注射用尼扎替丁治疗消化性溃疡出血205例

目的:研究注射用尼扎替丁治疗消化性溃疡出血的疗效及安全性.方法:采用多中心、随机、双盲、阳性药物平行对照研究.将2008-09/2009-12收集的205例经胃镜证实的消化性溃疡出血患者随机分为两组,试验组102例给予尼扎替丁0.1g,每日3次,对照组103例给予法莫替丁20mg,每日2次,连续5d.结果:共有201例患者可供疗效评价.试验组的临床显效率为85.0%,总有效率为99.0%,对照组的临床显效率为82.2%,总有效率为98.0%,两组间差异无统计学意义(P>0.05).两组不良反应主要为白细胞减少、转氨酶轻度升高和贫血(P>0.05).结论:注射用尼扎替丁是治疗消化性溃疡合并上消化系出血有效且安全的药物.     

Novel role of Sarco/endoplasmic reticulum calcium ATPase 2 in development of colorectal cancer and its regulation by F36, a curcumin analog

Sarco/endoplasmic reticulum calcium ATPase (SERCA) enzymes play important roles in several signal transduction pathways that control proliferation, differentiation and apoptosis. Here, we reported that SERCA2 expression was positively correlated with tumor node metastasis (TNM) stages (n = 75, P = 0.0251) and grades (n = 63, P = 0.0146) of patients with colorectal cancer. The animal experiments demonstrated that SERCA2 expression was consistent with PCNA staining of intestinal tissues of male C57BL/6J-Apc^Min/JNju mice. Besides, SERCA2 expression was also increased in undifferentiated HT-29 cells as compared with that in differentiated HT-29 gal cells. Moreover, SERCA2 overexpression promoted proliferation and migration of SW480 cells via activating MAPK and AKT signaling pathways, while silence of SERCA2 inhibited the proliferation and migration of SW480 cells. In addition, we identified that a curcumin analog, F36, exhibited more potent inhibitory effect in colorectal cancer cells than curcumin through inhibiting SERCA2 expression. Taken together, our findings indicate that SERCA2 is involved in the malignant progress of colorectal cancer and maybe a therapeutic target for colorectal cancer treatment. Curcumin analog F36 shows enhanced anti-cancer activity in colorectal cancer cells by targeting SERCA2.     

卡介苗治疗肾移植术后膀胱癌的研究进展

肾移植可改善终末期肾病患者生活质量,是其最有效的治疗方法,但肾移植手术也是膀胱癌的高危因素。膀胱癌是泌尿外科常见的恶性肿瘤,有易复发的特点。卡介苗膀胱灌注治疗是高危非肌层浸润性膀胱癌的一线疗法,能直接杀伤膀胱癌细胞。我们对卡介苗治疗肾移植术后膀胱癌的作用机制及临床应用进行综述,旨在为更好地利用卡介苗辅助治疗肾移植术后膀胱癌提供参考。     

肠系膜静脉血栓31例

目的:总结肠系膜静脉血栓形成(mesenteric venous thrombosis,MVT)的临床经验,探讨MVT形成的临床表现、诊断和治疗.方法:回顾性分析河北联合大学附属医院31例MVT住院患者的临床资料,调查其危险因素、既往血栓史、主诉和查体、实验室检查、放射学检查、治疗及预后.结果:1990-2010共收治MVT患者31例;男性24例,女性7例;平均年龄55.6岁;主要的临床表现为腹痛(100%)、呕吐(77.4%,24/31)、腹胀(64.5%,20/31)、便秘(41.9%,13/31);肝脏疾病、既往手术史、糖尿病和恶性肿瘤是MVT的主要高危因素;增强CT扫描是首选检查手段.7例患者接受单纯抗凝治疗,24例患者接受手术治疗;4例患者死亡.抗凝和手术治疗是MVT的主要治疗手段.结论:MVT临床表现无特异性;早期诊断,及时治疗是改善预后的关键.     

妊娠间隔对经产妇妊娠结局的影响多中心回顾性研究

目的探讨不同妊娠间隔(IPI)对经产妇妊娠结局的影响。方法基于全国14个省区市共21家医院开展多中心回顾性研究,通过查阅病历收集2011—2018年间两次妊娠均在同一家医院分娩的经产妇的年龄、身高、孕前体重、IPI、既往史、妊娠合并症和并发症、分娩孕周、分娩方式、妊娠结局等资料。根据不同IPI分为4组:<18个月组、18~23个月组、24~59个月组和≥60个月组,分析其临床特征和妊娠结局。根据WHO的推荐,以24~59个月组作为参照,比较各组经产妇的妊娠结局。进一步根据年龄、妊娠期糖尿病(GDM)史、巨大儿分娩史和早产史进行分层分析,探讨不同特征经产妇中IPI对其妊娠结局的影响。结果本研究共纳入经产妇8026例,其中<18个月组、18~23个月组、24~59个月组和≥60个月组分别为423、623、5512和1468例。(1)<18个月组、18~23个月组、24~59个月组和≥60个月组的妊娠年龄、本次妊娠前体质指数(BMI)、剖宫产史比例、GDM发生率、妊娠期高血压发生率以及剖宫产术分娩比例均逐渐增加,分别比较,差异均有统计学意义(P均<0.05)。(2)校正混杂因素后,与24~59个月组经产妇相比,≥60个月组经产妇的早产、胎膜早破和羊水过少的发生风险分别增加42%(OR=1.42,95%CI为1.07~1.88,P=0.015)、46%(OR=1.46,95%CI为1.13~1.88,P=0.004)和64%(OR=1.64,95%CI为1.13~2.38,P=0.009),其他组均未见不良妊娠结局的发生风险增加(P均>0.05)。(3)根据妊娠年龄分层,校正混杂因素后,与24~59个月组比较,高龄经产妇≥60个月组羊水过少的发生风险明显增加(OR=2.87,95%CI为1.41~5.83,P=0.004);非高龄经产妇<18个月组胎膜早破的发生风险明显增加(OR=1.59,95%CI为1.04~2.43,P=0.032),≥60个月组胎膜早破(OR=1.58,95%CI为1.18~2.13,P=0.002)和早产(OR=1.52,95%CI为1.07~2.17,P=0.020)的发生风险均显著增加。根据有无GDM史分层,校正混杂因素后,与24~59个月组比较,≥60个月组有GDM史经产妇产后出血的风险显著增加(OR=5.34,95%CI为1.45~19.70,P=0.012),无GDM史经产妇胎膜早破的发生风险显著增加(OR=1.44,95%CI为1.10~1.90,P=0.009)。根据有无巨大儿分娩史分层,校正混杂因素后,与24~59个月组比较,≥60个月组有巨大儿分娩史经产妇剖宫产术分娩的比例显著增加(OR=4.11,95%CI为1.18~14.27,P=0.026),无巨大儿分娩史经产妇胎膜早破的发生风险显著增加(OR=1.46,95%CI为1.12~1.89,P=0.005)。根据有无早产史分层,校正混杂因素后,与24~59个月组比较,≥60个月组无早产史经产妇胎膜早破的发生风险显著增加(OR=1.47,95%CI为1.13~1.92,P=0.004)。结论IPI≥60个月或<18个月均会造成经产妇不良妊娠结局的发生风险增加,应通过对育龄期妇女孕前咨询和产后保健的健康教育,指导育龄期妇女再次妊娠时保持适宜的IPI,以降低不良妊娠结局的发生风险。     

Overexpression of ERβ inhibits the proliferation through regulating TNG-β signaling pathway in osteosarcoma

The present study aimed to explore the potential anti-tumor effect of ERβ overexpression and investigate its related mechanism in osteosarcoma. Cell cycle and apoptosis rates were measured by flow cytometry. Cell proliferation and formation of autophagosome were assessed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay and dansylcadaverine (MDC) staining assay. Cell migration and invasion were detected by wound healing assay and transwell assay. Western blot analysis was designed to detect the protein expressions of surviving, Bax, LC-3 П, Beclin-1, ERβ, TβRⅠ, TβRⅡ, Smad2, Smad3 and Smad7. Real-Time fluorogenic PCR was designed to examine the mRNA expressions of surviving, Bax, ERβ, TβRⅠ, TβRII, Smad2, Smad3 and Smad7. The results showed that ERβ overexpression inhibited cell proliferation, migration and invasion, blocked cell cycle, and induced apoptosis and autophagy. Additionally, ERβ overexpression significantly inhibited the expression of surviving, TβRⅠ, TβRⅡ, Smad2 and Smad3. Meanwhile, the expressions of Bax, LC-3 П, Beclin-1 and Smad7 were dramatically upregulated by ERβ overexpression. In conclusion, ERβ overexpression could inhibit cell proliferation, migration and invasion, block cell cycle, and promote apoptosis and autophagy in OS by downregulating TNG-β signaling pathway.     

Human bone marrow mesenchymal stem cells-derived exosomes protect against nerve injury via regulating immune microenvironment in neonatal hypoxic-ischemic brain damage model

Neonatal hypoxic-ischemic (HI) brain injury is a serious injury caused by various perinatal factors, which has become a heavy mental burden to the family. The molecular mechanism underlying neonatal hypoxic-ischemic brain injury remains largely unknown. Human bone marrow mesenchymal stem cells (hBMSCs) have caused wide public concern due to the immunomodulatory properties. Exosomes can polarize human microglia and thus changed it into an anti-inflammatory phenotype to reduce the release of pro-inflammatory factors. However, it is unclear whether hBMSCs-exosomes have effect on neonatal hypoxic-ischemic brain injury. In this study, we aimed at investigating the role of hBMSCs-exosomes in regulating immune response and nerve injury in neonatal hypoxic-ischemic brain damage model. In the research, we identified the exosome secretion of hBMSCs could transferred into human microglia (HMC). Moreover, we determined the importance of hBMSCs-exosomes in regulating HMC polarization and inflammatory response. Our research findings might provide a new insight into slowing the disease progression of neonatal hypoxic-ischemic brain injury.