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在我国教育体制改革推进过程中,国家和社会对高等教育教学水平的要求不断提高,我们发现传统中医各专业教学内容比较固定,人才培养模式单一的问题越来越明显。如何将课堂学习知识运用到今后的工作实践中去,如何解决教学与实践脱节的问题,使学生能真正做到学以致用是提高教学质量和效果至关重要的环节。笔者在近几年的教学工作中体会到组织胚胎学课程教学应该结合中医院校所设专业特点有针对性的进行,希望可以在一定程度上弥补传统教学模式中教学内容缺乏变化,缺乏特色的不足之处。 相似文献
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目的:观察一次法根管治疗术对老年人前牙慢性根尖炎的疗效。方法:前牙慢性根尖炎老年患者80例,40例采用一次法根管治疗术治疗,40例采用传统多次法根管治疗术治疗,记录两组术后(多次法为第一次术后)24 h、第7天患牙疼痛发生率、同时采集患者上述两时点静脉血2 mL,采用Sysmex全自动血球分析仪检测白细胞( WBC)计数,散射比浊法测定血清C-反应蛋白( CRP),观察患牙疼痛发生率、WBC计数、CRP变化及1年后患牙临床疗效。结果:两组患者术后24 h、第7天患牙疼痛发生率、WBC计数、CRP检测比较,差异无统计学意义(P>0.05),1年后临床疗效的评定两组比较,差异无统计学意义(P>0.05)。结论:一次法根管治疗术在老年人前牙慢性根尖炎手术治疗效果与传统多次法相当,值得临床推广。 相似文献
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目的研究慢性氟中毒大鼠脑组织中细胞外信号调节蛋白激酶(Extracellular signal regulated kinases,Ras-Erk1/2)通路主要激酶表达变化及其对转录因子环一磷酸腺苷反应单元结合蛋白(cAMP Responsive Element Binding Protein,CREB)的影响。方法 SD(Sprague dawley)大鼠随机分为3组,即正常组、饮水中小剂量加氟(5 mg/L)组、大剂量加氟(50 mg/L)组,实验期为6个月。实验结束时,用氟离子选择电极法测定大鼠尿氟及血氟含量,尼氏染色检查神经细胞尼氏小体改变,蛋白印迹(Western-blotting)方法检测脑组织中小鸟苷三磷酸结合蛋白(small GTP-binding protein,Ras)、Erk1/2、CREB信号转导激酶的蛋白表达水平,实时荧光定量聚合酶链式反应(Real-time Polymerase Chain Reaction,Re-al-time PCR)方法检测c-fos基因mRNA表达水平。结果与对照组相比,染氟组大鼠有不同程度的氟斑牙及血氟尿氟升高;大脑皮质和海马部位神经细胞尼氏小体减少;脑组织中Ras、phospho-Erk1/2t、otal-Erk1/2及phospho-CREB蛋白表达水平上升(F值分别为19.9、114.59、4.6 9、7.6,P〈0.05),以大剂量染氟组尤为明显t,otal-CREB在各组间未见明显改变;大剂量染氟组c-fos基因mRNA表达明显升高,而小剂量染氟组该基因mRNA表达降低。结论过多的氟可引起大鼠脑组织神经细胞损伤,脑组织中Ras-Erk1/2信号激酶通路过度激活可刺激转录因子CREB磷酸化,从而影响c-fos基因的表达,该过程可能参与慢性氟中毒脑损伤机制。 相似文献
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目的:利用多波长反相高效液相色谱法(RP-HPLC)建立对民间验方仲氏止痛散加减后的止痛方中6种有效成分的含量进行同时测定的方法。方法:使用Diamond C18色谱柱(4.6 mm×250 mm,5μm),柱温30℃,甲醇-乙腈-0.1%氨水为流动相,以1 mL·min-1梯度洗脱,检测波长230 nm(芍药苷)、235 nm(乌头碱、次乌头碱)、280 nm(延胡索乙素)、280 nm(原阿片碱)、235 nm(新乌头碱)。结果:6个成分峰面积与浓度呈良好的线性(r>0.999 4),芍药苷、延胡索乙素、原阿片碱、乌头碱、次乌头碱、新乌头碱的加样回收率分别为97.2%(RSD 1.4%),96.5%(RSD 1.2%),102.5%(RSD 0.7%),96.8%(RSD0.7%),100.8%(RSD 1.1%),98.5%(RSD 1.1%)。结论:利用RP-HPLC同时测定止痛方中的几种有效成分,简便易行,为止痛方相关制剂的质量控制提供一定的依据。 相似文献
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目的 观察慢性氟中毒大鼠脑组织中细胞外调节蛋白激酶(ERK1/2)信号转导通路下游作用底物三元复合物因子Phospho-Elk-1的表达和分布,探讨慢性氟中毒所致学习记忆损害的发生机制.方法 SD 大鼠72只,体质量100~120 g,按体质量随机分为3组,每组24只,雌雄各半.对照组饮用自来水(含氟量<0.5 mg/L),低氟组和高氟组饮用加入氟化钠的自来水(P质量浓度分别为5.0、50.0 mg/L).6个月后,称取大鼠体质量,观察氟斑牙发生情况,用氟离子选择电极法检测大鼠尿氟及骨氟;用Morris水迷宫方法的定向航行实验检测大鼠学习能力,空间探索实验检测大鼠记忆能力;用免疫组织化学方法检测大鼠脑组织中Phospho-Elk-1在蛋白水平的表达和分布.结果 低氟组和高氟组大鼠体质量[(449.2±77.1)、(312.8 ±89.7)g]较对照组[(635.5±76.2)g]显著下降(P均<0.05),出现不同程度氟斑牙(x2=7.83,P<0.05),尿氟[(2.56±0.91)、(5.73±3.14)mg/L]及骨氟[(709.2±37.4)、(1306.3 ±102.4)mg/kg]较对照组[(0.92±0.30)mg/L、(348.5 ±89.2)mg/kg]明显升高(P均<0.05).低氟组和高氟组大鼠逃避潜伏期[(7.4±4.1)、(12.2±5.7)s]较对照组[(4.8±2.7)s]明显延长(P均<0.05),第1次穿越平台区时同[(4.18±1.10)、(5.89±0.56)s]较对照组[(1.17±0.75)s]显著延长(P均<0.05),均以高氟组尤为明显(P均<0.05).低氟组和高氟组大鼠海马CA1区(167.4±8.3、163.2±9.4)、CA2区(175.7±5.0、183.3±4.2)、CA3区(165.2±11.6、162.9±4.4)、CA4 区(168.7±6.9、169.5±5.3)、齿状回(185.2 ±4.0、193.1±6.1)及尾壳核(181.4±3.8、179.8±5.5)神经细胞Phospho-Elk-1表达水平较对照组(142.4±8.1、144.9±8.4、143.6±5.8、116.8±9.1、140.2±7.8、163.1±13.1)显著增加(P均<0.05).结论 慢性氟中毒可引起大鼠脑组织海马及尾壳核区域Pbospho-Elk-1表达水平升高,这种改变可能与大鼠学习记忆能力下降机制有一定关系.Abstract: Objective To investigate the expression and distribution of the downstream substrate of extracellular regulated protein kinase(ERK1/2) pathway, ternary complex factor phospho-Elk-1, in rat brains with chronic fluorosis, and reveal the mechanism of the impaired learning and memory ability caused by chronic fluorosis. Methods Seventy-two SD rats, weighing 100 - 120 g, were randomly divided into 3 groups, 24 in each group (half male and half female). The rats in control group were fed with tap water (fluoride < 0.5 mg/L); low- and high-dose fluoride groups were fed with tap water with different concentrations of NaF(5.0,50.0 mg/L F-, respectively). After 6 months, body weight was weighed, dental fluorosis was determined by observation and urinary fluoride and bone fluoride were detected by fluorine ion-selective electrode; the learning ability of rats was measured by navigation test of Morris water maze, and memory ability by spatial probe test in Morris water maze; the expression and distribution of phospho-Elk-1 in different brain regions were detected by immunohistochemistry method. Results In low- and high-fluoride groups, the body weight of rat[(449.2 ± 77.1), (312.8 ± 89.7)g] was significantly decreased than that of control [(635.5 ± 76.2 )g, all P< 0.05], the varying degrees of dental fluorosis were observed(x2 = 7.83, P<0.05), urinary fluoride[(2.56 ±0.91),(5.73 ±3.14)mg/L] and bone fluoride[(709.2 ± 37.4) ,(1306.3 ± 102.4) mg/kg] were significantly higher than those in controls[(0.92 ± 0.30)mg/L,(348.5 ± 89.2)mg/kg, all P< 0.05]. The escape latency of low- and high-fluoride groups[ (7.4 ± 4.1), (12.2 ± 5.7)s] was longer than that of control [(4.8 ± 2.7 )s, all P < 0.05] and the escape latency in high-fluoride group was significantly longer than that in other groups (all P < 0.05); in spatial probe test, the time of first crossing platform was longer in rats with fluorosis [(4.18 ± 1.10),(5.89 ± 0.56)s] as compared to control[(1.17 ± 0.75)s, all P< 0.05]. Expressions of phospho-Elk-1 in the hippocampus CA1(167.4 ± 8.3,163.2 ± 9.4), CA2(175.7 ± 5.0,183.3 ± 4.2), CA3(165.2 ± 11.6,162.9 ± 4.4), CA4(168.7± 6.9,169.5 ±5.3), fascia dentate (185.2 ±4.0,193.1 ±6.1) and caudate putamen( 181.4 ± 3.8, 179.8 ± 5.5) in low- and high-fluoride groups were higher than those of controls(142.4 ± 8.1,144.9 ± 8.4,143.6 ± 5.8, 116.8 ± 9.1,140.2 ± 7.8,163.1 ± 13.1, all P< 0.05). Conclusion Chronic fluorosis can cause increased expression of phospho-Elk-1 in the hippocampus and caudate putamen region of rat brains, which might be related to the mechanisms of decreased learning and memory ability of rats overexposed to fluoride. 相似文献