LOX-1介导ox-LDL诱导的血管内皮细胞MCP-1的表达

目的：观察血凝素氧化低密度脂蛋白受体-1（LOX-1）对氧化LDL（ox-LDL）诱导的人脐静脉内皮细胞(human unbilical vein endothelial cells, HUVECs)表达单核细胞趋化蛋白（monocyte chemoattractant protein-1, MCP-1）基因及蛋白的影响。 方法： 用RT-PCR和Western blot的方法观察ox-LDL对培养的HUVECs表达LOX-1和MCP-1基因及蛋白的影响，然后用LOX-1的受体阻滞剂爱兰苔胶（carrageenan） 和聚肌苷酸［polyinosinic acid，poly(I)］与HUVECs预先作用后，再观察内皮细胞表达LOX-1和MCP-1基因和蛋白的变化。 结果： 用不同浓度的ox-LDL（0 mg/L、10 mg/L、20 mg/L 、50 mg/L、100 mg/L）与HUVECs培养24 h后，LOX-1和MCP-1的mRNA和蛋白的表达明显增加，呈浓度依赖性；用Carrageenan 和polyinosinic acid与HUVECs预先作用2 h后，再加入50 mg/L的ox-LDL培养24 h，与未加Carrageenan和polyinosinic acid相比，HUVECsLOX-1和MCP-1的mRNA和蛋白的表达明显减少。 结论： ox-LDL可以调节培养的HUVECsLOX-1和MCP-1基因和蛋白的表达，LOX-1作为ox-LDL的特异性受体，可能介导了ox-LDL诱导血管内皮细胞分泌MCP-1，从而在动脉粥样硬化的发生发展中起着重要的作用。     

内毒素致家兔氧提取功能障碍的研究

作者复制了家兔病理性氧供依赖性(POSD)模型。采用渐进性低氧法降低总氧运输量(TO_2),从而考察机体氧运输及氧摄取的变化特点。结果表明,在TO_2-VO_2的关系中,对照组可清楚地分为“非依赖”与“依赖”两部分;内毒素组从呼吸空气开始,从未出现坪区,内毒素组和对照组依赖段的斜率,即氧提取率分别为0.473和0.730,两者差别显著(P<0.05)。内毒素组的动静脉血氧含量差值(CaO_2-CVO_2)在渐进性低氧过程中逐渐变小(P<0.01,ANOVA),对照组则呈相反变化趋势,故其组间差别越来越大,表明内毒素组氧提取率降低。     

延胡索中季铵生物碱的高分辨基质辅助激光解吸电离质谱研究

目的：研究中药中季铵生物碱的基质辅助激光解吸电离质谱行为。方法：以延胡索为例，采用2，5-二羟基苯甲酸为基质，以样品和基质混合均匀点样，直接分析中药生物碱提取物；利用高分辨质谱数据确定生物碱化合物的元素组成。结果：从延胡索中检出并鉴定了去氢紫堇碱等5种季铵生物碱。结论：基质辅助激光解吸电离质谱为中药中季铵生物碱提供了一种快速分析方法。     

近视眼后极部视网膜厚度与眼轴长度的相关性研究

目的:探讨近视眼后极部不同区域的视网膜厚度与眼轴长度的关系。方法:采用视网膜厚度分析仪(retinalthicknessan-alyzer,RTA)测定45例(85眼)近视患者后极部视网膜厚度,并分析视网膜厚度与眼轴长度的相关性。结果:近视眼后极部视网膜平均厚度与性别、年龄无关,与眼轴长度明显相关,随着近视眼眼轴延长,近视屈光度明显增加,后极部视网膜厚度明显变薄,其中以黄斑周围区比黄斑区视网膜变薄更明显。结论:近视眼眼轴延长不仅会引起屈光度的近视化,还导致后极部视网膜厚度明显变薄。     

高效液相色谱法测定氨咖甘片中咖啡因及氨基比林的含量和溶出度

目的:建立同时测定氨咖甘片中咖啡因及氨基比林的含量和溶出度的高效液相色谱分析方法.方法:采用ODS色谱柱(150 mm×4.6 mm,5μm),流动相为甲醇-水(45:55),检测波长285 nm,流速:1.0 mL·min-1.采用外标法分别测定咖啡因和氨基比林的含量及溶出度.结果:标准曲线的线性范围为咖啡因0.01～0.20 g·L-1,氨基比林0.06～0.95 g·L-1.加样回收率咖啡因为99.5%～100.7%,氨基比林为98.4%～100.0%.结论:本方法快速、可靠、简单、灵敏,适用于该制剂的质量分析检验.     

老年慢性左心衰竭与右心衰竭患者心肺运动试验特点比较

目的 比较老年慢性左心衰竭与右心衰竭患者心肺运动试验（CPET）特点。方法 入选老年非瓣膜性慢性左心衰竭患者25例[男性20例，年龄（60.2±4.7）岁]，以及年龄、性别、纽约心脏联合会（NYHA）心功能分级匹配的慢性右心衰竭患者25例[男性19例，年龄（61.3±5.7）岁]，排除合并肺部疾病、神经肌肉疾病或贫血等患者，对比其CPET特点。结果 两组患者年龄、性别、体质量指数（BMI）、NYHA心功能分级无明显差异，超声心动图左心室舒张末内径左心衰竭组明显大于右心衰竭组，分别为（66.1±9.0）和（40.4±5.4）mm，左心衰竭组左室射血分数明显低于右心衰竭组，分别为（32.5±11.9）%和（65.8±8.1）%（P＜0.001）。CPET结果显示，左心衰竭组峰值氧耗量（peak VO2）为（1056.6±340.5）ml/min，峰值单位千克体质量的氧耗量（peak VO2/kg）为（15.1±2.7）ml/（min·kg），peak VO2占预计值的百分比为（52±13）%，右心衰竭组分别为（750.9±269.1）ml/min，（11.0±3.2）ml/（min·kg）和（39±11）%，右心衰竭组较左心衰竭组明显降低（P＜0.05）。右心衰竭组峰值氧脉搏（VO2/HR）明显低于左心衰竭组[（6.3±2.2） vs （8.5±3.0）ml/（min·beat），P＝0.016]。右心衰竭组氧耗量与功率比值斜率（VO2/WR slope）明显低于左心衰竭组[（5.1±1.1） vs （6.4±1.8）ml/（min·W），P＝0.014]。与左心衰竭组相比，右心衰竭组每分通气量/每分二氧化碳生量成斜率（VE/VCO2 slope）明显升高[（34.7±8.2） vs （49.5±12.6），P＜0.001]。结论 与左心疾病所致左心衰竭患者相比，即使是相似的NYHA心功能分级，右心衰竭患者运动状态下的心肺功能更差，VE/VCO2 slope更高。     

KRAS mutation and immunohistochemical profile in intraductal papillary neoplasm of the intrahepatic bile ducts

Intraductal papillary neoplasm of bile duct (IPNB) is characterized by a spectrum of diseases ranging from low-grade intraepithelial neoplasia to invasive carcinoma. In the present study, we aimed to investigate immunophenotypic features and KRAS mutations in relation to pathological subtypes and grades in Chinese patients with IPNBs. A total of 46 patients with IPNBs and 11 invasive adenocarcinomas arising in IPNBs (invasive IPNBs) were enrolled and clinicopathological data were analyzed. It was found that CK7 was expressed in 42 of the 46 neoplastic lesions. HepPar1 was expressed in 11 of the 46 noninvasive IPNBs, but not in invasive IPNBs. Additionally, CK19 was frequently expressed in both noninvasive IPNBs and invasive IPNBs. The intestinal-type IPNBs had a significantly higher percentage of MUC2 expression relative to the pancreaticobiliary (P = 0.015) and gastric-type IPNBs (P < 0.001). High-grade IPNBs and invasive IPNBs showed increased expression of cyclin D1, Ki-67, p53, mCEA, and CA19-9. The rate of KRAS mutation was significantly higher in high-grade IPNBs (P = 0.001) and invasive IPNBs (P = 0.006) than that in low- to intermediate-grade IPNBs. Additionally, KRAS mutation was significantly associated with tumor size, and Ki-67 expression. In conclusion, the expression of cyclin D, Ki-67, p53, mCEA and CA19-9 and KRAS mutation status are significantly correlated with histological grades of IPNBs.     

A simple hydrazone as a multianalyte (Cu2+, Al3+, Zn2+) sensor at different pH values and the resultant Al3+ complex as a sensor for F−

A new colorimetric and fluorescence molecular chemosensor based on triazole hydrazone can be used as a multi-probe for selective detection of Al³⁺, Zn²⁺, and Cu²⁺ by monitoring changes in the absorption and fluorescence spectral patterns. Results show that Al³⁺ and Zn²⁺ ions can induce remarkable fluorescence enhancement at pH 6.0 and pH 10.0, respectively, while the addition of Cu²⁺ ions leads to a significant UV-visible absorption enhancement in the visible range at pH 6.0. In addition, the resultant Al³⁺ complex could act as an ‘on–off’ fluorescence sensor for F⁻. The fluorescence sensor was also used to monitor intracellular Al³⁺, Zn²⁺, and F⁻ in Hela cells.

A fluorescent probe for Al³⁺ and Zn²⁺ was synthesised, and the resultant Al³⁺-complex was used for the detection of F⁻.     

In Vivo Protective Effects of Diosgenin against Doxorubicin-Induced Cardiotoxicity

Doxorubicin (DOX) induces oxidative stress leading to cardiotoxicity. Diosgenin, a steroidal saponin of Dioscorea opposita, has been reported to have antioxidant activity. Our study was aimed to find out the protective effect of diosgenin against DOX-induced cardiotoxicity in mice. DOX treatment led to a significant decrease in the ratio of heart weight to body weight, and increases in the blood pressure and the serum levels of lactate dehydrogenase (LDH), creatine phosphokinase (CPK) and creatine kinase myocardial bound (CK-MB), markers of cardiotoxicity. In the heart tissue of the DOX-treated mice, DOX reduced activities of antioxidant enzymes, including superoxide dismutase (SOD) and glutathione peroxidase (GPx), were recovered by diosgenin. Diosgenin also decreased the serum levels of cardiotoxicity markers, cardiac levels of thiobarbituric acid relative substances (TBARS) and reactive oxygen species (ROS), caspase-3 activation, and mitochondrial dysfunction, as well as the expression of nuclear factor kappa B (NF-κB), an inflammatory factor. Moreover, diosgenin had the effects of increasing the cardiac levels of cGMP via modulation of phosphodiesterase-5 (PDE5) activity, and in improving myocardial fibrosis in the DOX-treated mice. Molecular data showed that the protective effects of diosgenin might be mediated via regulation of protein kinase A (PKA) and p38. Our data imply that diosgenin possesses antioxidant and anti-apoptotic activities, and cGMP modulation effect, which in turn protect the heart from the DOX-induced cardiotoxicity.