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。     

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.     

老年COPD病患营养治疗的疗效观察

目的观察营养状况及营养支持治疗对COPD患者治疗及预后的重要性。方法 76例COPD住院患者随机分为营养支持组(A组)和常规对照组(B组),各38例,观察在住院期间临床总有效率,平均住院时间,营养状况,血清尿酸,肺功能变化。结果 A组临床总有效率明显高于B组;平均住院时间A组明显短于B组;营养状况、血清尿酸、肺功能A组明显优于B组。结论在常规治疗的基础上,应用营养支持治疗可以明显改善老年COPD患者营养状况、肺功能,提高临床疗效,减少住院天数。     

高血压患者同型半胱氨酸、尿酸、超敏C-反应蛋白及脂蛋白a检测的临床意义

目的:研究高血压患者血清同型半胱氨酸(HCY)、尿酸(UA)、超敏C-反应蛋白(hs-CRP)及脂蛋白a(LPa)含量的变化。方法:选择高血压患者110例作为观察组,另选择同期进行体检的健康者110例作为对照组。检测两组受检者血清同型半胱氨酸、尿酸、超敏C-反应蛋白及脂蛋白a水平,并进行统计学分析。结果:观察组中的HCY、UA、hs-CRP及LPa血清水平显著高于对照组,差异有统计学意义(P<0.05)。在观察组中,HCY、UA、hs-CRP及LPa单一检测及4项联检的阳性率显著高于对照组,差异有统计学意义(P<0.05)。结论:高血压患者同型半胱氨酸、尿酸、超敏C-反应蛋白及脂蛋白a水平显著高于正常人,检测HCY、UA、hs-CRP及LPa可给临床治疗提供参考,值得临床推广应用。     

Inhibition of Organic Anion Transporting Polypeptide 1B1 and 1B3 by Betulinic Acid: Effects of Preincubation and Albumin in the Media

Betulinic acid (BA), a plant-derived pentacyclic triterpenoid, may interact with the members of the organic anion transporting polypeptide 1B subfamily. Here, we investigated the interactions of BA and its analogs with OATP1B1/3 and rat Oatp1b2 in vitro and in vivo. BA inhibited the activity of OATP1B1/3 and rat Oatp1b2 in vitro. Systemic exposure of atorvastatin was substantially altered with the intravenous co-administration of BA (20 mg/kg). Preincubation (incubation with inhibitors, followed by washout) with BA led to a sustained inhibition of OATP1B3, which recovered rapidly in the media containing 10% fetal bovine serum. The addition of albumin to the media decreased intracellular concentrations of BA and expedited the recovery of OATP1B3 activity following preincubation. For asunaprevir and cyclosporin A (previously known to inhibit OATP1B3 upon preincubation), the addition of albumin to the media shortened recovery time with asunaprevir, but not with cyclosporin A. Overall, our results showed that BA inhibits OATP1B transporters in vitro and may incur hepatic transporter-mediated drug interactions in vivo. Our results identify BA as another OATP1B3 inhibitor with preincubation effect and suggest that the preincubation effect and its duration is impacted by altered equilibrium of inhibitors between intracellular and extracellular space (e.g., albumin in the media).