益气养阴治疗Ⅱ型糖尿病158例

糖尿病与祖国医学的消渴病症状相似。笔者通过多年来临床治疗糖尿病所得,发现糖尿病以“气阴两虚”为主要表现者颇多。自1996年至1999年4年间,采用益气养阴为主治疗Ⅱ型糖尿病临床效果满意,现报告如下。1一般资料本组158例患者根据WHO诊断标准均确诊为Ⅱ型糖尿病。其中住院患者     

不同浓度七氟烷对小儿先天性心脏病心内直视手术血流动力学及心肌酶的影响

目的:对比不同浓度七氟烷对先天性心脏病(简称先心病)心内直视手术患儿血流动力学、心肌酶的影响。方法:选取择期行先心病心内直视手术患儿75例,男36例、女39例,年龄5～11岁,根据七氟烷吸入浓度分为S1组、S2组、S3组,各25例。麻醉诱导：静脉注射0.05～0.10 mg/kg咪达唑仑、0.2～0.3 mg/kg依托咪酯、1.0～2.0μg/kg舒芬太尼以及0.8 mg/kg罗库溴铵;麻醉维持：麻醉诱导后行气管插管,自机械通气起S1、S2、S3组患儿分别持续吸入体积分数2.0%、2.5%、3.0%七氟烷,同时持续静脉泵注9～12μg·kg^-1·min^-1罗库溴铵、2.0～2.5μg·kg^-1·h^-1舒芬太尼、0.2～0.7μg·kg^-1·h^-1右美托咪定直至手术结束。记录3组患儿体外循环(CPB)时间、主动脉阻断(ACC)时间、转机时间、机械通气时间;分别于术前(T0)、麻醉诱导后(T1)、切皮后(T2)、劈胸骨后(T3)、术毕(T4)、术后6 h(T5...     

淋巴滤泡中补体成分沉积的意义

目的:观察补体成分在淋巴组织中的表达,探讨不同发育阶段淋巴滤泡中补体激活与免疫球蛋白沉积及滤泡树突状细胞之间的关系。方法:采用免疫组化方法对淋巴组织标本进行IgG、IgM、IgA、C3c、C4c、C1q和C4d标记,同时对其部分标本进行双标染色。结果:淋巴组织次级滤泡的Ⅰ~Ⅳ期的生发中心才出现不同程度的IgG、IgM、IgA、C3c、C4c、C1q、C4d阳性表达;免疫球蛋白与补体成分重叠沉积,并呈不规则网线状包绕在滤泡树突状细胞周围。其中以C4d的阳性表达最强。结论:淋巴滤泡生发中心有大量免疫球蛋白和补体成分围绕滤泡树突状细胞沉积,可能与中心淋巴细胞的发育和选择有关。     

慢性肺心病病人血清及发中锌铜的测定

本实验研究了21例正常人及43例慢性肺心病急性发作期病人血清及发中锌、铜含量。结果表明重度呼衰病人血清锌含量明显低于正常人,也低于轻、中度呼衰病人。病人组血清铜含量明显高于正常人。发中锌、铜含量病人组与正常人无显著差别。实验证明慢性肺心病病人,尤其重症,存在某些微量元素变化,可能参与某些病理生理过程。     

乳腺癌雌激素受体α基因启动子甲基化与其蛋白表达的关系

目的：检测乳腺癌雌激素受体α（estrogen receptor α,ERα）基因启动子区CpG岛甲基化状态,探讨乳腺癌ERα启动子甲基化与其蛋白表达及临床病理的关系。方法：采用免疫组化EnVisionTM二步法检测20例正常乳腺组织、44例乳腺癌组织ERα基因的表达,同时运用甲基化特异性PCR（Methylation-Specific PCR,MSP）及测序法分别检测ERα基因启动子A区和B区CpG岛的甲基化状态。结果：32例ERα阳性乳腺癌组织中,ERα启动子A区、B区甲基化率分别为28.2%和18.8%。12例ERα阴性乳腺癌组织中,ERα启动子A区、B区甲基化率分别为66.7%和58.3%。ERα阳性乳腺癌组、ERα阴性乳腺癌组、乳腺癌组的ERα启动子A、B区甲基化率均较正常组显著增高（P〈0.05）;ERα阴性乳腺癌组的ERα启动子A、B区甲基化率较ERα阳性乳腺癌组均显著增高（P〈0.05）。乳腺癌组织ERα表达与启动子区甲基化之间呈显著负相关。结论：乳腺癌组织ERα基因表达沉默与其启动子A区、B区CpG岛甲基化相关,后者有可能成为乳腺癌预后不良的分子检测指标。     

A risk prediction model for contrast-induced nephropathy associated with gadolinium-based contrast agents

ObjectiveThis is the first study to explore the risk factors for nephropathy caused by gadolinium-based contrast agents and establish a prediction model to identify high-risk patients.MethodsA total of 1404 patients who received gadolinium-based contrast agents in our hospital were included. The participants were randomly assigned in a 7:3 ratio to the modeling and validation groups. The modeling group was divided into a contrast-induced nephropathy group and a non-contrast-induced nephropathy group. The clinical characteristics before the use of contrast agents were compared between the two groups. The risk factors for contrast-induced nephropathy were analyzed by logistic regression. A nomogram that could predict the incidence of contrast-induced nephropathy was plotted. The validation group was used to verify the predictive model.ResultsThe incidence of contrast-induced nephropathy caused by gadolinium-based contrast agents was 3.92% (55/1404). The logistic stepwise regression analysis showed that sex, systolic pressure (SBP), absolute neutrophil count, albumin, fasting blood glucose level, and furosemide use were significant predictors of contrast-induced nephropathy caused by gadolinium-based contrast agents. The above predictors were then included in the nomogram construction. The area under the receiver operating characteristic (ROC) curve was 0.82 (p < 0.001). The specificity and sensitivity corresponding to the optimal cutoff point (0.039) based on the area under the ROC curve were 71.9% and 80.5%, respectively.ConclusionSex, SBP, absolute neutrophil count, albumin, fasting blood glucose levels, and furosemide use are significant predictors of contrast-induced nephropathy caused by gadolinium-based contrast agents. Therefore, the incidence of contrast-induced nephropathy may be estimated by the prediction model established in this study before the use of contrast agents.     

Subtoxic concentration of doxorubicin enhances TRAIL-induced apoptosis in human prostate cancer cell line LNCaP

Most tumor cells are sensitive to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis but sparing to normal cells, thus providing therapeutic potential for clinical use. Some tumor cells are resistant to TRAIL-induced cell death while the sensitivity could be recruited with the existence of some chemical agents. In this study, human prostatic cancer cell line LNCaP was found to be resistant to TRAIL-induced apoptosis while it could be restored to TRAIL sensitivity with combination treatment of low concentration of doxorubicin. TRAIL receptor-1 (DR4) and TRAIL receptor-2 (DR5) were upregulated under the treatment of doxorubicin and verified to be responsible for TRAIL-mediated signal transduction. Furthermore, caspase-8 and caspase-3 were activated and drove their autocleavage into programmed cell death. Interestingly, apoptosis-inhibitory protein c-FLIP, but not Bcl-2 and XIAP was downregulated after doxorubicin treatment. Taken together, these findings suggested that the pathway of cell apoptosis induced by TRAIL was intact but under negative control. Subtoxic concentration of doxorubicin effectively boosted TRAIL sensitivity via depletion of antiapoptotic protein. These findings support the new strategies for killing tumors with TRAIL and chemical agents.     

过表达或抑制IL-18对大鼠深静脉血栓形成的影响

目的 :探讨白介素(interleukin,IL)-18对大鼠深静脉血栓(deep vein thrombosis,DVT)模型血栓形成的影响。方法 :构建IL18-p CDH-GFP、IL18-LMP-sh RNAmir1病毒载体。SD大鼠(n=27)随机均分为3组。过表达组:尾静脉注入IL-18慢病毒过表达载体(IL18-p CDH-GFP,100μl);抑制组:注入IL-18逆转录病毒抑制载体(IL18-LMP-sh RNAmir1,100μl);对照组:注入无菌生理盐水(100μl)。注射24 h后,SD大鼠行狭窄法下腔静脉(inferior vena cava,IVC)血栓造模,造模后24 h解剖观察IVC血栓形成情况,并取材称量血栓重量及长度;血栓静脉管壁行实时荧光定量PCR检测IL-18表达情况。结果:IL18-p CDH-GFP、IL18-LMPsh RNAmir1病毒载体的体外细胞实验具备理想的过表达率及抑制率。各组大鼠造模后24 h可见稳定血栓形成。IL-18过表达组的平均成栓长度和重量较IL-18抑制组、对照组明显增加(P<0.05),real-time PCR结果显示过表达组中IL-18在大鼠静脉壁表达量明显增加(F=3.784,P<0.05)。结论:IL-18表达量增加,对大鼠DVT造模后IVC血栓形成有促进作用,而表达减少亦对成栓有影响,其表达状况与深静脉血栓的发生、发展有关,IL-18介导的促炎反应在静脉血栓疾病发病机制中可能起重要作用。