BACKGROUND:Post cardiac arrest brain injury (PCABI) results from global ischemia-reperfusion. Circular RNAs (circRNAs) are stable regulators of post transcriptional networks that may modulate neuronal survival and metabolism after ischemic injury. We investigated the role and mechanism of mmu_circ_0000376 (circ_0000376) in PCABI. METHODS:Through integrated bioinformatics analysis of circular RNA/microRNA/messenger RNA datasets via the GEO platform, a regulatory network involving circ_0000376/mmu-let-7b-5p/CCND1 was identified. We validated its circular structure, stability, and cytoplasmic localization in HT22 neuronal cells. Through in vitro and in vivo experiments modulating circ_0000376 expression, we investigated cellular functions by assessing cell viability, apoptosis (Annexin V/PI staining, TUNEL, caspase/Bcl-2 family proteins), and mitochondrial/energy parameters (ATP, glucose consumption, lactate, G6PD activity). RESULTS:Circ_0000376 is a stable, cytoplasmic circRNA. Overexpression of Circ_0000376 reduced ischemia-reperfusion injury induced ROS, preserved ATP and glycolytic flux, increased G6PD activity, decreased apoptosis, and restored CCND1 and Bcl 2 while lowering Bax and cleaved caspases. Bioinformatic and reporter assays showed circ_0000376 sponges mmu-let-7b-5p, relieving repression of CCND1. mmu-let-7b-5p overexpression or CCND1 knockdown reversed circ_0000376 mediated protection. AAV mediated circ_0000376 overexpression in mice decreased hippocampal apoptosis and restored CCND1 in vivo. CONCLUSIONS:Circ_0000376/mmu-let-7b-5p/CCND1 axis mitigates neuronal apoptosis and metabolic dysfunction after ischemic injury. Targeting this ceRNA network may offer a novel neuroprotective strategy for PCABI.

Acute pancreatitis (AP)-induced intestinal barrier disruption drives fatal systemic complications. We engineered human umbilical cord mesenchymal stem cell-derived extracellular vesicles (hUC-MSC-EVs) to deliver emodin-a bioactive compound limited by poor bioavailability-for targeted intestinal protection. In TNF-α-stimulated intestinal epithelial cells (CCD-841CON), EV-loaded emodin (EVs-Emodin) synergistically suppressed NLRP3 inflammasome activation, pyroptosis, reactive oxygen species production, and inflammatory cytokines, outperforming monotherapies. EVs-Emodin restored cell viability and curtailed apoptosis. In taurocholate-induced AP mice, intravenous EVs-Emodin attenuated systemic inflammation, promoted the expression of Occludin and ZO-1, mitigated intestinal tissue lesions, promoted epithelial regeneration, inhibited inflammasome activation, and alleviated mitochondrial damage. hUC-MSC-EVs overcome emodin's delivery limitations, providing a synergistic strategy to protect the intestinal barrier via NLRP3/pyroptosis inhibition and oxidative stress mitigation, offering a promising therapeutic approach for AP-associated intestinal injury.

Background Sepsis complicates acute pancreatitis (AP), increasing mortality risk. Few studies have examined how sepsis and its onset timing affect mortality in AP. This study evaluates the association between sepsis occurrence and all-cause mortality in AP, focusing specifically on the impact of sepsis onset timing. Methods This multicenter retrospective cohort study included 494 ICU-admitted AP patients from the MIMIC-IV database and 91 from our center. Patients were grouped by sepsis occurrence and onset timing. Clinical outcomes were in-hospital and 90-day all-cause mortality. Machine learning identified key variables associated with mortality. Multivariable regression analyzed the impact of sepsis and its onset timing on mortality. To reduce baseline differences, propensity score matching (PSM) based on time to sepsis was conducted. After PSM, Kaplan-Meier survival analyses incorporated data from our center for validation. Restricted cubic spline analysis examined any nonlinear relationship between sepsis onset timing and mortality. Results Patients with sepsis had significantly higher in-hospital and 90-day mortality rates than those without sepsis ( p < 0.05). Sepsis was identified as a significant risk factor for in-hospital mortality and remained significantly associated after adjusting for key variables ( p < 0.05). However, sepsis onset timing did not significantly impact in-hospital or 90-day mortality. These findings were validated after PSM and with our center's data. No nonlinear relationship between sepsis onset timing and mortality was found. Conclusion Sepsis significantly increases all-cause mortality in AP patients, but the timing of its onset has limited impact. Continuous monitoring and intervention for sepsis during hospitalization are recommended to improve prognosis.

BACKGROUND:Fluid resuscitation in acute pancreatitis (AP) patients requires precise titration because both excess and insufficient volumes may worsen outcomes. This study aimed to develop a weight-normalized fluid balance index (FBI) and assess its association with in-hospital mortality in critically ill AP patients. METHODS:This retrospective cohort study utilized data from the MIMIC-IV 3.0 database and the emergency intensive care unit (EICU) of our hospital (validation cohort) and was based on inclusion and exclusion criteria. Using the R package cutoff, an FBI of 145 mL/kg was identified as the optimal risk stratification threshold. The primary outcome was in-hospital all-cause mortality. Machine learning was used to screen covariates for inclusion in multivariable Cox models. Cox regression and restricted cubic spline (RCS) models were used to evaluate the relationship between FBI and mortality. Propensity score matching (PSM) was applied to minimize baseline confounding. After PSM, Kaplan-Meier survival curves were generated, and the results were validated via data from our center. RESULTS:In this study, 547 AP patients from the MIMIC-IV database and 156 from the EICU of our hospital were included. In the MIMIC-IV cohort, the overall in-hospital mortality rate was 8.96%. Patients with FBI ≥145 mL/kg had significantly higher in-hospital mortality than did those with FBI <145 mL/kg (P<0.05). High-risk classification remained an independent predictor of death after full adjustment (hazard ratio [HR] 1.99, 95% confidence interval [95% CI]: 1.08-3.69). Post-PSM Kaplan-Meier analysis confirmed significantly higher in-hospital mortality in the high-risk group (P<0.05). This result was corroborated by our validation cohort. RCS analysis further demonstrated a non-linear increase in in-hospital mortality with increasing FBI values. CONCLUSION:An FBI ≥145 mL/kg may be associated with increased in-hospital mortality in critically ill AP patients.

Background:Intestinal ischemia/reperfusion (II/R) is a severe condition with high mortality and limited treatment options. Extracellular vesicles that are derived from bone marrow mesenchymal stem cells (BM-MSC-EVs) exhibit therapeutic potential in alleviating II/R injury. However, the mechanism by which BM-MSC-EVs fulfill this function requires further characterization. The ubiquitin-proteasome system plays an essential role in II/R, but the functions of individual ubiquitination regulators such as ubiquitin-specific proteases (USPs) in this process remain incompletely understood. Methods:An II/R cellular model was established by using IEC-6 intestinal epithelial cells with oxygen-glucose deprivation/reperfusion (OGD/R) treatment. The expression of USPs was evaluated by using quantitative polymerase chain reaction and Western blot. The role of USP38 on the viability, apoptosis, migration, and reactive oxygen species (ROS) levels in OGD/R-treated IEC-6 cells were measured by using CCK-8, Annexin V/PI staining, transwell assay, and 2',7'-dichlorofluorescin diacetate (DCFDA) staining, respectively. The interaction between USP38 and BIRC5 was explored by using co-immunoprecipitation (Co-IP) and the ubiquitination level and stability of BIRC5 were examined by using Western blot. USP38-overexpressing BM-MSC-EVs were produced to treat OGD/R-treated IEC-6 cells. Results:USP38 expression was significantly downregulated in OGD/R-treated IEC-6 cells. Incubation of these cells with BM-MSC-EVs substantially elevated the USP38 expression, resulting in improved viability, reduced apoptosis, enhanced migration, and decreased ROS levels. Furthermore, overexpression of USP38 in BM-MSC-EVs further enhanced their protective effect on OGD/R-treated IEC-6 cells. At the molecular level, USP38 interacts with and stabilizes BIRC5 by decreasing its ubiquitination. Knock-down of BIRC5 abolished the protective effect of excessive USP38 on OGD/R-treated IEC-6 cells. Conclusion:USP38 protects intestinal epithelial cells from I/R injury by enhancing the stability of BIRC5.

Pancreatitis is a rapidly expanding global non-communicable disease, marked by substantial disparities across populations. However, comprehensive long-term assessments of global health inequalities remain scarce. This study examined inequality in the pancreatitis burden from 1990 to 2021, identified principal determinants, and forecasted future trends across countries with varying Socio-demographic Index (SDI) levels. Using data from the Global Burden of Disease 2021, we assessed inequalities in the prevalence, incidence, and disability-adjusted life years of pancreatitis via the Slope Index of Inequality (SII) and Concentration Index (CI). Decomposition analysis was used to identify drivers of change, and a Bayesian age-period-cohort model projected trends to 2030. Between 1990 and 2019, the SII decreased from 13.83 to 8.61, signaling a reduction in absolute health inequality. Nevertheless, beginning in 2020, the SII turned negative, reaching -10.79 in 2021, indicating a structural reversal in disease burden distribution from high- to low-SDI countries. Concurrently, the CI declined from -0.04 to -0.10, suggesting worsening relative inequality. Decomposition revealed population growth and aging as primary drivers of the rising burden, while epidemiological improvements contributed minimally, particularly in low-SDI regions. Projections suggest that while global age-standardized rates may continue to decrease through 2030, the proportional burden in low-SDI countries is expected to rise steadily. The global socioeconomic distribution of pancreatitis burden is experiencing a profound shift, with inequalities increasingly concentrated in low-SDI areas. Driven by demographic trends, this shift underscores the necessity for targeted global strategies to mitigate disparities and bolster health system resilience.

ABSTRACT The triglyceride–glucose body mass index (TyG‐BMI) is an emerging composite metabolic indicator in cardiovascular research. However, the link between TyG‐BMI and target organ damage (TOD) in essential hypertension (EH) remains uncertain. This study investigated the association between TyG‐BMI and TOD in patients with EH. We conducted a retrospective cohort study involving 493 individuals with EH. Participants were divided at the cohort‐specific median into high and low TyG‐BMI groups. Over a median follow‐up of 23 months, 191 participants experienced TOD. Kaplan–Meier curves showed a significantly higher cumulative incidence of TOD in the high TyG‐BMI group than in the low TyG‐BMI group ( p < 0.05). In multivariable logistic regression, TyG‐BMI remained an independent correlate of TOD (adjusted OR = 1.83, 95% CI: 1.08–3.10; p < 0.05). Least absolute shrinkage and selection operator–Cox regression further selected TyG‐BMI, age, and smoking status as key predictors of TOD. Subgroup analyses revealed that the TyG‐BMI–TOD association was stronger among younger or middle‐aged, normal‐weight, non‐diabetic, non‐smoking subjects ( p < 0.05). Finally, the TyG‐BMI‐based model achieved predictive accuracy comparable to that of a conventional risk‐factor model. In conclusion, TyG‐BMI is independently associated with TOD in EH patients. Its predictive value closely mirrors that of combined traditional risk factors, highlighting TyG‐BMI as a promising clinical marker.

Abstract Endothelial dysfunction is acknowledged as a marker for subclinical target organ damage (STOD) in hypertension, though its therapeutic potential has not yet been clarified. This study assessed whether early endothelial function improvement (EEFI) reduced STOD in patients with essential hypertension (EH). We conducted a retrospective cohort analysis of 456 EH patients initially free from STOD. Endothelial function was assessed using brachial artery flow-mediated dilation (FMD), with values ≤ 7.1% indicating dysfunction. Patients were initially categorized by endothelial status (dysfunction: n = 180, normal: n = 276), and further divided into improved or unimproved groups based on changes within three months post-enrollment. During a median follow-up of 25 months, 177 patients developed STOD. The incidence of STOD was significantly higher in patients with initial dysfunction compared to those with normal function. Kaplan–Meier analysis indicated that the improved group had a lower cumulative incidence of STOD compared to the unimproved group (p < 0.05). Multivariable Cox regression confirmed EEFI as an independent protective factor against STOD in EH patients (p < 0.05), regardless of their baseline endothelial status, especially in those under 65 years old, non-smokers, and with low-density lipoprotein cholesterol levels ≤ 3.4 mmol/L. In conclusion, EEFI significantly reduces STOD incidence in EH patients, particularly in specific subgroups, emphasizing the need for early intervention in endothelial function to prevent STOD.

目的:探讨乌司他丁联合生长抑素在重症急性胰腺炎临床治疗中的应用效果.方法:将 70 例重症急性胰腺炎患者分为观察组(乌司他丁联合生长抑素)和对照组(生长抑素),各 35 例,观察两组患者的治疗效果.结果:观察组患者的ICU治疗时间、住院时间比对照组更短(P<0.05).对比炎性因子指标,观察组患者治疗 3d后的肿瘤坏死因子-α(TNF-α)水平、C 反应蛋白(CRP)水平、白细胞介素-6(IL-6)水平低于对照组(P<0.05),治疗 7d 后的 TNF-α水平、CRP 水平、IL-6 水平低于对照组(P<0.05).对比腹痛症状,观察组患者治疗后 3d的疼痛 VAS评分、治疗后 7d 的疼痛 VAS 评分低于对照组(P<0.05).观察组患者治疗后 3d 的急性生理学及慢性健康状况评分系统(APACHEⅡ)评分、治疗后 7d的APACHEⅡ评分均低于对照组(P<0.05).结论:应用乌司他丁联合生长抑素治疗重症急性胰腺炎,可获得良好的治疗效果.

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 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.

H2S can also protect nerve cells. The objective of the study is to investigate the effects of hydrogen sulfide (H2S) on the expressions of brain-derived neurotrophic factor (BDNF) and its receptors, tyrosine protein kinase B (TrkB) and p75 neurotrophin receptor (p75NTR), in brain tissues of rats with cardiac arrest and cardiopulmonary resuscitation (CA/CPR) following the restoration of spontaneous circulation (ROSC).

目的 调查急诊眩晕患者头颅CT临床实用价值.方法 收集以头晕、眩晕或行走不稳为主诉的1085例急诊眩晕患者资料,主要包括个人基本信息、就诊方式、头颅CT和头颅磁共振成像(MRI)检查、急诊滞留时间及医疗费用等,并进行相关统计分析.结果 1085例急诊眩晕患者中,有358例完成头颅CT检查,CT检查使用率33.0%.从接受CT检查及未接受CT检查的患者临床资料来看,老年患者、救护车送入患者,以及既往有脑卒中、高血压、糖尿病病史的患者容易被安排接受CT检查(P<0.05);且与未接受CT检查患者的急诊滞留时间(67.4±9.7)min、医疗费用(263.4±67.8)元比较,接受CT检查患者的急诊滞留时间为(96.5±12.7)min,增加43.2%,医疗费用为(535.8±78.4)元,增加103.4%,差异均具有统计学意义(P<0.05).358例完成头颅CT检查的患者中,有14例具有临床意义的阳性病灶,阳性率仅为3.9%.有112例经CT检查呈阴性的急诊眩晕患者在急诊科治疗后症状无缓解,而后接受住院治疗并进行头颅MRI检查,结果证实其中15例患者存在新发脑梗死灶.结论 在急诊眩晕患者的临床诊断中,头颅CT具有一定的辅助诊断价值但十分有限,眩晕的确诊更应注重于患者的病史及详细的床边临床检查.

目的 探讨血常规和CRP联合检测对急性上呼吸道感染的诊断价值.方法 对本院急诊科就诊的254例患者采血,检测血常规和CRP；并同时用咽拭子或痰样做细菌培养.依据细菌培养的结果将患者分为细菌感染组(A组)和非细菌感染组(B组),同时以55例健康体检者的资料作为正常对照组(C组).应用受试者工作特征曲线(ROC曲线)对单项指标及联合指标的诊断价值进行评估.结果 254例中共检出50例细菌感染(A组),其WBC、中性粒细胞百分比(NEU)和CRP显著升高,与B组和C组比较差异均有统计学意义(P＜0.01).各种指标ROC曲线下面积分别为0.920( WBC)、0.975(NEU)、0.995 (CRP)、0.985( WBC+ NEU)和0.999( WBC+ NEU+ CRP).通过ROC曲线分析,各项指标最佳诊断界值分别为11.9×109/L(WBC)、75.4％(NEU)和27.8 mg/L(CRP).结论 联合检测血常规和CRP可帮助明确急性上呼吸道感染细菌感染情况,进一步提高诊断效率。

A total of 192 patients with sepsis were tested by Montreal Cognitive Assessment (MoCA) for a preliminary diagnosis of whether or not there was sepsis associated encephalopathy (SAE) according to their test results.SAE was diagnosed or excluded after consultations and comprehensive analysis on the basis of clinical manifestations and auxiliary examination results.The scores of the patients in this group were (25.7 ± 3.3) points.The sensitivity of MoCA for screening SAE was 0.776 and its specificity 0.963.The rate of diagnostic coincidence between MoCA and comprehensive analysis for SAE was 0.880.The diagnostic concordance between two diagnostic methods of SAE was excellent (kappa value =0.753 ± 0.048,P =0.000).The area under the receiver operating characteristic (ROC) curve of MoCA for screening SAE was 0.929 ± 0.019 (P =0.000) ; the optimal cutoff value was 25.5 points; and its sensitivity was 0.779 and specificity 0.962.And negative correlations existed between score of MoCA and age,disease course and co-existing shock or multiple organ dysfunction syndrome (P ＜ 0.05).

Objective This study was designed to explore the effects of atorvastatin,an inhibitor of HMG-CoA reductase on the experimental autoimmune encephalomyelitis(EAE) in Wistar rats.Methods Atorvastatin was administered at two different doses to Wistar rats EAE model.A scale of 0-5 according to the symptoms scored the severity of EAE.The numbers of inflammation lesion in the brain and spinal cord were counted by optical microscopy.The serum levels of interferon-γ and interleukin-4 were determined by enzyme-linked immunosorbent assay.Results Compared to the untreated group,the atorvastatin groups only partially developed EAE with a lighter degree of malfunction.The numbers of inflammation lesion reduced significantly in atorvastatin treated groups.The serum level of interferon-γ increased in atovarstatin treated groups with the development of EAE,but was lower than that in the untreated group.The serum levels of interleukin-4 in atorvastatin groups were higher at the onset.Higher dose atorvastatin showed better protection against EAE development.Conclusion To a certain extent atorvastatin could effectively ameliorate EAE in rats. The effects were in a dose-dependent fashion,which might be mechanistically related to the balance between Th1/Th2 cytokines.

恩经复致精神障碍罕见,现报告1例如下. 1 病例 男,51岁.因进行性四肢无力、麻木16 d于2004年9月14日入院.患者既往体健,无精神病史,无精神因素.查体:双侧闭眼、皱额、露齿不能,双上肢肌力Ⅳ级、双下肢肌力Ⅱ～Ⅲ级,四肢肌张力低,四肢远端浅感觉减退,腱反射(-),其他无异常.血常规、肝功能、肾功能、电解质、血糖和血脂均正常.心电图正常.神经肌电图示:周围神经损害(混合性).腰穿脑脊液检查:白细胞60×106/L,单核0.95,多核0.05,蛋白质1.81 g/L,其余正常.