养心氏片对动脉粥样硬化模型小鼠的作用机制研究

目的探讨养心氏片治疗动脉粥样硬化(AS)的可能作用机制。方法以高脂饲料喂养雄性载脂蛋白E基因敲除(ApoE~(-/-))小鼠12周,复制AS模型。将AS小鼠随机分成模型组,养心氏片高剂量组、中剂量组、低剂量组及阳性对照组,每组8只。另设雄性C57BL/6J小鼠8只作为正常对照组。养心氏片高剂量组、中剂量组、低剂量组及阳性对照组给药量分别相当于70 kg成人临床剂量的2倍、1倍、0.5倍及1倍。养心氏片高剂量组、中剂量组、低剂量组给予养心氏片,剂量分别为1.40 g/(kg·d)、0.70 g/(kg·d)、0.35 g/(kg·d)灌胃,阳性对照组给予阿托伐他汀剂量为2.57 mg/(kg·d)灌胃,共给药12周。采用苏木素-伊红(HE)染色法观察小鼠升主动脉病理学变化,Image J软件测定小鼠升主动脉斑块校正后斑块面积。采用实时定量PCR(qPCR)法检测各组小鼠主动脉组织核转录因子-κB(NF-κB)、单核细胞趋化蛋白-1(MCP-1)、血管内皮细胞黏附分子-1(VCAM-1)、白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)mRNA的表达。结果与模型组比较,养心氏片高剂量组、中剂量组、低剂量组及阳性对照组升主动脉斑块校正后斑块面积呈现不同程度的降低(P0.05),以养心氏片高剂量组小鼠升主动脉斑块校正后斑块面积最低,而养心氏片高剂量组小鼠升主动脉斑块校正后斑块面积与阳性对照组相比差异无统计学意义(P0.05)。与正常对照组比较,模型组小鼠主动脉组织NF-κB、MCP-1、VCAM-1、IL-6、TNF-αmRNA的表达水平明显升高(P0.05),各药物干预组小鼠主动脉组织NF-κB、MCP-1、VCAM-1、IL-6、TNF-αmRNA表达水平较模型组均显著降低(P0.05),与养心氏片高剂量组相比,养心氏片中剂量组及低剂量组小鼠主动脉NF-κB、MCP-1、VCAM-1、IL-6、TNF-αmRNA表达升高(P0.05),而养心氏片高剂量组小鼠主动脉NF-κB、MCP-1、VCAM-1、IL-6、TNF-αmRNA表达与阳性对照组相比差异无统计学意义(P0.05)。结论养心氏片可抗动脉粥样硬化,并具有剂量依赖性,养心氏片给药组以养心氏片高剂量组抗AS效果最佳,其机制可能与降低AS小鼠升主动脉斑块校正后斑块面积及下调主动脉NF-κB信号通路相关因子mRNA表达有关。     

生芪降糖颗粒对2型糖尿病大鼠血糖、血脂及血管内皮素表达的影响

目的 探讨生芪降糖颗粒对糖尿病大鼠血糖、血脂及血管内皮素表达的影响.方法 制作2型糖尿病大鼠模型,随机分为生芪降糖颗粒低剂量组、中剂量组、高剂量组、文迪雅组、对照组.正常组给予蒸馏水灌胃,模型组分别给予生芪降糖颗粒低剂量、中剂量、高剂量、文迪雅、蒸馏水灌胃,至血糖下降至正常组水平或与造模时比较有统计学差异为治疗有效.测定各组血糖、总胆固醇(TC)、甘油三酯(TG)、胰岛素、主动脉内皮素1(ET-1)的变化及ET-1mRNA表达.结果 药物干预后生芪降糖颗粒中、高剂量组和文迪雅组血糖、TC、TG和胰岛素明显下降(P均<0.01).文迪雅组和生芪降糖颗粒高剂量组ET-1和主动脉El-1mRNA表达量较对照组均显著下降(P均<0.01).结论 ①生芪降糖颗粒有抗糖尿病作用,并呈剂量依赖性;②生芪降糖颗粒降低ET-1mRNA的表达,可保护和改善糖尿病大鼠主动脉内皮和心肌的功能.     

表没食子儿茶素没食子酸酯对2型糖尿病大鼠主动脉Ⅰ、Ⅳ型胶原及纤维连接蛋白表达的影响

目的探讨表没食子儿茶素没食子酸酯(EGCG)对2型糖尿病大鼠主动脉Ⅰ、Ⅳ型胶原(ColⅠ、ColⅣ)、纤维连接蛋白(FN)表达的影响及可能机制。方法通过高脂喂养加腹腔注射小剂量链脲佐菌素(STZ)构建2型糖尿病大鼠模型。雄性SD大鼠分为正常对照组8只,模型组、EGCG低、中、高剂量组,每组10只。EGCG给药组大鼠每周灌胃7 d。实验结束后检测大鼠血液血糖(GLU)、糖化血红蛋白(GHb)、糖化血清蛋白(GSP)和主动脉超氧化物歧化酶(SOD)、丙二醛(MDA)、ColⅠ、ColⅣ、FN水平的变化。结果与正常对照组相比,糖尿病模型组的血液GLU、GHb、GSP水平和主动脉氧化应激水平及主动脉ColⅠ、ColⅣ、FN表达均显著升高(P0.01);与模型组相比,EGCG中、高剂量组血液GLU、GHb、GSP水平和主动脉氧化应激水平及主动脉ColⅠ表达均显著降低(P0.05),EGCG高剂量组主动脉ColⅣ、FN表达显著降低(P0.05)。结论 EGCG对2型糖尿病大鼠主动脉胶原合成异常增加具有明显的改善作用,机制可能与EGCG的降血糖、抗氧化及降低氧化应激下游与胶原代谢相关的信号通路效应有关。     

TRALI大鼠肺泡活化巨噬细胞及共刺激分子CD40、ICAM-1的表达变化分析

目的探讨输血相关急性肺损伤(TRALI)大鼠肺泡活化巨噬细胞及共刺激分子CD40、血浆及肺组织中细胞间粘附分子-1(ICAM-1)的表达变化及其意义。方法选取60只SPF级、6-7周龄的雄性SD大鼠,采用随机数字表法分为假手术组(腹腔注射等量生理盐水)、对照组(腹腔注射2mg/kg脂多糖)、模型组(静脉输注脂多糖5mg/kg)和TRALI组(腹腔注射2mg/kg脂多糖+静脉输注血浆1m L/只)各15只,采用RTPCR技术检测活化巨噬细胞中Toll样受体4(TLR4)mRNA的表达,采用Northern bolt检测CD40 mRNA的表达,采用免疫组化染色检测ICAM-1蛋白的表达,采用酶联免疫吸附法(ELISA)检测血清中肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-β)、ICAM-1的水平。结果模型组和TRALI组的活化巨噬细胞中TLR4 mRNA、肺组织中CD40 mRNA、ICAM-1蛋白表达水平显著高于假手术组和对照组(P0.05),TRALI组的活化巨噬细胞中TLR4 mRNA、肺组织中CD40 mRNA、ICAM-1蛋白表达水平显著的低于模型组(P0.05);模型组和TRALI组的血清中TNF-ɑ、IL-β、ICAM-1的水平显著的高于假手术组和对照组(P0.05),TRALI组的血清中TNF-ɑ、IL-β、ICAM-1的水平显著的低于模型组(P0.05)。结论 TRALI大鼠肺TLR4 mRNA、CD40 mRNA、ICAM-1蛋白高表达,这可能与促进炎症因子释放,引起肺损伤有关。     

中药五灵脂对动脉粥样硬化大鼠细胞间黏附分子-1的影响

目的 观察中药五灵脂(FT)水提取物对实验性动脉粥样硬化(AS)大鼠细胞间黏附分子-1(ICAM-1)表达及动脉内膜病变的影响,探讨五灵脂抗AS作用的机制.方法 健康雄性清洁级6周龄Wistar大鼠60只,按体重随机分为4组,每组15只:空白对照组、模型组、五灵脂低剂量组(FWL)、五灵脂高剂量组(FTH).采用高脂饮食结合腹腔注射维生素D3注射液复制AS模型,模型复制成功后给予五灵脂水提取物不同剂量(2.5、10g/kg)灌胃干预.用药6w后采用酶联免疫吸附法测大鼠血清可溶性细胞间黏附分子-1(sICAM-1)水平,免疫组化观察主动脉ICAM-1表达,透射电镜观察主动脉内膜病变情况.结果 成功复制了大鼠AS模型.与空白对照组比较,模型组大鼠血清sICAM-1含量显著升高(P＜0.01).同给药前相比,给药后FTL、FTH大鼠血清sICAM-1含量显著降低(P＜0.01),也显著低于模型组(P＜0.01).免疫组化结果显示,模型组大鼠主动脉内皮细胞ICAM-1表达强阳性,药物干预后FTL、FTH大鼠ICAM-1表达明显减少(P＜0.01),FTH低于FTL(P＜0.05)但仍显著高于空白对照组(P＜0.01).电镜显示,FTL、FTH大鼠主动脉病变明显轻于模型组,FTH病变轻于FTL.结论 FT能降低实验性AS大鼠ICAM-1表达,减轻血管内皮病变程度,高剂量优于低剂量,这可能是其抗AS的分子机制之一.     

表观遗传修饰炎症相关基因在高血糖“代谢记忆”中的作用及机制

目的研究表观遗传修饰炎症相关基因在高血糖"代谢记忆"中的作用及相关机制。方法将Wistar大鼠分为正常对照组、高糖组和代谢记忆组,对比3组内皮细胞一氧化氮(NO)活性水平、单核细胞趋化蛋白(MCP-1)、细胞间黏附分子(ICAM-1)和白细胞介素(IL)-6 mRNA表达水平、活性氧(ROS)水平、内源性NO合酶(eNOS)基因表达和eNOS(Ser-1177)磷酸化水平。结果正常对照组NO含量显著高于高糖组和代谢记忆组,而MCP-1、ICAM-1和IL-6 mRNA表达则显著低于高糖组和代谢记忆组(P0.01);代谢记忆组NO含量显著高于高糖组,而MCP-1、ICAM-1和IL-6 mRNA表达则显著低于高糖组(P0.01)。正常对照组的超氧化物阴离子荧光探针(DHE)和活性氧簇细胞渗透性指示剂(CM-H2DCFDA)荧光强度显著低于高糖组和代谢记忆组(P0.01);代谢记忆组DHE和CM-H2DCFDA荧光强度显著低于高糖组(P0.01)。正常对照组eNOS mRNA和蛋白表达水平显著低于高糖组和代谢记忆组,而Ser-1177磷酸化水平显著高于高糖组和代谢记忆组(P0.01);代谢记忆组eNOS mRNA和蛋白表达水平显著低于高糖组,而Ser-1177磷酸化水平显著高于高糖组(P0.01)。结论早期高血糖可持续损伤血管内皮细胞舒张功能,进而令其功能紊乱,即使血糖水平恢复正常,仍然存在着持久的eNOS高表达,产生高血糖代谢记忆。     

硫化氢对自发性高血压大鼠血管炎症反应的调节作用

目的 探讨新型气体信号分子硫化氢(H2S)对自发性高血压大鼠(SHR)血管炎症反应的调节作用.方法 4周龄Wistar-Kyoto(WKY)雄性大鼠和SHR雄性大鼠分为4组:WKY大鼠对照组、SHR对照组、SHR+硫氢化钠(NaHS,H2S供体)组及SHR+炔丙基甘氨酸(PPG,H2S生成关键酶抑制剂)组,饲养至9周.尾容积法测清醒时大鼠血压,免疫组织化学方法检测主动脉内皮细胞膜细胞间黏附分子-1(ICAM-1)、核转录因子-κB p65(NF-κB p65)和核转录因子抑制因子-α(IκB-α)的蛋白表达,原位杂交分析检测主动脉内皮细胞ICAM-1 mRNA的表达.结果 SHR对照组血压显著高于WKY对照组(P<0.05),主动脉内皮细胞ICAM-1、ICAM-1 mRNA、胞核NF-κB p65明显高(P均<0.01),胞浆IκB-α蛋白表达明显低(P<0.01).SHR+NaHS组血压显著低于SHR对照组,主动脉内皮细胞ICAM-1、ICAM-1 mRNA、胞核NF-κB p65蛋白表达明显低(P<0.05),胞浆IκB-α蛋白表达明显增高(P<0.05),SHR+PPG组主动脉内皮细胞ICAM-1、ICAM-1mRNA、胞核NF-κB p65蛋白表达更高(P<0.05),胞浆IκB-α蛋白表达显著低(P<0.05).结论 H2S可通过抑制SHR血管炎症发挥抗高血压效应.H2S的抗血管炎症效应可能通过上调IκB-α的表达,降低NF-κB p65的表达,抑制ICAM-1 mRNA的转录和蛋白表达实现.     

电针丰隆穴对高脂血症大鼠肝脏SR-BI、PPARγ的调控及炎症相关因子的影响

目的:探讨电针丰隆穴对高脂血症大鼠血脂水平、肝脏组织的清道夫受体BI(scavenger receptor clas s B type I,SR-BI)、过氧化物酶体增殖物激活型受体γ(peroxi some proliferator-activated receptor-γPPARγ)的mRNA相对表达量及腹腔巨噬细胞炎症相关因子细胞间黏附因子-1(intercellular adhesion molecule-1,ICAM-1)、白介素-1β(intefleukin-1β,IL-1β)、IL-10含量的影响及其相关作用机制.方法:将SD大鼠随机分为空白对照组、模型对照组、电针1组、电针2组这4组,每组10只.治疗结束后检测各组血脂含量,肝脏组织中SR-BI、PPARγ的mRNA相对表达量.最后分离出大鼠腹腔中的巨噬细胞,应用流式细胞仪检测炎症相关因子ICAM-1、IL-1β、IL-10的含量.结果:与空白对照组比较,模型对照组TG.变化并不明显(p0.05),而总胆固醇(total chole sterol,TC)、低密度脂蛋白-胆固醇(loW density lipoprotein cholesterol,LDL-C)明显上升(P0.01),高密度脂蛋白-胆固醇(high density lipoprotein cholesterol,HDL-C).明显下降(P0.01);与模型对照组比较,电.针l组及电针2组的TG和HDL-C变化并不明显(P0.05),大鼠血清TC、LDL-C均有显著下降(P0.01);与电针1组比较,电针2组TC、LDL-C均有降低(P0.01,P0.05).与空白对照组比较,除了电针2组外,其余两组SR-BI、PPAR7均有显著降低(P0.05,P0.01);与模型对照组比较,电针1组和电针2组的SR-BI、PPARγ均有显著升高(P0.05,P0.01),其中电针2组更为显著(P0.01).与空白对照组比较,除电针2组外,模型对照组和电针1组的炎症因子ICAM-1、IL-1β均有显著性升高(P0.05,P0.01),而模型对照组的抗炎因子IL-10有显著下降(P0.01);与模型对照组比较,电针1组和电针2组的炎症因子ICAM-1、IL-1β均有非常显著性减少(P0.01),而抗炎因子IL-10的含量有非常显著性升高(p0.01).结论:通过电针丰隆穴治疗能降低高脂血症模型大鼠的TC、LDL-C水平,升高HDL-C水平,增加肝脏SR-BI、PPARγmRNA相对表达量,减少大鼠巨噬细胞内炎症因子ICAM-1、IL-1β并增加抗炎因子IL-10的含量,达到治疗高脂血症的目的.     

西红花苷通过C/EBP-β/PGC-1α/UCP3途径对缺血缺氧损伤心肌的保护作用

目的探讨西红花苷对异丙肾上腺素所致心肌缺血缺氧模型大鼠的保护作用,并验证其作用机制是否与C/EBP-β/PGC-1α/UCP3信号通路有关。方法皮下注射异丙肾上腺素建立大鼠缺血缺氧模型后,分别灌胃给予西红花苷不同剂量干预(25、50、100 mg/kg)。比较各组大鼠血清LDH-1、CK-MB、MDA、TNF-α、NO水平以及大鼠CI及心肌梗死面积;比较各组心肌Akt、ERK1/2、C/EBP-β、PGC-1α、UCP3蛋白及基因表达水平。结果与空白对照组比较,模型组大鼠存活率极显著降低(P0.01),血清LDH-1、CK-MB、MDA、TNF-α、NO水平、CI及心肌梗死面积均极显著升高(P0.01);心肌纤维排列紊乱且炎性细胞浸润明显;心肌Akt、ERK1/2蛋白表达均显著升高(P0.05),C/EBP-β、UCP3蛋白及mRNA表达均极显著升高(P0.01),PGC-1α蛋白及mRNA表达极显著降低(P0.01)。与模型组比较,阳性对照组大鼠存活率显著升高(P0.05),血清LDH-1、CK-MB、MDA、TNF-α、NO水平、心肌梗死面积均极显著降低(P0.01),CI显著降低(P0.05),心肌纤维排列整齐且炎性细胞浸润明显减轻;Akt、ERK1/2蛋白表达均极显著升高(P0.01),C/EBP-β蛋白及mRNA表达均极显著降低(P0.01),PGC-1α蛋白表达极显著升高(P0.01)而mRNA表达显著升高(P0.05),UCP3蛋白表达无差异而mRNA表达显著升高(P0.05)。与模型组、对照组比较,西红花苷中、高剂量均可显著提高大鼠存活率(P0.05);显著降低大鼠血清LDH-1、CK-MB、MDA、TNF-α及NO水平(P0.05);显著降低CI及心肌梗死面积(P0.05);减轻炎症浸润且提高心肌细胞完整程度;显著升高心肌Akt、ERK1/2蛋白表达水平(P0.05);显著降低心肌C/EBP-β蛋白及mRNA表达水平(P0.05),显著升高PGC-1α、UCP3蛋白及mRNA表达水平(P0.05);其中高剂量组综合效果较好。结论西红花苷对大鼠缺血缺氧损伤心肌具有明显的保护作用,其机制可能与调节C/EBP-β/PGC-1α/UCP3信号通路相关。     

菩人丹超微粉对糖尿病大鼠视网膜细胞间黏附分子-1表达的影响

目的探讨探讨菩人丹超微粉(PRD)对糖尿病大鼠视网膜细胞间黏附分子(ICAM-1)表达的影响。方法 36只Wistar大鼠随机分为3组,正常对照组、糖尿病模型组和PRD治疗组,每组12只。糖尿病模型组和PRD治疗组大鼠均采用链脲佐菌素连续腹腔注射建立2型糖尿病大鼠模型。模型成功建立后,PRD治疗组大鼠给予PRD灌胃,时间为3个月。采用SP免疫组织化学染色法、Western印迹法检测视网膜ICAM-1蛋白的表达;逆转录聚合酶链反应(RT-PCR)检测视网膜ICAM-1 mRNA的表达。结果糖尿病模型组与正常对照组比较,大鼠视网膜ICAM-1蛋白及mRNA表达均明显升高(P0.01),PRD治疗组与糖尿病模型组比较,大鼠视网膜ICAM-1蛋白及mRNA表达均明显降低(P0.01)。结论 PRD可通过下调ICAM-1的表达,抑制糖尿病大鼠视网膜炎症反应,发挥对糖尿病视网膜损伤的保护作用。     

胰岛素瘤的解剖分布特点分析

目的胰岛素瘤是最常见的胰腺神经内分泌肿瘤，因其临床表现多样，导致诊断困难。影像学诊断尤其是超声内镜(EUS)在胰岛素瘤的诊断中起着重要作用，拥有较高的敏感性和特异性。本研究拟通过明确胰岛素瘤的解剖分布特点，以期有助于提高影像学的诊断准确率和降低漏诊率，尤其是在教育和培训实践中对于EUS的学习者更具有指导价值。 方法回顾性分析解放军总医院第一医学中心病案资料数据库1993年1月至2019年11月经外科手术、病理确诊为胰岛素瘤的患者的临床资料，检索方法采取搜索术后病理诊断为"胰岛素瘤"的病例，通过查阅病例的方法，提取出胰岛素瘤的大小和解剖分布等数据，进一步分析其特点。 结果共检索到确诊为胰岛素瘤的患者116例，其中，男45例、女71例，年龄13～76岁，平均年龄(44.4±14.85)岁。胰岛素瘤单发110例(94.8%)、多发6例(5.2%)。位置分布：头颈部46例(39.7%)，单发45例、多发1例；体尾部68例(58.6%)，单发65例、多发3例；全胰腺多发2例(1.7%)。病变大小特点：最大径0.4～3.4 cm，平均大小(1.53±0.58)cm。≤1 cm 29例、>1 cm而≤1.5 cm41例、>1.5 cm而≤2.0 cm28例，≤3 cm 15例，>3 cm 3例。年龄与肿瘤的大小相关，≤44岁患者肿瘤平均大小为(1.36±0.51)cm、>44岁患者肿瘤平均大小为(1.70±0.60)cm，P<0.05。头颈部的肿瘤大于体尾部的肿瘤，头颈部肿瘤平均大小(1.66±0.63)cm，体尾部(1.42±0.52)cm，P<0.05。 结论胰岛素瘤在胰腺体尾部较头颈部更好发；绝大多数单发，但可以全胰腺多发；多数小于1.5 cm，肿瘤的大小与患者年龄和肿瘤的解剖分布相关。     

Pathogenesis of carcinoma of the papilla of Vater

Most adenomas and carcinomas of the small intestine and extrahepatic bile ducts arise in the region of the papilla of Vater. In familial adenomatous polyposis (FAP) it is the main location for carcinomas after proctocolectomy. In many cases symptoms due to stenosis lead to diagnosis at an early tumor stage. In about 80%, curative intended resection is possible. Operability is the most relevant prognostic factor. Most ampullary carcinomas resp. carcinomas of the papilla of Vater develop from adenomatous or flat dysplastic precursor lesions. They can be sited in the ampulloduodenal part of the papilla of Vater, which is lined by intestinal mucosa. They also can develop in deeper parts of the ampulla, which are lined by pancreaticobiliary duct mucosa. Intestinal-type adenocarcinoma and pancreaticobiliary-type adenocarcinoma represent the main histological types of ampullary carcinoma. Furthermore, there exist unusual types and undifferentiated carcinomas. Many carcinomas of intestinal type express the immunohistochemical marker profile of intestinal mucosa (keratin 7?, keratin 20+, MUC2+). Carcinomas of pancreaticobiliary type usually show the immunohistochemical profile of pancreaticobiliary duct mucosa (keratin 7+, keratin 20?, MUC2?). Even poorly differentiated carcinomas, as well as unusual histological types, may conserve the marker profile of the mucosa they developed from. These findings underline the concept of histogenetically different carcinomas of the papilla of Vater which develop either from intestinal- or from pancreaticobiliary-type mucosa of the papilla of Vater. Molecular alterations in ampullary carcinomas are similar to those of colorectal as well as pancreatic carcinomas, although they appear at different frequencies. In future studies, molecular alterations in ampullary carcinomas should be correlated closely with the different histologic tumor types. Consequently, the histologic classification should reflect the histogenesis of ampullary tumors from the two different types of papillary mucosa.     

Demonstration of the mechanism of action of biguanides

Summary Palmitic acid oxidation in rat diaphragm homogenate is depressed by biguanide concentrations that are still incapable of inhibiting oxidative phosphorylation. Glucose oxidation is not directly effected by the same biguanide concentrations: however, the inhibitory effect of palmitic acid on glucose oxidation is partly removed by biguanides. Inhibition of fatty acid oxidation, which accounts for most of the metabolic effects caused by these drugs, can be regarded as the fundamental mechanism of action of biguanides. There is some evidence suggesting that these drugs might interact with carnitine, thus preventing long-chain fatty acids from being transported across the mitochondrial membrane to the site of oxidation. Traduzione a cura degli AA.     

Lack of correlation of degree of villous atrophy with severity of clinical presentation of coeliac disease

BACKGROUND AND AIM: Both the clinical presentation and the degree of mucosal damage in coeliac disease vary greatly. In view of conflicting information as to whether the mode of presentation correlates with the degree of villous atrophy, we reviewed a large cohort of patients with coeliac disease. PATIENTS AND METHODS: We correlated mode of presentation (classical, diarrhoea predominant or atypical/silent) with histology of duodenal biopsies and examined their trends over time. RESULTS: The cohort consisted of 499 adults, mean age 44.1 years, 68% females. The majority had silent coeliac disease (56%) and total villous atrophy (65%). There was no correlation of mode of presentation with the degree of villous atrophy (p=0.25). Sixty-eight percent of females and 58% of males had a severe villous atrophy (p=0.052). There was a significant trend over time for a greater proportion of patients presenting as atypical/silent coeliac disease and having partial villous atrophy, though the majority still had total villous atrophy. CONCLUSIONS: Among our patients the degree of villous atrophy in duodenal biopsies did not correlate with the mode of presentation, indicating that factors other than the degree of villous atrophy must account for diarrhoea in coeliac disease.     

血吸虫童虫生长发育及其机制的研究进展

血吸虫童虫是宿主免疫系统攻击的重要靶标,包括皮肤型、肺型和肝门型童虫。宿主分子对童虫生长发育具有重要作用。童虫生长发育机制包括免疫调节、信号转导、性别发育及凋亡等。肌动蛋白、组织蛋白酶、烯醇化酶和葡萄糖基转移酶等分子为血吸虫童虫生长发育的重要分子。本文对血吸虫童虫生长发育及其机制的研究进展做一综述。     

氯硝柳胺悬浮剂的毒性评价

目的评价氯硝柳胺悬浮剂的毒性，为现场大规模应用灭螺提供依据。方法按照中华人民共和国国家标准GB 15670-1995《农药登记毒理学试验方法》和鱼类毒性试验方法进行。结果经口、经皮肤的LDso雌、雄性大鼠均>5 000 mg/kg，经呼吸道的LCso雌、雄性大鼠均>5 000mg/m3，该药经口、经皮肤、经呼吸道毒性均属微毒类药物；兔眼用药后，观察期内无不良反应，对眼无刺激性；皮肤用药后对皮肤无刺激性。与氯硝柳胺原药、氯硝柳胺乙醇胺盐原药和氯硝柳胺乙醇胺盐可湿性粉剂相比，氯硝柳胺悬浮剂对鱼急性毒性最低。结论氯硝柳胺悬浮剂属微毒类药物，对鱼的毒性低于其乙醇胺盐可湿性粉剂，适合于现场应用。     

124例耐多药结核分枝杆菌基因突变特征分析

目的对临床分离的耐多药结核分枝杆菌相关基因的突变特征进行分析。方法对124例耐多药结核分枝杆菌以及50株敏感株的耐药相关基因(包括异烟肼inh A、kat G、oxyR-ahp C间隔区以及利福平rpo B)进行序列测定,分析其基因突变情况。结果异烟肼耐药inh A基因突变率为14.5%;kat G基因突变率为70.2%(87/124),主要位于315位;oxyR-ahp C间隔区突变率为15.3%;inh A、kat G两种基因同时突变率75.0%,三种基因同时突变率为89.5%。利福平rpo B基因突变的检出率高达95.2%,突变主要发生在531、526、516位点。结论我省耐多药菌异烟肼耐药相关基因最常见突变为kat G 315、inh A C-T(-15)、axyR-ahp C间隔区(-10)C-T,利福平为rpo B531、526、516。结合MDR-TB耐药相关基因的特征分析,可以建立一种快速、准确、特异的适合于我省的检测结核菌耐多药性的新方法。     

Assessment of quality of life of parents of children with juvenile chronic arthritis

The aim of the study was to assess the quality of life (QOL) and the psychological status of parents of children with juvenile chronic arthritis (JCA). The QOL, anxiety and depression of the parents of 28 children with JCA were evaluated and compared to those of the parents of 28 healthy children. Mothers of JCA children and mothers of healthy children reported similar QOL. The reported anxiety and depression levels were similar for mothers and fathers in both groups. The parents of children with pauciarticular-type JCA reported lower QOL and higher levels of anxiety and depression than the parents of children with other types, namely polyarticular and systemic JCA. These findings may be explained by the fact that the pauciarticular patients had shorter disease duration and were less frequently seen in the outpatient clinic. The QOL of mothers of children with JCA was found to be slightly impaired in the group of children with pauciarticular JCA. Future larger studies are needed to confirm these results, as the number of subjects in the three groups was rather low. Received: 26 September 2001 / Accepted: 8 February 2002     

Numerical Simulation of the Effect of Rate of Change of Glucose on Measurement Error of Continuous Glucose Monitors

Background

A 5-day in-patient study designed to assess the accuracy of the FreeStyle Navigator® Continuous Glucose Monitoring System revealed that the level of accuracy of the continuous sensor measurements was dependent on the rate of glucose change. When the absolute rate of change was less than 1 mg•dl⁻¹•min⁻¹ (75% of the time), the median absolute relative difference (ARD) was 8.5%, with 85% of all points falling within the A zone of the Clarke error grid. When the absolute rate of change was greater than 2 mg•dl⁻¹•min⁻¹ (8% of the time), the median ARD was 17.5%, with 59% of all points falling within the Clarke A zone.

Method

Numerical simulations were performed to investigate effects of the rate of change of glucose on sensor measurement error. This approach enabled physiologically relevant distributions of glucose values to be reordered to explore the effect of different glucose rate-of-change distributions on apparent sensor accuracy.

Results

The physiological lag between blood and interstitial fluid glucose levels is sufficient to account for the observed difference in sensor accuracy between periods of stable glucose and periods of rapidly changing glucose.

Conclusions

The role of physiological lag on the apparent decrease in sensor accuracy at high glucose rates of change has implications for clinical study design, regulatory review of continuous glucose sensors, and development of performance standards for this new technology. This work demonstrates the difficulty in comparing accuracy measures between different clinical studies and highlights the need for studies to include both relevant glucose distributions and relevant glucose rate-of-change distributions.     

Angiographic diagnosis of the degree of serosal invasion of carcinoma of the colon

Angiography using Prostaglandin El^® was performed on 38 patients with carcinoma of the colon in order to diagnose the degree of serosal cancer invasion. The findings at angiography were classified into four groups:1) AG-S3, abnormal change (irregularity and/or encasement) up to marginal vessels; 2) AG-S2, abnormality up to vasa recta; 3) AG-S1, abnormality of penetrating branches of vasa recta within the wall of the colon; and 4) AG-S0, no distinct findings of abovementioned vessels. These angiographic findings were compared with both macroscopic and microscopic serosal cancer invasion. Angiographic diagnosis is in accord with the macroscopic findings in 84.2 percent of cases. Angiographic diagnosis is in accord with the microscopic findings in 32.4 percent of cases. Macroscopic findings confirm the angiographic diagnosis precisely but the conflict with microscopic findings should not be overlooked. This may be the result of inflammatory change, adhesion, and fibrosis around carcinoma of the colon.