良性前列腺增生与前列腺慢性炎症的相关性研究进展

良性前列腺增生（BPH）是老年男性常见的泌尿系统疾病，其发病与前列腺慢性炎症之间存在显著相关。感染因子、尿液返流、代谢综合征、衰老过程和自身免疫应答在内的几种刺激，通过相应分子途径引起前列腺免疫细胞的组织定位和组成成分发生广泛改变，从而导致免疫系统失调，之后引发的组织损伤和缓慢愈合，导致了BPH发生和进展。本文通过总结良性前列腺增生与前列腺慢性炎症的相关性的临床研究结果，前列腺免疫细胞在病理生理机制层面与前两者之间的内在联系，以及抗炎药物对BPH-LUTS的干预作用，以其为BPH-LUTS的药物研发提供参考。     

膀胱肿瘤切除术后尿路感染病原学和危险因素

目的观察膀胱肿瘤切除术后患者尿路感染发生情况与病原学特征,分析诱发尿路感染的危险因素,并提出合理且具备针对性的冲洗对策,为未来膀胱肿瘤切除术后尿路感染的预防提供合理参考。方法回顾性分析连云港市第一人民医院2016年1月-2019年1月接受经尿道膀胱肿瘤切除术治疗的451例膀胱肿瘤患者的临床资料,收集患者病例资料,全部患者术后均定期取尿液标本进行细菌培养,参照相关标准判定患者尿路感染情况,记录患者一般情况,包括一般人口学资料(性别、年龄、体质量、受教育程度等),同时记录患者糖尿病的疾病合并情况,将术后尿路感染可能的危险因素纳入初步分析,Logistic多因素回归分析膀胱肿瘤切除术后发生尿路感染的危险因素。结果451例膀胱肿瘤切除术患者术后第3天尿液中细菌培养阳性例数为80例,阳性率为17.74%,在使用抗菌药物后,患者尿液中细菌培养阳性率逐渐降低,各时点尿液细菌阳性培养率比较,差异有统计学意义(P<0.05);经多因素Logistic回归分析检验证实,高龄、血糖水平控制不佳、术前留置导尿管、多发肿瘤是膀胱肿瘤切除术后尿路感染的危险因素(OR>1,P<0.05);80例术后尿液细菌培养阳性患者共分离出87株菌株,其中革兰阴性菌66株占75.86%,革兰阳性球菌21株占24.14%。结论膀胱肿瘤切除术后患者有较高的尿路感染风险,革兰阴性菌是主要的感染病原菌,年龄、基础疾病、肿瘤位点、术前导尿管留置等是影响因素,这类患者应引起临床高度重视。     

A comparison of the relationships between psychosocial factors,occupational strain,and work ability among 4 ethnic teacher groups in China

The present study compared the level of occupational strain and work ability among Han, Hui, Uygur, Hui, and Kazakh teachers, and explored ethnic differences based on the associations of psychosocial factors at work, occupational strain, and work ability. A cross-sectional survey was conducted among 2,941 teachers in primary and secondary schools in Xinjiang Province, China. Psychosocial factors, occupational strain, and work ability were measured using the Occupation Stress Inventory—Revised Edition (OSI-R) and Work Ability Index. Han and Hui teachers experienced reduced work ability compared with Uygur and Kazakh teachers, and this finding was caused, in part, by exposure to psychosocial factors at work. The vocational and psychological strains caused by these factors play an important role in reduced work ability among all ethnic teacher groups. The findings indicate the importance of taking action to reduce occupational strain for promoting teachers' work ability in multiethnic workplaces.     

柴芍四金汤预防ERCP术后胆总管结石复发的临床观察

目的 研究柴芍四金汤预防ERCP术后胆总管结石复发的临床疗效。方法 选取昆山市中医医院脾胃肝胆科2014年1月至2016年12月因胆总管结石行ERCP取石病例120例，按随机数字表法将120例病例随机分为治疗组和对照组，每组各60例，治疗组口服自拟柴芍四金汤，每日1剂，水煎400 mL，分早晚两次温服，随证加减；对照组口服熊去氧胆酸250 mg/次，3次/d，2组均连续药物治疗6月，观察术后2周血清中总胆红素（Tbil）、直接胆红素（Dbil）、碱性磷酸酶（ALP）、谷氨酰转肽酶（GGT）指标、术后半年临床症状（包括腹痛、腹胀、恶心、纳差）及术后6月、12月、18月胆总管结石复发情况。结果 治疗组术后6月、12月及18月结石复发率略低于对照组，但两者差异无统计学意义（ P >0.05）；治疗组在改善腹痛、腹胀、恶心、纳差症状方面优于对照组（ P <0.05）；治疗组在改善血清Tbil、Dbil、ALP、GGT水平方面优于对照组（ P <0.01）。结论 柴芍四金汤能有效预防ERCP术后胆总管结石的复发，且能改善胆总管结石引起的临床症状及血清生化指标。      

苯扎贝特治疗儿童ApoE Tokyo(Arg25Cys)突变型脂蛋白肾病1例

脂蛋白肾病(Lipoprotein glomerulopathy,LPG),1989年首次由日本学者Saito报道,LPG主要累及肾脏,且以肾小球病变为主[1]。几乎所有患者均有不同程度的蛋白尿,多数表现为肾病综合征,少数表现为轻微蛋白尿和镜下血尿,部分患者伴有不同程度的贫血及高血压,血脂异常易被忽略为肾病综合征的低蛋白血症所致。载脂蛋白E(apolipoprotein E,ApoE)增高是LPG血脂改变的主要特点[2-3]。LPG为一种与脂质代谢紊乱密切相关的肾脏疾病,目前世界范围内有报道的病例不足200例,儿童报道仅10余例[2]。本病进展缓慢,临床常误诊为原发性肾病综合征[4]。因此,为增强对LPG的认识,提高诊治水平,现分析1例确诊的儿童LPG临床资料,总结LPG的临床特点、诊断、治疗及预后。     

Lysophosphatidylcholine‐induced cytotoxicity and protection by heparin in mouse brain bEND.3 endothelial cells

A pathological feature in atherosclerosis is the dysfunction and death of vascular endothelial cells (EC). Oxidized low‐density lipoprotein (LDL), known to accumulate in the atherosclerotic arterial walls, impairs endothelium‐dependent relaxation and causes EC apoptosis. A major bioactive ingredient of the oxidized LDL is lysophosphatidylcholine (LPC), which at higher concentrations causes apoptosis and necrosis in various EC. There is hitherto no report on LPC‐induced cytotoxicity in brain EC. In this work, we found that LPC caused cytosolic Ca²⁺ overload, mitochondrial membrane potential decrease, p38 activation, caspase 3 activation and eventually apoptotic death in mouse cerebral bEND.3 EC. In contrast to reported reactive oxygen species (ROS) generation by LPC in other EC, LPC did not trigger ROS formation in bEND.3 cells. Pharmacological inhibition of p38 alleviated LPC‐inflicted cell death. We examined whether heparin could be cytoprotective: although it could not suppress LPC‐triggered Ca²⁺ signal, p38 activation and mitochondrial membrane potential drop, it did suppress LPC‐induced caspase 3 activation and alleviate LPC‐inflicted cytotoxicity. Our data suggest LPC apoptotic death mechanisms in bEND.3 might involve mitochondrial membrane potential decrease and p38 activation. Heparin is protective against LPC cytotoxicity and might intervene steps between mitochondrial membrane potential drop/p38 activation and caspase 3 activation.