Delirium is a common complication in patients with hemorrhagic stroke (HS) admitted to intensive care, but its association with peripheral oxygen saturation (SpO2) remains uncertain. We analyzed 1935 adults with HS from the Medical Information Mart for Intensive Care IV (MIMIC-IV, v3.1). SpO2 was recorded and categorized as low (<95%), moderate (95-98%), or high (>98%) after intensive care unit (ICU) admission. Delirium was identified using the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU). Associations were assessed with multivariable logistic regression, restricted cubic spline (RCS) modeling, subgroup analyses, and receiver operating characteristic (ROC) curves for SpO2, Glasgow Coma Scale (GCS), and their combination. Delirium occurred most frequently in the high SpO2 group (29.6%), followed by the low (19.7%) and moderate groups (17.6%). Compared with the moderate group, high SpO2 was consistently associated with increased delirium risk (adjusted odds ratio: 1.855-1.998; all P < .001), while low SpO2 showed no independent association. RCS analysis demonstrated a U-shaped relationship with the lowest risk between 95% and 98%. Subgroup analyses confirmed consistency across patient characteristics. Combining SpO2 with GCS improved prediction (AUC = 0.702) compared with either alone. High SpO2 (>98%) was independently associated with increased delirium risk, while low SpO2 (<95%) showed a nonlinear trend but was not statistically significant in fully adjusted categorical models. Maintaining SpO2 around 95% to 98% and integrating SpO2 with GCS may aid early risk stratification.

BACKGROUND:Out-of-hospital cardiac arrest (OHCA) in China has a high incidence and poor survival, highlighting an urgent need for rapid identification of reversible aetiologies. Conventional transthoracic echocardiography during resuscitation can be limited by imaging quality and prolonged chest compression interruptions. Transoesophageal echocardiography (TEE) is a feasible alternative that allows for continuous real-time imaging during compressions, but its utility in Chinese OHCA patients remains uncertain. METHODS:This prospective, single-centre exploratory study enrolled 45 consecutive selected adults with non-traumatic OHCA (NT-OHCA) of unclear aetiology who were eligible for TEE. Of all enrolled patients, 43 completed standardised TEE image acquisition, while 2 cases with TEE-unrecognisable aetiology were excluded from aetiological analysis. The per-protocol analysis finally included 41 patients in whom TEE was successfully completed. Certified emergency physicians performed simplified TEE examinations (five standard views) during active resuscitation. Door-to-TEE interval, diagnostic yield, TEE-guided interventions and clinical outcomes were recorded according to Utstein guidelines. RESULTS:TEE yielded diagnostic-quality images in all patients (43/43), with a median door-to-TEE time of 13 min (IQR: 6.5-22). Reversible aetiologies were identified in 39.0% (16/41), most commonly acute aortic dissection (50.0%, 8/16), followed by massive pulmonary embolism (25.0%), hypertrophic cardiomyopathy (18.8%) and hypovolaemia (6.3%). TEE guided interventions in 56.3% (9/16) of identified cases. Return of spontaneous circulation (ROSC) and 28-day survival rates were 41.5% and 12.2%, respectively, with no significant differences between aetiology-identified and unidentified groups (ROSC: 37.5% vs 44.0%, p>0.05; 28-day survival: 6.3% vs 16.0%, p>0.05). Sensitivity analysis of the 43-case complete imaging cohort and the total 45 enrolled cases further verified the stability and reliability of the diagnostic results. CONCLUSIONS:During mechanical cardiopulmonary resuscitation, TEE rapidly identified suspected aetiologies in 39% (16/41) of NT-OHCA cases, notably revealing frequent acute aortic dissections. Lacking a comparator group, TEE's feasibility as a complementary tool requires further controlled investigation.

There is a lack of comprehensive research on intensive care unit acquired weakness (ICU-AW), which hinders the early detection and diagnosis of this condition. This study aims to investigate the diagnostic and prognostic significance of miR-140-5p in ICU-AW patients and assess its potential utility as a biomarker for ICU-AW. The expression level of miR-140-5p was assessed using real-time quantitative PCR in ICU-AW patients. The diagnostic and prognostic value of miR-140-5p in ICU-AW patients was evaluated through ROC curve, correlation, Cox regression, and Kaplan–Meier survival analysis. Additionally, the target gene of miR-140-5p was predicted, followed by enrichment analysis on the Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway. The expression of miR-140-5p was up-regulated in ICU-AW patients and showed a significant association with MRC and SOFA sores. miR-140-5p demonstrated potential diagnostic utility in discriminating ICU-AW patients from the controls. ICU-AW patients exhibiting low miR-140-5p expression levels tended to have a more favorable prognosis. Enrichment analyzed based on GO and KEGG suggested miR-140-5p might facilitate intercellular communication via exosomes. The miR-140-5p exhibits promise as a potential biomarker for diagnosing and prognosticating the outcomes of ICU-AW.

Objective This study aimed to explore the effects of bone marrow mesenchymal stem cell (BMSC)-derived exosomal miR-146a-5p on microglial polarization and the potential underlying mechanisms in oxygen-glucose deprivation (OGD)-exposed microglial cells. Methods Exosomes were isolated from BMSCs, and their characteristics were examined. The effects of BMSC-derived exosomes on microglial polarization were investigated in OGD-exposed BV-2 cells. Differentially expressed miRNAs were identified and their biological function was explored using enrichment analyses. The regulatory role of miR-146a-5p in microglial polarization was studied via flow cytometry. Finally, the downstream target gene Traf6 was validated, and the role of the miR-146a-5p/Traf6 axis in modulating microglial polarization was investigated in OGD-exposed BV-2 cells. Results BMSC-derived exosomes were successfully isolated and characterized. A total of 10 upregulated and 33 downregulated miRNAs were identified. Exosomal treatment resulted in significant changes in microglial polarization markers. miR-146a-5p was found to be significantly downregulated in OGD-exposed microglial cells treated with exosomes. Manipulation of miR-146a-5p expression modulated microglial polarization. Moreover, the miR-146a-5p/Traf6 axis regulated microglial polarization. Conclusion Our findings demonstrate that BMSC-derived exosomal via miR-146a-5p modulates microglial polarization by targeting Traf6, providing a potential thermal target for the treatment of neurological diseases involving microglial activation.

目的:探究预后营养指数(PNI)、γ-谷氨酰转移酶/白蛋白比值(GAR)与老年急性冠脉综合征患者短期预后的相关性.方法:选择2017年1月—2019年12月期间在我院行经皮冠状动脉介入治疗(PCI)的老年急性冠脉综合征患者120例(观察组).另选这一时期内体检健康志愿者100例(对照组).检测比较两组外周血PNI、GAR水平差异.随访1年,根据患者有无不良心血管事件发生(MACE),将其分为MACE组(28例)与非MACE组(92例),详细记录患者病历资料如血脂指标、心功能指标等.采用多因素logistics回归分析影响急性冠脉综合征患者MACE发生的危险因素.应用ROC曲线分析PNI、GAR对急性冠脉综合征患者MACE发生的预测价值.结果:观察组外周血PNI、GAR值与对照组外周血PNI、GAR值相比,差异有统计学意义(P＜0.05).MACE组外周血PNI值低于非MACE组,GAR值高于非MACE组,差异有统计学意义(P＜0.05).多因素logistics回归分析示,Gensini评分升高、PNI降低及GAR升高是急性冠脉综合征患者MACE发生的独立危险因素(P＜0.05).ROC曲线结果示,PNI、GAR及二者结合预测急性冠脉综合征患者MACE发生的AUC分别为0.767、0.801、0.906,敏感度分别为0.791、0.806、0.687,特异度分别为0.652、0.609、0.913.结论:入院时外周血PNI降低、GAR升高与急性冠脉综合征的临床预后密切相关,早期联合检测PNI、GAR对判断急性冠脉综合征患者预后状况有较高参考价值.

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 研究罗格列酮对重症急性胰腺炎大鼠肾组织中一氧化氮(NO)及核因子(NF)-κB/p65表达的影响.方法试验动物分为模型组、对照组和罗格列酮组,模型组和罗格列酮组构建重症急性胰腺炎大鼠模型,对照组只翻动十二指肠,罗格列酮组用罗格列酮腹腔注射.取各组大鼠肾组织,硝酸还原酶法检测NO含量,酶联免疫吸附(ELISA)法检测诱导型一氧化氮合酶(iNOS)活性,免疫组化法检测NF-κB/p65表达,Western印迹检测肿瘤坏死因子(TNF)-α和细胞间黏附分子(ICAM)-1表达.结果模型组和罗格列酮组肾组织中NO含量、iNOS活性、NF-κB/p65水平、TNF-α水平、ICAM-1水平较对照组明显升高(均P<0.05),而罗格列酮组较模型组均明显降低(均P<0.05).结论 罗格列酮能够降低重症急性胰腺炎肾组织中NO含量和NF-κB/p65、TNF-α、ICAM-1水平.

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 通过了解急诊患者流行病学特征,为急诊科人员配置、抢救器材的准备提供依据,提高救治成功率.方法 采用描述性方法对我院2014年急诊科抢救室患者的性别、年龄、就诊时间、就诊月份、抢救室滞留时间、疾病谱等资料进行流行病学调查分析.结果 随着急诊患者增多抢救室患者也同步增多,尤其是6,7,8月是急诊患者高峰;抢救室接诊患者人数与滞留时间呈显著正相关;急诊入抢救室人数随年龄增高比例逐渐增多,90岁以上组入抢救室比例达43.49%;60岁以下患者滞留时间中位数无差异,60岁以上随着年龄的增长,滞留时间延长;晚期肿瘤患者滞留时间较非晚期者时间长;多发伤患者滞留时间明显长于非多发伤患者;抢救室疾病谱分析前5位分别是神经系统、消化系统、创伤、心血管系统、呼吸系统.结论 急诊医学专业应根据急诊主要人群、高发年龄、不同就诊时间、主要疾病谱、滞留时间较长的疾病等因素合理安排急诊人员配备,进行重点培训,保持急诊工作有序安全进行.

目的系统评价国内有关纳洛酮治疗急性乙醇中毒的有效性和安全性。方法计算机检索CBMdisc(2001～2008)、CNKI(2001～2008)和重庆维普。以"纳洛酮"和"急性酒精中毒"或"急性乙醇中毒"为关键词检索文献,收集有关纳洛酮治疗急性乙醇中毒的随机对照试验和半随机对照试验,有两名评价员检索资料并交叉核对,所得文献数据采用Cochrane协作组提供的RevMan4.2软件进行Meta分析。结果初步检索相关文献385篇,通过质量评价,纳入的3项研究,包括患者178例,其中纳洛酮治疗组88例,对照组90例。纳洛酮治疗组的患者清醒时间明显比对照组短,其差异有统计学意义。结论纳诺酮可明显缩短急性乙醇中毒患者的昏迷时间,使昏迷患者提前清醒,但是由于国内大部分文献方法学质量差,同时缺乏对纳洛酮药物不良反应的报道。这一结论尚需更多设计严格的高质量研究加以证实。

75%以上的腹水是肝硬化引起的.腹水增多提示严重门脉高压和肝功能不全,往往是肝硬化由代偿期转为失代偿期的重要标志.肝硬化患者初次诊断后10年内腹水发生率超过50%,并发腹水的患者其3年生存率不足50%,难治性腹水1年病死率超过50%[1].

目的:探讨肝硬化并胆囊结石的临床特点及其发病机制.方法:回顾性分析我院2003-2/2006-2住院的131例肝硬化患者,并以同期门诊行体检者790例作为对照组,分析的指标包括肝硬化并胆囊结石患者的性别差异、与对照组性别差异、肝病性胆囊改变在肝硬化胆囊结石发生中的作用、肝硬化并脾功能亢进在肝硬化胆囊结石发生中的作用.结果:肝硬化胆囊结石的发生率为41.22%,对照组胆结石的发生率为6.96%;肝硬化患者胆囊结石的发生率无性别差异(P＞0.05);男性与女性肝硬化患者与对照组比较,胆囊结石发生率均有显著差异(39.58% vs 5%,P＜0.05;48.57% vs 10.53%,P＜0.05);肝病性胆囊改变及肝硬化并脾功能亢进在胆囊结石发生中起着重要作用.肝病性胆囊改变患者胆囊结石发病率明显高于无肝病性胆囊改变者(48.39% vs 26.32%,P＜0.05),肝硬化并脾功能亢进胆囊结石的发生率与对照组比较差异也有显著性(54.44% vs 6.96%,p＜0.05).结论:肝硬化患者易发生胆囊结石,与性别无关而与肝功能、胆囊运动功能障碍、脾功能亢进等有关.

目前因计划生育或医学原因自愿要求终止中期妊娠的情况仍较常见.我们分别采用利凡诺羊膜腔内注射联合米非司酮、米非司酮配伍米索前列醇用于中期妊娠引产,并与单用利凡诺引产比较,效果良好,现报道如下.

随着人们生活水平的日渐提高,无痛人工流产成了避孕失败的最佳补救措施.为此,我院应用氯胺酮复合咪唑安定静脉注射,取得了无痛人工流产的满意效果,现报道如下.