氯沙坦治疗心功能不全临床观察

目的 :探讨血管紧张素 (ANG)Ⅱ受体拮抗剂氯沙坦治疗心功能不全中的临床疗效。方法 :选择NHYA心功能分级为ⅡⅣ级、EF≤ 5 0 %的病人 6 8例 ,随机单盲分为氯沙坦和福辛普利组 ,于服药前及服药 6个月观察临床症状、超声心功图。结果 :两组用药后左室射血分数 (EF)、心输出量 (CO)、心脏指数 (CI)及左室舒张末内径等指标均有改善(均为P <0 .0 5 ) ;氯沙坦组血尿酸 (UA)水平降低 (P <0 .0 5 ) ,而对照组无明显变化 (P >0 .0 5 ) ;福辛普利组 4例出现干咳 ,而氯沙坦组无病例出现。结论 :尽管氯沙坦和福辛普利均能改善左心室收缩、舒张功能 ,但氯沙坦可同时降低血尿酸水平 ,且耐受性好。     

熊果酸体外抗胃癌细胞SGC7901机制的研究

目的探讨熊果酸(urso lic ac id,UA)体外抑制胃癌细胞SGC 7901生长的作用机制。方法体外培养人胃癌细胞株SGC 7901,M TT法观察不同浓度UA作用不同时间对细胞生长的影响;不同浓度UA(0~40μm o l/L)处理SGC 7901细胞24 h后,倒置显微镜观察细胞形态变化;荧光染料Hoechst 33258染色和流式细胞仪检测细胞凋亡情况;W estern B lotting法检测凋亡相关蛋白B cl-2和B ax的表达。结果20~40μm o l/L UA可抑制SGC 7901的生长,并呈浓度和时间依赖性,其作用12、24、36、48 h的IC50分别为(57.50±1.18)、(34.28±2.05)、(27.54±1.11)、(24.83±1.02)μm o l/L。20~40μm o l/L UA作用24 h后,SGC 7901细胞变圆,出现不同程度的漂浮;同时细胞被阻滞于G0/G1期并发生凋亡,随药物浓度升高,凋亡率增加,凋亡相关蛋白B cl-2表达减少,B ax无明显变化。结论熊果酸对SGC 7901细胞具有较强的抗肿瘤活性,其机制可能与细胞毒作用、增殖抑制作用以及下调凋亡相关蛋白B cl-2表达而促进凋亡有关。     

熊果酸对卵巢癌细胞转移的抑制作用

目的 熊果酸(UA)对人卵巢癌细胞株HO-8910PM黏附、侵袭及趋化运动的影响,并探讨其可能的作用机制。方法 采用MTT法方法检测熊果酸对HO-8910PM细胞黏附能力的影响;Transwell小室进行人工重组基底膜侵袭实验检测熊果酸对HO-8910PM细胞侵袭及运动的影响;采用RT-PCR和Western blot方法检测熊果酸对HO-8910PM细胞中MMP-2 mRNA、MMP-9 mRNA和蛋白的表达的影响。结果 在黏附试验中,不同浓度熊果酸作用细胞24h后,抑制率分别为44.03%、46.62%和55.11%,与对照组比较具有统计学意义(P＜0.05)。不同浓度的熊果酸在体外作用24h后可以显著抑制HO-8910PM细胞的侵袭能力,穿膜细胞数与对照组比较具有统计学意义(P＜0.01)。熊果酸处理后细胞趋化运动能力降低与对照组比较差异有统计学意义(P＜0.05)。不同浓度熊果酸作用24小时后,HO-8910PM细胞MMP-2 mRNA、MMP-9 mRNA表达量明显低于正常对照组(P＜0.05),Western blot结果显示:HO-8910PM细胞MMP-2、MMP-9蛋白表达量受到明显抑制(P＜0.05)。结论 熊果酸抑制人卵巢癌细胞株HO-8910PM黏附、侵袭和转移的生物学行为,其作用机制可能与熊果酸显著抑制MMP-2、MMP-9表达水平有密切关系。     

不同中医治法对高尿酸血症大鼠模型血清尿酸水平的影响比较

目的：探讨不同中医治法对高尿酸血症大鼠模型血清尿酸水平的影响。方法：设立空白对照组、模型组、西药治疗组与中药复方6个治疗组（滋肾阴、温肾阳、健脾、活血、化痰、利湿），除空白对照组外，其余各组采用腺嘌呤联合乙胺丁醇法建立大鼠高尿酸血症动物模型，造模第21d开始给予各治疗组相应治疗，连续2周。检测造模第21d、35d的血清尿酸水平，观察其变化情况。结果：滋肾阴、温肾阳、健脾、活血、化疫、利湿各组中药均具有降低血清尿酸的作用，与模型组比较，有显著性差异（P〈0．05），其中利湿组和化痰组血清尿酸水平下降较其他组明显（P〈0．05），但与西药治疗组比较，无显著性差异（P〉0．05）。结论：不同中医治法均可降低血清尿酸，其中以利湿、化痰法治疗效果明显，对高尿酸血症具有预防及治疗作用．     

血清胆红素、尿酸、血脂水平含量与冠心病的相关性分析

目的研究血清胆红素、尿酸、血脂水平与冠心病的关系。方法应用日立7180全自动生化仪分别测定52例临床确诊的冠心病患者和42例正常人的血清胆红素、尿酸、血脂（总胆固醇、甘油三酯、高密度脂蛋白、低密度脂蛋白）的含量。采用病例对照的研究方法,对两组结果进行比较分析。结果冠心病组血清胆红素,HDL的水平明显低于正常对照组（P〈0.01）,CH、TG、LDL、UA的水平明显高于对照组（P〈0.01）,且男性尿酸水平明显高于女性,差异有统计学意义（P〈0.05）。结论冠心病的发病危险与胆红素、HDL呈负相关,与CH、TG、LDL、UA呈正相关。     

Advances in Percutaneous Coronary Interventions for Elderly Patients

Coronary heart disease (CHD) is one of the leading causes of morbidity and the most common cause of death in older adults. Paradoxically, elderly patients tend to be systematically excluded from randomized-controlled cardiovascular trials, which complicates decision-making in this population. Management of CHD in the elderly is frequently more difficult in virtue of chronic comorbid conditions and aging-intrinsic dynamics. Despite these challenges, the number of elderly and very elderly patients undergoing percutaneous coronary interventions (PCI) is increasing. Elderly patients in many registries and large clinical series exhibit even a greater benefit from interventional procedures than younger patients, but they have a higher rate of overall complications. We present an overview of the current available evidence of PCI in older adults with stable and unstable CHD, including comparisons between drug-eluting and bare-metal stents, transfemoral and transradial access, and methods of revascularization. Adjuvant antiplatelet and antithrombotic therapies are also discussed.     

老年高血压患者颈动脉粥样硬化病变及相关因素

目的探讨老年高血压患者的颈动脉粥样硬化病变程度及其与血脂、血尿酸、C-反应蛋白的关系。方法应用彩色多普勒超声检测22例正常老年人(对照组)、47例老年高血压患者(A组)、43例老年高血压合并冠心病患者(B组)的颈动脉内中膜厚度(IMT)、粥样硬化斑块、血流参数[收缩期峰值流速(Vmax)、阻力指数(RI)];同时检测血脂、血尿酸(UA)及C反应蛋白(CRP)。结果A组与对照组比较,平均IMT、最大IMT及CRP增高(均为P<0.001),斑块发生率、Vmax、RI、胆固醇(TC)、低密度脂蛋白(LDL-C)、UA增高(均为P<0.05);B组与A组比较,平均IMT、最大IMT、RI及CRP增加更为明显(均为P<0.001),斑块发生率、Vmax、TC、甘油三酯(TG)、LDL-C、UA也有相应变化(均为P<0.05)。结论老年颈动脉粥样硬化病变与许多危险因素有关,防治应采取综合措施。     

Dissociation of uterine eosinophilia and water imbibition from other estrogen-induced responses by nafoxidine pretreatment

We investigated the effect of pretreatment of immature rats with 5 or 50 micrograms nafoxidine (UA), or with 0.05 micrograms 17 beta-estradiol (E2) on several uterine responses elicited by treatment with a test injection of 15 micrograms E2, administered 48 h after pretreatment. Early (6 h) and late (24 h) responses were measured, including wet weight, RNA, protein and glycogen content and number of blood eosinophils per uterus. The results showed that, like a 24 h pretreatment with 5 micrograms UA, a 48 h pretreatment with either of the UA doses dissociated the early wet weight response from the late responses to E2 treatment, only the former being restored. In the case of E2 pretreatment, both types of response to E2 treatment were reinstalled. By contrast, uterine eosinophilia, induced 6 and 24 h after E2 treatment, was not only restored but even markedly amplified following any of the 3 pretreatments. This was obtained without amplification of the early wet weight response and with various levels of the other parameters at the time of administration of the test E2 injection (i.e. due to the pretreatment alone). From this it may be concluded that if the previously documented correlation between estrogen-induced eosinophilia and edema actually reflects the existence of a causal link between the 2 responses, as postulated by Tchernitchin in 1972, this would be with eosinophils controlling edema, rather than the reverse. Testable working hypotheses for the mechanism of amplification of the eosinophil response are proposed.