放疗病房发生医院感染的原因分析

为了解放疗病房医院感染的发病情况，对1995年8月～1996年7月间所有的放疗科的160例住院病人进行回顾性分析。结果发现年医院感染发病率为19．4％（31／160），年例次发病率为21．3％（34／l160）。有无基础病的发病率差异显著，接受抗癌治疗的病人处在多种致病危险因素之中。以抑制免疫功能、降低抵抗力为主要致病原因。感染发生的疾病前三位为临床败血症、急性支气管炎、肺部感染。因此，提醒人们发生在放疗病房的医院感染有其特殊性，要加强对放疗科各级医务人员的医院感染知识的教育，以便对发生的感染能够及时、有效的控制。     

吴立文教授治疗慢性前列腺炎经验

吴立文教授根据多年临床经验,认为慢性前列腺炎是由湿、热、虚、瘀等因素引起,临证时从病机、病性、论治三方面入手,强调以祛除湿邪为重点,活血化瘀贯彻始终,酌情配合扶正治疗。     

TRAIL与羟基喜树碱联用协同杀伤人肺腺癌A549细胞

目的：探讨羟基喜树碱与肿瘤坏死因子相关凋亡诱导配体（tumor necrosis factor-related apoptosis inducing ligand，TRAIL）联用对肺腺癌A549细胞是否具有协同杀伤作用，并对其机制进行初步研究。方法：MTT法检测细胞毒性作用，流式细胞仪检测细胞凋亡和线粒体膜电位，Western blot分析bcl-2和bcl-xl蛋白水平变化。结果：单用100ng／mL TRAIL，4、40和400μg／mL羟基喜树碱对A549细胞杀伤率分别为13．9％、3．0％、23．4％和76．7％，联合用药的抑制率分别为43．6％、52．5％和83．1%。100ng／mL TRAIL和4μg/mL羟基喜树碱有协同作用，可使细胞线粒体膜电住降低，但不影响bcl-2和bcl-xl蛋白表达。结论：TRAIL与羟基喜树碱联用对肺腺癌A549细胞有明显的协同杀伤作用，其机制可能与羟基喜树碱降低A549细胞线粒体膜电位有关。     

饮食在大肠癌发生发展中致病作用的研究进展

大肠癌是常见的恶性肿瘤之一，全世界大肠癌的发病率每年以2％的速度上升，在西欧、北美国家中发病率较高，可达35-50／10万，亚、非、拉国家发病率较低；在美国所有死于癌症的病人中，大肠癌居第二位，其中85％-90％的病人癌发生与环境和饮食因素有关。近年来从我国各地资料显示：随着人民生活水平的提高，饮食结构的改变，结肠癌发病率呈逐年上升趋势，其年平均增长率为4％，现已成为市区第四位常见癌症。据统计，1992年上海市大肠癌的年发病率为28．35／10万，已接近欧美国家水平。遗传学和临床研究认为，大肠癌发病可能是遗传易感性和饮食因素协同作用所致，其中环境、生活习惯、尤其是与饮食方式有密切关系。     

β-七叶皂甙钠治疗慢性肺心病心衰的临床观察

目的：探讨β-七叶皂甙钠对慢性肺源性心脏病心力衰竭的疗效及治疗机制。方法：160例肺心病心力衰竭患者随即分为两组，对照组给予常规治疗，治疗组在常规治疗的基础上加用β-七叶皂甙钠20mg，加入10％葡萄糖注射液250ml，以30-40滴／分，每日1次，静滴，10天为1个疗程。结果：治疗组的显效率和总有效率明显高于对照组（P〈0.01），且治疗组的血液流变学及血气分析各项指标较治疗前显著改善（P〈0．01或P〈0．05）；而对照组仅红细胞压积有显著改善（P〈0．05），其它指标无显著性差异。结论：β-七叶皂甙钠对肺心病心力衰竭疗效显著，且不良反应少，值得临床推广。     

A Survey on Intelligent Screening for Diabetic Retinopathy

Diabetic retinopathy (DR) is one of the leading causes of vision loss and can be effectively avoided by screening, early diagnosis and treatment. In order to increase the universality and efficiency of DR screening, many efforts have been invested in developing intelligent screening, and there have been great advances. In this paper, we survey DR screening from four perspectives: 1) public color fundus image datasets of DR; 2) DR classification and related lesion-extraction approaches; 3) existing computer-aided systems for DR screening; and 4) existing issues, challenges, and research trends. Our goal is to provide insights for future research directions on DR intelligent screening.     

根据新版核查要点浅析某儿童医院临床试验质控常见问题

目的:分析与总结苏州大学附属儿童医院临床试验机构质控中发现的问题。 方法:按照国家药品监督管理局食品药品 审核查验中心最新发布的核查要点对 2021 年 1 月-2023 年 6 月机构质控报告中的问题进行整理与归类。 结果:本机构临床试 验项目质控中发现的问题主要集中在研究人员资质文件收集、知情同意书签署、异常值评判、试验数据记录等方面。 结论:临床 试验机构、伦理委员会、研究者和申办方均应履行各自职责,对试验质量全程把关,保障受试者的权益与安全、保证临床试验数 据的真实性。     

两种术式在缓解恶性输尿管梗阻疗效中的对比研究

目的 探讨恶性输尿管梗阻（malignant ureteral obstruction,MUO）现有的临床治疗方案和经验,讨论恶性输尿管梗阻时使用经皮肾脏穿刺引流（percutaneous nephrostomy,PN）或输尿管支架置入术（ureteral stenting,US）的临床适用范围,明确2种术式在缓解恶性输尿管梗阻时肾功能损伤的有效性。方法 回顾性纳入重庆医科大学附属第一医院泌尿外科2021年1月至2023年5月诊断为恶性输尿管梗阻的患者,严格筛选纳入及排除标准后共有76例患者入组并随机分为PN组（n=22）与US组（n=54）,对患者基本特征及围术期、术后半年随访数据进行病例对照研究以反映肾功能在2组中的差异,采用SPSS 21.0版本对数据进行处理分析。结果 2组患者在性别（P=0.017）、手术侧肾积水程度（P=0.000）的比较,差异有统计学意义。2组患者术前3 d比较尿素氮（P=0.002）、血肌酐（P=0.003）,术后1 d尿素氮（P=0.017）、血肌酐（P=0.005）,差异有统计学意义。术后3 d与术后6个月2组患者在肾功能比较中差异均无统计学意义。结论 恶性输尿管梗阻以宫颈癌多发,其次为位膀胱癌、结直肠癌等。US可选择梗阻或积水较轻、慢性输尿管梗阻、肾功能损伤较轻的患者,可作为缓解输尿管梗阻的首选治疗方案。PN临床常对中至重度肾积水、肾功能损伤较重或者急性肾功能不全的恶性输尿管梗阻患者进行治疗,可作为US失败的替代方案。     

Nanofused Hierarchically Porous MIL-101(Cr) for Enhanced Methyl Orange Removal and Improved Catalytic Activity

Hierarchically porous MIL-101(Cr) (H-MIL-101(Cr)) with meso/macro-pores was directly prepared via nanofusion progress by using butyric acid as a modulating agent. In the methyl orange (MO) adsorption experiments, H-MIL-101(Cr) showed a high adsorption capability of 369.8 mg g⁻¹, which was 1.52-fold greater than that of pristine MIL-101(Cr) (P-MIL-101(Cr)). While in the oxidation reaction of indene and 1-dodecene tests, H-MIL-101(Cr) presented much higher catalytic efficiency, with turnover frequency (TOF) values of 0.7242 mmol g⁻¹ min⁻¹ and 0.1492 mmol g⁻¹ min⁻¹, respectively, which were 28% and 34% greater than that in the case of P-MIL-101(Cr). Thus, compared with P-MIL-101(Cr), H-MIL-101(Cr) exhibited better removal efficiency and higher levels of activity in the oxidation reactions of indene and 1-dodecene. The unique structure of H-MIL-101(Cr) also contributed to its superior performance in these processes.     

PXR activation impairs hepatic glucose metabolism partly via inhibiting the HNF4α–GLUT2 pathway

Drug-induced hyperglycemia/diabetes is a global issue. Some drugs induce hyperglycemia by activating the pregnane X receptor (PXR), but the mechanism is unclear. Here, we report that PXR activation induces hyperglycemia by impairing hepatic glucose metabolism due to inhibition of the hepatocyte nuclear factor 4-alpha (HNF4α)‒glucose transporter 2 (GLUT2) pathway. The PXR agonists atorvastatin and rifampicin significantly downregulated GLUT2 and HNF4α expression, and impaired glucose uptake and utilization in HepG2 cells. Overexpression of PXR downregulated GLUT2 and HNF4α expression, while silencing PXR upregulated HNF4α and GLUT2 expression. Silencing HNF4α decreased GLUT2 expression, while overexpressing HNF4α increased GLUT2 expression and glucose uptake. Silencing PXR or overexpressing HNF4α reversed the atorvastatin-induced decrease in GLUT2 expression and glucose uptake. In human primary hepatocytes, atorvastatin downregulated GLUT2 and HNF4α mRNA expression, which could be attenuated by silencing PXR. Silencing HNF4α downregulated GLUT2 mRNA expression. These findings were reproduced with mouse primary hepatocytes. Hnf4α plasmid increased Slc2a2 promoter activity. Hnf4α silencing or pregnenolone-16α-carbonitrile (PCN) suppressed the Slc2a2 promoter activity by decreasing HNF4α recruitment to the Slc2a2 promoter. Liver-specific Hnf4α deletion and PCN impaired glucose tolerance and hepatic glucose uptake, and decreased the expression of hepatic HNF4α and GLUT2. In conclusion, PXR activation impaired hepatic glucose metabolism partly by inhibiting the HNF4α‒GLUT2 pathway. These results highlight the molecular mechanisms by which PXR activators induce hyperglycemia/diabetes.Key words: Pregnane X receptor, Hepatocyte nuclear factor 4-alpha, Glucose transporter 2, Hepatic glucose uptake, Diabetes, Drug-induced hyperglycemia