Identification of dynamic signatures associated with smoking‐related squamous cell lung cancer and chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a risk factor for the development of lung cancer. The aim of this study was to identify early diagnosis biomarkers for lung squamous cell carcinoma (SQCC) in COPD patients and to determine the potential pathogenetic mechanisms. The GSE12472 data set was downloaded from the Gene Expression Omnibus database. Differentially co‐expressed links (DLs) and differentially expressed genes (DEGs) in both COPD and normal tissues, or in both SQCC + COPD and COPD samples were used to construct a dynamic network associated with high‐risk genes for the SQCC pathogenetic process. Enrichment analysis was performed based on Gene Ontology annotations and Kyoto Encyclopedia of Genes and Genomes pathway analysis. We used the gene expression data and the clinical information to identify the co‐expression modules based on weighted gene co‐expression network analysis (WGCNA). In total, 205 dynamic DEGs, 5034 DLs and one pathway including CDKN1A, TP53, RB1 and MYC were found to have correlations with the pathogenetic progress. The pathogenetic mechanisms shared by both SQCC and COPD are closely related to oxidative stress, the immune response and infection. WGCNA identified 11 co‐expression modules, where magenta and black were correlated with the “time to distant metastasis.” And the “surgery due to” was closely related to the brown and blue modules. In conclusion, a pathway that includes TP53, CDKN1A, RB1 and MYC may play a vital role in driving COPD towards SQCC. Inflammatory processes and the immune response participate in COPD‐related carcinogenesis.     

新型冠状病毒的动物源性和传染源控制

根据现有的数据,新型冠状病毒(2019 novel coronavirus,2019-nCoV)比严重急性呼吸综合征冠状病毒(severe acute respiratory syndrome coronavirus,SARS-CoV)的传染性强、传播速度快、疫情规模大、病死率低。其传染性、传播速度和疫情规模似乎具有甲型流感病毒(influenza A virus)的特点。尽管2019-nCoV来源于何种动物尚无定论,但它与SARS-CoV同属冠状病毒,具有共同之处。如果流行过后 2019-nCoV没能在人群中持续传播和存在(如同SARS-CoV一样),则控制野生动物传染源乃重中之重;如果2019-nCoV获得了能在人群中持续传播的能力,预防控制策略将与SARS-CoV明显不同,疫苗便成为至关重要的手段。     

严重急性呼吸综合征冠状病毒2型 IgM / IgG、病毒核酸和白细胞介素6的联合检测在2019冠状病毒病诊断和治疗中的价值

探讨严重急性呼吸综合征冠状病毒2型(severe acute respiratory syndrome coronavirus 2,SARS-CoV-2)免疫球蛋白M(Immunoglobulin M,IgM)/免疫球蛋白G(Immunoglobulin G,IgG)、病毒核酸和白细胞介素6(interleukin 6, IL-6)的联合检测在2019冠状病毒病(coronavirus disease 2019, COVID-19)诊断和治疗中的临床价值。本研究按照《新型冠状病毒肺炎诊疗方案(试行第七版)》的标准收集了93例确诊病例(51例危重型、18例重型,15例轻型和9例普通型)和20例疑似病例(核酸检测阴性但临床症状和CT检测结果均符合标准)。选取110例儿科、妇科、肿瘤、血液和消化等疾病患者并排除COVID-19作为对照组。采用全自动化学发光免疫分析技术和电化学发光技术检测所有研究对象血清中SARS-CoV-2 IgM/IgG和IL-6。用实时荧光定量反转录聚合酶链反应对病例组和对照组的咽拭子进行SARS-CoV-2核酸检测。结果发现,血清IgM、IgG和IL-6在疑似病例中的阳性率分别为85%、75%和0%,在确诊病例中的阳性率分别为98.9%、95.7%和75.2%(其中危重型分别为100%、100%和100%,重型分别为94.4%、100%和97.9%,轻型分别为100%、93.3%和5%、普通型分别为100%、66.7%和0%)。IL-6和 SARS-CoV-2 IgM/IgG表达水平的改变与患者疾病的严重程度存在一定的关联性,差异有统计学意义(χ²＝273.51,χ²＝149.37;P＜0.05)。血清IL-6和SARS-CoV-2 IgM/IgG的联合检测可作为诊断和治疗COVID-19的监测指标,也可作为SARS-CoV-2核酸检测假阴性的有效互补。     

乌司他丁联合连续性肾脏替代治疗对严重脓毒症患者炎症反应和血流动力学的影响

目的:探讨乌司他丁联合连续性肾脏替代(CRRT)治疗对严重脓毒症患者炎症反应和血流动力学的影响。方法:选取2015年5月～2019年4月期间我院收治的严重脓毒症患者119例,将所有患者根据随机数字表法分为对照组(n=59)和研究组(n=60),对照组给予CRRT治疗,研究组在对照组基础上联合乌司他丁治疗,比较两组患者临床疗效、炎症反应指标、血流动力学参数,记录两组患者住院时间及28d内病死率。结果:研究组治疗7 d后的临床总有效率高于对照组(P0.05)。两组治疗7 d后血清白介素-6(IL-6)、降钙素原(PCT)、肿瘤坏死因子-α(TNF-α)水平均下降,且研究组低于对照组(P0.05)。两组患者治疗7 d后心率、平均动脉压(MAP)、血乳酸下降,氧合指数升高(P0.05),研究组治疗7 d后氧合指数高于对照组,血乳酸则低于对照组(P0.05)。研究组住院时间短于对照组(P0.05),两组28d内病死率比较无统计学差异(P0.05)。结论:乌司他丁联合CRRT治疗严重脓毒症患者的疗效确切,可有效抑制机体炎症反应,改善血流动力学,减少住院时间,具有一定的临床应用价值。     

人免疫球蛋白联合IMP/CS和PS/TS对重症肺部感染患者炎性因子及T细胞亚群的影响

目的:人免疫球蛋白(HIG)联合亚胺培南西司他丁钠(IMP/CS)和哌拉西林他唑巴坦钠(PS/TS)治疗重症肺部感染的临床疗效。方法:选择2013年3月～2018年7月复旦大学附属华山医院北院收治的重症肺部感染患者99例为研究对象,采用随机数字法分为A组(33例,采用HIG+IMP/CS+PS/TS治疗)、B组(33例,采用IMP/CS+PS/TS治疗)和C组(33例,采用PS/TS治疗),比较三组有效率、炎性因子、T细胞亚群和不良反应。结果:A组临床总有效率为96.97%,高于B组的78.79%,B组高于C组的60.61%(P0.05)。治疗7 d后,三组C反应蛋白(CRP)、白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、CD8~+水平较治疗前降低,CD4~+和CD4~+/CD8~+较治疗前升高,差异有统计学意义(P0.05)。治疗7 d后,A组CRP、IL-6、TNF-α、CD8~+水平低于B组,B组低于C组(P0.05);治疗7d后,A组CD4~+和CD4~+/CD8~+高于B组,B组高于C组(P0.05)。三组治疗期间均无药物相关不良反应的发生。结论:HIG联合IMP/CS和PS/TS治疗重症肺部感染患者安全有效,能有效改善患者的炎性反应,调节免疫功能,促进患者恢复。     

布地奈德福莫特罗联合噻托溴铵吸入剂治疗慢阻肺疗效及对CRP、SaO2、PH水平影响

摘要 目的：探究布地奈德福莫特罗联合噻托溴铵吸入剂对慢阻肺治疗效果及对患者C-反应蛋白（C reaction protein,CRP）、血氧饱和度（arterial oxygen saturation,SaO₂）以及肺动脉高压（pulmonary Hypertension,PH）的影响。方法：选择2016年至2019年于我院接受治疗的82例慢性阻塞性肺病患者,按照随机数字表法将其均分为两组（各41例）,对照组单纯接受布地奈德福莫特罗治疗,研究组在对照组基础上加用噻托溴铵吸入剂施治,对比两组治疗有效率,治疗前后的第1秒用力呼气容积（forced expiratory volume in one second,FEV₁）、用力肺活量（forced vital capacity,FVC）、第1秒用力呼气容积占预计值百分比（Percentage of FEV₁ in the predicted value,FEV₁%）、二氧化碳分压（carbon dioxide partial pressure,PaCO₂）、SaO₂、PH值、CRP。结果：（1）研究组治疗有效率明显高于对照组（P<0.05）;（2）治疗前两组FEV₁、FVC、FEV₁%对比无差异（P>0.05）,治疗后研究组上述指标均高于对照组（P<0.05）;（3）治疗前两组SaO₂、PaCO₂、PH值对比无差异（P>0.05）,治疗后研究组SaO₂、PH值均高于对照组,PaCO₂低于对照组（P<0.05）;（4）治疗前两组CRP水平无差异（P>0.05）,治疗后研究组上述因子水平均低于对照组（P<0.05）。结论：布地奈德福莫特罗联合噻托溴铵吸入剂对慢阻肺具有较好的治疗效果,能够显著改善患者肺功能及血气指标,同时还能够缓解患者炎性状态。     

A Prognostic Model to Predict Recovery of COVID-19 Patients Based on Longitudinal Laboratory Findings

Virologica Sinica - The temporal change patterns of laboratory data may provide insightful clues into the whole course of COVID-19. This study aimed to evaluate longitudinal change patterns of key...     

The protective effects of C16 peptide and angiopoietin-1 compound in lipopolysaccharide-induced acute respiratory distress syndrome

C16 peptide and angiopoietin-1 (Ang-1) have been found to have anti-inflammatory activity in various inflammation-related diseases. However, their combined role in acute respiratory distress syndrome (ARDS) has not been investigated yet. The objective of this study was to investigate the effects of C16 peptide and Ang-1 in combination with lipopolysaccharide (LPS)-induced inflammatory insult in vitro and in vivo. Human pulmonary microvascular endothelial cells and human pulmonary alveolar epithelial cells were used as cell culture systems, and an ARDS rodent model was used for in vivo studies. Our results demonstrated that C16 and Ang-1 in combination significantly suppressed inflammatory cell transmigration by 33% in comparison with the vehicle alone, and decreased the lung tissue wet-to-dry lung weight ratio to a maximum of 1.53, compared to 3.55 in the vehicle group in ARDS rats. Moreover, C  +  A treatment reduced the histology injury score to 60% of the vehicle control, enhanced arterial oxygen saturation (SO₂), decreased arterial carbon dioxide partial pressure (PCO₂), and increased oxygen partial pressure (PO₂) in ARDS rats, while also improving the survival rate from 47% (7/15) to 80% (12/15) and diminishing fibrosis, necrosis, and apoptosis in lung tissue. Furthermore, when C  +  A therapy was administered 4 h following LPS injection, the treatment showed significant alleviating effects on pulmonary inflammatory cell infiltration 24 h postinsult. In conclusion, our in vitro and in vivo studies show that C16 and Ang-1 exert protective effects against LPS-induced inflammatory insult. C16 and Ang-1 hold promise as a novel agent against LPS-induced ARDS. Further studies are needed to determine the potential for C16 and Ang-1 in combination in treating inflammatory lung diseases.     

Psoralen attenuates bleomycin‐induced pulmonary fibrosis in mice through inhibiting myofibroblast activation and collagen deposition

Idiopathic pulmonary fibrosis (IPF) is a progressive disease characterized by excessive deposition of extracellular matrix (ECM) and chronic inflammation with limited therapeutic options. Psoralen, a major active component extracted from Psoralea corylifolia L. seed, has several biological effects. However, the role of psoralen in IPF is still unclear. Here, we hypothesized that psoralen played an essential role in IPF in the inhibition of fibroblast proliferation and inflammatory response. A murine model of IPF was established by injecting bleomycin (BLM) intratracheally, and psoralen was administered for 14 days from the 7^th to 21^st day after BLM injection. Our results demonstrated that psoralen treatment reduced body weight loss and improved the survival rate of mice with IPF. Histological and immunofluorescent examination showed that psoralen alleviated BLM‐induced lung parenchymal inflammatory and fibrotic alteration. Furthermore, psoralen inhibited proliferation and collagen synthesis of mouse fibroblasts and partially reversed BLM‐induced expression of α‐smooth muscle actin at both the tissue and cell level. Moreover, psoralen decreased the expression of transforming growth factor‐β1, interleukin‐1β, and tumor necrosis factor‐α in the lungs of BLM‐stimulated mice. Our results reveale for the first time that psoralen exerts therapeutic effects against IPF in a BLM‐induced murine model.