教学医院青年医师提高教学能力途径的探索

医学院校师资力量的培养已成当务之急。青年医师应系统学习教育理论、积极观摩、开展教学查房及经验交流、利用互联网、阅读文献、重视学术实践,以不断提高临床教学能力。     

糖尿病高风险人群糖化血红蛋白与微血管并发症的关系

目的 探讨在广州地区的糖尿病高风险人群中HbA1C与糖尿病微血管并发症之间的关系,并评价其对糖尿病的诊断价值.方法 对208例糖尿病高风险患者进行HbA1C、血糖、眼底彩色照相及微量白蛋白尿测定.以受试者工作特征(ROC)曲线比较HbA1C、空腹血糖(FPG)、餐后2 h血糖(2hPG)的诊断效果.结果 高风险人群中糖尿病视网膜病变患病率为14.9%,微量白蛋白尿患病率为12%.HbA1C、FPG和2hPG分别为5.8%、7.0 mmol/L和10.9 mmol/L时视网膜病变的发病率显著增加.HbA1C、FPG和2hPG分别为5.8%、6.4mmol/L和10.7mmol/L时微量白蛋白尿发病率明显增加.结论 HbA1C为5.8%时糖尿病高风险人群微血管并发症患病率显著增加,HbA1C和2hPG判断微血管并发症的效果无明显差异,FPG相对偏低.

Abstract：

Objective To explore the association of HbA1C with microvascular complications,and to evaluate the diagnostic value of HbA1C in diabetes mellitus in high-risk populations of Guangzhou.Methods HbA1C,blood glucose,fundus photography,and microalbuminuria were detected in 208 permanent residents with high-risk factors of diabetes.The receiver operating characteristiC(ROC)curves were used to estimate the area of HbA1C,fasting plasma glucose(FPG),postprandial 2 h plasma glucose(2hPG)under the curve for discriminating microvascular complications.Results There were 14.9% adults suffering from diabetic retinopathy and 12% microalbuminuria in high risk populations of diabetes.The optimal cutoff points of HbA1C,FPG,and 2hPG in detecting retinopathy were 5.8%,7.0 mmol/L,and 10.9 mmol/L respectively.The thresholds for increasing prevalence of microalbuminuria were5.8% for HbA1C,6.4 mmol/L for FPG,and 10.7 mmol/L for 2hPG.Conclusions The prevalence of diabetic microvascular complications increases dramatically at the concentration of HbA1C 5.8%.As a diagnostic value for microvascular complications,there is no significant difference between HbA1C and 2hPG.     

波动性高糖对胰岛β细胞增殖及Skp2-p27表达的影响

目的 探讨波动性高糖对INS-1细胞增殖、凋亡及对细胞周期进程的影响,并研究其可能的分子机制.方法 采用细胞计数试剂盒(cell counting kit-8)检测细胞增殖活性,流式细胞仪测定细胞周期及细胞ROS水平,Annexin-V/PI双标流式细胞术检测细胞凋亡.应用Western印迹检测细胞周期调控蛋白p27及Skp2的表达水平.结果 (1)波动性高糖及持续性高糖均明显抑制INS-1细胞的生长,且波动性高糖对细胞增殖的抑制作用更为显著.(2)波动性高糖及持续性高糖均明显增加INS-1细胞的凋亡,且波动性高糖作用更为显著.(3)波动性高糖及持续性高糖能明显抑制细胞周期进程,使INS-1细胞周期更多滞留在G0/G1期,G2/M期与S期细胞比例下降,波动性高糖作用更显著.(4)波动性高糖及持续性高糖均能显著增强细胞周期调控蛋白p27的表达,同时减弱Skp2蛋白的表达水平.结论 波动性高糖较持续性高糖更能够抑制INS-1细胞的增殖和诱导凋亡,可能是通过减弱Skp2蛋白的表达水平,增加p27蛋白的活性,使细胞阻滞在G0/G1期,抑制细胞周期进程,从而减弱细胞的增殖活性.

Abstract：

Objective To investigate the effect of intermittent high glucose on proliferation, apoptosis, and cell cycle progression of INS-1 cells, and the possible intracellular pathways activated by intermittent high glucose. Methods Cell viability was evaluated by cell counting kit, the cell cycle was determined by flow cytometry,Annexin-V/PI double-labeled cell apoptosis detection kit was used to monitor cell apoptosis. Cell cycle related protein Skp2 and p27 expressions were detected by Western blot. Results ( 1 ) Both intermittent and constant high glucose significantly inhibited the growth of INS-1 cells, and the former effect was more significant. ( 2 ) Intermittent and constant high glucose levels significantly increased apoptosis in INS-1 cells, and the former effect was more significant. (3) Intermittent and constant high glucose levels significantly inhibited the cell process, the G0/G1 cell cycle arrest also was induced by intermittent high glucose, resulting in lowered proportion of the G2/M phase and S phase of INS-1 cells. (4) Intermittent and constant high glucose significantly decreased the level of protein Skp2 and increased the level of cell cycle related protein p27. Conclusion Intermittent high glucose levels affect INS-1 cell growth and proliferation, as well as induce cell apoptosis, probably by decreasing the level of protein Skp2 and increasing the level of p27 in the cells, resulting in arrest of progression through the G1 phase to the S phase of INS1 cells, and thus impairment of cell proliferation.     

间歇性高糖对胰岛β细胞生长及细胞周期进程的影响

背景:间歇性高糖可阻滞胰岛β细胞生长,增加β细胞的凋亡,但具体作用机制尚不清。目的:观察间歇性高糖对大鼠胰岛素细胞增殖、凋亡及对细胞周期进程的影响。方法:实验对大鼠胰岛素细胞进行培养,分为正常糖对照组,恒定性高糖组和间歇性高糖组,分别含葡萄糖5.5,30,30和5.5mmol/L间歇换液。采用细胞计数试剂盒检测细胞增殖活性,流式细胞仪测定细胞周期,Annexin-V/PI双标流式细胞术检测细胞凋亡,应用Westernblot检测细胞周期调控蛋白CyclinD1的表达水平。结果与结论:与正常糖对照组相比,恒定性高糖组及间歇性高糖组均明显抑制大鼠胰岛素细胞细胞的生长(P<0.01),增加大鼠胰岛素细胞的凋亡(P<0.01),明显抑制细胞周期进程,使大鼠胰岛素细胞的细胞周期更多滞留在G0/G1期(P<0.01),能显著减弱细胞周期调控蛋白CyclinD1的表达(P<0.01)。与恒定性高糖组相比,间歇性高糖以上各指标作用均更显著(P<0.01)。结果证实,间歇性高糖能够抑制大鼠胰岛素细胞的生长,增殖和诱导凋亡,其机制可能是通过降低CyclinD1的活性,使细胞阻滞在G0/G1期,抑制细胞周期进程,从而减弱细胞的增殖活性。     

PPARγ通路对模拟微重力条件下大鼠骨髓间充质干细胞向成骨细胞分化的影响

目的观察过氧化物酶体增殖物激活受体γ（PPARγ）通路对模拟微重力条件下大鼠骨髓间充质干细胞（BMSC）向成骨细胞
分化的影响,并通过调节PPARγ信号通路开闭影响这一分化过程。方法以大鼠BMSCs作对象,以回转器模拟微重力效应。
将细胞随机分为5组,包括实验组：模拟微重力组、模拟微重力+10 μmol/L吡格列酮组、模拟微重力+10 μmol/L GW9662组、模
拟微重力+10 μmol/L吡格列酮+10 μmol/L GW9662组;对照组：正常重力组。体外成骨诱导14 d后,利用茜素红进行成骨结节
染色、油红-O进行脂肪细胞染色,并计算成脂率;测定各组细胞ALP活性;利用RT-PCR技术检测各组细胞PPARγmRNA表达水
平。结果吡格列酮明显抑制BMSCs向成骨细胞分化,GW9662通过抑制PPARγ的激活而增加BMSCs向成骨细胞分化。结
论推测PPARγ信号通路的激活是模拟微重力条件下抑制BMSCs向成骨细胞分化的主要因素之一,而通过抑制这条通路的激
活可以有效预防及治疗失重导致的骨质疏松症。
     

中老年糖尿病高危人群血脂异常现状调查

目的探讨广州市中老年糖尿病高危人群血脂异常的分布情况及其危险因素。方法选取广州市5个社区年龄≥45岁且无糖尿病史居民619名,采用芬兰糖尿病风险积分(FINDRSC)表筛查糖尿病高危人群,FINDRSC≥9分者即为糖尿病高危人群并纳入研究。结果共208例糖尿病高危人群纳入研究。血脂异常患病率75.0%。单纯型血脂异常者占22.6%,混合型血脂异常者占52.4%。Logistic回归分析显示,WC(OR=1.063,95%CI:1.018~1.111)、臀围(OR=1.077,95%CI:1.022~1.134)、BMI(OR=1.154,95%CI:1.035~1.286)、FPG(OR=2.050,95%CI:1.316~3.195)、2hPG(OR=1.115,95%CI:1.012~1.228)、高血压(OR=2.220,95%CI:1.093~4.513)和FINDRSC(OR=1.320,95%CI:1.093~1.594)进入回归方程。结论广州市糖尿病高危人群血脂异常患病率较高,肥胖、高血压、高血糖和FINDRSC是血脂异常的危险因素。