急性胰腺炎(acute pancreatitis,AP)是一种以胰腺组织水肿和坏死为主要病理特征的急腹症.约11％～32％的初发AP患者会发展为复发性急性胰腺炎(recurrent acute pancreatitis,RAP)[1-2],远期危害较大[3-5].高脂血症性急性胰腺炎(hyperlipidemic acute pancreatitis,HLAP)发病率逐年升高[6-7],较其他病因所致的AP更年轻化[8]、重症化[9-10],且合并症多[8],易发展为复发性高脂血症性急性胰腺炎(recurrent hyperlipidemic acute pancreatitis,R-HLAP)[3,11].如果能在初发HLAP患者中甄别出复发高风险人群,及时采取有效防治措施,则可能避免RAP发生.故本文回顾性分析本院诊治且能随访跟踪的初发HLAP患者临床资料,探讨发生R-HLAP的影响因素,构建预测R-HLAP的列线图并验证及评价,为临床早期筛选高风险复发人群制定防治策略.

目的 探讨长链非编码RNA(LncRNA)MEG3减轻缺血再灌注肠黏膜屏障功能损害的机制,为肠缺血再灌注损伤的临床治疗提供潜在策略.方法 使用人结肠腺癌Caco-2细胞建立缺氧缺糖(OGD)模型.采用CKK-8法检测对照组、OGD处理组和OGD处理后合并LncRNA MEG3过表达或抑制表达后Caco-2细胞存活率,Annexin V-异硫氰酸荧光素(FITC)/碘化丙啶(PI)细胞凋亡检测试剂盒检测各组细胞凋亡,定量逆转录聚合酶链式反应检测各组细胞LncRNA MEG3表达的差异,采用跨皮细胞电阻(TEER)检测法测定肠黏膜TEER值,并分析肠屏障功能.结果 经OGD处理的各组LncRNA MGE3表达明显降低,细胞存活率降低且细胞凋亡增加,导入shMEG3后进一步降低Caco-2细胞LncRNA MEG3表达及细胞存活率,并且加剧细胞凋亡,过表达LncRNA MEG3可增加OGD处理的各组Caco-2细胞存活率,减少其凋亡,并减轻其肠屏障功能损害.结论 LncRNA MEG3在体外实验中可减轻肠黏膜细胞缺血再灌注损伤,保护肠黏膜屏障功能.

Objective:To explore the characteristics of T lymphocyte subsets and cytokines in hyperlipidemia-induced acute pancreatitis (HLAP) and its prognostic value.Methods:This study included 184 patients with acute pancreatitis (AP) admitted to the First Affiliated Hospital of Xiamen University from January 2018 to May 2021. Based on disease etiology, there were 92 HLAP cases and 92 non-hyperlipidemia-induced AP (NHLAP) cases. Stratified by disease severity according to 2012 Atlanta classification criteria, the patients were divided into the severe subgroup (SAP) and non-severe subgroup (NSAP). Peripheral venous blood samples were taken from all patients on day 1, 3, and 5 after admission. T lymphocyte subsets were determined by flow cytometry, and cytokines were detected by flow fluorometry. The number of CD4 +% and CD8 +% and the expression of cytokines were compared by Student’s t test or Mann-Whitney U analysis. Logistic regression analyses were performed to identify risk factors for severe AP, and a receiver operating characteristic (ROC) curve was constructed to predict severe AP. Statistical significance was taken as P<0.05. Results:Compared with the NHLAP group, patients in the HLAP group had lower CD4 +%, while higher levels of IL-2 on day 1 ( P<0.05), and had also lower CD4 +%, while higher levels of IL-4, IL-6, and IL-10 on day 3 ( P<0.05). Furthermore, IL-6 and IL-10 levels of the HLAP group were significantly increased compared to the NHLAP group on day 5 ( P<0.05). IL-10 levels in the SAP subgroup were significantly higher than those in the NSAP subgroup on day 1 ( P<0.05). Compared with the NSAP subgroup, the SAP subgroup had elevated levels of IL-2, IL-4, IL-6, IL-10 and IFN-γ on day 3 (all P<0.05), and had lower CD4 +%, while increased levels of IL-6 and IL-10 on day 5 (all P<0.05). Multivariate Logistic regression analysis showed that IL-10 was an immune indicator of independent risk factor for severe AP in the HLAP group on day 1 ( OR=1.139, 95% CI: 1.038-1.251, P<0.05). Finally, ROC analysis showed that the area under the curve of IL-10 to assess HLAP with severe AP was 0.772, and the best cut-off value for predicting severe AP was 5.6 pg/mL, with a sensitivity of 83.3% and a specificity of 68.8%. Conclusions:Changes of CD4 +% and cytokines are different between the HLAP and NHLAP groups. IL-10 can be used as a predictor of early disease severity in patients with HLAP.

BACKGROUND:Cardiac arrest (CA), a common disease with a high mortality rate, is a leading cause of ischemia/reperfusion (I/R)-induced dysfunction of the intestinal barrier. Long non-coding RNAs (lncRNAs) play crucial roles in multiple pathological processes. However, the effect of the lncRNA maternally expressed 3 (MEG3) on intestinal I/R injury and the intestinal barrier has not been fully determined. Therefore, this study aimed to investigate the function of MEG3 in CA-induced intestinal barrier dysfunction. METHODS:The oxygen and glucose deprivation (OGD) model in the human colorectal adenocarcinoma Caco-2 cells and in vivo cardiac arrest-induced intestinal barrier dysfunction model in Sprague-Dawley (SD) rats were established. The effect and underlying mechanism of MEG3 on the intestinal barrier from cardiac arrest-induced ischemia/reperfusion injury were analyzed by methyl thiazolyl tetrazolium (MTT) assays, Annexin V-FITC/PI apoptosis detection kit, Terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) staining, quantitative polymerase chain reaction (qPCR) assays, Western blot analysis, luciferase reporter gene assays, transepithelial electrical resistance (TEER) measurements, immunofluorescence analysis, and enzyme-linked immunosorbent assay (ELISA) assays. RESULTS:Interestingly, we found that MEG3 could protect Caco-2 cells from oxygen-glucose deprivation (OGD)/reoxygenation-induced I/R injury by modulating cell proliferation and apoptosis. Moreover, MEG3 relieved OGD-induced intestinal barrier dysfunction in vitro, as demonstrated by its significant rescue effect on transepithelial electrical resistance and the expression of tight junction proteins such as occludin and claudin-1 (CLDN1), which were impaired in OGD-treated Caco-2 cells. Mechanistically, MEG3 inhibited the expression of inflammatory factors including interleukin (IL)-1β, tumor necrosis factor (TNF)-α, interferon-gamma (IFN)-γ, inflammatory factors including interleukin (IL)-10, and transforming growth factor beta (TGFb)-1, as well as nuclear factor-kappa B (NF-κB) signaling. In response to OGD treatment in vitro, MEG3 also activated the expression of sirtuin 1 (SIRT1) by Caco-2 cells via sponging miR-34a-3p. Furthermore, MEG3 relieved CA-induced intestinal barrier dysfunction through NF-κB signaling in vivo. CONCLUSIONS:LncRNA MEG3 can protect the intestinal barrier from cardiac arrest-induced I/R injury via miR-34a-3p/SIRT1/NF-κB signaling. This finding provides new insight into the mechanism by which MEG3 restores intestinal barrier function following I/R injury, presenting it as a potential therapeutic candidate or strategy in intestinal injury.

目的 分析急性上消化道出血患者的电子胃镜完成情况.方法 回顾性分析2019年1-12月就诊于厦门大学附属第一医院急诊科的所有急性上消化道出血患者,将就诊后的患者分为5个时间段,对比分析电子胃镜完成情况、不同时间段住院费用、住院时间、责任病灶检出数与胃镜下治疗情况.结果 共收集890例急性上消化道出血患者,410例患者完成电子胃镜,责任病灶检出率和内镜下止血治疗比率最高的时间分别为患者就诊后12～24 h 时段和6～12 h时段,与≥48 h时段比较,差异有统计学意义(P＜0.05).613例患者住院治疗,57.7％(354/613)患者完成电子胃镜检查,就诊后12～24 h时段完成电子胃镜检查患者的住院时间和住院费用最低,与未做电子胃镜及≥48 h时段比较,差异有统计学意义(Z=4.380、5.010,P＜0.05).结论 患者就诊后12～24 h接受电子胃镜检查有利于急诊上消化道出血患者病情诊治.

Objective: To investigate the role of lncRNA ANRIL in the modulation of myocardial cell apoptosis in acute myocardial infarction (AMI). Methods: AMI mice model was established, and lncRNA ANRIL, IL-33 and ST2 expressions were detected by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. The apoptosis of myocardial cells was detected by TUNEL assay. RNA pull-down and RNA immunoprecipitation (RIP) assays were used to confirm the interaction between lncRNA ANRIL and USP17. Results: Compared with sham group, lncRNA ANRIL and ST2 expression levels were up-regulated, and the apoptosis of myocardial cells was increased in heart tissues of AMI group. Compared with normoxia group, the apoptosis of mouse myocardial cell HL-1 and primary murine myocardial cells was increased, and lncRNA ANRIL and ST2 expression levels were up-regulated in hypoxia group. We also found up-regulation of IL-33 in AMI group and hypoxia group. Besides, lncRNA ANRIL affected deubiquitinase USP17-mediated degradation of IL-33. Interfering lncRNA ANRIL reduced the apoptosis of myocardial cells through IL-33/ST2 pathway. In vivo experiments found that interfering lncRNA ANRIL relieved myocardial cell apoptosis and improved heart function in AMI mice. Conclusion: LncRNA ANRIL regulated myocardial cell apoptosis through IL-33/ST2 pathway.

目的 探讨AutoPuslse心肺复苏机与传统人工复苏的效果.方法 选择2014年9月至2017年11月198例心肺复苏患者(全为院内抢救)随机分为两组AutoPuslse组和传统组,分别用AutoPuslse心肺复苏机(99例)和传统人工复苏(99例)进行复苏.比较两组复苏的成功率及生存率.排除就诊时间这一影响因素后,比较两种方法对心肺复苏成功率及存活率的影响.结果 AutoPuslse心肺复苏复苏效果明显优于传统人工复苏且并发症少,差异具有统计学意义(P<0.05).结论 应用AutoPuslse辅助心肺复苏,可以取得较好的效果,适合临床应用.

Objective To investigate the biomechanical properties of human calcaneus by finite element method.Methods Through CT scanning,Mimics,Geomagic and other software,the finite element model of calcaneus was established.The stress distribution and displacement tendency of calcaneus under normal standing and external force were analyzed.Results Under normal standing,the calcaneal stress was uniformly distributed and small.Under extemal force,the entire calcaneus stress increased significantly,and the stress on calcaneocuboid articular surface also obviously increased.Conclusions The analysis of the stress and strain distribution on calcaneus in neutral position under different loading,and the investigation on biomechanical properties of calcaneus and mechanism of calcaneal fracture will provide theoretical basis for clinical treatment of calcaneal fractures.

肺奴卡菌病是由奴卡菌侵犯肺部引起的亚急性、慢性局限性或播散性化脓性或肉芽肿性疾病,可经血源播散至皮肤或中枢神经系统、肾脏等部位或器官.由于是一种少见病,且临床和影像学表现缺乏特异性,故容易误诊或漏诊而延误治疗或治疗不规范而影响预后.本文报道 1 例肺奴卡菌病伴发脑梗死病例,并复习相关文献,希望有助于提高对奴卡菌病的认识.

目的：观察Glidoscope视频喉镜气管插管和直接喉镜气管插管在心肺复苏中的应用及其对心肺复苏效果的影响。方法48例心肺复苏患者按其就诊顺序分为视频喉镜组及直接喉镜组，记录每例患者插管所用时间、患者1次吃插管成功率、记录每例患者因配合气管插管胸外按压中断时间、插管成功2、5、10分钟呼气末二氧化碳分压数值及恢复自主循环例数并作统计学分析。结果两组患者使用视频喉镜组明显缩短平均插管时间、一次插管成功率明显提高、由插管所造成的按压中断明显减少、视频喉镜组插管成功2、5、10分钟呼气末二氧化碳分压平均数值明显高于直接喉镜组、恢复自主循环例数视频喉镜组明显多于直接喉镜组。结论视频喉镜在心肺复苏中有重要应用价值。

<正>水仙(Chinese Narsissus)是中国的十大名花之一,是人们冬季喜爱养植的一种观赏花卉,每年冬季大量上市。去掉根部的水仙茎叶,与"蒜薹"相似,故误食水仙花茎叶时有发生,水仙的茎叶含对人体有毒的成分,误食可引起急性食物中毒〔1〕。2008-2010年本院收治误食水仙花引起的食物中毒2起共8例。

目的探究脑血管病合并肺部感染患者发病的原因。方法采用针对性的方法进行治疗和护理。结果 50例患者中38例患者成功治愈,治愈为76%,8例患者死亡,死亡率为16%,4例患者病情缓解,但病情出现反复的情况。结论 脑血管合并肺部感染的患者的死亡率较高,其发病原因比较复杂,不同的患者出现的症状也有所差异,需要对其进行针对性的治疗和护理,以便患者能更快更好地恢复。