Acute upper gastrointestinal bleeding (AUGIB) is a life-threatening condition with substantial mortality, and early, accurate risk stratification is essential to improve outcomes. The endothelial activation and stress index (EASIX) is a novel composite marker reflecting endothelial injury and systemic stress; however, its prognostic value in AUGIB remains uncertain. This study aimed to evaluate the predictive value of EASIX for in-hospital adverse outcomes in patients with AUGIB and to develop a prediction model integrating clinical variables. In this single-center retrospective cohort study, we consecutively enrolled 483 patients hospitalized with AUGIB between January and December 2023. Clinical data were extracted from electronic medical records, and log₂(EASIX) was calculated at admission. Candidate predictors were selected using least absolute shrinkage and selection operator (LASSO) regression to reduce overfitting, and Firth penalized logistic regression models were developed to predict in-hospital mortality and ICU admission in view of the relatively low event rate. Model performance was evaluated using receiver operating characteristic (ROC) analysis, calibration plots, and decision curve analysis, with internal validation by bootstrap resampling (B = 1000). Subgroup and sensitivity analyses were conducted to assess robustness. In-hospital mortality occurred in 55 patients (11.39

Previous published data have confirmed that the addition of a citric acid meal improves the accuracy of the 13C-urea breath test (13C-UBT). However, some studies have suggested that a citric acid test meal may not be necessary. Thus, the aim of this study was to evaluate the combination of a 13C-UBT with a citric acid meal for the diagnosis of Helicobacter pylori (Hp) infection in a Chinese population, particularly for patients with results in the gray zone. In this paired self-controlled study, all subjects had previously undergone 13C-UBTs without citric acid meals and were randomly divided into two groups based on different doses of citric acid (a low-dose citric acid group and a high-dose citric acid group, comprising meals with 0.68 g and 3.84 g citric acid powder, respectively). Positive rapid urease test (CLO) test and histology results were considered the 'gold standard'. The mean delta over baseline (DOB) value, sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV) and accuracy were compared between the two groups, particularly for patients with results in the gray zone. In total, 285 patients were tested. Of these patients, 189 were included in the low-dose citric acid group, and 96 were included in the high-dose citric acid group. Among patients with a positive 13C-UBT result without citric acid [delta over baseline (DOB) value ≥ 4‰, n = 174] and a negative 13C-UBT result without citric acid (DOB value < 4‰, n = 111), 8.0% (14/174) were false positive, and 0.9% (1/111) was false negative as determined by gold standard. Of 14 patients with false positive, 78.6% (11/14) false positive were in the gray zone of 4–10‰. However, there were no false positive 13C-UBT results with citric acid in the the gray zone of 4–10‰. In the comparison of the commercial 13C-UBT with the 13C-UBT in the low-dose citric acid group, the sensitivity, specificity, PPV, NPV and accuracy at 15 min were as follows: 99.1% vs. 99.1%, 97.5% vs. 88.9%, 98.2% vs. 92.2%, 98.8% vs. 98.6% and 98.4% vs. 94.7%, respectively. In the the gray zone of 4.0–10.0‰, the comparison of the commercial 13C-UBT with the 13C-UBT in the low-dose citric acid group, the sensitivity, specificity, PPV, and accuracy at 15 min were as follows: 94.4% vs. 100.0%, 100.0% vs. 0%, 100.0% vs. 75.0% and 95.8% vs. 75.0%, respectively. No significant difference was observed between the 15-min and 30-min measurement intervals in the low- and high-dose citric acid groups, including patients with results in the gray zone. The low-dose citric acid test, with an optimal measurement interval of 15 min, was highly accurate in the diagnosis of Hp infection in the Chinese population, especially for individuals with results in the gray zone.

Liver cirrhosis, characterized by diffuse necrosis, insufficient regeneration of hepatocytes, angiogenesis, severe fibrosis, and the formation of pseudolobules, is a progressive, chronic liver disease induced by a variety of causes. It is clinically characterized by liver function damage and portal hypertension, and many complications may occur in its late stage. Based on the updated practice guidelines, expert consensuses, and research advances on the diagnosis and treatment of cirrhosis, the Chinese Society of Gastroenterology of Chinese Medical Association established the current consensus to standardize the clinical diagnosis and management of liver cirrhosis and guide clinical practice. This consensus contains 43 statements on the etiology, pathology and pathogenesis, clinical manifestations, major complications, diagnosis, treatment, prognosis, and chronic disease control of liver cirrhosis. Since several practice guidelines and expert consensuses on the complications of liver cirrhosis have been published, this consensus emphasizes the research progress of liver cirrhosis itself.

Introduction: Early detection and accurate pathological assessment are critical to improving prognosis of pancreatic cancer. EUS has been widely used in diagnosing pancreatic lesions and can obtain histological diagnosis by endoscopic ultrasound-guided fine needle aspiration (EUS-FNA). However, comprehensive assessment of the interobserver agreement (IOA) among cytopathologists evaluating EUS-FNA specimens is still limited. Therefore, this study evaluated IOA among cytopathologists for EUS-FNA specimens of solid pancreatic lesions, especially in false-negative cases of cytological diagnosis and analyzed the factors that influence cytological diagnosis of EUS-FNA so as to improve the diagnostic efficiency of EUS-FNA. Methods: We retrieved EUS-FNA samples of pancreatic solid lesions from 2017 to 2021 and collected their clinical/cytological data. Two cytopathologists independently reviewed these cases using a quoted, novel standardized cytology scoring tool. Ultimately, we calculated IOA among cytopathologists and performed a binary logistic regression analysis to evaluate factors influencing the cytological diagnosis of EUS-FNA. Results: 161 patients were included, and 60 cases with a clinical diagnosis of pancreatic cancer but a cytological diagnosis of benign and atypical constituted the false-negative group. IOAs for cytological diagnosis of overall patients and the false-negative group were in perfect/moderate agreement with Kendall’s W values of 0.896 and 0.462, respectively. The number of diagnostic cells in the scoring tool had the highest level of agreement (κ = 0.721) for overall patients. There was at best moderate agreement on other quantity and quality parameters for both all cases and false-negative group. Logistic regression analysis showed the number of diagnostic cells (OR = 6.110, p < 0.05) and amount of blood (OR = 0.320, p < 0.05) could influence cytological diagnosis. Conclusions: The false-negative rate of our study as high as 37.26% (60/161) is mainly related to strict standards of cytopathologists, and their ability to standardize pancreatic cytology is still improving. Suboptimal agreement among cytopathologists for cytological diagnosis and the number of diagnostic cells may be associated with the occurrence of false-negative diagnosis. Further regression analysis confirmed that the number of diagnostic cells and obscuring blood were important factors in cytological diagnosis. Therefore, refinement of cytological diagnostic criteria, standardization of specimen quality evaluation, and training of cytopathologists may improve the agreement of cytopathologists, thus improving the repeatability of cytological diagnosis and reducing the occurrence of false-negative events.

目的 探讨中脑胶质细胞神经营养因子(MANF)在利福平(RFP)诱导的人肝癌细胞(HepG2)胆汁酸转运体的适应性表达中的作用.方法 使用慢病毒稳转构建对照组细胞株(Y07)和敲减组细胞株(Y25),于对数生长期的Y07和Y25细胞中加入RFP 200μmol/L处理48 h.利用qRT-PCR和Western blot检测MANF、胆盐输出泵(BSEP)、多药耐药相关蛋白2/3/4(MRP2、MRP3、MRP4)、多药耐药蛋白1(MDR1)、有机溶质转运体a/β(OSTα/β)、有机阴离子转运蛋白(OATP2B1)的蛋白和基因表达程度.检测增殖细胞核抗原(PCNA)、增殖细胞标志物Ki67蛋白和基因表达程度评价各组细胞增殖水平变化;检测C/EBP同源蛋白(CHOP)、天冬氨酸半胱氨酸特异性蛋白酶-3(Caspase-3)蛋白和基因表达程度变化评估各组细胞凋亡情况.用试剂盒检测各组细胞培养液上清中的损伤标志物丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、碱性磷酸酶(ALP)、总胆红素(TBIL)、直接胆红素(DBIL)、总胆汁酸(TBA)的水平.结果 在蛋白和基因水平,RFP可诱导HepG2细胞的MANF、BSEP、MRP2、MRP3、MRP4、MDR1、OSTα、OSTβ、OATP2B1的上升(P<0.05),而MANF敲减后BSEP、MRP2、MRP3、MRP4、MDR1、OSTα、OSTβ、OATP2B1的蛋白和基因表达水平均下降(P<0.05).在RFP作用下,敲减MANF后PC-NA、Ki67的蛋白表达相对较高,CHOP、Caspase-3蛋白和基因表达上升(P<0.05),肝细胞损伤标志物水平上升(P<0.05).结论 RFP可诱导HepG2细胞胆汁酸转运体的表达上升(P<0.05),而敲减MANF后的HepG2在RFP诱导下胆汁酸转运体的表达会明显下降(P<0.05),同时细胞损伤加重,提示MANF在RFP诱导的适应性反应中起保护作用.

Melatonin possesses potent hepatoprotective properties, but it remains to be elucidated whether melatonin has a therapeutic effect on monocrotaline (MCT)-induced hepatic sinusoidal obstruction syndrome (HSOS). In this study, male Sprague Dawley rats were intraperitoneally injected with melatonin or the same volume of vehicle at 0 and 24 h after MCT intragastric administration. Next, hematoxylin-eosin staining and electron microscopy were performed to evaluate the hepatic sinusoidal injury of rats. Endothelial cell marker RECA-1 was observed by immunohistochemistry. Hepatic oxidative stress was analyzed by detecting malondialdehyde, glutathione S-transferase, and reactive oxygen species. Assessment of liver function was carried out by analysis of serum aspartate aminotransferase, alanine aminotransferase, total bilirubin, and albumin levels. Real-time polymerase chain reaction and Western blot analysis were used to identify liver Sirtuin-3 (SIRT3) and active matrix metallopeptidase 9 (MMP-9) expression. Besides, liver sinusoidal endothelial cells (LSECs) were used for the in vitro functional verification experiment. Specifically, liver histology of the melatonin-treated groups showed that the pathological damages caused by MCT were significantly attenuated, total HSOS scores were decreased, and the elevation of serum hyaluronic acid observed in the model group was also reduced. Moreover, melatonin treatment also improved the survival of rats after partial hepatectomy. Administration of melatonin ameliorated MCT-induced LSECs injury, hepatic oxidative stress, and hepatic dysfunction. Furthermore, melatonin treatment increased SIRT3 expression while attenuating MMP-9 activity in liver tissues. Cell experiment also demonstrated that SIRT3 might mediate the protective effect of melatonin on LSECs. Collectively, our study provided the potential rationale for the application of melatonin for the prevention of MCT-induced HSOS.

目的 探讨药物性胆汁淤积型肝损伤患者基本信息、临床特征、影像学表现及转归.方法 回顾性分析近5 年来的住院患者中诊断为药物性胆汁淤积型肝损伤的病例资料,记录其临床数据,至少随访6 个月.结果 共有105 例药物性胆汁淤积型肝损伤患者,中位年龄 55 岁,男性占比54.3%,多无特异性临床症状.所涉及的药物近80 余种,前3 位依次为中药(34.3%)、抗肿瘤药(22.9%)、抗生素(10.5%).49 例行磁共振胰胆管成像患者中,有 7 例(14.3%)患者存在硬化性胆管炎样改变.105 例患者中治愈53 例(50.5%),好转 41 例(39.0%),未愈 7 例(6.7%),死亡4 例(3.8%),总有效率为89.5%.结论 药物性胆汁淤积型肝损伤主要发生于老年患者,涉及药物种类较多,以中药最为多见.药物还可引起类似于硬化性胆管炎样改变,因此应将药物性胆汁淤积型肝损伤作为胆汁淤积和胆管造影异常患者的鉴别诊断之一.基础肝病对患者预后无影响.二元Logistic逐步回归分析示:Roussel Uclaf因果关系评价法(RUCAM)评分低、血红蛋白水平低、住院时间短以及白细胞计数高是药物性胆汁淤积型肝损伤患者转归的独立危险因素.

本文报道了1例以复发性胰腺假性囊肿为主要表现的胰管离断综合征，经过2次内镜下囊肿胃引流以及4次经内镜逆行胰胆管造影术治疗，最终成功放置胰管支架进行胰管断裂桥接治疗，术后囊肿吸收，患者恢复良好。此病例有助于临床医师认识胰管离断综合征，尤其是对于反复发作的胰腺假性囊肿更应当警惕本病。

通过体内和体外实验方法观察依诺肝素对野百合碱导致肝窦阻塞综合征(HSOS)的治疗及其可能机制。结果显示，野百合碱可导致大鼠HSOS，并降低大鼠肝窦内皮细胞的存活率。与野百合碱比较，依诺肝素治疗可减轻野百合碱所致HSOS大鼠的肝窦阻塞，并可提高肝窦内皮细胞的存活率。此外，野百合碱可使大鼠肝脏、肝窦内皮细胞中Slit2、Robo4蛋白质和mRNA表达下降，但依诺肝素能够上调野百合碱所致HSOS大鼠肝脏、肝窦内皮细胞中Slit2、Robo4蛋白质和mRNA的表达。

Aberrant TGF-beta/Smad7 signaling has been reported to be an important mechanism underlying the pathogenesis of ulcerative colitis. Therefore, the present study aimed to investigate the effects of a number of potential anti-colitis agents on intestinal epithelial permeability and the TGF-beta/Smad7 signaling pathway in an experimental model of colitis. A mouse model of colitis was first established before anti-TNF-alpha and 5-aminosalicyclic acid (5-ASA) were administered intraperitoneally and orally, respectively. Myeloperoxidase (MPO) activity, histological index (HI) of the colon and the disease activity index (DAI) scores were then detected in each mouse. Transmission electron microscopy (TEM), immunohistochemical and functional tests, including Evans blue (EB) and FITC-dextran (FD-4) staining, were used to evaluate intestinal mucosal permeability. The expression of epithelial phenotype markers E-cadherin, occludin, zona occludens (ZO-1), TGF-beta and Smad7 were measured. In addition, epithelial myosin light chain kinase (MLCK) expression and activity were measured. Anti-TNF-alpha and 5-ASA treatments was both found to effectively reduce the DAI score and HI, whilst decreasing colonic MPO activity, plasma levels of FD-4 and EB permeation of the intestine. Furthermore, anti-TNF-alpha and 5-ASA treatments decreased MLCK expression and activity, reduced the expression of Smad7 in the small intestine epithelium, but increased the expression of TGF-beta. In mice with colitis, TEM revealed partial epithelial injury in the ileum, where the number of intercellular tight junctions and the expression levels of E-cadherin, ZO-1 and occludin were decreased, all of which were alleviated by anti-TNF-alpha and 5-ASA treatment. In conclusion, anti-TNF-alpha and 5-ASA both exerted protective effects on intestinal epithelial permeability in an experimental mouse model of colitis. The underlying mechanism may be mediated at least in part by the increase in TGF-beta expression and/or the reduction in Smad7 expression, which can inhibit epithelial MLCK activity and in turn reduce mucosal permeability during the pathogenesis of ulcerative colitis.

目的 利用乳果糖氢呼气试验(LHBT)检测肝硬化和慢性肝炎肝纤维化(CHF)患者中小肠细菌过度生长(SIBO)的发生率,探讨其与炎症因子及氧化应激相关指标的关系.方法 选取38例CHF患者和60例肝硬化患者以及31例健康对照组,利用LHBT的方法评估各组SIBO发生率.然后将受试者分为SIBO阳性组和SIBO阴性组,比较两组间临床症状和实验室检查,并检测其血清脂多糖(LPS)、白细胞介素(IL)-6、肿瘤坏死因子(TNF)-α、IL-10水平以及二胺氧化酶(DAO)、超氧化物岐化酶(SOD)、谷胱甘肽(GSH)、过氧化氢酶(CAT)水平,并对所检测的LPS、IL-6、TNF-α、IL-10、DAO、SOD、GSH、CAT的浓度与LHBT集值的相关性进行统计学分析.结果 ①CHF组和肝硬化组以及对照组SIBO阳性率分别为36.84％、60.00％和9.68％,差异有统计学意义(P<0.01);②SIBO阳性组患者和阴性组患者在Child-Pugh(CTP)分级及腹水的表现上差异有统计学意义(P<0.05);③SIBO阳性患者血清中LPS、IL-6、DAO、CAT、SOD水平高于SIBO阴性患者(P<0.05),IL-10、TNF-α以及GSH水平与SIBO阴性组差异无统计学意义;④ 患者LHBT集值与LPS、IL-6、DAO、SOD、CAT呈正相关(P<0.05),与TNF-α、IL-10、GSH的相关性差异无统计学意义.结论 CHF以及肝硬化患者较健康对照组更易发生SIBO,且与外周血中多种炎症因子和氧化应激指标水平升高相关.SIBO可能通过肠道菌群失调导致的炎症反应和氧化应激等途径加重CHF和肝硬化患者的病情变化.

Background Crohn's disease (CD), an inflammatory bowel disease (IBD), is a complex and heterogeneous disease characterized by nonspecific transmural inflammation of the gastrointestinal tract. CD has a variety of potential causes with no effective treatment available yet. Current clinical laboratory findings from patients do not provide direct indication of the status of mucosal inflammation in the intestine. Recently, it has been found that intestinal inflammation is generally associated with increased levels of 5-hydroxytryptamine (5-HT), which acts as an important gastrointestinal signaling molecule in intestinal homeostasis by stimulating specific receptors. Most previous researches were carried out in vitro or with animal models, and there was a lack of authentic clinical research. In this study, clinical specimens from patients with Crohn's disease were used to investigate the expression of 5-hydroxytryptamine 7 receptor (5-HT7R) in the induction and development of chronic non-specific inflammatory bowel disease. Methods Patients with CD admitted to the Department of Gastroenterology in the First Affiliated Hospital of Anhui Medical University between June 2014 and January 2018 were recruited, among which 28 were in active disease and 32 were in remission. In addition, 20 patients who had no obvious abnormality by colonoscopy in the hospital during the same time period were recruited into the control group. Data of clinical disease activity (CDAI), CD endoscopic score (SES-CD) and magnetic resonance score (MaRIA) were collected from those two groups of patients. The expression and distribution of 5-HT7R were investigated and their correlations with clinical CDAI, MaRIA, and endoscopic SES-CD scores were analyzed. Results Our study demonstrated that 5-HT7R is expressed in intestinal neurons and CD11(C)-positive cells in human colon. In CD11c/CD86 double-positive cells in the bowel, 5-HT7R expression was significantly increased in the inflammatory area in the bowel of CD patients, and it was closely related to disease severity, MaRIA, and SES-CD scores. Conclusion The expression of 5-HT7R was significantly correlated with the degree of gut inflammation in CD patients and could be a potential biomarker for disease activity and the therapeutic efficacy in patients with Crohn's Disease.

氯法齐明导致的小肠损伤临床罕见，其主要症状包括腹痛、营养不良和黑便。当长期服用氯法齐明患者出现腹痛腹泻、体重减轻时，若不及时停药，可能出现致死性的并发症，应引起临床重视。本文报道1例经小肠镜检查并病理明确的氯法齐明导致的小肠损伤，供临床参考。

目的 分析发热伴血小板减少综合征(SFTS)并发胰腺损伤患者的临床特点,为提高对该病的诊疗水平提供参考.方法 回顾性分析2018年1月至2020年12月收治的SFTS并发胰腺损伤患者临床资料,对患者人口学资料、临床特点、血清脂肪酶和淀粉酶检测结果、治疗方案和转归等资料进行统计分析.结果 32例SFTS并发胰腺损伤患者发病高峰在4～8月,患者年龄在50岁以上者29例(90.63％),农民19例(59.38％).本病临床表现差异大,主要症状包括发热31例(96.88％)、乏力18例(56.25％)等.32例患者中,并发急性胰腺炎者2例(6.25％),并发高脂肪酶血症者19例(59.38％),并发高淀粉酶血症者8例(25.00％).结论 SFTS并发胰腺损伤患者以高脂肪酶血症和高淀粉酶血症多见;临床应加强对本病的鉴别诊断,避免过度诊疗,节约医疗资源.

目的 探讨慢性萎缩性胃炎(CAG)患者可操作的与胃癌风险联系的胃炎评估(OLGA)及可操作的与胃癌风险联系的肠化生评估(OLGIM)分期系统和血清胃蛋白酶原(PG)浓度相关性,分析其在随访期间胃癌发生情况及其危险因素.方法 对既往内镜诊断为CAG并经病理证实符合腺体萎缩伴或不伴肠化(IM)、低级别上皮内瘤变(LGIN)的患者进行内镜监测.根据新悉尼系统活检标准对随访患者进行组织学活检,并根据组织学结果进行OLGA及OLGIM分期,0～Ⅱ期为胃癌低风险,Ⅲ～Ⅳ期为胃癌高风险.同时利用酶联免疫吸附法(ELISA)测定血清PG和胃泌素-17(G-17)水平.结果 纳入164例患者,平均年龄为(57.48±10.71)岁,男/女为102/62.所有患者均曾被诊断为胃黏膜萎缩伴或不伴IM、LGIN,平均随访时间为(4.2±3.3)年,至少进行了2次内镜随访.与OLGA分期及OLGIM分期低风险组相比,高风险组中G-17增加,胃蛋白酶原Ⅰ(PGI)及胃蛋白酶原比值(PGR)降低,差异有统计学意义(P＜0.05).随访过程中,共检出胃癌6例(3.65％),其中男性4例,早期胃癌5例,进展期胃癌1例,慢性萎缩性胃炎肿瘤进展率每年为0.58％.COX回归分析显示,年龄大于60岁,萎缩伴低级别上皮内瘤变为萎缩性胃炎发生胃癌的危险因素.结论 慢性萎缩性胃炎是胃癌前状态,采用内镜病理随访有助于早期发现胃癌.60岁以上重度萎缩性胃炎伴低级别上皮内瘤变者,建议每1～2年复查高清胃镜.

目的 探讨敲低中脑星型胶质细胞源性神经生长因子(MANF)对利福平(RFP)诱导HepG2细胞损伤的影响及机制.方法 慢病毒转染技术构建MANF敲低稳转细胞株(MANF Y25)及其对照细胞株(MANF Y07).实验分为4组:MANF Y07+ DMSO组、MANF Y07+ RFP组、MANF Y25+ DMSO组、MANF Y25+RFP组.给予HepG2细胞100μmol/L RFP 24 h后,Western blot和qRT-PCR检测各组细胞MANF及未折叠蛋白反应(UPR)相关基因葡萄糖调节蛋白78 (GRP78)、蛋白酶R样内质网激酶(PERK)、真核翻译启动因子2α(eIF2α)、活化转录因子4(ATF4)、CCAAT/增强子结合蛋白(CHOP)、Tribbles同源蛋白3(TRIB3)、肌醇需求激酶1(IRE1)、剪接型X-盒结合蛋白1(XBP1-S)、非剪接型X-盒结合蛋白1(XBP1-U)、活化转录因子6(ATF6)的蛋白及基因表达水平;Annexin V-PE/7-AAD双染法检测各组细胞凋亡率;CCK-8法检测各组细胞增殖变化;试剂盒检测各组细胞培养上清液中细胞损伤标志物谷丙转氨酶(ALT)、谷草转氨酶(AST)、碱性磷酸酶(AKP)、总胆红素(TBIL)、间接胆红素(IBIL)相对含量变化.结果 在蛋白水平,RFP激活MANF、GRP78、p-eIF2α、ATF4、ATF6的蛋白表达;在基因水平,RFP诱导HepG2细胞MANF、GRP78、PERK、eIF2α、ATF4、CHOP、TRIB3的基因表达,并且MANF敲低后GRP78、p-PERK、p-eIF2α、ATF4、ATF6蛋白表达水平及上述UPR相关基因的基因表达水平进一步上调(P＜0.05),MANF敲低后细胞凋亡率升高(P＜0.01),细胞增殖能力降低(P＜0.01),细胞培养上清液中ALT、AST、AKP、TBIL、IBIL水平升高(P＜0.05),说明细胞损伤加重.结论 RFP可激活UPR,敲低MANF后这种效应进一步加强,同时细胞损伤加重,表明MANF可能通过调节URP而在RFP诱导HepG2细胞损伤中发挥保护作用.

目的 分析非胰腺炎相关高脂肪酶血症患者的临床特点,提高临床诊疗水平.方法 回顾分析2018年1月至2019年3月安徽医科大学第一附属医院38例非胰腺炎相关高脂肪酶血症住院患者临床资料,分析其临床表现、实验室生化检查及基础疾病等资料.结果 38例非胰腺炎相关高脂肪酶血症患者,其中意识不清10例,余患者39.3％(11/28)表现有非胰腺炎相关的腹痛.38例患者血清脂肪酶平均升高5.93±3.68倍,平均进行1.37±0.59次腹部影像学检查;47.4％(18/38)患者接受了抑制胰酶治疗.常见的基础疾病包括肾功能不全(36.8％,14/38)和发热伴血小板减少综合征(26.3％,10/38).肾功能不全组血清脂肪酶大于非肾功能不全组(P＜0.05).23.7％(9/38)高脂肪酶血症患者同时合并高淀粉酶血症.结论 高脂肪酶血症见于多种基础疾病,常合并高淀粉酶血症,详细病史和影像学检查是避免过度诊疗的关键.

Accumulating evidence has revealed that long noncoding RNAs (lncRNAs) play essential roles in regulating cellular process of various cancers. There have been many studies on the biological functions of lncRNAs in colorectal cancer (CRC). In this research, we explored the role and mechanism of lncRNA ovarian tumor domain containing 6B antisense RNA1 (OTUD6B-AS1) in CRC. Here, we detected OTUD6B-AS1 expression in CRC tissues and cells by RT-qPCR. Functional experiments were performed to test alterations in different cellular processes. Moreover, to verify the binding ability among the indicated RNA molecules, we carried out RIP, RNA pull-down and luciferase reporter assays. According to our data, OTUD6B-AS1 expression was low in CRC tissues and cells. Functionally, overexpression of OTUD6B-AS1 inhibited cell proliferation, migration, invasion and EMT, and promoted cell apoptosis. Bioinformatic analysis and mechanistical experiments confirmed that OTUD6B-AS1 could act as a competitive endogenous RNA (ceRNA) to upregulate Proline-Rich Nuclear Receptor Coactivator 2 (PNRC2) expression by sequestering miR-21-5p. Further rescue experiments validated the inhibitory function of the OTUD6B-AS1/miR-21-5p/PNRC2 axis in cellular process of CRC. Overall, OTUD6B-AS1 inhibits cellular development in CRC by sponging miR-21-5p and upregulating PNRC2, providing a novel insight into the exploration on CRC treatment.

Background and AimsAbnormal transforming growth factor-β (TGF-β)/Smad7 signaling pathway may be an important mechanism of IBD.Therefore, this study was to investigate whether anti-colitis drugs modulate intestinal epithelial permeability in experimental colitis and to determine its TGF-β/Smad7 signaling pathway. MethodsA murine colitis model was induced, and then anti-TNF-α and 5-ASA were administered intraperitoneally and orally respectively. Myeloperoxidase(MPO) activity, histological index(HI) of colon and the disease activity index(DAI) scores of mice were detected. Transmission electron microscopy (TEM), immunohistochemical and functional tests which included two methods: one was Evans blue(EB) and the other was FITC-dextran(FD-4), were used to evaluate intestinal mucosal permeability. The expression of epithelial E-cad, Occludin, ZO-1, TGF –β and Smad7 were analyzed. Epithelial MLCK expression and activity were determined.ResultsAnti-TNF-α and 5-ASA both effectively reduced the DAI score and HI, and decreased colonic MPO activity, plasma levels of FD-4 and EB permeation of the intestine. Moreover, anti-TNF-α and 5-ASA downregulated the MLCK expression and activity and the expression of Smad7 in the small intestinal epithelium, and increased the expression of TGF-β(P < 0.050). In colitis mice, TEM revealed partial ileal epithelial injury, intercellular TJs and the expression of E-cadherin, ZO-1 and occludin were decreased, which were alleviated by anti-TNF-α and 5-ASA.ConclusionsAnti-TNF-α and 5-ASA both showed a significant effect on intestinal epithelial permeability in experimental colitis. The mechanism can be clarified as the increase of TGF-β expression or the decrease of Smad7 expression which could inhibit epithelial MLCK and then reduce the mucosal permeability of ulcerative colitis.

Rifaximin has been recommended as a prophylactic drug for hepatic encephalopathy (HE) and spontaneous bacterial peritonitis (SBP). This study aims to explore whether low-dose rifaximin can prevent overall complications and prolong survival in cirrhotic patients. In this multi-centre randomized open-labelled prospective study, 200 patients with decompensated cirrhosis were randomly assigned at a ratio of 1:1. Patients in rifaximin group were administered 400 mg rifaximin twice daily for 6 months, and all other therapeutic strategies were kept unchanged in both groups as long as possible. The primary efficacy endpoints were the incidence of overall complications and liver transplantation-free survival. The secondary endspoints were the incidence of each major cirrhosis-related complication, as well as the Child–Pugh score and class. The major baseline characteristics were similar in the two groups except for HE. The cumulative incidence and frequency of overall complications were significantly lower in rifaximin group than in the control group (p < 0.001). Though liver transplantation-free survival was not significantly different between the two groups, subgroup analysis showed rifaximin markedly prolonged liver transplantation-free survival in patients with Child–Pugh score ≥ 9 (p = 0.007). Moreover, rifaximin markedly reduced the episodes of ascites exacerbation (p < 0.001), HE (p < 0.001) and gastric variceal bleeding (EGVB, p = 0.031). The incidence of adverse events was similar in the two groups. Low-dose rifaximin significantly decreases the occurrence of overall complications, leading to prolonged survival in patients with advanced stages of cirrhosis in this trail. Further study should be carried out to compare the effect of this low-dose rifaximin with normal dose (1200 mg/day) rifaximin in preventing cirrhosis-related complications. NCT02190357