维生素E对小鼠日本血吸虫病肝纤维化的治疗作用及其机制

目的: 探讨维生素E (Vit E)抗小鼠日本血吸虫病肝纤维化作用及其机制. 方法: 用日本血吸虫尾蚴皮肤敷贴法感染小鼠,构建日本血吸虫病肝纤维化模型,以肝纤维化达Ⅱ级或Ⅱ级以上作为开始Vit E治疗标志. 实验分5组: 正常对照组、模型组及Vit E高、中、低剂量组(每日150, 50, 5 mg/kg), 8 wk末处死动物,HE和VG染色对肝组织进行病理学检查,分光光度法检测肝组织丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性,免疫组化SP法检测肝星状细胞(HSC)标记物α-平滑肌动蛋白(α-SMA)表达,RT-PCR方法检测肝脏α1(I)型前胶原mRNA表达. 结果: Vit E降低模型组肝脏MDA含量[(5.00±0.31) μmol/g vs (11.66±1.84) μmol/g, P＜0.05],提高SOD活性[(249.84±26.22) μkat/g vs (120.11±42.61) μkat/g, P＜0.05];减少α-SMA阳性表达 [(0.41±0.02) vs (0.68±0.02), P＜0.05];降低肝脏胶原含量[(0.23±0.01) vs (0.60±0.11), P＜0.05]和α1(I)型前胶原基因表达[(0.28±0.01) vs (0.85±0.15), P＜0.05]. 结论: Vit E具有抗小鼠日本血吸虫病肝纤维化作用,其机制与抗脂质过氧化作用、抑制HSC活化和增殖、降低α1(I)型前胶原基因表达和胶原合成有关.     

过氧化物酶体增殖物激活受体γ抑制高磷诱导血管平滑肌细胞钙化

目的 探讨过氧化物酶体增殖物激活受体γ(peroxisome proliferators activated receptor γ,PPARγ)对高磷诱导的小鼠血管平滑肌细胞(vascular smooth muscle cells,VSMCs)钙化的抑制作用.方法 体外培养小鼠血管平滑肌细胞,先分正常对照组、高磷组(HP,2.6 mmol/L),观察高磷对VSMCs的影响,再分为正常对照组、高磷组(HP,2.6 mmol/L)、罗格列酮组(RGL,10 μmol/L)、高磷(2.6 mmol/L)±罗格列酮(10 μmol/L)组(HP+RGL),观察PPARγ激动剂罗格列酮对高磷诱导的VSMCs钙化的抑制作用.茜素红S(alizarin red S)染色观察高磷对细胞钙盐沉积的影响.Western blot检测PPARγ、血管平滑肌22alpha蛋白标志物(SM22α)、骨形成蛋白2(BMP2)和成骨特异性转录因子2(Runx2)的表达变化.结果 与正常对照组相比,高磷处理后的VSMCs的钙盐沉积明显升高[(0.08 ±0.02)vs(0.19 ±0.03),P＜0.01],成骨细胞标志物BMP2[(0.26 ±0.02) vs (0.74±0.03),P＜0.01]及Runx2表达[(0.29 ±0.03) vs (0.91 ±0.04),P＜0.01)],明显升高.同时PPARγ[(0.93±0.04)vs(0.58±0.02),P＜0.05]及平滑肌细胞标志物SM22α表达减少[(1.02±0.09) vs(0.77±0.03),P＜0.05],而加入罗格列酮后,高磷状态下VSMCs的钙盐沉积明显降低[(0.19±0.02) vs(0.12±0.03),P＜0.05],PPARγ[(0.63 ±0.04)vs(0.85 ±0.03),P＜0.05]和SM22α[(0.69 ±0.02) vs(0.99±0.03),P＜0.01]表达明显上升,相反,BMP2[(1.02±0.04) vs (0.48±0.05),P＜0.01]及Runx2[(1.00 ±0.06) vs (0.67 ±0.03),P＜0.01]的表达则明显受抑.结论 高磷诱导VSMCs向成骨细胞分化和钙化可能与下调PPARγ的表达有关,而罗格列酮可通过激活PPARγ抑制高磷状态下VSMCs钙化的发生.     

对氧磷酶2对氧化低密度脂蛋白诱导的乳鼠心肌细胞损伤的影响

目的 探讨对氧磷酶2(paraoxonase 2,PON2)在氧化低密度脂蛋白(oxidized low density lipoprotein,ox-LDL)诱导的乳鼠心肌细胞(neonatal rat ventricular cells,NRVCs)损伤中的作用及机制.方法 分离SD大鼠(出生1～3d,雌雄不限,共90只)心肌细胞.细胞分为:①对照组(未进行任何干预)、②0.1 μmol/Lox-LDL组(ox-LDL干预24 h)、③10 μmol/Lsalubrinal+ox-LDL组(salubrinal预处理1h后加入ox-LDL干预24 h)、④20 μg/mLPON2+ox-LDL组(PON2预处理1h后加入ox-LDL干预24 h)、⑤2.5μmol/LMn(Ⅲ)TBAP+ ox-LDL组[(Mn(Ⅲ)TBAP预处理1h后加入ox-LDL干预24 h].通过MTT法和Caspase-3/7活性检测试剂盒分别检测细胞活性和细胞凋亡变化(n=6);Western blot检测心肌细胞内质网应激和氧化应激蛋白表达情况(n=4).结果 与对照组相比,ox-LDL明显降低心肌细胞活性[(0.417 ±0.047) vs(O.883 ±0.064),P ＜0.01]显著增加心肌细胞凋亡[(11 505 ±817)vs(6417 ±439),P ＜0.01].与ox-LDL组相比,PON2、salubrinal和Mn(Ⅲ)TBAP干预后,细胞活性显著升高[(0.567 ±0.066) 、0.649 ±0.082) 、0.539 ±0.049) vs0.417 ±0.047),P ＜0.01],细胞凋亡显著下降[(7 776 ±488) 、(7 545 ±547)、(7 960±480)vs (11 505 ±817),P ＜0.01).与对照组相比,ox-LDL显著增加PON2蛋白表达[(0.86 ±0.223) vs (0.561 ±0.13),P ＜0.05]、内质网应激蛋白eIF-2αphox、caspase-12和氧化应激蛋白Nox2/gp91 phox、p47 phox表达[(1.309 ±0.274) vs (0.780 ±0.186) 、(1.294±0.273) vs (0.606 ±0.064) 、(1.342 ±0.274) vs(0.788 ±0.137) 、(1.178 ±0.194) vs (0.629 ±0.125),P＜0.01].与ox-LDL组相比,PON2干预后,PON2蛋白表达明显升高[(1.190 ±0.151) vs (0.860±0.222),P＜0.05];eIF-2αphox 、caspase-12、Nox2/gp91 phox和p47 phox蛋白表达明显降低[(0.924 ±0.170) vs(1.309 ±0.274) 、(0.895 ±0.202) vs (1.294 ±0.273) 、(0.957 ±0.190) vs (1.342 ±0.274) 、(0.799±0.232) vs(1.178 ±0.194),P ＜0.05].与PON2作用类似,salubrinal干预后,eIF-2αphox和caspase-12蛋白表达明显降低[(1.010±0.096) vs(1.309±0.274)、(0.788±0.042)vs(1.294±0.273),P＜0.01],Mn(Ⅲ)TBAP干预后,Nox2/gp91 phox和p47 phox蛋白表达明显降低[(0.898 ±0.190) vs(1.342±0.274) 、(0.769±0.158) vs(1.178 ±0.194),P ＜0.01],二者均显著升高PON2蛋白表达[(1.248±0.259) 、(1.176 ±0.248) vs(0.860 ±0.222),P ＜0.05].结论 PON2可能通过代偿性升高抑制氧化应激和内质网应激而减轻ox-LDL诱导的心肌细胞损伤.     

二氢杨梅素激活磷酸腺苷活化蛋白激酶抑制高糖诱导的血管内皮细胞凋亡

目的 探讨二氢杨梅素对高糖诱导血管内皮细胞凋亡的影响及其与磷酸腺苷活化蛋白激酶(AMP-activated protein kinase,AMPK)的关系.方法 体外培养原代人脐带静脉内皮细胞(human umbilical vein endothelial cells,HUVECs),分为正常对照组(5.56 mmoL/L葡萄糖)、高糖处理组(33.36 mmol/L葡萄糖)、甘露醇高渗对照组(5.56 mmol/L葡萄糖+27.8 mmol/L甘露醇)、AMPK激动剂5-氨基咪唑4-甲酰胺-1-β-D-呋喃核糖苷(5-Aminoimidazole-4-carboxamide-1-β-D-ribofuranoside,AICAR)(10 nmol/L)+高糖处理组、二氢杨梅素(1μmol/L)+高糖处理组、AMPK抑制剂compound C(5 mmol/L) +AICAR+高糖处理组和AMPK抑制剂compound C(5 mmol/L)+二氢杨梅素+高糖处理组.处理36 h后,CCK-8法检测细胞增殖活力,Annexin V-FITC/PI双标记流式细胞仪检测细胞凋亡,Western blot法检测AMPK、p-AMPK、乙酰辅酶A羧化酶(Acetyl-CoA carboxylase,ACC)和p-ACC蛋白水平.结果 与正常对照组比较,高糖处理组细胞活力明显降低(P＜0.05),细胞凋亡率显著增加(P＜0.05),p-AMPK、p-ACC水平显著降低(P＜0.05);二氢杨梅素或AICAR预处理均明显抑制高糖诱导的HUVECs细胞活力下降、细胞凋亡增加和p-AMPK、p-ACC水平降低(P＜0.05);Compound C预处理明显抑制AICAR和二氢杨梅素对高糖诱导HUVECs细胞凋亡的保护作用(P＜0.05).结论 二氢杨梅素通过促进AMPK活化抑制高糖诱导的血管内皮细胞凋亡.     

磷酸腺苷激活的蛋白激酶在慢性应激诱发小鼠非酒精性脂肪肝中的作用

目的 探讨磷酸腺苷激活的蛋白激酶(AMPK)及其激动剂5-氨基咪唑-4-甲酰胺核苷酸(AICAR)在慢性应激诱发小鼠非酒精性脂肪肝(NAFLD)中的作用.方法 建立小鼠慢性应激模型,设对照组、应激组、应激加AICAR给药组和AICAR给药组,每组6只.采用ELISA法检测小鼠血浆促炎性细胞因子(肿瘤坏死因子a,γ干扰素)浓度,采用自动生化分析仪检测小鼠血浆丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、总胆固醇、三酰甘油、游离脂肪酸的水平,采用苏木精-伊红染色和油红O染色检测肝细胞脂肪变性,采用蛋白质印迹法检测肝组织AMPK蛋白表达;然后用AICAR处理慢性应激小鼠并检测上述指标的变化.结果 慢性应激导致小鼠肝细胞脂肪变性,肝功能损害(ALT、AST水平升高,P＜0.01),血浆促炎性细胞因子浓度升高(P＜0.05),血浆游离脂肪酸水平升高(P＜0.01)以及肝组织AMPK蛋白表达降低(P＜0.01).AICAR改善了肝细胞脂肪变性,并缓解了上述指标的变化.结论 慢性应激可能通过AMPK信号通路诱发NAFLD,AMPK激动剂AICAR可缓解慢性应激导致的NAFLD.     

盐酸青藤碱介导Hedgehog信号通路治疗小鼠溃疡性结肠炎分子机制的研究

  目的  研究盐酸青藤碱(SH)对小鼠溃疡性结肠炎(UC)的保护作用及可能机制。   方法  将24只小鼠采用随机数字表法分为正常组、模型组、SH低、高剂量组(SH 20 mg/kg、60 mg/kg)4组,每组6只;记录疾病活动指数(DAI)和结肠组织病理学评分,检测Shh mRNA及相关蛋白和细胞因子的表达。   结果  与正常组相比,模型组DAI评分[(3.44±0.27)分vs. 0分, P＜0.001]升高,组织病理学评分升高[(7.67±0.52)分vs. 0分,P＜0.001],Shh mRNA降低(P＜0.05),Shh、Smo、Ptch1、Gli1蛋白表达水平降低(均P＜0.01),TNF-α、IL-1β、IL-6升高(均P＜0.001);与模型组相比, SH低、高剂量组DAI评分[(2.50±0.18)分、(1.89±0.17)分vs. (3.44±0.27)分, P < 0.001]降低, 组织病理学评分降低[(5.17±0.75)分、(3.33±0.52)分vs. (7.67±0.52)分, P < 0.001],Shh、Smo、Ptch1、Gli1蛋白升高(均P＜0.001),TNF-α、IL-1β、IL-6降低(均P＜0.01)。   结论  SH可治疗小鼠UC,其机制可能是SH上调了Hedgehog信号通路活性,从而降低了TNF-α、IL-1β、IL-6含量。      

慢性缺氧诱导小鼠心肌细胞自噬及其机制

目的 观察慢性缺氧对小鼠心肌细胞自噬水平的影响,并初步探讨AMPKα2敲除对该过程的作用.方法 采用野生型与AMPKα2-/-雄性C57小鼠均分为野生型常氧组、野生型缺氧组、敲除型常氧组和敲除型缺氧组(n=10).常氧组于空气环境中饲养,缺氧组于10％ O2的低氧舱内饲养.4周后野生型小鼠取静脉血标本,测红细胞及血红蛋白水平;取心脏标本用Western blot检测AMPKα2及自噬相关蛋白LC3-Ⅱ/LC3-Ⅰ比值与p62的变化,用免疫荧光染色法检测心肌冰冻切片LC3变化.敲除型小鼠取心脏标本用Western blot检测心肌组织LC3-Ⅱ/LC3-Ⅰ比值变化.结果 ①野生型小鼠中,与常氧组比较,缺氧组红细胞与血红蛋白水平显著增加[红细胞:(9.33 ±0.15)×1012/L vs(12.78±0.66)×1012/L,P ＜0.05;血红蛋白:(135 ±3)g/L vs (192 ±4)g/L,P＜0.05];②野生型小鼠中,与常氧组相比,缺氧组心肌组织LC3-Ⅱ/LC3-Ⅰ比值显著增加[(0.49 ±0.29) vs(1.70 ±0.24),P＜0.05];p62表达明显降低[(1.32±0.57) vs (0.71 ±0.19),P＜0.05];免疫荧光结果显示,缺氧组心肌组织LC3荧光较常氧组增多;③在常氧条件下,与野生型小鼠比较,AMPKα2-/-小鼠心肌组织LC3-Ⅱ/LC3-Ⅰ比值降低,但差异无统计学意义[(0.78 ±0.08) vs (0.73 ±0.34),P＞0.05];在缺氧条件下,与野生型小鼠比较,AMPKα2-/-小鼠心肌组织LC3-Ⅱ/LC3-Ⅰ比值显著降低[(2.08±0.72) vs (1.01 ±0.21),P＜0.05];④野生型小鼠中,与常氧组比较,缺氧组AMPKα2蛋白表达水平并无显著增加[(1.14±0.13) vs(1.25±0.19),P＞0.05].结论 慢性缺氧可能通过AMPKα2依赖的途径增强心肌细胞自噬,该自噬可能是心肌细胞对慢性缺氧的适应机制.     

心肌细胞来源NCoR1对小鼠心肌梗死损伤的保护作用

  目的  探究心肌细胞来源的核受体辅抑制因子1(NCoR1)对小鼠心肌梗死损伤发挥的作用。  方法  构建心肌细胞NCoR1特异性敲除小鼠并根据不同手术处理分为假手术野生型组、假手术基因敲除组、心肌梗死野生型组和心肌梗死基因敲除组,每组各50只小鼠。统计各组小鼠在心肌梗死28 d的生存率和心功能水平;通过病理染色判断梗死面积与纤维化程度;测定小鼠血清心肌酶[磷酸肌酸激酶(CK-MB)、乳酸脱氢酶(LDH)]及炎症指标[肿瘤坏死因子α(TNF-α)、白介素6(IL-6)]水平。  结果  与野生型小鼠相比,基因敲除组小鼠存活率更低,左心室射血分数[(30.39±5.13)% vs. (9.46±2.10)%]和左心室缩短分数[(14.62±2.69)% vs. (4.26±0.96)%]均明显下降,而左室容积[(101.50±14.07)μL vs. (197.50±22.41)μL]明显升高(均P＜0.05);小动物PET/CT提示心肌梗死后野生型小鼠对18F-FDG的摄取量更高[(2.74±0.06)MBq vs. (1.60±0.03)MBq],梗死程度[(36.22±0.86)% vs. (47.17±1.27)%]和纤维化程度[(32.70±0.85)% vs. (46.38±1.31)%]更低(均P＜0.05);血清学指标显示敲除小鼠心肌损伤更重且炎症水平更高(均P＜0.05)。  结论  心肌细胞中NCoR1在小鼠心肌梗死中发挥重要的保护作用。      

AMPK腺病毒载体在小鼠骨骼肌中的表达和作用

目的:探讨注射AMPK腺病毒在小鼠骨骼肌中的表达和作用。方法:C57BL/6小鼠随机分为4组:（1）无任何处理的空白对照组。（2）肌肉注射腺病毒空载体（Ad-GFP）组。（3）肌肉注射Ad-GFP,48 h后腹腔注射AMPK激活剂AICAR组。(4)肌肉注射GFP标记的激活型AMPK腺病毒（Ad-AMPK-CA）组。注射腺病毒72 h后,处死小鼠,通过小动物成像系统测定骨骼肌中的荧光强度,检测腺病毒的表达,用Western Blot方法检测ACC的磷酸化。结果:与空白对照组比较,注射腺病毒组的平均荧光强度显著增高。与病毒空载体组比较,注射AICAR组和Ad-AMPK-CA组的ACC磷酸化水平显著升高。结论:AMPK腺病毒能在小鼠骨骼肌中表达目的蛋白,调节AMPK的作用。     

LIGHT在低氧性肺动脉高压形成中的作用及机制

目的 初步探讨LIGHT在低氧性肺动脉高压(hypoxic pulmonary hypertension,HPH)形成中的作用及其机制.方法 将20只8周龄雌性C57BL/6J小鼠[体质量(17.90 ±0.91)g]和20只8周龄雌性LIGHT-/-C57BL/6J小鼠[体质量(17.55 ±0.93)g]分为4组(n=10):①野生小鼠常氧组(WT-C组)、②野生小鼠低氧组(WT-H组)、③LIGHT KO小鼠常氧组(LIGHT KO-C组)、④HGHT KO小鼠低氧组(LIGHT KO-H组).WT-H组和LIGHT KO-H组小鼠置于模拟6000 m低压舱内连续低氧饲养30 d,WT-C组和LIGHT KO-C组小鼠舱外(海拔308 m)常规饲养.检测右心室收缩压(right ventricular systolic pressure,RVSP)和右心肥厚指数(right ventricular hypertrophy index,RVHI);HE染色观察肺小动脉结构;免疫组化检测LIGHT及其受体HVEM、LTβR表达;荧光定量PCR和Western blot检测肺组织LIGHT、HVEM和LTβR、IL-6的mRNA和蛋白水平.流式细胞术检测肺组织中各类炎症细胞的比例.结果 与WT-C组相比,WT-H组肺组织中LIGHT的mRNA和蛋白水平均显著增高(P＜0.05),WT-H组RVSP和RVHI明显升高(P＜0.05),肺小动脉明显增厚;与HGHT KO-C组相比,LIGHT KO-H组小鼠的RVSP、RVHI和肺小动脉厚度显著增加(P＜0.05),但与WT-H组相比,LIGHTKO-H组的RVSP、RVHI和肺小动脉增厚程度明显降低(P＜0.05).与WT-C组相比,WT-H组LIGHT受体HVEM表达增加,LTβR表达降低,差异具有统计学意义(P＜0.05).LIGHT KO-H组与WT-H组相比,肺组织IL-6mRNA和蛋白水平显著降低(P＜0.05).流式细胞检测发现,与WT-C组相比,WT-H组小鼠肺组织中单核细胞比例降低[(3.88±0.87)％ vs (11.03±1.71)％,P ＜0.05],间质巨噬细胞比例升高[(15.56±2.69)％ vs (8.57±2.17)％,P ＜0.05];与WT-H组相比,LIGHT KO-H组的肺组织单核细胞增加[(6.55±1.01)％ vs (3.88±0.87)％,P ＜0.05],而间质巨噬细胞的比例降低[(10.87±1.68)％vs.(15.56±2.69)％,P ＜0.05].结论 慢性低氧诱导肺组织中HGHT表达增加与HPH发病机制密切相关.LIGHT可能通过HVEM信号途径促进细胞增殖、上调肺组织IL-6表达、促进肺间质巨噬细胞产生,参与HPH的形成.     

Value of D-Dimers in patients with acute aortic dissection

Objective: To evaluatel the value of D-dimers in patients with acute aortic dissection (AAD). Methods: This study consisted of 16 patients with AAD and 27 non-AAD patients. Serum D-dimets were measured by Sta-Liatest D-DI immunoturbidimetric assay. Results: D-dimer level was higher (P ＜ 0.001) in patients with AAD(7.91 ± 5.52 μg/ml) than that in non- AAD group(1.57±1.24 μg/ml). D-dimer was positive (＞0.4 μg/ml) in all patients with AAD and in 10 control group patients (37%). Among patients with acute AAD, D-dimers tended to be higher in Stanford A than in Stanford B (8.67 ± 4.31 μg/ml vs. 3.24±1.27 μg/ml, P ＜0.01). D-dimer values tended to be higher in more extended disease(3.84 ± 1.65 μg/ml, 8.57 ± 3.58 μg/ml and 11.87 ± 5.69 μg/ml in thoracic aorta, thoracic and abdominal aorta, thoracic and abdominal aorta and iliacal arteries, respectively, P ＜ 0.05 for both 8.57 ± 3.58 and 11.87 ± 5.69 vs. 3.84 ± 1.65 ). Including the control group into the analysis, we found a sensitivity of 100%, a negative predictive value of 100%, and a specificity of 66% and a positive predictive value of 64% for D-dimer in diagnosis of AAD in our patients with suspected AAD. Conclusion: D-dimer was elevated in patients with AAD. A negative D-dimer test result could be useful in excluding AAD.     

Research of combined liver-kidney transplantation model in rats

Objective： To set up a simple and reliable rat model of combined liver-kidney transplantation. Methods： SD rats served as both donors and recipients. 4℃ sodium lactate Ringer＇s was infused from portal veins to donated livers,and from abdominal aorta to donated kidneys, respectively. Anastomosis of the portal vein and the inferior vena cava （IVC） inferior to the right kidney between the graft and the recipient was performed by a double cuff method, then the superior hepatic vena cava with suture. A patch of donated renal artery was anastomosed to the recipient abdominal aorta. The urethra and bile duct were reconstructed with a simple inside bracket. Results： Among 65 cases of combined liver-kidney transplantation, the success rate in the late 40 cases was 77.5%. The function of the grafted liver and kidney remained normal. Conclusion： This rat model of combined liver-kidney transplantation can be established in common laboratory conditions with high success rate and meet the needs of renal transplantation experiment.     

BLOOD PRESSURE CHANGE WITH AGE IN SALT-SENSITIVE TEENAGERS

Objective To observe blood pressure change with age in salt-sensitive teenagers whose salt sensitivity were determined by repeated testing.Methods Salt sensitivity was determined through intravenous infusion of normal saline combined with volume-depletion by oral diuretic furosemide in 55 teenagers. After five years, salt sensitivity was re-examined and subject blood pressure was followed up. Blood pressure changes in salt-sensitive teenagers were compared to that of non-salt sensitive teenagers over five years.Results After 5 years, the repetition rate of salt sensitivity determined by intravenous saline loading is 92.7%. In teenagers with salt sensitivity on the baseline, both the systolic blood pressure increments and increment rates were much higher than non-salt sensitive teenagers (12.7±12.1 mmHg vs. 2.8±5.2 mmHg, P＜ 0.01; 12.2%± 12.0% vs. 2.5% ±4.4%, P＜ 0.001,respectively). There was a similar trend for diastolic blood pressure (8.4 ± 6.4 mmHg vs. 3.7 ± 6.4 mmHg, P = 0.052; 13.2% ±10.6 % vs. 6.8%± 10.1%, P = 0.053, respectively).Conclusions Salt sensitivity determined by intravenous saline loading showed good reproducibility. Blood pressure increments with age were much higher in salt-sensitive teenagers than non-salt sensitive teenagers, especially in terms of systolic blood pressure.     

APPLICATION OF LORNOXICAM TO PATIENT-CONTROLLED ANALGESIA IN PATIENTS UNDERGOING ABDOMINAL SURGERIES

FOR anesthesiologis s ,treatingpostoperativepainhas alwaysbeen a problem.Althoughopioidshave been provedtobe effective,theirsideeffectscouldnotbeignored.With thedevelopmentofscienceand pharmacology,many drugs with aspectsof satisfactoryanalgesicefficacyand couldbe welltoleratedby patientshave been developed.And lornoxicamisone of them, which isa non-steroidalanti-inflammatorydrug (NSAID ), with analgesic, anti-infl-ammatory,andantipyreticproperties.Itseliminationhalf-time(3 to 5 hours) isle…     

安心颗粒对急诊经皮冠状动脉介入术后生活质量影响的研究

目的：评价使用安心颗粒对急诊经皮冠状动脉介入术（PPCI）术后生活质量的影响.方法：将160例接受PPCI的急性ST段抬高型心肌梗死患者随机分为安心颗粒组（术前顿服安心颗粒8.8g,术后安心颗粒4.4 g/次,每日2次）和对照组（仅接受基础药物治疗）.所有患者均服用阿司匹林、氯吡格雷和阿托伐他汀.分别在入院时、出院前1d、出院后180 d时,应用心肌梗死多维度量表（MIDAS）、中文版SF-36评价量表对患者生活质量评分.并观察术后30 d以内的出血并发症、血小板减少症发生情况.结果：入院时和出院前1d,两组患者的心肌梗死MIDAS、SF-36量表评分比较无差异（P＞0.05）;出院后180 d时,与对照组比较,安心颗粒组MIDAS、SF-36评分明显减低（P＜0.05）;组内与入院时比较,两组出院前1d、出院后180 d时,MIDAS、SF-36评分均降低（P＜0.05）.两组患者在随访期间均无大量出血、少量出血、重度和极重度血小板减少症发生,安心颗粒组有4例、对照组有7例发生不明显出血（P＞0.05）.两组发生轻度血小板减少症的患者数比较无差异（P＞0.05）.结论：PPCI使用安心颗粒,能改善急性ST段抬高型心肌梗死患者的生活质量,且不增加出血风险.     

The comparative studies of the influences of Urapidil and Nicardipine on sino-atrial node function, atrio-ventricular node function and hemodynamics

Objective:To investigate the influences of urapidil and nicardipine on rabbit sinus function,atrio-ventricular node function and hemodynamics.Methods:Thirty-two Angora's rabbits were selected and randomly divided into four groups.U1 group:urapidil 0.25 mg/kg;U2 group:urapidil 0.5 mg/kg;N1 group:nicardipine 10 μg/kg;N2 group:nicardipine 20 μg/kg.All these medicine were administrated within 30 seconds.Measurements were taken before and after the administration of urapidil or nicardipine for the following data:mean blood pressure(MAP),heart rate(HR),sino-atrial conduction time(SACT),maximal sinoatrial recovery time(SNRTmax)corrected sinus node recovery time(CSNRT),index of sinus node recovery time(SNRTI),Wenckebach A-V conduction frequency (WB),and P-R interval.Results:Significant MAP and HR changes were identified in all of the four groups before and after administration of both urapidil and nicardipine.No significant changes could be found in the rest of the parameters.Intergroup analysis showed that SACT and CSNRT of N1 and N2 groups were shorter than those of the U2 group(P＜0.01);the MAP decreased(P＜0.01)and the HR increased drastically(P＜0.01).Conclusions:Neither urapidil(0.25 mg/kg,0.5 mg/kg)nor nicardipine(10μg/kg,20μg/kg)has any significant influence on rabbit sinus function or rabbit atrio-ventricular node function.Nicardipine could be a better choice than urapidil for parafunctional sinus node patients.     

Dynamic Changes in Serum Estradiol and Progesterone levels in Patients of Premenstrual Syndrome with Adverse Flow of Liver-qi

Objective:To probe into the influence of changes of ovarian hormones on the pathogenesis of the specific sub-type premenstrual syndrome(PMS)and reveal partial microcosmic mechanisms of adverse flow of liver-qi.Methods:Estradiol(E2)and progesterone(P)levels in serum were determined at different phases of menstrual cycle by radioimmunoassay.Results:In the group of PMS with adverse flow of liver-qi.the secretive peak value Of E2 and P at the follicular phase significantly decreased,and the secretive peak value at the luteal phase did not come into being.Conclusions:Low E2 and P secretive peak at the follicular phase and absence of secretive peak at the luteal phase is one of the microcosmic mechanisms of PMS with adverse flow of liver-qi.One of the pathophysiologic mechanisms of specific sub-type PMS is probably the continuous low level of E2and P.     

Real-time Three-dimensional Echocardiography in Assessment of Left Ventricular and Right Ventricular Volumes

Real-time three-dimensional echocardiography (RT3DE)is a new ultrasound technique that enables dynamic threedimensional visualization and quantification of the heart in real time. Investigation of feasibility and methodology of RT3DE in determining left ventricular (LV) and right ventricular (RV) volumes, RT3DE was performed in 35 normal adults using Philips SONOS 7500 system with a 2-4 MHz matrix array transducer. The 60°×60° "pyramid" volume database was obtained and analyzed on a TomTec echo workstation. Both LV and RV volumes were calculated with four 3DE methods (i.e. apical 2, 4, 8, and 16-plane) through manually tracing ventricular endocardial borders in end diastole and end systole. Stroke volumes were then calculated. LV volume was also measured by 2DE Simpson's rule using GE VIVID 7 ultrasound machine.     

SCREENING FOR A 21-CHROMOSOME ABNORMALITY IN PREIMPLANTED EMBRYOS OF ELDERLY WOMEN

Increasing maternal age is the only etiological factor unequivocally linked to Down's syndrome in humans. The occurrence rate of newborns with Down's syndrome is about 1/220 in women over 35 years old. However, the occurrence rate in embryos fertilized in vitro, of the elder woman is unclear. Using FISH we screened the number of chromosome 21 in preimplanted embryos of 5 elderly women (average age, 38.4 years) to study the feasibility and necessity of screening trisomy 21 in embryos in patients over 35 years old at the in vitro fertilization (IVF) center.     

Scientific principles and rigorous processes should be followed in developing clinical guidelines for therapeutic interventions of integrative medicine

A clinical guideline for the therapeutic interventions of integrative medicine may be defined as a written document which states a series of recommendations on therapeutic interventions of integrative medicine for a special disease or condition. The guideline may provide assistance to medical professionals in making clinical decisions aimed at improving the clinical outcome of patients and reducing the costs of medical care（~＇4~. Recommendations issued by a guideline should be based on the best available evidence in both Western and Chinese medicine. For fulfilling this purpose, the development of clinical guidelines for therapeutic interventions in the field of integrative medicine should follow scientific principles and undergo a rigorous processes.