浙江省高校学生功能性消化不良流行病学调查及其与心理因素的关系

目的 了解浙江省高校学生功能性消化不良(FD)患病情况及其与心理因素的关系.方法 选取浙江省两所高校学生,采用多级分层随机整群抽样方法,以罗马Ⅲ成人功能性胃肠病诊断调查问卷(ROMEⅢ-DQ)及心理学症状自评量表(SCL-90)对其进行分析调查.统计学处理采用x2检验和t检验.结果 共调查浙江省高校学生1870名,FD患病率为5.78％;女性患病率高于男性(7.53％比4.14％,x2=9.884,P＜0.05);高校四年级学生FD患病率最高,各年级之间差异有统计学意义(x2=13.83,P＜0.05).FD亚型中餐后不适综合征明显多于上腹痛综合征;FD患者与其他功能性胃肠病重叠以功能性排便障碍和功能性便秘最多.SCL-90调查中FD组各项因子评分均高于健康对照组.结论 FD在浙江省高校学生中有较高的患病率,心理因素与其发病有相关性.     

乳糖酶添加剂对早产儿乳糖不耐受有效性及安全性：一项前瞻性、多中心、随机对照研究

目的 探讨乳糖酶添加剂对早产儿乳糖不耐受改善的有效性以及安全性。方法 2018年1月至2019年12月对上海交通大学医学院附属新华医院、上海市第一妇婴保健院、浙江大学医学院附属儿童医院和苏州大学附属儿童医院收治的有乳糖不耐受症状并符合入组标准的早产儿进行研究,将研究对象随机分为乳糖酶治疗组及对照组,各80例。乳糖酶治疗组患儿每顿母乳或早产儿配方奶中加入4滴（180mg）乳糖酶,同时予双歧杆菌三联活菌散口服及腹部按摩作为辅助治疗。对照组患儿则在每顿奶中加入同等剂量的安慰剂,并予与治疗组相同的益生菌和腹部按摩进行辅助治疗。在干预后第1周末和第2周末比较两组患儿临床症状、体重、粪便pH值、粪便还原糖等指标。结果 乳糖酶治疗组和对照组分别有78例、77例完成研究。干预后第1周末,乳糖酶治疗组还原糖阳性率较对照组低（P<0.05）;干预后第2周末,乳糖酶治疗组患儿腹胀发生率较对照组低（P<0.05）,还原糖阳性率低于对照组（P<0.05）,同时乳糖酶治疗组患儿喂养增加量高于对照组（P<0.05）。研究过程中两组均未发现患儿对乳糖酶添加剂或益生菌产生不良反应。结论 外源性乳...     

难治性胃食管反流病

近年来,有学者发现部分胃食管反流病(GERD)患者对质子泵抑制剂(PPI)治疗无效,由此提出了"难治性GERD"的概念。通过对难治性GERD病例进行研究,已发现部分GERD相关病理生理机制,并在此基础上提出了一些新的检测技术和治疗方法,以使这部分患者的症状能有所改善。本文就难治性GERD的研究现状作一概述。     

质子泵抑制剂对双氯芬酸诱导小肠黏膜损伤保护机制研究

目的 探讨不同质子泵抑制剂(PPI)对大鼠非甾体类抗炎药(NSAID)所致小肠损伤是否具有保护作用及可能的保护机制.方法 将72只SD大鼠均分为空白对照组、模型对照组和奥美拉唑治疗组、埃索美拉唑治疗组、雷贝拉唑治疗组、兰索拉唑治疗组.除空白对照组外其余各组予双氯芬酸7.5mg· kg-1 ·d-1灌胃,1次／d,制备NSAID相关性小肠损伤大鼠模型.各治疗组分别予奥美拉唑30mgmg·kg-1 ·d-1、埃索美拉唑30mg· kg-1·d-1、兰索拉唑45mg·kg-1·d-1、雷贝拉唑15mg· kg1·d1,1次／d灌胃.连续给药5d,处死后取小肠组织,观察其大体和病理学损伤变化,应用Western印迹检测、实时PCR分析小肠组织转录因子红细胞系-2p45相关因子-2(Nrf2)蛋白及mRNA表达,免疫组织化学染色行小肠组织Nrf2的定性及定位分析,黄嘌呤氧化酶法和硫代巴比妥法检测小肠组织超氧化物歧化酶(SOD)和丙二醛(MDA)活性.结果 实验造模成功率100％.空白组对照组大鼠存活率为12/12;模型对照组存活率为9/12;奥美拉唑治疗组存活率为10/12;埃索美拉唑治疗组存活率为11/12;雷贝拉唑治疗组存活率为11/12;兰索拉唑治疗组存活率为10/12.雷贝拉唑、埃索美拉唑、兰索拉唑治疗组大体和病理损伤积分均明显低于模型对照组(P＜0.05).小肠组织SOD活性雷贝拉唑治疗组明显高于模型对照组(P＜0.05),而MDA活性雷贝拉唑、埃索美拉唑治疗组明显低于模型对照组(P＜0.05).Western印迹检测显示雷贝拉唑治疗组小肠组织Nrf2蛋白表达量较模型对照组升高(P＜0.05).实时PCR结果雷贝拉唑治疗组小肠组织Nrf2 mRNA表达较空白对照组和模型对照组明显升高(P值分别＜0.01和0.05).结论 不同PPI对NSAID小肠损伤的保护作用不同,但奥美拉唑的保护作用不明显.其中雷贝拉唑防止NSAID小肠损伤的机制可能通过上调转录因子Nrf2的表达及促进其活化来实现.     

非甾体抗炎药肠损伤大鼠模型小肠组织中蛋白酶激活受体2的表达与肥大细胞分布

Objective To identify the expression and significance of protease-activated receptor-2 (PAR-2) and mast cell ( MC) in the rat model of small intestinal mucosal damage by a short-term administration of diclofenac. Methods Twenty-four SD-rats were divided into 2 groups ( control group and model group, 12 rats each) by random digit table. The rats in the control group were treated with 1 ml distilled water per 250 g, once a day while those in the model group diclofenac 7. 5 mg/kg per day. Their terminal ileum was harvested at Day 5 after an intraperitoneal injection. Toluidine blue dyeing was employed to determine the distribution of MC and its count in intestinal mucous membrane. Immunohistochemistry,Western blot and real-time PCR (polymerase chain reaction) were employed analyze the location, expression and change of PAR-2 mRNA in intestinal mucous membrane. Results The count of MC was obviously higher in the model group than that in the control group( 10. 3 ±2. 2 vs 4. 2 ± 1. 2, P ＜0.05 ). PAR-2 was expressed on the mucous surface, recesses epidermis and lamina propria inflammatory cells. And positive dyes were located within cytoplasm. As compared with the control group, the expression of PAR-2 mRNA was higher(2. 63 ±0. 26 vs 1, P ＜0. 05)and its protein expression higher in the model group(24. 3 ±2.4 vs 17. 5 ±3. 5, P＜0. 05). Conclusion Both PAR-2 and mast cell are involved in the pathogenesis of small intestinal mucosa injury induced by diclofenac in rats. PAR-2 may be activated by tryptase released from mast cells and participate in the pathogenesis of small intestinal injury as induced by non-steroidal antiinflammatory drugs.     

新型冠状病毒感染新生儿院间转运应急预案——浙江大学医学院附属儿童医院经验

自2019年12月以来，2019冠状病毒病（COVID-19）疫情已成为目前最严峻的公共卫生问题。新生儿作为免疫功能不成熟的特殊人群，已有COVID-19病例报道。鉴于疑似/确诊COVID-19新生儿应转运到定点医院隔离救治，为建立健全相应急救转运机制，特编写COVID-19新生儿急救转运预案。该预案提出了新生儿COVID-19的转运指征、组织管理、防护策略、工作流程、消毒处置方法等，旨在为疑似或确诊新生儿COVID-19的院间转运提供相关指导与建议。     

非甾体抗炎药肠损伤大鼠模型小肠组织中蛋白酶激活受体2的表达与肥大细胞分布

Objective To identify the expression and significance of protease-activated receptor-2 (PAR-2) and mast cell ( MC) in the rat model of small intestinal mucosal damage by a short-term administration of diclofenac. Methods Twenty-four SD-rats were divided into 2 groups ( control group and model group, 12 rats each) by random digit table. The rats in the control group were treated with 1 ml distilled water per 250 g, once a day while those in the model group diclofenac 7. 5 mg/kg per day. Their terminal ileum was harvested at Day 5 after an intraperitoneal injection. Toluidine blue dyeing was employed to determine the distribution of MC and its count in intestinal mucous membrane. Immunohistochemistry,Western blot and real-time PCR (polymerase chain reaction) were employed analyze the location, expression and change of PAR-2 mRNA in intestinal mucous membrane. Results The count of MC was obviously higher in the model group than that in the control group( 10. 3 ±2. 2 vs 4. 2 ± 1. 2, P ＜0.05 ). PAR-2 was expressed on the mucous surface, recesses epidermis and lamina propria inflammatory cells. And positive dyes were located within cytoplasm. As compared with the control group, the expression of PAR-2 mRNA was higher(2. 63 ±0. 26 vs 1, P ＜0. 05)and its protein expression higher in the model group(24. 3 ±2.4 vs 17. 5 ±3. 5, P＜0. 05). Conclusion Both PAR-2 and mast cell are involved in the pathogenesis of small intestinal mucosa injury induced by diclofenac in rats. PAR-2 may be activated by tryptase released from mast cells and participate in the pathogenesis of small intestinal injury as induced by non-steroidal antiinflammatory drugs.     

中医学专业学生西医临床实践技能的现状和需求分析

为了解中医学专业学生西医临床实践技能的现状和需求情况,采用问卷调查法对我校05-07级168名中医学专业本科及硕士生进行抽样调查。83.0%的学生认为有必要进行西医临床实践技能的专业培训;非常期望能加强临床诊断思维,体格检查,常见急症的处理,医患关系处理,X线、心电图诊断等技能。因此中医学专业学生提高西医临床实践技能较迫切,应在后期教学和实习中有针对性的加强。     

难治性胃食管反流病中西医治疗现状

难治性胃食管反流病可能与胃酸抑制不充分、非酸反流、食管高敏感性等因素有关.西医通常通过更换质子泵抑制剂、调整质子泵抑制剂剂量或者联用H2受体拮抗剂来有效控制胃酸;通过促进动力、肌松药、黏膜保护剂控制非酸反流;Stretta射频技术、腹腔镜下Nissen胃底折叠术对重症、难治性胃食管反流病也是一种有效的治疗方法.中医辨证...     

质子泵抑制剂对NSAIDs相关小肠损伤大鼠HO-1表达的影响

背景：长期使用非甾体消炎药（NSAIDs）可引起小肠黏膜炎症性病变。质子泵抑制剂（PPI）除抑酸外还具有抗炎和抗氧化作用,并可上调胃黏膜血红素加氧酶-1（HO．1）的表达。目的：探讨不同PPI对NSAIDs相关小肠损伤大鼠HO-1表达的影响。方法：将Sprague—Dawley大鼠随机分为空白对照组、模型组和4组PPI治疗组。给予大鼠双氯芬酸钠7．5mg／kg灌胃,以制备NSAIDs相关小肠损伤大鼠模型。各PPI治疗组分别以奥美拉唑30mg／kg、埃索美拉唑30mg／kg、雷贝拉唑15mg／kg、兰索拉唑45mg／kg灌胃治疗。实验第6d,处死所有大鼠,观察小肠组织大体和病理变化．以实时荧光定量PCR和蛋白质印迹法分别检测小肠组织HO-1mRNA和蛋白表达。结果：埃索美拉唑、雷贝拉唑、兰索拉唑治疗组大体和病理评分均显著低于模型组（P〈0．05）,雷贝拉唑、兰索拉唑治疗组小肠组织HO-1mRNA和蛋白表达较模型组明显升高（P〈0．05）,而奥美拉唑治疗组上述指标与模型组相比均无明显差异。结论：不同PPI对NSAIDs相关小肠损伤的保护作用不同．其机制可能与上调HO-1mRNA和蛋白表达有关-但奥美拉畔无明碌保护作用-