肠道菌群失调与皮肤科常见结缔组织病相关性概述

【摘要】 越来越多的研究发现，肠道菌群与结缔组织病具有相关性。本文概述肠道菌群的特点及其在结缔组织病中的作用机制，重点阐述肠道菌群失调在红斑狼疮、系统性硬化病、干燥综合征中的相关性、可能作用机制及相关假说。通过益生菌调节肠道菌群失调可作为这些常见结缔组织病的治疗手段之一。     

上海市成人脂肪肝患病率及其危险因素流行病学调查

目的 明确上海市成人脂肪肝的患病率及其主要危险因素。 方法 通过随机多级分层整群抽样对杨浦区和浦东新区各4个居委会16岁以上居民进行调查,内容涉及问卷咨询、体格检查、75 g葡萄糖耐量试验、血脂检测、以及肝脏实时超声检查。 结果 3175名成人完成调查,约占上海市人口的2.26／10000。其中男性1218名,女性1957名,平均年龄(52.4±15.1)岁。B超共检出脂肪肝661例,占20.82％,其中酒精性、可疑酒精性、非酒精性脂肪肝分别占3.48％、4.08％及92.43％。经年龄和性别调整后,上海市成人脂肪肝患病率为17.29％,酒精性脂肪肝、可疑酒精性脂肪肝、非酒精性脂肪肝患病率分别为0.79％、1.15％、15.35％。无论是男性还是女性,脂肪肝患病率均随年龄增长而增加,50岁之前男性脂肪肝患病率显著高于女性(x2=13.934,P<0.01),而50岁以后女性脂肪肝患病率显著高于男性(x2=4.146,P<0.05)。脂肪肝组年龄、体重指数(BMI)、腰围、血压、空腹及餐后血糖、甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、肥胖、糖尿病、高血压病、血脂异常和胆石症患病率等均显著高于对照组,高密度脂蛋白胆固醇(HDL-C)水平以及文化程度显著低于对照组。多元回归分析显示:男性、文化程度、腰围、BMI、HDL-C、TG、空腹血糖水平、糖尿病、     

奥美沙坦通过减低整合素β5的表达促进心肌肥大的消退

目的研究整合素β5和心肌肥大的关系,比较新型血管紧张素Ⅱ-Ⅰ型受体拮抗剂(ARB)奥美沙坦和血管紧张素转换酶抑制剂(ACEI)替莫普利对心肌肥大的作用.方法雄性脑卒中易感型自发性高血压大鼠(SHRSP)33只,5周龄雄性京都种Wistar(WKY)大鼠11只,随机分为SHRSP空白组,SHRSP的奥美沙坦给药组(10 mg·kg-1·d-1),SHRSP的替莫普利给药组(10 mg·kg-1·d-1),WKY作为对照组.给药6周后,取出心脏称重,制作标本进行病理学检查,检测血管紧张素Ⅱ-1型受体(AT1)以及整合素β5的表达量.结果奥美沙坦和替莫普利的使用使SHRSP的收缩压降低,但奥美沙坦比替莫普利的促心肌肥大消退作用更显著.半定量RT-PCR测定表明,SHRSP的AT1和整合素β5的表达量明显高于WKY,奥美沙坦和替莫普利的使用降低了两者的表达量,奥美沙坦的作用更显著.AT1和整合素β5的表达成正相关关系.结论奥美沙坦在抑制心肌细胞肥大和降低AT1、整合素β5的表达量方面比替莫普利有更多获益.整合素β5的表达受抑参与了心肌肥大的消退.整合素β5在心肌细胞的表达可能受到血管紧张素Ⅱ(AngⅡ)通过AT1受体的调节.     

Relationship between Fas/FasL expression and apoptosis of colon adenocarcinoma cell lines

INTRODUCTIONFas/ FasL system has been identified as a keymediator of apoptosis in tumor cells[1-4]. Theoccurrence and development of neoplasm are closelyrelated to apoptosis[5-7] Most chemotherapeuticdrugs kill cancer cells mainly by inducingapoptosis[8-14].'     

Efficacy and safety of tumor necrosis factor-α blockers for ulcerative colitis: A systematic review and meta-analysis of published randomized controlled trials

To evaluate the efficacy and safety of TNF-α blockers for ulcerative colitis. A systematic search for randomized controlled trials (RCTs) of TNF-α blockers for treatment of ulcerative colitis (UC) were performed in PubMed, Web of Science, Embase and cochrane clinical trial. We estimated Pooled estimates of the odds ratio (OR) and relevant 95% confidence interval (CI) using fixed effects model or random effects model as appropriate. Heterogeneity, publication bias, and subgroup analyses were conducted. Nine randomized controlled studies met the selection criteria with a total of 2518 patients. Five studies compared Infliximab with placebo. Two studies compared Infliximab to corticosteroids. Two studies compared Adalimumab to placebo. One study compared subcutaneous golimumab to placebo. Short-term response, short-term remission, long-term remission and mucosal healing were better in the TNF-α blocker group than in the control group (p < 0.05). TNF-α blockers decreased the colectomy rate and serious adverse reactions (p < 0.05). The TNF-α blockers were superior to controls in achieving short-term clinical response/remission, long-term remission and mucosal healing and decreased the colectomy rate and serious adverse reactions.     

糖尿病大鼠视网膜中内质网应激蛋白、HIF-1α和血管内皮生长因子的表达

目的：探索糖尿病大鼠视网膜中内质网应激相关BIP (蛋白重链结合蛋白)、HIF-1α(低氧诱导因子-1α)和VEGF (血管内皮生长因子)的表达及意义。
　　方法：72只雄性SD大鼠,随机分为6组：正常2月对照组(C2m),糖尿病2月组(D2m),正常4月对照组(C4m),糖尿病4月组(D4m),正常6月对照组(C6m),糖尿病6月组(D6m),每组各12只。实验组给予一次性腹腔注射65mg/kg STZ建立糖尿病模型。 ELISA法检测BIP、HIF-1α和VEGF表达水平,免疫组化法观察大鼠BIP、HIF-1α和VEGF视网膜内定位情况。
　　结果：BIP表达随DM 病程的延长而增加( P<0.05),且DM各组与对照组相比,其差异均有统计学意义( P<0.01)。 HIF-1α在DM组中表达较对照组增加,其差异有统计学意义(P<0.05),但DM组各组间差异无统计学意义。 VEGF蛋白在D2 m组与对照组间差别无统计学意义,但 D4 m、D6 m 与对照组间差别有统计学意义( P<0.05),且D4 m和D6 m两组间差别有统计学意义。免疫组化：BIP在对照组视网膜神经节细胞层中少量表达,DM组主要分布于视网膜内核层和神经节细胞层;HIF-1α在对照组基本不表达, DM组各层均有表达;VEGF在对照组大鼠中视网膜各层中少量表达,而DM组大鼠的内核层、外核层及视网膜血管、神经节细胞层中 VEGF 阳性表达。
　　结论：糖尿病大鼠视网膜组织中的 BIP、HIF-1α、VEGF均较对照组增加且随糖尿病病程进展而增加,内质网应激和低氧诱导因子途径均可能在糖尿病视网膜病变的进展中起重要作用。     

后巩膜加固术在高度近视性黄斑病变手术中的应用

近视性黄斑病变致盲率高,常用治疗手段为玻璃体切割术,然而单纯玻璃体切割术对于已出现严重后巩膜葡萄肿的超高度近视患者疗效欠佳。近年来临床应用玻璃体切割术联合后巩膜加固术治疗高度近视继发眼底病变,特别在黄斑劈裂及黄斑裂孔病例中,疗效肯定,前景可期。我们针对近年来后巩膜加固术的材料与术式变迁作一全面综述,并进一步讨论其应用于眼底手术中的发展远景。     

Long non-coding RNA TP73-AS1 promotes pancreatic cancer growth and metastasis through miRNA-128-3p/GOLM1 axis

BACKGROUNDPrevious studies have suggested that long non-coding RNAs (lncRNA) TP73-AS1 is significantly upregulated in several cancers. However, the biological role and clinical significance of TP73-AS1 in pancreatic cancer (PC) remain unclear. AIMTo investigate the role of TP73-AS1 in the growth and metastasis of PC.METHODSThe expression of lncRNA TP73-AS1, miR-128-3p, and GOLM1 in PC tissues and cells was detected by quantitative real-time polymerase chain reaction. The bioinformatics prediction software ENCORI was used to predict the putative binding sites of miR-128-3p. The regulatory roles of TP73-AS1 and miR-128-3p in cell proliferation, migration, and invasion abilities were verified by Cell Counting Kit-8, wound-healing, and transwell assays, as well as flow cytometry and Western blot analysis. The interactions among TP73-AS1, miR-128-3p, and GOLM1 were explored by bioinformatics prediction, luciferase assay, and Western blot. RESULTSThe expression of TP73-AS1 and miRNA-128-3p was dysregulated in PC tissues and cells. High TP73-AS1 expression was correlated with a poor prognosis. TP73-AS1 silencing inhibited PC cell proliferation, migration, and invasion in vitro as well as suppressed tumor growth in vivo. Mechanistically, TP73-AS1 was validated to promote PC progression through GOLM1 upregulation by competitively binding to miR-128-3p. CONCLUSIONOur results demonstrated that TP73-AS1 promotes PC progression by regulating the miR-128-3p/GOLM1 axis, which might provide a potential treatment strategy for patients with PC.