无转移颈淋巴结,差异有统计学意义(P<0.05);在诊断下咽癌颈转移淋巴结的敏感度、特异度、准确度中,CT分别为90.4％、75.7％、85.5％,MRI分别为93.2％、83.3％、90.0％,CT、MRI联合时分别为97.3％、91.7％、95.5％,差异有统计学意义(P<0.05).结论 CT、MRI 可单独作为诊断下咽癌颈转移淋巴结的方法,二者联合时具有更佳的诊断效能.

目的 应用解剖学无纸化实验考试方法并进行调查分析.方法 将前期解剖学资源体系作为题库基础,建立和应用无纸化考试方法,并对180名学生进行无纸化测试和问卷调查.结果 绝大多数学生认为无纸化考试方法考点明确清晰、软件操作方便、考试更加客观公正而且考试环境更好,希望应用此种方式.结论 基于资源体系建设的解剖学无纸化实验考试改革具有诸多优势,有很强的现实意义和拓展价值.

目的:探讨粒细胞集落刺激因子(G-CSF)对1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTTP)所致小鼠帕金森病(PD)模型中脑黑质致密部(SNpc)及纹状体(STR)多巴胺(DA)能神经元的影响.方法:正常健康雄性C57BL/6J小鼠随机分为对照组、MPTP组及MPTP+ G-CSF组,采用腹腔注射MPTP法制作小鼠PD模型,MPTP+G-CSF组于最后一次MPTP注射后再腹腔注射G-CSF.爬杆实验观察小鼠的行为学改变;尼氏染色技术观察各组小鼠黑质致密部神经元数量及形态学变化;免疫组织化学法检测酪氨酸羟化酶(TH)在各组小鼠中脑黑质致密部及纹状体的表达;Western Blot法检测各组小鼠中脑TH蛋白的表达量.结果:与对照组相比,MPTP组小鼠较对照组爬杆用时显著延长(P＜0.05),尼氏染色显示黑质致密部神经元数量显著减少(P＜0.05),黑质致密部、纹状体TH表达量显著减少(P ＜0.05);MPTP+ G-CSF组较MPTP组爬杆用时显著缩短(P＜0.05),神经元丢失减少(P＜0.05),神经元形态较完整;与MPTP组比较,MPTP+ G-CSF组黑质致密部、纹状体TH表达水平显著增高(P＜0.05).结论:G-CSF能够改善PD小鼠运动功能,减少黑质致密部多巴胺能神经元丢失,增加TH表达水平.

目的 探讨微课结合翻转课堂教学模式在系统解剖学教学中的应用效果.方法 对全日制本科临床医学专业系统解剖学教学进行改革,选择小班进行微课结合翻转课堂教学,通过期末成绩及调查问卷评价教学效果.结果 微课结合翻转课堂教学模式完善了课程设计、课程实施、课后评价,为系统解剖学教学提供了新思路,学生期末成绩及教学满意度均较高.结论 微课结合翻转课堂教学模式可提高教学质量,激发学生学习兴趣,改善教学效果,有重要的推广意义.

Objective To investigate the effect of selective cyclooxygenase (COX-2) inhibitor celecoxib on the expression of COX-2,motor function and learning and memory after traumatic brain injury in rats.Methods The mice were divided into control group,sham operation group,model group and experimental group.The model of closed craniocerebral trauma was established by Marmarou method,the control group did not receive any treatment.The experimental group was given 250 mg· kg-1 celecoxib,intraperitoneal injection immediately after injury,and every 6 h a time.The control group,sham operation group and model group were injected intraperitoneally with the same amount of 0.9％ NaC1.Real-time quantitative polymerase chain reaction (qPCR) was used to detect the expression of COX-2 mRNA,Western blot and immunohistochemical staining were used to detect the expression of COX-2 protein,the neurological impairment score (NSS) was used to measure motor function after trauma in rats,Morris water maze test to test the learning and memory function.Results The relative expression of COX-2 mRNA in control group,sham operation group,model group and experimental group were 1.10 ±6.96,1.27 ±2.10,2.18 ±5.24 and 1.69 ±4.62,there was significant difference between model group and experimental group (P ＜ 0.05).Western blotting showed that the expression of COX-2 protein in control group,sham operation group,model group and experimental group were 0.88 ± 3.26,0.93 ± 2.25,2.26 ± 1.43 and 1.65 ± 4.62,there was significant difference between model group and experimental group (P ＜ 0.05).Immunohistochemical staining showed that the expression of COX-2 in control group,sham operation group,model group and experimental group were 68.53 ±2.66,70.05 ±3.10,97.38 ±6.14,80.40 ±7.32,there was significant difference between model group and experimental group (P ＜ 0.05).The NSS of control group,sham operation group,model group and experimental group were 0.96 ± 0.37,1.13 ± 0.24,16.26 ± 4.56,7.97 ±3.49,there was significant difference between model group and experimental group (P ＜0.05).The time required for the search platform in control group,sham operation group,model group and experimental group on 11 d after traumatic brain injury were (28.25 ±9.10),(27.35 ± 10.32),(57.36 ± 18.20),(57.21 ±20.38) s.There was significant difference between model group and experimental group (P ＜ 0.05).Conclusion Celecoxib can reduce the inflammatory response after craniocerebral injury by specific inhibition of COX-2,and further improve the motor and learning and memory dysfunction after craniocerebral trauma in rats.

目的 研究塞来昔布对大鼠颅脑创伤后Fas表达及认知功能的影响,探讨其对颅脑创伤后神经的保护作用及其机制.方法 96只Wistar大鼠随机分为对照组、假手术组、模型组和药物组,参照Marmarou方法构建大鼠闭合型脑创伤模型,采用实时荧光定量PCR和免疫组织化学法分别检测Fas、Caspase-8的mRNA和蛋白表达,TUNEL法检测神经细胞凋亡情况,Y型迷宫实验检测大鼠认知功能.结果 模型组较对照组、假手术组Fas、Caspase-8的mRNA和蛋白表达均显著增高(P＜0.05);药物组较模型组Fas、Caspase-8的mRNA和蛋白表达均显著降低(P＜0.05),但仍高于对照组和假手术组(P＜0.05).模型组较对照组、假手术组凋亡细胞显著增多(P＜0.05);药物组较模型组凋亡细胞数显著减少(P＜0.05),但仍高于对照组和假手术组(P＜0.05).模型组较对照组、假手术组大鼠记忆成绩次数明显减少(P＜0.05),药物组较模型组大鼠记忆成绩次数明显增加(P＜0.05),但仍低于对照组与假手术组(P＜0.05).结论 塞来昔布通过下调颅脑创伤后Fas介导的凋亡程序,以发挥对大鼠颅脑创伤后神经元的保护作用,并改善大鼠的认知功能.

对医学全日制本科临床专业大学三年级进行局部解剖学实验教学视频应用并开展调查与分析,调查围绕局部解剖学实验视频的播放内容、时间、效果等情况,分析局部解剖学教学视频在实验教学中的作用及学生的认同程度,以改进局部解剖学实验的教学方法,提高教学质量.

目的:以自发性Ⅱ型糖尿病动物模型db/db小鼠为研究对象,探讨高血糖环境下胰岛、心肌、肝脏、肾脏及海马组织病理学的改变.方法:以同种系但不发病杂合子db/m小鼠为正常对照组,检测体重及口服糖耐量变化,取胰腺、心肌、肝脏、肾脏及海马组织甲醛固定后石蜡包埋,HE染色观察病理学变化.结果:与db/m小鼠相比,db/db小鼠体重显著升高,口服糖耐量异常,胰岛形态紊乱,胰岛内细胞数量减少、结构紊乱;心肌细胞排列紊乱,肌细胞边界模糊;肾小球明显增大,肾小管空泡变性,断裂;肝细胞索排列紊乱,肝细胞气球样变.结论:db/db小鼠可以很好地模拟T2MD临床症状,是一种适用于研究T2MD发病机制及寻找治疗药物的动物模型.

目的:利用1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)所致帕金森病(Parkinson's disease,PD)模型,探讨红景天苷(Sal)发挥多巴胺能神经元保护作用的可能机制.方法:将72只雄性C57/BL小鼠随机分为3组,每组24只.对照组腹腔注射生理盐水;模型组腹腔注射MPTP(每日30 mg/kg);治疗组腹腔注射MPTP(每日30 mg/kg)后1h腹腔注射Sal(每日50 mg/kg),连续注射7d,观察每组小鼠行为学表现,使用爬杆法测定小鼠运动能力;采用免疫组织化学图像分析,测定模型小鼠中脑黑质区酪氨酸羟化酶(TH)和烟酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化酶催化亚基(NOX2)阳性表达量;采用蛋白质印迹法,测定模型小鼠中脑TH、血管紧张素1型受体(AT1)和NOX2蛋白表达情况;使用试剂盒测定活性氧簇(ROS)产生水平.结果:与对照组相比,模型组小鼠表现出典型的帕金森病样行为学表现,运动能力明显减退;TH阳性细胞减少61.1％,TH蛋白表达降低67.6％,AT1、NOX2表达与ROS生成均上升(P＜0.01).与模型组相比,Sal治疗组小鼠行为学症状减轻,运动能力提高,TH表达升高,AT1、NOX2表达与ROS生成下降(P＜0.01).结论:Sal在一定程度上可通过抑制肾素-血管紧张素系统(RAS)轴中AT1、NOX2过度表达与ROS过度生成,减轻氧化应激反应,从而发挥多巴胺能神经元保护效应.

①目的 应用脂多糖(Lipopoly saccharide,LPS)建立帕金森病大鼠模型并对其进行行为学评估.②方法 雄性SD大鼠60只,随机分为观察组(40只)和对照组(20只).应用立体定位技术向观察组大鼠右侧脑室内注入LPS(5μg/μL,注射速度为1μL/min,20分钟注完)制成大鼠模型,应用转棒法和旋转法对大鼠运动协调行为进行评估,观察LPS诱发的大鼠行为学变化.向对照组大鼠右侧脑室注射生理盐水20μL,注射速度为1μL/min,20分钟注完.③结果 LPS造模后,40只大鼠中有31只(78％)在转棒实验中在棒时间显著缩短;有35只(88％)在旋转实验中出现向注射侧的旋转行为,同时伴有运动迟缓、肌肉强直、活动量减少等症状,提示帕金森大鼠模型复制成功.④结论 采用LPS成功建立帕金森病大鼠模型,为进一步研究帕金森病发病机制提供了新的实验方向;行为学检测也为帕金森病动物模型的评价提供了新的实验依据.

麻醉解剖学在大三上学期开设,是从麻醉学角度研究人体局部配布规律及临床应用的一门学科,是麻醉学专业的主干课程之一.目前各个院校麻醉解剖学理论教学基本上是"局部解剖为主,麻醉解剖为辅"的授课模式;采用的教材基本是按照绪论、头部、颈部、胸部、腹部、脊柱、盆部及会阴、上肢、下肢等各个局部编排,局部解剖学知识篇幅较重;涉及到的麻醉学相关解剖如临床麻醉、疼痛诊疗、危重病监测与治疗等内容多散在各个章节,与临床实际操作结合不紧密,迫切需要融入一些整合性的专题解剖学知识.因此本教研室尝试开展了麻醉解剖学整合专题交流活动,以提高学生实际运用知识能力与合作交流能力.

目的 探讨婴幼儿不同分型中耳炎的治疗策略,预防抗生素滥用.方法 对该院2015年1月—2016年12月门急诊收治的婴幼儿中耳炎患者1 080例(其中急性中耳炎864例,分泌性中耳炎179例,非渗出性中耳炎26例,咽鼓管功能障碍11例)做回顾性研究.结果 1 080名中耳炎患儿依家长自愿分为血清降钙素原组(PCT组)和经验治疗组(非PCT组),动态检测PCT组抗生素使用时间及使用率均小于非PCT组,差异有统计学意义(P＜0.01),而治疗时间和有效率差异无统计学意义(P＞0.05).结论 采用降钙素原(PCT)动态检测指导婴幼儿中耳炎治疗可降低抗生素的使用,在取得良好治疗效果的同时,避免抗生素滥用,降低药品花费.

Aim To investigate the effects of celecoxib on cyclooxygenase-2(COX-2) and caspase-9 expression and motor function after traumatic brain injury in rats.Methods The rats were divided into control group, sham operation group, trauma group and treatment group.The model of closed craniocerebral trauma was established by Marmarou method, the gene expression of COX-2 and Caspase-9 was detected by real-time quantitative PCR(qPCR), the protein expressions of COX-2 and Caspase-9 were detected by immunohistochemical staining, and the motor function of the rats was evaluated by the neurological impairment score(NSS).Results The gene and protein expression of COX-2 and Caspase-9 in traumatic group was significantly higher than in other three groups (P<0.05), the expression of COX-2 and Caspase-9 in treatment group was significantly lower than in traumatic group(P<0.05), but still higher than the sham operation group and the normal group(P<0.05);compared with the trauma group, the motor function of the treatment group could be effectively improve (P<0.05), but compared with the control group and the sham operation group, the difference was statistically significant(P<0.05).Conclusion Celecoxib can reduce the inflammatory response after craniocerebral injury by specific inhibition of COX-2, and further reduce the expression of Caspase-9, thereby reducing the apoptosis of nerve cells, and improving motor function after traumatic brain injury in rats.