Background LncRNAs are key regulators in cancer. The current study explored the role of lncRNA LINC00261 (LINC00261) in lung cancer (LC). Methods Expression of LINC00261 in LC tissues and cells was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Pearson's Chi square test and Kaplan-Meier analysis were performed to evaluate the correlations between LINC00261 expression and clinical characteristics, and overall survival time. A549 and SPC-A1 cells were transfected with LINC00261 overexpression plasmid, cell viability, cell number, and apoptosis were detected by CCK-8 assay, colony formation, and flow cytometry. Moreover, wound-healing and transwell assay were performed to detect cell metastasis and invasion. Expressions of proteins related to cell proliferation and metastasis were determined by Western blot. Xenograft was constructed, and tumor size and weight were measured and the effects of LINC00261 overexpression on tumor growth were detected. Bioinformatics analysis, dual-luciferase reporter assay, qRT-PCR, correlation analysis, and functional rescue experiments were conducted on clinical cases and LC cells to explore the molecular mechanism of LINC00261 in LC. Results In LC, LINC00261 expression was down-regulated, and was associated with more advanced TNM stage, metastasis and a shorter survival time. LINC00261 overexpression inhibited the growth and metastasis of LC cells in vitro and tumor growth in vivo. Furthermore, miR-1269a directly interacted with LINC00261 and FOXO1. The expressions of miR-1269a and FOXO1 were dysregulated by LINC00261 in LC. Additionally, miR-1269a promoted the progression of LC through targeting FOXO1. Conclusions Down-regulation of LINC00261 expression has a prognostic value in LC, and overexpression LINC00261 inhibits LC progression via targeting miR-1269a/FOXO1 axis.

目的 研究缺氧诱导因子-1α(HIF-1α)低表达对肺癌A549细胞增殖、侵袭能力的影响,并探讨相关机制.方法 取A549细胞进行缺氧培养,用于模拟肿瘤内部低氧微环境,设置为缺氧处理组,取正常培养的A549细胞设为正常组,比较两组HIF-1α表达.取对数期A549细胞,进行HIF-1α-siRNA、HIF-1α-pLentiGFP、对照质粒pLentiGFP转染,分别设为低表达组、高表达组、对照组,取不作处理的细胞设为空白组,比较四组HIF-1α表达、增殖能力、侵袭能力、趋化因子受体(CXCR4)及上皮型钙黏附蛋白(E-cadherin)表达.结果 缺氧处理组HIF-1αmRNA、蛋白相对表达量高于正常组(P<0.05);对照组、低表达组、高表达组转染效率均>75％;与空白组、对照组比较,低表达组HIF-1αmRNA、蛋白相对表达量降低,24、48、72 h MTT实验A值降低,穿膜细胞数/视野减少,CXCR4蛋白相对表达量降低,E-cadherin蛋白相对表达量升高(P<0.05),高表达组HIF-1αmRNA、蛋白相对表达量升高,24、48、72 h MTT实验A值升高,穿膜细胞数/视野增加,CXCR4蛋白相对表达量升高,E-cad-herin蛋白相对表达量降低,差异均有统计学意义(P<0.05).结论 HIF-1α 低表达对肺癌肺癌A549细胞增殖及侵袭能力具有抑制作用,可能通过下调CXCR4,上调E-cadherin蛋白表达实现.

目的 研究黄芪多糖(APS)对支气管哮喘模型小鼠气道上皮中胸腺间质淋巴细胞生成素(thymic stromal lymphopoietin,TSLP)和树突状细胞(dendritic cell,DCs)表达的影响.方法 饲养雌性BALB/c小鼠30只,随机将其分为对照组、哮喘模型组和黄芪多糖组,各组采取相应的干预措施.通过支气管哮喘激发试验、肺组织病理学和酶联免疫吸附试验(ELISA)评价哮喘模型造模是否成功;肺组织中TSLP mRNA的相对表达水平采用实时荧光定量PCR(qRT-PCR)检测;蛋白免疫印迹实验(Western blot)检测肺组织中TSLP蛋白的表达;流式细胞术检测支气管肺泡灌洗液(bronchoalveolar lavage fluid,BALF)中DCs表面CD40、CD80和CD86的表达水平.结果 哮喘模型组小鼠气道反应性增高和肺组织HE染色结果均为哮喘的典型表现且哮喘模型组BALF中IL-13、IL-5和IL-4的表达水平显著高于黄芪多糖组和对照组(P＜0.001);黄芪多糖组和对照组小鼠肺组织中TSLP mRNA的表达水平与哮喘模型组相比较低(P＜0.001),TSLP mRNA的表达水平在黄芪多糖组与对照组之间差异无统计学意义(P＞0.05);黄芪多糖组与对照组小鼠肺组织中TSLP蛋白的表达与哮喘模型组相比较弱;黄芪多糖组与对照组BALF中DCs表面CD54、CD80、CD86的表达明显低于哮喘模型组(P＜0.001),黄芪多糖组与对照组之间差异无统计学意义(P＞0.05).结论 黄芪多糖可明显抑制哮喘模型小鼠气道上皮细胞TSLP水平和DCs表面CD54、CD80、CD86的表达,并减轻气道炎症反应.

目的 探讨银杏叶提取物(GBE)治疗慢性阻塞性肺疾病急性加重期(AECOPD)的效果.方法 选取2017年1月至2018年12月于河南省胸科医院接受治疗的98例AECOPD患者为受试对象,根据随机数字表法分为观察组与对照组,每组49例.对照组予以常规对症治疗,观察组在其基础上服用GBE进行治疗.比较两组患者治疗前及治疗2周后炎性因子、血气分析指标及血管内皮功能指标变化.结果 治疗2周后,两组患者血清白细胞介素-8(IL-8)、血清肿瘤坏死因子-α(TNF-α)水平较治疗前均有显著下降(P均<0.05),且观察组明显低于对照组(P<0.05).治疗2周后,两组患者动脉血氧分压(PaO 2)、动脉血氧饱和度(SaO 2)均较治疗前显著提升(P均<0.05),且观察组明显高于同期对照组(P<0.05);而动脉血二氧化碳分压(PaCO 2)均较治疗前显著下降(P<0.05),且观察组明显低于同期对照组(P<0.05).治疗2周后,两组患者血清一氧化氮(NO)、血栓调节蛋白(TM)均较治疗前显著提升(P均<0.05),且观察组明显高于同期对照组(P<0.05);而血管假血友病因子(vWF)均较治疗前显著下降(P<0.05),且观察组明显低于同期对照组(P<0.05).结论 GBE可明显改善AECOPD症状,提升患者血管内皮细胞,调节血气分析指标,且能显著降低炎性因子水平.

目的 评估NLR、CD64及CRP对医院获得性肺炎(HAP)的诊断及预后的价值.方法 随机收集2018年5月-2019年12月在河南省胸科医院呼吸科门诊体检的健康志愿者41例为健康对照组,普通呼吸科病房确诊为医院获得性肺炎患者39例为普通组,随机收集入住ICU确诊为HAP患者40例为重症组.根据出院时结局分为死亡组及生存组.比较各组NLR、CID64、CRP与SOFA评分的差异及相关性.结果 普通组与重症组合并后,NLR、CD64与CRP的曲线下面积(AUC)分别为0.838、0.881、0.804,最佳诊断临界值分别为10.37、8.97％、10.21 mg/L,特异性分别为89.31％、90.34％、85.91％,敏感性分别为55.91％、66.39％、48.21％;重症组的NLR、CD64、CRP、SOFA评分明显高于普通组(P＜0.05),重症组的NLR、CD64、CRP明显高于对照组(P＜0.05),普通组的NLR、CD64、CRP明显高于对照组(P＜0.05).死亡组的NLR、CD64、CRP、SOFA评分明显高于生存组(P＜0.01).NLR、CID64、CRP与SOFA评分均为正相关,相关系数分别为0.81、0.86、0.62(P＜0.01).结论 NLR、CD64、CRP有助于对医院获得性肺炎的诊断和预后的评估,且NLR、CD64的作用要大于CRP.

目的 探讨抑制环氧合酶-2(COX-2)基因表达对TGF-β1诱导的人胚肺成纤维细胞系MRC-5活力、胶原合成和转化及Notch信号通路的影响.方法 将MRC-5细胞分为对照组、TGF-β1组、NC组和COX-2-siRNA组,各组细胞处理48 h,Western blotting检测COX-2、胶原合成相关的COL-Ⅰ和COL-Ⅲ、EMT标志物α-SMA及Notch信号通路受体Notch1及配体Jagged1的蛋白表达;CCK8法检测各组细胞活力.结果 TGF-β1组COX-2的表达显著高于对照组,COX-2-siRNA组COX-2的表达显著低于TGF-β1组(P<0.05),NC组COX-2的表达与TGF-β1组差异无统计学意义(P>0.05);与对照组比较,TGF-β1组细胞活力及COL-Ⅰ、COL-Ⅲ、α-SMA、Notch1和Jagged1的蛋白表达均显著升高(P<0.05),与TGF-β1组比较,COX-2-siRNA组细胞活力及COL-Ⅰ、COL-Ⅲ、α-SMA、Notch1和Jagged1的蛋白表达均显著降低(P<0.05).结论 抑制COX-2基因表达中可能通过降低MRC-5细胞活力、抑制细胞胶原合成和转化,并下调Notch信号通路,从而对肺纤维化起保护作用.

目的 探讨肺癌患者血清转化生长因子(TGF)-β、白细胞介素(IL)-6水平及肺功能的影响.方法 该院收治的肺癌患者170例,根据是否吸烟分为吸烟组和对照组,每组85例,应用酶联免疫吸附法检测两组患者血清TGF-β和IL-6水平,并比较两组肺活量(FVC)、第1秒用力呼气容积(FEV1)、最大呼气中期流量(MMEF)以及用力呼气50%肺活量(FEF50%).结果 吸烟组患者血清TGF-β水平显著高于对照组(P<0.05),而两组IL-6水平比较无统计学意义(P>0.05);吸烟组FVC、FEV1、MMEF以及FEF50%均显著低于对照组(P<0.05).结论 吸烟的肺癌患者血清TGF-β水平明显高于非吸烟患者,且患者的肺功能明显降低,但其对患者血清IL-6水平则无明显影响.

目的 探讨尿激酶治疗结核性包裹性胸腔积液的效果.方法 选取2014年7月至2016年4月河南省胸科医院治疗的78例结核性包裹性胸腔积液患者,按治疗方法分为观察组和治疗组,观察两组患者临床症状缓解情况、胸水吸收情况、胸膜增厚情况及肺功能情况.结果 治疗组患者胸水吸收时间较对照组短,胸膜厚度较对照组小,FEV1%及FVC%均大于对照组,总有效率较对照组高.结论 尿激酶治疗结核性包裹性胸膜炎效果较好,值得临床推广.

OBJECTIVE To investigate the pathogen distribution and bacterial sensitivity test results in patients with advanced lung cancer ,so as to provide the basis for clinical treatment .METHODS A total of 174 cases of pulmo‐nary infection in patients with advanced lung cancer clinical data admitted to hospital from Mar .2014 to May 2015 were collected .All patients were collected for bacterial cultures of sputum specimens to analyze in patients the pathogen type distribution and drug susceptibility results .SPSS 11 .0 was used for data analysis .RESULTS A to‐tal of 237 strains of pathogens were cultured ,including mainly 144 strains of gram‐negative bacteria ,accounting for 60 .76% ,51 strains of fungi ,accounting for 21 .52% ,and 42 strains of gram‐positive bacteria ,accounting for 17 .72% .Susceptibility results showed K lebsiella pneumoniae ,Acinetobacter baumannii ,Pseudomonas aerugino‐sa to imipenem lower than 10 .00% .Staphylococcus aureus to levofloxacin ,gentamicin and sulfamethoxazole/tri‐methoprim had resistance rate of 25 .00% .CONCLUSION There are wide variety of pathogens caused lung infec‐tion in patiens with advanced lung cancer .The clinical use of antibiotics should be reasonable based on susceptibili‐ty results .