Acute respiratory distress syndrome (ARDS) is characterized by uncontrolled inflammation, which manifests as leukocyte infiltration and lung injury. However, the molecules that initiate this infiltration remain incompletely understood. We evaluated the effect of the nuclear alarmin IL-33 on lung damage and the immune response in LPS-induced lung injury. We established a LPS-induced lung injury mouse model. We used genetically engineered mice to investigate the relationship among the IL-33/ST2 axis, NKT cells, and ARDS. We found that IL-33 was localized to the nucleus in alveolar epithelial cells, from which it was released 1 h after ARDS induction in wild-type (WT) mice. Mice lacking IL-33 (IL-33-/-) or ST2 (ST2-/-) exhibited reduced neutrophil infiltration, alveolar capillary leakage, and lung injury in ARDS compared with WT mice. This protection was associated with decreased lung recruitment and activation of invariant nature killer (iNKT) cells and activation of traditional T cells. Then, we validated that iNKT cells were deleterious in ARDS in CD1d-/- and V alpha 14 Tau g mice. Compared with WT mice, V alpha 14 Tau g mice exhibited increased lung injury in ARDS, and the CD1d-/- mice showed outcomes opposite those of the V alpha 14 Tau g mice. Furthermore, we administered a neutralizing anti-ST2 antibody to LPS-treated WT and V alpha 14 Tau g mice 1 h before LPS administration. We found that IL-33 promoted inflammation through NKT cells in ARDS. In summary, our results demonstrated that the IL-33/ST2 axis promotes the early uncontrolled inflammatory response in ARDS by activating and recruiting iNKT cells. Therefore, IL-33 and NKT cells may be therapeutic target molecules and immune cells, respectively, in early ARDS cytokine storms.

Introduction:Sepsis is a syndrome characterized by high morbidity and mortality rates. One of its most severe complications is acute lung injury, which exhibits a multitude of clinical and biological features, including macrophage pyroptosis. This study investigates the regulatory effects of exosomes derived from Bone Marrow-Derived Mesenchymal Stem Cells (BMSCs) on sepsis-associated acute lung injury (ALI) and explores the potential mechanisms mediated by exosomal miRNAs.Methods:Exosomes were isolated from primary BMSCs of adult C57BL/6J mice using differential centrifugation. Their uptake and distribution in both in vitro and in vivo contexts were validated. Key sepsis-associated hub gene signal transducer and activator of transcription 3 (STAT3) and its upstream non-coding miR-125b-5p were elucidated through a combination of bioinformatics, machine learning, and miRNA sequencing. Subsequently, the therapeutic potential of BMSC-derived exosomes in alleviating sepsis-induced acute lung injury was substantiated. Moreover, the functionalities of miR-125b-5p and STAT3 were corroborated through miR-125b-5p inhibitor and STAT3 agonist interventions, employing gain and loss-of-function strategies both in vitro and in vivo. Finally, a dual-luciferase reporter assay reaffirmed the interaction between miR-125b-5p and STAT3.Results:We isolated exosomes from primary BMSCs and confirmed their accumulation in the mouse lung as well as their uptake by macrophages in vitro. This study identified the pivotal sepsis-associated hub gene STAT3 and demonstrated that exosomes derived from BMSCs can target STAT3, thereby inhibiting macrophage pyroptosis. MiR-125b-5p inhibition experiments showed that exosomes mitigate macrophage pyroptosis and lung injury by delivering miR-125b-5p. STAT3 overexpression experiments validated that miR-125b-5p reduces macrophage pyroptosis and lung injury by suppressing STAT3. Furthermore, a dual-luciferase reporter assay confirmed the binding interaction between miR-125b-5p and STAT3.Conclusion:Exosomes derived from BMSCs, serving as carriers for delivering miR-125b-5p, can downregulate STAT3, thereby inhibiting macrophage pyroptosis and alleviating sepsis-associated ALI. These significant findings provide valuable insights into the potential development of ALI therapies centred around exosomes derived from BMSC.

右美托咪定是一种非苯二氮类镇静剂,具有良好的镇静、抗炎、抗应激和稳定血流动力学的作用,对呼吸系统抑制作用微弱.布托啡诺是一种新型的阿片类药物,具有减少呼吸抑制、胃肠道不适、躯体依赖等不良反应的优势.右美托咪定复合布托啡诺可提供更加有效的镇静、镇痛作用,且具有阿片节省作用,维持血流动力学稳定,减少呼吸抑制、恶心呕吐、低血压、心动过缓、谵妄等不良反应的优点,主要用于临床麻醉、术后镇痛、重症监护病房镇静镇痛治疗、舒适化医疗等临床实践中.

The cardiovascular complications contribute to a majority of diabetes associated morbidity and mortality, accounting for 44% of death in those patients with type 1 diabetes mellitus (DM) and 52% of deaths in type 2 DM. Diabetes elicits cardiovascular dysfunction through 2 major mechanisms: ischemic and non-ischemic. Non-ischemic injury is usually under-recognized although common in DM patients, and also a pathogenic factor of heart failure in those diabetic individuals complicated with ischemic heart disease. Diabetic cardiomyopathy (DCM) is defined as a heart disease in which the myocardium is structurally and functionally abnormal in the absence of coronary artery disease, hypertensive, valvular, or congenital heart disorders in diabetic patients, theoretically caused by non-ischemic injury solely. Current therapeutic strategies targeting DCM mainly address the increased blood glucose levels, however, the effects on heart function are disappointed. Accumulating data indicate endothelial dysfunction plays a critical role in the initiation and development of DCM. Hyperglycemia, hyperinsulinemia, and insulin resistance cause the damages of endothelial function, including barrier dysfunction, impaired nitric oxide (NO) activity, excessive reactive oxygen species (ROS) production, oxidative stress, and inflammatory dysregulation. In turn, endothelial dysfunction promotes impaired myocardial metabolism, intracellular Ca2+ mishandling, endoplasmic reticulum (ER) stress, mitochondrial defect, accumulation of advanced glycation end products, and extracellular matrix (ECM) deposit, leads to cardiac stiffness, fibrosis, and remodeling, eventually results in cardiac diastolic dysfunction, systolic dysfunction, and heart failure. While endothelial dysfunction is closely related to cardiac dysfunction and heart failure seen in DCM, clinical strategies for restoring endothelial function are still missing. This review summarizes the timely findings related to the effects of endothelial dysfunction on the disorder of myocardium as well as cardiac function, provides mechanical insights in pathogenesis and pathophysiology of DCM developing, and highlights potential therapeutic targets.

Background and PurposeCalcific Aortic Valve Disease (CAVD) is a crucial component of degenerative valvular disease in old age and with the increasing prevalence of the aging population. we hope that by modeling valvular osteogenesis and intervening with endoplasmic reticulum stress inhibitor TUDCA to observe the effect of endoplasmic reticulum stress on valve osteogenesisMethodsIn this study, rabbit heart valvular interstitial cells (VICs) were isolated and cultured. They treated with ox-LDL (Oxidized Low Density Lipoprotein) stimulation to establish a model of valvular osteogenic transformation. BMP2 (Bone Morphogenetic Protein 2), PERK (Protein kinase R-like endoplasmic reticulum kinase), CHOP (CCAAT/enhancer-binding protein homologous protein) and transcriptional regulatory factor ATF4 (Activating Transcription Factor 4 )were recorded after intervention with ER stress inhibitor TUDCA. The effects of er stress on valvular osteogenic transformation were analyzed.ResultAfter stimulation of VICs with ox-LDL, the expression levels of BMP2, PERK, CHOP, and ATF4 increased. However, TUDCA treatment can alleviate the increased expression levels of BMP2, PERK ATF4, and CHOP under ox-LDL stimulation to a certain extent.ConclusionThe endoplasmic reticulum stress signaling pathway is involved in ox-LDL-induced calcification of rabbit valve interstitial cells. Inhibition of endoplasmic reticulum stress using TUDCA can improve the progression of rabbit aortic valve calcification.

目的:探讨非甲状腺疾病综合征(NTIS)对新型冠状病毒肺炎(COVID-19)患者的预后价值.方法:回顾性收集2020年1月14日-2月28日华中科技大学同济医学院附属同济医院收治确诊的COVID-19患者,根据游离三碘甲状腺原氨酸(FT3)值分为NTIS组(FT3＜3.1 pmol/L)和非NTIS组.采用Logistic回归分析和Kaplan-Meier曲线分析NTIS与COVID-19预后的相关性.绘制受试者工作特征(ROC)曲线以确定FT3对住院死亡率的预测性能.结果:共纳入384例患者,其中NTIS组92例和非NTIS组292例,与非NTIS组比较,NTIS组炎症反应强烈,凝血功能障碍复杂,心脏损伤及全身其他器官损伤较多,但淋巴细胞绝对值、百分比较低.Logistic回归分析显示,NTIS与COV-ID-19 严重程度(aOR=3.795)、急性呼吸窘迫综合征并发症(aOR=3.768)和急性心脏损伤并发症(aOR=3.698),以及住院死亡率(aOR=5.017)独立相关.Kaplan-Meier曲线显示NTIS组患者生存趋势较差,风险比为5.98.ROC曲线显示FT3预测轻症患者住院死亡率的临界值为3.395 pmol/L,重症/危重患者为3.035 pmol/L.结论:NTIS与COVID-19患者的不良预后相关.FT3值可作为COVID-19患者死亡率的预测指标.

Background: The epidemic of COVID-19 presents a special threat to older adults. However, information on kidney damage in older patients with COVID-19 is limited. Acute kidney injury (AKI) is common in hospitalized adults and associated with poor prognosis. We sought to explore the association between AKI and mortality in older patients with COVID-19. Methods: We conducted a retrospective, observational cohort study in a large tertiary care university hospital in Wuhan, China. All consecutive inpatients older than 65 years with COVID-19 were enrolled in this cohort. Demographic data, laboratory values, comorbidities, treatments, and clinical outcomes were all collected. Data were compared between patients with AKI and without AKI. The association between AKI and mortality was analyzed. Results: Of 1764 in-hospital patients, 882 older adult cases were included in this cohort. The median age was 71 years (interquartile range: 68-77), 440 (49.9%) were men. The most presented comorbidity was cardiovascular diseases (58.2%), followed by diabetes (31.4%). Of 882 older patients, 115 (13%) developed AKI and 128 (14.5%) died. Patients with AKI had higher mortality than those without AKI (68 [59.1%] vs 60 [7.8%]; p < .001). Multivariable Cox regression analysis showed that increasing odds of in-hospital mortality are associated with higher interleukin-6 on admission, myocardial injury, and AKI. Conclusions: Acute kidney injury is not an uncommon complication in older patients with COVID-19 but is associated with a high risk of death. Physicians should be aware of the risk of AKI in older patients with COVID-19.

Background: Phenotypes have been identified within heterogeneous disease, such as acute respiratory distress syndrome and sepsis, which are associated with important prognostic and therapeutic implications. The present study sought to assess whether phenotypes can be derived from intensive care patients with coronavirus disease 2019 (COVID-19), to assess the correlation with prognosis, and to develop a parsimonious model for phenotype identification. Methods: Adult patients with COVID-19 from Tongji hospital between January 2020 and March 2020 were included. The consensus k means clustering and latent class analysis (LCA) were applied to identify phenotypes using 26 clinical variables. We then employed machine learning algorithms to select a maximum of five important classifier variables, which were further used to establish a nested logistic regression model for phenotype identification. Results: Both consensus k means clustering and LCA showed that a two-phenotype model was the best fit for the present cohort ( N = 504). A total of 182 patients (36.1%) were classified as hyperactive phenotype, who exhibited a higher 28-day mortality and higher rates of organ dysfunction than did those in hypoactive phenotype. The top five variables used to assign phenotypes were neutrophil-to-lymphocyte ratio (NLR), ratio of pulse oxygen saturation to the fractional concentration of oxygen in inspired air (Spo 2 /Fio 2 ) ratio, lactate dehydrogenase (LDH), tumor necrosis factor α (TNF-α), and urea nitrogen. From the nested logistic models, three-variable (NLR, Spo 2 /Fio 2 ratio, and LDH) and four-variable (three-variable plus TNF-α) models were adjudicated to be the best performing, with the area under the curve of 0.95 [95% confidence interval (CI) = 0.94–0.97] and 0.97 (95% CI = 0.96–0.98), respectively. Conclusion: We identified two phenotypes within COVID-19, with different host responses and outcomes. The phenotypes can be accurately identified with parsimonious classifier models using three or four variables.

Background To date, specific cytokines associated with development of acute respiratory distress syndrome (ARDS) and extrapulmonary multiple organ dysfunction (MOD) in COVID-19 patients have not been systematically described. We determined the levels of inflammatory cytokines in patients with COVID-19 and their relationships with ARDS and extrapulmonary MOD. Methods The clinical and laboratory data of 94 COVID-19 patients with and without ARDS were analyzed. The levels of inflammatory cytokines (interleukin 6 [IL-6], IL-8, IL-10, and tumor necrosis factor α [TNF-α]) were measured on days 1, 3, and 5 following admission. Seventeen healthy volunteers were recruited as controls. Correlations in the levels of inflammatory cytokines with clinical and laboratory variables were analyzed, furthermore, we also explored the relationships of different cytokines with ARDS and extrapulmonary MOD. Results The ARDS group had higher serum levels of all 4 inflammatory cytokines than the controls, and these levels steadily increased after admission. The ARDS group also had higher levels of IL-6, IL-8, and IL-10 than the non-ARDS group, and the levels of these cytokines correlated significantly with coagulation parameters and disseminated intravascular coagulation (DIC). The levels of IL-6 and TNF-α correlated with the levels of creatinine and urea nitrogen, and were also higher in ARDS patients with acute kidney injury (AKI). All 4 inflammatory cytokines had negative correlations with PaO 2 /FiO 2 . IL-6, IL-8, and TNF-α had positive correlations with the APACHE-II score. Relative to survivors, non-survivors had higher levels of IL-6 and IL-10 at admission, and increasing levels over time. Conclusions The cytokine storm apparently contributed to the development of ARDS and extrapulmonary MOD in COVID-19 patients. The levels of IL-6, IL-8, and IL-10 correlated with DIC, and the levels of IL-6 and TNF-α were associated with AKI. Relative to survivors, patients who died within 28 days had increased levels of IL-6 and IL-10.

Background: Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) is the causative agent of coronavirus disease 2019 (COVID-19). Lung lesions are considered to be the main damage caused by SARS-CoV-2 infection. In addition, liver injury has also been reported to occur during the course of the disease in severe cases. However, the effect of antiviral treatment on liver injury in critically ill patients is not yet clear.Methods: We retrospectively evaluated the effect of antiviral treatment and antiviral drug arbidol on liver injury in COVID-19 critically ill patients. Baseline characteristics were collected from patients who were admitted to intensive care units of Tongji Hospital in Wuhan, China, and confounders were balanced by propensity score matching (PSM) and inverse probability of treatment weighting (IPTW) analyses.Results: Both the PSM (OR =2.77; 95% CI: 1.03, 7.48; P=0.045) and the IPTW-adjusted (OR =2.33; 95% CI: 1.02, 5.34; P=0.047) results showed that COVID-19 critically ill patients receiving antiviral treatment had a significantly higher risk of liver injury. However, arbidol treatment did not have a significant effect on liver injury (IPTW: OR =2.11; 95% CI: 0.79, 5.67; P=0.14).Conclusions: Our results show that although arbidol treatment does not seem to be significantly associated with liver injury complications, the overall use of antiviral drugs increases the risk of liver injury for critically ill patients with COVID-19. Antiviral drugs are widely used to treat COVID-19, but we recommend that for critically ill patients, antiviral treatment should be used with caution considering both effectiveness and potential adverse effects.

目的:探讨抑制Wnt/β-catenin信号通路对脓毒症急性肺损伤(ALI)的影响.方法:选取(250±10)g健康成年SD雄性大鼠50只,随机分为3组:对照组10只、脓毒症ALI组(CLP组)20只、脓毒症ALI治疗组(CLP+XAV939组)20只.统计各组大鼠体重下降率及死亡率,取肺组织观察肺组织病理学变化,通过蛋白印迹法(WB)、免疫组化(IHC)、免疫荧光(IF)、实时定量PCR等技术检测Wnt/β-catenin信号通路关键蛋白(TNF-α、β-catenin、Cyc-lin D、LRP5/6)表达在3组之间的差异性.结果:CLP组48h内死亡率为40％,而对照组和CLP+XAV939组无大鼠死亡.对照组大鼠术后48 h体重无变化,而CLP组大鼠体重下降20％,CLP+XAV939组下降10％.组织病理学表现,对照组可见完整的肺泡结构,未见炎症细胞浸润;CLP组见肺泡水肿和塌陷,肺泡间隔增厚增宽并有大量炎症细胞浸润,肺血管充血明显;CLP+XAV939组可见基本完整的肺组织结构,炎症细胞数量及分部范围较CLP组减小.WB显示,与对照组比较,CLP组、CLP+XAV939组Wnt/β-catenin信号通路关键蛋白表达量上升,且CLP组高于CLP+XAV939组(P＜0.01或P＜0.05).实时定量PCR示,CLP组β-catenin mRNA表达量较对照组增高(P＜0.05),CLP+XAV939组与对照组无差异.IHC示,与对照组比较,CLP组和CLP+XAV939组肺内多种细胞内β-catenin蛋白表达量明显增多,且CLP组多于CLP+XAV939组(P＜0.05).IF示,与对照组比较,CLP组和CLP+XAV939组肺内LRP5/6表达量明显升高,且CLP组高于CLP+XAV939组(P均＜0.05).结论:Wnt/β-catenin信号通路参与脓毒症ALI过程,腹腔注射XAV939抑制Wnt/β-catenin信号通路可减轻ALI.

Background The novel 2019 coronavirus (COVID-19) has caused a global pandemic, and often leads to extrapulmonary organ injury. However, the risk factors for extrapulmonary organ injury are still unclear. We aim to explore the risk factors for extrapulmonary organ injury and the association between extrapulmonary organ injury and the prognosis in COVID-19 patients. Methods We implemented a single-center, retrospective, observational study, in which a total of 349 confirmed COVID-19 patients admitted to Tongji Hospital from January 25, 2020, to February 25, 2020, were enrolled. We collected demographic, clinical, laboratory, and treatment data from electronic medical records. Potential risk factors for extrapulmonary organ injury of COVID-19 patients were analyzed by a multivariable binary logistic model, and multivariable Cox proportional hazards regression model was used for survival analysis in the patients with extrapulmonary organ injury. Results The average age of the included patients was 61.73±14.64 years. In the final logistic model, variables including aged 60 or older [odds ratio (OR) 1.826, 95% confidence interval (CI): 1.060–3.142], acute respiratory distress syndrome (ARDS) (OR 2.748, 95% CI: 1.051–7.185), lymphocytes count lower than 1.1×109/L (OR 0.478, 95% CI: 0.240–0.949), level of interleukin-6 (IL-6) greater than 7 pg/mL (OR 1.664, 95% CI: 1.005–2.751) and D-Dimer greater than 0.5 μg/mL (OR 2.190, 95% CI: 1.176–4.084) were significantly associated with the extrapulmonary organ injury. Kaplan-Meier curve and log-rank test showed that the probabilities of survival for patients with extrapulmonary organ injury were significantly lower than those without extrapulmonary organ injury. Multivariate Cox proportional hazards model showed that only myocardial injury (P=0.000, HR: 5.068, 95% CI: 2.728–9.417) and circulatory system injury (P=0.000, HR: 4.076, 95% CI: 2.216–7.498) were the independent factors associated with COVID-19 patients’ poor prognosis. Conclusions Older age, lymphocytopenia, high level of D-Dimer and IL-6, and the severity of lung injury were the high-risk factors of extrapulmonary organ injury in COVID-19 patients. Myocardial and circulatory system injury were the most important risk factors related to poor outcomes of COVID-19 patients. It may help clinicians to identify extrapulmonary organ injury early and initiate appropriate treatment.

新型冠状病毒肺炎是由一种新型冠状病毒所引发的急性感染性肺炎[1～3].2020年2月,世界卫生组织(World Health Organization,WHO)将该病毒命名为新型冠状病毒(SARS-CoV-2),所致疾病命名为2019冠状病毒病(coronavirus disease 2019,COVID-19).COVID-19重症患者的救治较为困难,病死率较高.本文总结一线抗疫临床经验,并结合文献梳理了对重症患者的氧疗、呼吸支持处理策略,供一线医生参考.

The number of pertinent researches of COVID-19 has increased rapidly but they mainly focused on the description of general information of patients with confirmed infection. We aimed to bridge the gap between disease classification and clinical outcome in intensive care patients, data of which are scarce and such classification could help in individual evaluation and provide effective triage for treatment and management. Specifically, we collected and filtered out 151 intensive care patients with complete medical records from Tongji hospital in Wuhan, China. We constructed a fully Bayesian latent variable model for integrative clustering of six data categories, including demographic information, symptoms, original comorbidities, vital signs, blood routine tests and inflammatory marker measurements. We identified four prognostic types of COVID-19 in intensive care patients, presenting a stepwise distribution in age, respiratory condition and inflammatory markers, suggesting the prognostic efficacy of these indicators. This report, to our knowledge, is the first attempt of dealing with classification of COVID-19 in intensive care patients. We acknowledge the limitation of ignoring the effect of treatment, but we believe such classification is enlightening for better triage, allowing for a more rational allocation of scarce medical resources in a resource constrained environment.

With the dramatic increase of confirmed cases of coronavirus disease (COVID-19) and the increasing death toll in China, timely and effective management of severely and critically ill patients appears to be particularly important. Previous studies on COVID-19 mainly described the general features of patients (1). However, little attention has been paid to clinical characteristics and outcomes of intensive care patients, data on whom are scarce but are of paramount importance to reduce mortality. Some of the results of these studies have been previously reported in the form of an abstract (2).

A review The outbreak of COVID-19 caused by a novel coronavirus known as SARS-CoV-2 has initiated the first-grade national response in China and listed as a public health emergency of international concern (PHEIC) by WHO In this article, the authors summarized their front-line clin experience in fighting against COVID-19 in combination with literature review to illustrate the clin manifestations and diagnostic and therapeutic measures for COVID-19 patients, especially the identification and treatment strategies for severe COVID-19 patients, aiming to provide reference for the front-line clinicians

目前心房纤颤治疗方式可分为药物治疗和手术治疗[1],其中微创手术导管下射频消融术在临床的运用越来越广泛,带来临床获益的同时也可能产生一些的手术并发症,射频治疗后的心房食管瘘就是其中一项严重的手术并发症[2].由于患者射频消融点多位于在左心房或者肺静脉口或窦周围,而食管与左心房位置紧密,因此在手术同时容易损伤食管,一旦心房与食管有瘘口形成时,即造成心房食管瘘(atrial esophageal fistula,AEF),产生一系列临床症状[2].目前文献报道AEF发病率有所差别,资料显示占射频消融手术患者的0.1％～0.25％[2],虽然发病率小但是其发病后往往出现致命情况[3].同时由于AEF在术后发病时间差异较大,临床症状不典型,往往在早期症状较多且相关性不紧密,容易被忽视,因此需要加强该疾病的认识.本文报道一例射频消融术后出现心房食管瘘的病例,同时进行文献复习,以期增加临床工作者对该疾病的认识.

To investigate autonomic substrates of brainstem-gut circuitry identified using trans-synaptic tracing with pseudorabies virus (PRV)-152, a strain that expresses enhanced green fluorescent protein, and PRV-614, a strain that expresses enhanced red fluorescent protein, injecting into the rat rectum wall. 3-7 days after PRV-152 injection, spinal cord and brainstem were removed and sectioned, and processed for PRV-152 visualization using immunofluorescence labeling against PRV-152. 6 days after PRV-614 injection, brainstem was sectioned and the neurochemical phenotype of PRV-614-positive neurons was identified using double immunocytochemical labeling against PRV-614 and TPH. We observed that the largest number of PRV-152- or PRV-614-positive neurons was located in the gigantocellular reticular nucleus (Gi), lateral paragigantocellular (LPGi), rostral ventrolateral reticular nucleus (RVL), solitary tract nucleus (Sol), locus coeruleus (LC), raphe magnus nucleus (RMg), subcoeruleus nucleus (SubCD). Double-labeled PRV-614/tryptophan hydroxylase (TPH) neurons were concentrated in the RMg, LPGi and Sol. These brainstem neurons are candidates for relaying autonomic command signals to the gut. The autonomic substrate of brainstem-gut circuitry likely plays an important role in mediating different aspects of stress behaviors.

OBJECTIVE To monitor the detection rate and drug resistance of Acinetobacter baumannii (ABA ) in Tongji Hospital ,and understand the prevalence status of ABA ,in order to provide references for the clinical pre‐vention and treatment of ABA infections .METHODS ABA strains clinically isolated from 2011 to 2015 from ICU of Tongji Hospital were statistically analyzed .Bacterial identification and drug sensitivity were detected by VITEK‐2 automatic bacteria identification system ,and the results of antimicrobial susceptibility were determined according to CLSI 2015 M100‐S25 criteria .All the data were analyzed by WHONET 5 .6 software .RESULTS Totally 1079 strains of Ab were detected from 5 084 positive specimens from ICU from 2011 to 2015 ,with the detection rate of 21 .22% ,including 1 026 strains of carbapenem‐resistant AB(CRAB) ,accounting for 95 .09% .The detection rate was generally on the rise in five years .Among the specimens ,88 .88% were sputum specimens ,6 .21% were blood specimens ,and 4 .91% were other types of specimens .In 5 years ,the resistance of Ab isolated from our ICU to cefoperazone / sulbactam ,minocycline had significantly changed ,to tigecyclin was lower ,to other antibi‐otics were all above 70% ,and to tobramycin ,and amikacin increased year by year .CONCLUSION The isolation rate and drug resistance of ABA are severe in the ICU of the hospital ,showing an upward trend .We should mas‐ter the epidemic trend and characteristics ,select the sensitive antibiotics according to the drug sensitivity results , and use the antibiotics reasonably .