Acute lung injury (ALI) is a severe condition with multifaceted causes, including inflammation and oxidative stress. This research investigates the influence of m6A (N6-methyladenosine) modification on GBP4, a protein pivotal for macrophage polarization, a critical immune response in ALI. Utilizing a mouse model to induce ALI, the study analyzed GBP4 expression in alveolar macrophages. By overexpressing or knocking down GBP4, the study assessed its impact on M1 macrophage polarization. The role of YTHDF1 was also explored through knockdown experiments to determine its effect on GBP4 expression and macrophage polarization. Increased GBP4 expression was noted in ALI model mice, promoting M1 macrophage polarization. YTHDF1 was found to enhance GBP4 expression by recognizing m6A sites on its mRNA, which was linked to reduced inflammation in MLE-12 cells upon YTHDF1 knockdown. The study emphasizes the crucial roles of GBP4 and YTHDF1 in ALI development and immune response regulation. It suggests m6A modification as a potential therapeutic target, contributing to the understanding of ALI’s molecular mechanisms and guiding future treatment strategies.

目的 探究支气管镜下肺泡灌洗对老年支气管扩张并感染患者肺功能、血气指标及炎症反应的影响.方法 研究选择开封市第三人民医院 2021 年 2 月至 2022 年 2 月收治的 202 例支气管扩张合并感染的老年患者作为研究的对象,按照随机数字表将 202 例患者分为试验组和对照组,每组 101 例.对照组进行常规保守治疗,试验组在此基础上进行支气管镜下肺泡灌洗.记录两组患者通气指标[第 1 秒用力呼气量(FEV1)、1 秒用力呼吸容积与用力肺活量的比值(FEV1/FVC)],血气指标[动脉血氧分压(PaO2)、动脉血二氧化碳分压(PaCO2)、动脉血氧饱和度(SaO2)],炎症因子[超敏C-反应蛋白(hs-CRP)、肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)-4 和IL-23],排痰量、感染控制及住院时间.结果 在肺通气功能指标方面,治疗后,两组FEV1、FEV1/FVC指标均增高,而试验组患者的FEV1、FEV1/FVC均高于对照组,差异有统计学意义(P＜0.05);两组患者的SaO2、PaO2 均较治疗前上升,试验组SaO2、PaO2显著高于对照组,PaCO2水平均治疗前显著降低,试验组PaCO2水平显著低于对照组,差异有统计学意义(P＜0.05);两组患者的炎症因子hs-CRP、TNF-α、IL-4、IL-23均降低,试验组降低程度优于对照组,差异有统计学意义(P＜0.05);试验组每日排痰量试验组多于对照组,感染控制时间和住院时间试验组短于对照组,差异有统计学意义(P＜0.05).结论 支气管镜下肺泡灌洗可有效改善老年支气管扩张合并感染患者的肺功能和血气指标,抑制其机体内炎性反应.

Introduction:The advent of metagenomics next-generation sequencing (mNGS) has garnered attention as a novel method for detecting pathogenic infections, including Non-Tuberculous Mycobacterial (NTM) and tuberculosis (TB).However, the robustness and specificity of mNGS in NTM diagnostics have not been fully explored.Methods:In this retrospective study, we enrolled 27 patients with NTM genomic sequences via mNGS and conducted a comprehensive clinical evaluation.Results:Pulmonary NTM disease was the most commonly observed presentation, with a subset of patients also presenting with extrapulmonary NTM infections.mNGS analysis identified six distinct NTM species, primarily Mycobacteriumavium complex (MAC), followed by Mycobacterium intracellulare andMycobacterium abscessus. Conventional routine culture methods encountered challenges, resulting in negative results for all available 22 samples. Among the 10 patients who underwent quantitative polymerase chain reaction (qPCR) testing, five tested positive for NTM.Discussion:It is important to note that further species typing is necessary to determine the specific NTM type, as traditional pathogen detection methods serve as an initial step. In contrast, when supplemented with pathogen data, enables the identification of specific species, facilitating precise treatment decisions. In conclusion, mNGS demonstrates significant potential in aidingthe diagnosis of NTMdisease by rapidly detecting NTM pathogens and guiding treatment strategies. Its enhanced performance, faster turnaround time (TAT), and species identification capabilities make mNGS a promising tool for managing NTM infections.

Background: There is still no agreement on whether corticosteroids can reduce mortality in patients with acute respiratory distress syndrome (ARDS). The aim of this study was to investigate the efficacy of low-dose corticosteroid administration in patients with ARDS. Methods: A prospective observational study of patients with ARDS in 17 hospitals in China was performed between March 2016 and February 2018. Propensity score matching was performed to adjust for differences in baseline characteristics between different groups. The effects of corticosteroids were assessed by using the Kaplan-Meier method and a multivariate Cox regression. Results: A total of 527 ARDS patients were enrolled in the study. Sixty-five patients (12.3%) were administered low-dose (methylprednisolone ≤1 mg·kg−1·d−1) corticosteroids. The median dose was equivalent to 0.67 (0.57–0.81) mg/kg methylprednisolone for a median duration of 10 days. The control group included 224 patients (42.5%) who had never receive corticosteroids. In the matched sample, the hospital mortality rates in the low-dose (n=40) and control groups (n=80) were 27.5% and 42.5% (P=0.110), respectively. The length of hospital stay was significantly longer in the low-dose corticosteroid group than in the control group (24.0 vs. 17.0, P=0.002), and the multivariate Cox regression analysis suggested that the low-dose group had a significantly lower risk of death than the control group (HR: 0.48; 95% CI: 0.24–0.97; P=0.040). Conclusions: The administration of low-dose corticosteroids may reduce mortality in patients with ARDS.

Abstract Background The anti-coagulation protocol of patients with hemorrhage risk primary disease who need extracorporeal membrane oxygenation (ECMO) supported is controversial. This study evaluated the feasibility of a new anti-coagulation strategy, that is heparin-free after 3000 IU heparin loaded in veno-venous ECMO (VV ECMO) supported acute respiratory failure patients with hemorrhage risk. Methods A retrospective study was performed in a series of hemorrhage risk patients supported with VV ECMO at the First Affiliated Hospital of Zhengzhou University, between June 2012 to Sept 2020. A total of 70 patients received a low heparin bolus of 3000 units for cannulation but without subsequent, ongoing heparin administration. Patients were divided into survival (n = 25) and non-survival group (n = 45). Data of coagulation, hemolysis and membrane lung function were calculated and analyzed. The complications of patients were recorded. Finally, the binary Logistic regression was conducted. Results The longest heparin-free time was 216 h, and the mean heparin-free time was 102 h. Compared with survivors, the non-survivors were showed higher baseline SOFA score and lower platelet counts in 0.5 h, 24 h, 48 h and 96 h after ECMO applied. However, there was no significant differences between survivors and non-survivors in ACT, APTT, INR, D-dimer, fibrinogen, LDH, blood flow rate, Δp and Ppost-MLO2 (all p < 0.05) of all different time point. Moreover, only the baseline SOFA score was significantly associated with mortality (p < 0.001, OR(95%CI): 2.754 (1.486–5.103)) while the baseline levels of ACT, APTT, INR, platelet, D-dimer, fibrinogen and LDH have no association with mortality. The percentage of thrombosis complications was 54.3% (38/70) including 3 oxygenator changed but there was no significant difference of complications in survival and non-survival groups (p > 0.05). Conclusions The anticoagulation protocol that no heparin after a 3000 units heparin bolus in VV ECMO supported acute respiratory failure patients with hemorrhage risk is feasible.

Background: The anti-coagulation protocol of patients with hemorrhage risk primary disease who need extracorporeal membrane oxygenation (ECMO) supported is controversial. This study evaluated the safety of heparin-free after 3000IU heparin loaded in veno-venous ECMO (VV ECMO ) supported acute respiratory failure patients with hemorrhage risk. Methods: A retrospective study was performed in a series of hemorrhage risk patients supported with VV ECMO at the First Affiliated Hospital of Zhengzhou University, between June 2012 to Sept 2020. A total of 70 patients received a low heparin bolus of 3000 units for cannulation but without subsequent, ongoing heparin administration. Patients were divided into survival (n=25) and non-survival group (n=45). Data of coagulation, hemolysis and membrane lung function were calculated and analyzed. The complications of patients were recorded. Finally, the binary Logistic regression was conducted. Results: The longest heparin-free time was 216 hours, and the mean heparin-free time was 102 hours. The percentage of thrombosis complications was 54.3% (38/70) including 3 oxygenator changed but there was no significant difference of complications in survival and non-survival groups (p>0.05). Compared with survivors, the non-survivors were showed higher baseline SOFA score and lower platelet counts in 0.5 hour, 24 hours, 48 hours and 96 hours after ECMO applied. However, there was no significant differences between survivors and non-survivors in ACT, APTT, INR, D-dimer, fibrinogen, LDH, blood flow rate, Δp and P post-ML O 2 (all p<0.05) of all different time point. Moreover, only the baseline SOFA score was significantly associated with mortality (p<0.001, OR(95%CI): 2.754 (1.486-5.103)) while the baseline levels of ACT, APTT, INR, platelet, D-dimer, fibrinogen and LDH have no association with mortality. Conclusions: The anticoagulation protocol that no heparin after a 3000 units heparin bolus in VV ECMO supported acute respiratory failure patients with hemorrhage risk is safe.

Objectives There are few studies of metagenomic next-generation sequencing (mNGS) in immunocompromised patients assisted by veno-venous extracorporeal membrane oxygenation (vv-ECMO). The present study is aimed to investigate the pathogen-detected effect and clinical therapy value of mNGS technologies in immunocompromised patients assisted by vv-ECMO. Methods Our study retrospectively enrolled 46 immunocompromised patients supported by vv-ECMO from Jan 2017 to June 2021 at the First Affiliated Hospital of Zhengzhou University, respectively. Patients were divided into the deterioration group (Group D) (n = 31) and improvement group (Group I) (n = 15) according to their outcomes. Baseline characteristics and etiological data of patients during hospitalization of 2 groups were compared. The pathogens detected by mNGS and antibiotic regimens guided by mNGS in immunocompromised patients assisted by vv-ECMO were analyzed. Results Compared with Group I, the deterioration patients showed a higher percentage of chronic obstructive pulmonary disease (COPD) (32.3% vs. 6.7%, p < 0.01) and were significantly older (47.77 ± 16.72 years vs. 32 ± 15.05 years, p < 0.01). Within 48 h of being ECMO assisted, the consistency of the samples detected by traditional culture and mNGS at the same time was good (traditional culture vs. mNGS detection, the positive rate of bronchoalveolar lavage fluid (BALF) culture: 26.1% vs. 30.4%; the positive rate of blood sample culture: 12.2% vs. 12.2%, p > 0.05). However, mNGS detected far more pathogen species and strains than conventional culture (30 strains vs. 78 strains, p < 0.01); the most popular pathogen was Klebsiella pneumoniae. Parts of patients had their antibiotic treatment adjustments, and the improvement patients showed less usage of broad-spectrum antibiotics. Conclusions mNGS may play a relatively important role in detecting mixed pathogens and personalized antibiotic treatment in immunocompromised patients assisted by vv-ECMO.

Objectives The metagenomic next-generation sequencing (mNGS) test is useful for rapid and accurate detection and identification of pathogenic microorganisms. The aim of the present study was to investigate the factors associated with in-hospital mortality in pneumocystis pneumonia (PCP) patients with mNGS-assisted diagnosis. Methods Our study enrolled 154 patients with mNGS-positive PCP from August 2018 to February 2022 at the First Affiliated Hospital of Zhengzhou University respectively. Patients were divided into the survivor group (n=98) and the death group (n=56) according to whether in-hospital death occurred. Baseline characteristics, patients’ pre-hospital symptoms and patients’ CT imaging performance during hospitalization were carefully compared between the two groups. Risk factors for the occurrence of in-hospital death were sought by selecting indicators that were significantly different between the two groups for modelling and performing multiple logistic regression analysis. Results Compared with the in-hospital death patients, the survivors were younger and had higher levels of albumin (ALB) (age: 50.29 ± 14.63 years vs 59.39 ± 12.27 years, p<0.001; ALB: 32.24 ± 5.62 g/L vs 29.34 ± 5.42g/L, p=0.002; respectively), while the levels of lactate dehydrogenase (LDH) and C-reactive protein CRP were lower (LDH: 574.67 ± 421.24 U/L vs 960.80 ± 714.94 U/L, p=0.001; CRP: 54.97 ± 55.92 mg/L vs80.45 ± 73.26 mg/L, p= 0.018; respectively). Multiple logistic regression analysis revealed that age, the baseline LDH and CRP levels were all positively associated with high in-hospital mortality [age: OR(95%CI): 1.115 (1.062-1.172), p<0.001; LDH: OR(95%CI): 1.002 (1.001-1.003), p<0.001; CRP: OR(95%CI): 1.008 (1.000-1.017), p=0.045; respectively] while the platelet counts was negatively associated with it [OR(95%CI): 0.986 (0.979-0.992), p<0.001]. Conclusions Old age, high baseline levels of LDH and CRP and low platelet counts were risk factors of the in-hospital mortality in mNGS positive PCP patients.

Background: The aim of this study was to investigate the mechanism of STAT3 in reducing the inflammatory responses in mice with viral myocarditis (VMC). Methods: Induce and generate viral myocarditis by using coxsackievirus B3 (CVB3) infected cardiomyocytespecific STAT3 conditional knockout (STAT3cKO) mice and BALB/c mice. Use RT-PCR and western blot techniques to detect the expression of related cytokines in the uninfected wild-type mice group (Control group), myocarditis wild-type mice group (Model group) and STAT3cKO group, as well as the differentiation of spleen T cells in each group. Eukaryotic expression plasmid pcDNA3-STAT3 can reduce the expression of inflammatory factors the in vitro cultured cardiomyocytes of the STAT3cKO group. Results: RT-PCR showed that compared with the Control group, the expression levels of VMC-related genes (NF kappa B, TNF-alpha, IL-1 beta and IL-1) and anti-inflammation-related cytokines (IL-10 and TGF-beta) in the Model group went up (*p < 0.05, **p < 0.01, ***p < 0.001); and also compared with the Control group, the rise in the expression levels of the above VMC-related genes in the STAT3cKO group was particularly significant (***p < 0.001, ****p < 0.0001) but there was no significant difference in the expression of IL-10 and TGF-beta. After 4 weeks, a second RT-PCR showed that the expression of inflammation-related genes in the STAT3cKO group continued to be activated (***p < 0.001, ****p < 0.0001). Western blotting was performed to detect the expression of p65, a key protein of the NF-kappa B signalling pathway. The results showed that the p65 protein content was increased and the IL-10 protein content was decreased in the STAT3cKO group; the results of the T cell differentiation test showed that the T cell differentiation rate increased in the STAT3cKO group (**p < 0.01). Eukaryotic expression plasmid pcDNA3-STAT3 could reduce the expression of NF-kappa B, TNF-alpha, IL-1 beta and IL-17 (**p < 0.01). Conclusion: The expression of STAT3 gene in VMC could to a certain extent inhibit the NF-kappa B signalling pathway and reduce the inflammatory responses of VMC.

感染性心内膜炎（IE）是由病原微生物侵入心内膜导致的感染，而右心感染性心内膜炎（RSIE）致脓毒性肺栓塞较为少见，表现为非特异性临床表现和影像学征象。本文报道1例RSIE致脓毒性肺栓塞病例，其经积极抗感染及外科手术治疗转归良好。

Sepsis-induced lung injury was the most common cause of death in patients. This study aimed to investigate whether PD-L1 regulates the inflammation in LPS-induced lung epithelial cells and vascular endothelial cells by interacting with the HIF-1α signaling pathway. Sepsis-induced lung injury mice were constructed by cecal ligation and puncture (CLP) procedure, and lipopolysaccharide (LPS)-induced lung epithelial cells and vascular endothelial cells simulate the sepsis-induced lung injury model in vitro. Hematoxylin-eosin (HE) staining detected the morphological changes of the lung tissues, and immunohistochemistry (IHC) detected the PD-L1 expression in lung tissues. Bicinchoninic acid (BCA) assay determined the protein concentration in bronchial alveolar lavage fluid (BALF). The number of PD-1 (+) cells in blood was detected by flow cytometry. The apoptosis in lung tissues and LPS-induced cells was analyzed by TUNEL assay. The inflammatory factor levels and HIF-1α in lung tissues and LPS-induced cells were analyzed by ELISA. The transfection effects of KD-PDL1 or KD-HIF1A in lung epithelial cells and vascular endothelial cells were confirmed by qRT-PCR analysis. The protein expression related to the PD-L1- and HIF-1α-related pathway was determined by Western blot analysis. As a result, LMT-28, as an IL-6 inhibitor, alleviated lung injury and suppressed the apoptosis and inflammation in lung tissues in BALF and the number of PD-1 (+) cells in blood. Sepsis-induced lung injury activated the PD-L1- and HIF-1α-related pathway, while LMT-28 could not completely inhibit the pathway. In addition, downregulation of PD-L1 or downregulation of HIF-1α suppressed the apoptosis and alleviated the inflammation in LPS-induced lung epithelial cells and vascular endothelial cells. Downregulation of PD-L1 had significant effects on lung epithelial cells but had greater effects on vascular endothelial cells. Downregulation of HIF-1α could decrease PD-L1 expression, and downregulation of PD-L1 could also suppress the protein expression of HIF-1α and related pathways. In conclusion, downregulation of PD-L1 alleviated the inflammation in LPS-induced lung epithelial cells and vascular endothelial cells by suppressing the HIF-1α signaling pathway.

Background Antibody-mediated rejection (AMR) occupies a major position for chronic rejection after kidney transplantation. Regulatory B cell (Breg) has been reported to have an inhibitory immune function, which contributes to the resistance for AMR. Methods A nested case–control study for nine healthy donors, 25 stable (ST) patients, and 18 AMR patients was performed to determine the type of Breg in maintaining immune tolerance and preventing AMR. Results Compared to the ST group, circulating interleukin (IL)-10+ Bregs, but not Bregs, significantly decreased. The receiver operating characteristic (ROC) curve analysis revealed that rather than the circulating Bregs, decreased circulating IL-10+ Breg levels were positively associated with AMR. However, kidney B cell and IL-10 infiltration was significantly increased in the AMR group with high expression of C-X-C motif chemokine 13 (CXCL13). In addition, circulating IL-10+ Bregs, rather than Bregs, remained higher than those at pre-operation, during the 90-day post-operation in immune homeostasis. Conclusion The circulating IL-10+ Breg levels are more appropriate measures for assessing the resistance of AMR after kidney transplantation.

Objective: To study the risk factors associated with the hospital survival rate of elder patients with acute respiratory distress syndrome (ARDS) in Medical/Respiratory Intensive Care Units (MICUs/RICUs) by evaluating the prognosis, and therefore to provide insight into patient treatment strategy. Methods: Twenty MICUs/RICUs of 19 general hospitals in mainland China participated in the multicenter prospective cohort study carried out from Mar 1st, 2016 to Feb 28th, 2018. Patients who met the criteria of Berlin ARDS and older than 65 years were recruited. Baseline data, risk factors of ARDS, ventilator setup and prognosis data were collected from all patients. Univariant and multivariant regression analysis were conducted to analyze the factors associated with the prognosis. Results: 170 elder ARDS patients (age≥65 years) met the Berlin ARDS criteria, among whom 8.8% (15/170), 42.9% (73/170) and 48.2% (82/170) patients had mild, moderate and severe ARDS, respectively. The most common predisposing factor for elder ARDS was pneumonia, which was present in 134 patients (78.8%). 37.6% (64/170) patients were treated with noninvasive mechanical ventilation (NIV), but 43.8% (28/64) cases experienced treatment failure. 76.5% (130/170) patients were treated with invasive mechanical ventilation. All patients 80 years or older were given invasive mechanical ventilation. 51.8% (88/170) cases had complications of non-pulmonary organ failure. 61.8% (105/170) patients deceased during hospital stay. Multivariant logistic analysis showed that the independent risk factors for hospital survival rate in elder patients with ARDS were SOFA score (P=0.030, RR=0.725, 95% CI 0.543-0.969), oxygen index after 24 hours of ARDS diagnosis (P=0.030, RR=0.196, 95% CI 0.045-0.853), accumulated fluid balance within 7 days after diagnosis of ARDS (P=0.026, RR=1.000, 95% CI 1.000-1.000) and shock (P=0.034, RR=0.140, 95% CI 0.023-0.863). Conclusion: Among 20 ICUs, the high mortality rate of elder patients with ARDS was correlated with higher 24 hour SOFA score, lower 24 hour oxygen index after ARDS diagnosis, more positive fluid balance within 7 days and concomitant shock. The conservative fluid strategy within 7 days of ARDS diagnosis may benefit the elder ARDS patients.

Non-small cell lung cancer (NSCLC) is the most common type of lung cancer, and numerous oncogenes are associated with this disease. Oxysterol-binding protein-related protein 8 (ORP8) is essential for cell growth, migration and the modulation of mitochondrial respiration and morphology. However, the underlying role of ORP8 in NSCLC remains unclear. In the present study, it was reported that the expression of ORP8 was low in NSCLC cells and tissues. The ORP8 expression levels were analyzed by immunohistochemistry (IHC), quantitative real-time PCR (qPCR) and western blot analysis. ORP8 overexpression inhibited cell growth and induced apoptosis in NSCLC cells with MTS, anchorage-independent growth and Hoechst 33342 staining assay. Further experiments demonstrated that ORP8 overexpression induced the apoptosis of NSCLC cells via the release of cytochrome c from mitochondria into the cytoplasm with western blot analysis and confocal microscopy results. In addition, qPCR analysis showed that miR-421 was upregulated in NSCLC cell lines, with the bioinformatics analysis, western blot analysis and Dual-Luciferase reporter assay, it was determined that miR-421 could target ORP8. The inhibition of cell proliferation via ORP8 overexpression was rescued by a miR-421 mimic, which aided in maintaining the proliferative potential of the cells. Overall, the present study revealed that ORP8 may be a candidate target in the prevention and treatment of NSCLC.

Objectives To evaluate the incidence and mortality of acute respiratory distress syndrome (ARDS) in medical/respiratory intensive care units (MICUs/RICUs) to assess ventilation management and the use of adjunct therapy in routine clinical practice for patients fulfilling the Berlin definition of ARDS in mainland China. Methods This was a multicentre prospective longitudinal study. Patients who met the Berlin definition of ARDS were included. Baseline data and data on ventilator management and the use of adjunct therapy were collected. Results Of the 18,793 patients admitted to participating ICUs during the study timeframe, 672 patients fulfilled the Berlin ARDS criteria and 527 patients were included in the analysis. The most common predisposing factor for ARDS in 402 (77.0) patients was pneumonia. The prevalence rates were 9.7% (51/527) for mild ARDS, 47.4% (250/527) for moderate ARDS, and 42.9% (226/527) for severe ARDS. In total, 400 (75.9%) patients were managed with invasive mechanical ventilation during their ICU stays. All ARDS patients received a tidal volume of 6.8 (5.8–7.9) mL/kg of their predicted body weight and a positive end-expository pressure (PEEP) of 8 (6–12) cmH 2 O. Recruitment manoeuvres (RMs) and prone positioning were used in 61 (15.3%) and 85 (16.1%) ventilated patients, respectively. Life-sustaining care was withdrawn from 92 (17.5%) patients. When these patients were included in the mortality analysis, 244 (46.3%) ARDS patients (16 (31.4%) with mild ARDS, 101 (40.4%) with moderate ARDS, and 127 (56.2%) with severe ARDS) died in the hospital. Conclusions Among the 18 ICUs in mainland China, the incidence of ARDS was low. The rates of mortality and withdrawal of life-sustaining care were high. The recommended lung protective strategy was followed with a high degree of compliance, but the implementation of adjunct treatment was lacking. These findings indicate the potential for improvement in the management of patients with ARDS in China. Trial registration Clinicaltrials.gov NCT02975908 . Registered on 29 November 2016—retrospectively registered.

目的 探讨心力衰竭患者血清脂联素(APN)及脂蛋白相关磷脂酶A2(LP-PLA2)的水平变化,并观察其与心力衰竭程度的关系.方法 收集160例心力衰竭患者作为试验组,根据纽约心脏协会分级(NYHA),分为NYHAⅡ组55例、NYHAⅢ组56例、NYHAⅣ组49例,同时选取150例健康体检者作为对照组;采用彩色多普勒超声显像仪,检测左心室射血分数(LVEF)水平,根据LVEF水平,分为LVEF＞40％组76例、LVEF≤40％组84例,采用酶联免疫吸附试验法(ELISA),测定血清APN、LP-PLA2水平,同时检测相关生化指标.结果 试验组N末端脑钠肽前体(NT-pro-BNP)水平较对照组明显升高,LVEF较对照组明显降低(P＜0.05);与NYHAⅡ级组患者比较,NYHAⅢ级组、NYHAⅣ级组患者APN、LP-PLA2、NT-pro-BNP明显升高(P＜0.05),与NYHAⅢ级组患者比较,NYHAⅣ级组患者APN、LP-PLA2、NT-pro-BNP明显升高(P＜0,05);LVEF＞40％患者血清APN、LP-PLA2、NT-pro-BNP水平均低于LVEF≤40％患者(P＜0.05).经Pearson直线相关分析,APN、LP-PLA2与NT-pro-BNP呈正相关(r=0.36,P＜0.05),APN、LP-PLA2与LVEF呈负相关(r=-0.426,P＜0.05).经二分类Logistic回归分析显示,NT-pro-BNP、APN、LP-PLA2与心力衰竭发生有关.结论 APN、LP-PLA2水平随着心力衰竭病情加重逐渐升高,可作为心力衰竭诊断及病情监测的新的标志物.

目的:探究孟鲁司特钠联合吸入用布地奈德混悬液治疗慢性阻塞性肺疾病(COPD)继发肺间质纤维化(PF)的效果.方法:选取2016年8月-2018年5月我院收治的COPD继发PF患者92例,按随机数字表法分为两组,各46例.对照组采取布地奈德混悬液(1 mg,bid,雾化吸入)治疗,试验组在此基础上采取孟鲁司特钠(10 mg,qn)治疗,连续治疗12周.比较两组治疗前后第1s用力呼气容积/用力肺活量(FEV1/FVC)、第1s用力呼气容积(FEV1)、6 min步行距离(6 MWD)及不良反应.结果:治疗后试验组FEV1、FEV1/FVC水平高于对照组,差异有统计学意义(P＜0.05);治疗后试验组6 MWD大于对照组,差异有统计学意义(P＜0.05);两组不良反应发生率比较,差异无统计学意义(P＞0.05).结论:孟鲁司特钠联合布地奈德混悬液治疗COPD继发PF,有助于改善患者的肺功能,提高运动耐力,且安全性较高.

人鼻病毒(HRV)是小核糖核酸病毒科中的一种RNA病毒,因其特别适应在鼻腔中生长,故被称为"鼻病毒".HRV不仅能引起普通感冒,还能导致急、慢性支气管炎等其他呼吸系统感染疾病.近年来也逐渐在下呼吸道感染患者中检测到,其引起的重症肺炎进展迅速,容易被临床医生误诊、漏诊.本文报道1例郑州大学第一附属医院呼吸ICU科收住的成人人鼻病毒感染引起的急性呼吸窘迫综合征病例.

With the continuous development of extracorporeal membrane oxygenation (ECMO) technology,the treatment of patients with severe clinical diseases is becoming more and more important.People who benefit from ECMO are also more aware of their complications.There have been a lot of researches about some serious complications such as thromboembolism,hemorrhage,and depipeation in ECMO.This paper introduces the cause and treatment progress of pneumothorax induced by mechanical ventilation in patients with ECMO.

Objective To investigate the changes of Th17 cell function by testing the transcription regulative factor RORγt and the main effect factor cytokine interleukin-17(IL-17)of Th17 cells,and the effect of human immunoglobulin on Th17 cell function in immunosuppressed mice with Pseudomonas aeruginose(PA)pneumonia.Methods Ninety BALB/c mice were divided into five groups randomly:control group,PA group,immunosuppressed group,immunosuppressed+PA group and human immunoglobulin group(named group A,B,C,D and E,n=18 each).All mice were sacrificed at 4,8 and 24 h after the establishment of the experimental models.Gross examination was performed and the lungs were excised for routine histological analysis.The expression level of RORγt mRNA was detected by reverse-transcriptase polymerase chain reaction(RT-PCR)and the concentration of IL-17 was measured in the peripheral blood by enzyme-linked immune sorbent assay(ELISA).Results Histological findings demonstrated that the lung tissues had no inflammatory changes in group A and C.But inflammatory changes,such as congestion of red blood cells in capillaries,edema,infiltration of many inflammatory cells and enlarged alveolar septum,occurred in group B,D,and E.Such changes were most significant at 8 h.The lung jury score was the highest in group D than in any other groups(P<0.01).The levels of RORγt mRNA in the lung were higher in group B,D and E than in group A and C(P<0.01),and they reached the peak at 4 h.The concentration of IL-17 in the peripheral blood was higher in group B,D and E than in group A and C(P<0.01),and it reached the peak at 8 h.All the observed indexes including the lung injury score,the level of RORγt mRNA and the concentration of IL-17 were much higher in group D than in group B(P<0.01),and they were even lower in group E than in group B(P<0.01).Conclusion The over-stimulation of Th17 cells derived from immunosupressed mice with PA pneumonia leads to excessive inflammatory responses and the organ and tissue injuries.Human immunoglobulin can inhibit the inflammatory reactions caused by Th17 cells,and therefore relieve the deterioration of the disease.