四川省西昌市吸毒人群首次吸毒情况的调查分析

目的:调查四川省西昌市吸毒人群首次吸毒的发生情况。方法:在四川省凉山彝族自治州西昌市戒毒所、拘留所和看守所调查吸毒人员的人口学特征,吸毒前吸烟和饮酒的情况,朋友、亲戚和家人吸毒的人数,首次吸毒的时间和使用毒品的方式和种类,吸毒前是否有被治安处理或违法行为。结果:共调查了619名吸毒人员,从出生到首次吸毒的发生率为4·08/100(95%可信区间为3·76-4·40)人年。在多因素Cox比例风险模型中,15a以前开始吸烟(危险率比值为1·58;95%可信区间为1·35-1·86),朋友中吸毒的人数(朋友中有1-4人吸毒危险率比值为1·25;95%可信区间为1·04-1·51,朋友中有5人及以上吸毒危险率比值为1·71;95%可信区间为1·39-2·09)和研究对象来源(拘留所和看守所危险率比值为1·52;95%可信区间为1·18-1·96)与首次吸毒的发生率有统计学意义。结论:需进一步了解首次吸毒发生的情况及其影响因素,为开展健康教育和行为干预来预防吸毒和有关疾病的传播提供科学依据。     

4-硫-5-(2-噻吩基)尿苷体外对黑色素肿瘤细胞增殖作用的影响

目的探究新化合物4-硫-5-(2-噻吩基)尿嘧啶核苷酸体外对黑色素瘤细胞的增殖作用影响。方法利用MTT法和磺酰罗丹明B染色法对比考察该化合物对人黑色素瘤细胞(A375)、小鼠黑色素肿瘤细胞(B16)和人正常皮肤细胞体外增殖的影响,并利用流式细胞术检测不同药物浓度下该化合物对人黑色素瘤细胞(A375)周期的影响。结果 4-硫-5-(2-噻吩基)尿嘧啶核苷酸苷体外对人和小鼠的黑色素瘤细胞无种属特异性,均表现出剂量依赖性的抑制作用,但对正常皮肤细胞却无抑制作用;流式细胞术显示:4-硫-5-(2-噻吩基)尿苷导致剂量依赖性的G2细胞累积,抑制细胞有丝分裂;同时具有诱导细胞凋亡的作用。结论 4-硫-5-(2-噻吩基)尿嘧啶核糖核苷酸对黑色素瘤有明显抑制作用,对正常皮肤细胞无抑制作用表明该化合物对细胞作用时具有选择性,有可能成为新型靶向抗癌药物的候选者。     

蟾酥脂质微球注射液的制备及其灭菌稳定性

目的研究蟾酥脂质微球注射液的处方工艺并考察制剂的灭菌稳定性。方法采用两级高压均质法制备蟾酥脂质微球注射液,分别考察油相组成、乳化剂用量、pH、灭菌方式对制剂灭菌稳定性的影响。结果采用质量分数为10.00%的油相[注射用中链脂肪酸甘油酯(MCT)与注射用大豆油(LCT)等比例混合],质量分数为1.20%的豆磷脂,质量分数为0.06%的油酸钠,均质前调节pH6.5,采用100℃旋转水浴灭菌30 min,制备所得的蟾酥脂质微球注射液在灭菌后仍保持良好的物理化学稳定性。结论粒子界面荷电性、空间位阻作用、pH、灭菌方式是影响蟾酥脂质微球注射液的物理化学稳定性的重要因素。     

毒蕈中毒致急性肝衰竭3例

3例患者（男2例,女1例）,年龄分别为14、4、37岁,食用自采野生蘑菇1d后出现恶心、呕吐、腹痛、腹泻等急性胃肠道症状。经治疗上述症状无明显缓解,且出现肝及心肌损害。4d后3例患者均出现皮肤及巩膜黄染,实验室检查示ALT1101～6580U/L,AST715～1965U/L,TBil38.5～153.2μmol/L,DBil16.9～63.1μmol/L,IBil21.6～90.1μmol/L;LDH1036～2234U/L,CK-MB18～36U/L,CK30～669U/L。临床确诊为毒蕈中毒、肝衰竭。先后给予3例患者白蛋白透析、血浆置换及对症、支持治疗。住院14d后患者病情好转出院。     

猪苓多糖对膀胱癌细胞钙离子浓度的影响

目的　观察猪苓多糖对人T2 4膀胱癌细胞内钙离子 (Ca2 )浓度的影响 ,探讨猪苓多糖抗癌机理。方法　体外培养人T2 4细胞经钙荧光指示剂 (calciumcrimson AM )负载后 ,用激光扫描共聚焦显微镜测定猪苓多糖作用前后细胞内Ca2 随时间的变化。结果　猪苓多糖低剂量 (0 .2mg·L- 1)使T2 4细胞内Ca2 降低 ,高剂量 (>1mg·L- 1)使T2 4细胞内Ca2 升高 ,最后维持在高钙水平上。猪苓多糖主要促进细胞核内Ca2 升高 ,细胞浆Ca2 无明显改变。结论　猪苓多糖可引起T2 4细胞内Ca2 水平的显著变化 ,而且这种变化主要表现在细胞核内 ,提示猪苓多糖可能有诱导细胞凋亡的作用     

家庭无创通气对慢性肺心病肺动脉高压的影响

目的探讨家庭无创机械通气对慢性肺源性心脏病（简称慢性肺心病）肺动脉高压的影响。方法慢性肺源性心脏病代偿期患者60例,随机分成治疗组30例（家庭无创机械通气联合常规治疗12周）和常规组30例（常规治疗12周）,测定治疗前后患者血浆ET-1、NO水平、血气变化及肺动脉压力等。结果①治疗组患者血浆NO水平明显升高（P<0.05）、血浆ET-1水平明显下降（P<0.05）。②治疗组肺动脉压、PaCO₂明显下降（P<0.05）,PaO₂明显升高（P<0.05）。③血浆NO水平变化与肺动脉压、PaCO₂呈负相关,与PaO₂呈正相关;血浆ET-1与肺动脉压、PaCO₂呈正相关,与PaO₂呈负相关。结论家庭无创机械通气治疗是慢性肺心病失代偿期患者肺动脉高压的重要治疗措施。     

紫杉醇在常见妇科恶性肿瘤中的应用

紫杉醇是一种新型抗微管类药物,自上市以来,该药就在妇科恶性肿瘤的治疗中得到了广泛应用。FDA已批准紫杉醇用于卵巢癌的一线治疗,而NCCN和FIGO指南也推荐其作为宫颈癌和子宫内膜癌的首选化疗药物。本文对紫杉醇的药理学机制进行了总结,归纳了该药的重要临床试验,着重比较在3种常见妇科恶性肿瘤中不同用药剂量、给药方式和联合用药的效果差异及不良反应,为紫杉醇的临床应用提供参考。     

Visual targeted therapy of hepatic cancer using homing peptide modified calcium phosphate nanoparticles loading doxorubicin guided by T1 weighted MRI

Effective treatment and real-time monitoring of hepatic cancer are essential. A multifunctional calcium phosphate nanoparticles loading chemotherapeutic agent doxorubicin and magnetic resonance imaging contrast agent diethylenetriaminepentaacetic acid gadolinium (A54-CaP/Gd-DTPA/DOX) was developed for visual targeted therapy of hepatic cancer via T1-weighted MRI in real-time. A54-CaP/Gd-DTPA/DOX exhibited a higher longitudinal relaxivity (6.02?mM^?1?s^?1) than commercial MR contrast agent Gd-DTPA (3.3765?mM^?1?s^?1). The DOX release from the nanoparticles exhibited a pH dependent behavior. The cellular uptake results showed that the internalization of A54-CaP/Gd-DTPA/DOX into BEL-7402 cells was1.9-fold faster than that of HepG2 cells via A54 binding. In vivo experiments presented that A54-CaP/Gd-DTPA/DOX had higher distribution and longer retention time in tumor tissue than CaP/Gd-DTPA/DOX and free DOX, and also displayed great antitumor efficacy (95.38% tumor inhibition rate) and lower toxicity. Furthermore, the Gd-DTPA entrapped in the nanoparticles could provide T1-weighted MRI for real-time monitoring the progress of tumor treatment.     

Activation of phospholipase D involved in both injury and survival in A549 alveolar epithelial cells exposed to H2O2

To determine the role of the phospholipase D (PLD) pathway in injury and survival of alveolar epithelial cells, A549 cells were exposed to H₂O₂ (500 μM) which resulted in time-dependent injury and bi-phasic increase of PLD activity at 5 min and at 3 h, respectively. n-Butanol (0.5%) inhibited PLD activation, attenuated cell injury at 5 min of H₂O₂ exposure, but enhanced injury at 3 h of exposure. This activation was inhibited by treatment with catalase (500 units/ml). Exogenous phosphatidic acid mimicked the effects of PLD activation, and diphenyliodonium (NADPH oxidase inhibitor) reversed the decline in cell viability induced by H₂O₂ exposure. Propranolol (phosphatidic acid phospholydrolase inhibitor) and quinacrine (phospholipase A2 inhibitor) had weak effects on H₂O₂-induced PLD activation but reversed H₂O₂-induced injury. We speculate that PLD activation at the initiation of H₂O₂ exposure predominantly results in NAPDH oxidase activation, which mediates A549 cell injury, but turns to mediating cell survival as the H₂O₂ attack continues, which might be mainly due to the accumulation of intracellular phosphatidic acid.