BACKGROUND:Osteopontin (OPN), a multifunctional bioactive protein, has been shown to be elevated in the serum and bronchoalveolar lavage fluid (BALF) of. individuals with asthma and modulate the airway smooth muscle cells (ASMCs) proliferation and migration, yet its underlying molecular mechanisms are not completely understood. The aim of the present study is to address this issue. METHODS:Primary rat ASMCs were cultured to verify the effects of OPN and focal adhesion kinase (FAK)/Src/yes-associated protein (YAP) axis on cell proliferation and migration. Cell proliferation was assessed by BrdU incorporation assay. Cell migration was assessed by Transwell assay. Immunofluorescence and immunoblotting analysis confirmed that OPN activated FAK/Src/YAP axis. Moreover, we established an ovalbumin (OVA)-induced asthma rat model to verify whether OPN/FAK/Src/YAP cascade axis was involved in airway remodeling and asthma progression. RESULTS:OPN induced YAP dephosphorylation and nuclear localization via the αVβ3 integrin mediated activation of FAK/Src pathway, and this in turn increased thrombospondin 1 (THBS1) expression leading to ASMCs proliferation and migration. Intriguingly, THBS1 further activated FAK/Src to form a positive feedback loop. Pre-treatment of cells with anti-αvβ3 neutralizing antibody, FAK inhibitor PF573228 or Src inhibitor Dasatinib blocked OPN-induced alterations of YAP, THBS1 and functions of ASMCs. In addition, OPN promotes airway remodeling in asthma by activating FAK/Src/YAP axis. CONCLUSIONS:Our study indicates that OPN stimulates ASMCs proliferation and migration by binding to αVβ3 and activating FAK/Src/YAP axis, suggesting that targeting this pathway might have potential value in the management of airway remodeling of asthma.

Objectives: Tigger transposable element-derived 1 (TIGD1) expression and its underlying functions and regulatory mechanisms in lung adenocarcinoma (LUAD) remain unknown. Therefore, we intended to explore the expression, potential functions, and regulatory mechanisms of TIGD1 in LUAD. Materials and methods: TIGD1 expression in LUAD tissues was determined by immunohistochemistry analysis of a tissue microarray. Functional experiments were conducted to determine how TIGD1 affects LUAD tumorigenesis and metastasis. The molecular mechanisms by which TIGD1 induces LUAD progression were determined. Results: TIGD1 was upregulated in LUAD tissues and was related to lymph node metastases. TIGD1 knockdown suppressed LUAD cell proliferation, migration, and invasion, while promoted cell apoptosis. Furthermore, decreased metastatic nodules were observed in the TIGD1 knockdown mouse metastasis model. Moreover, microarray analysis was performed to determine the potential downstream genes of TIGD1 in LUAD. Hallmark pathway analysis revealed that the downstream genes of TIGD1 were involved in epithelial-mesenchymal transition (EMT). Western blotting confirmed that vimentin and TWIST was downregulated in TIGD1 knockdown cells, while E-cadherin was upregulated. Ingenuity pathway and hallmark pathway analyses revealed that TIGD1 regulated the interleukin-6 signaling pathway and related gene members. Western blotting, quantitative real-time polymerase chain reaction, enzyme-linked immunosorbent assay indicated that downregulation of TIGD1 decreased interleukin-6 and CXCL1 expression. TIGD1 expression was negatively correlated with immune infiltration in LUAD. The upstream microRNA of TIGD1 was predicted, and subsequent luciferase reporter gene experiments confirmed the interactions between miR-137 and TIGD1. The expression of miR-137 was significantly downregulated in LUAD tissues and miR-137 suppressed the proliferation, migration, and invasion of LUAD cells, partially through negatively regulating the expression of TIGD1. Conclusion: Our findings suggest that TIGD1, which was regulated by miR-137, contributed to LUAD progression by promoting cell proliferation, migration, invasion, and EMT and suppressing cell apoptosis.

Through combined bioinformatics analysis, the goal of untrrec research was to develop and confirm the immune-related prognostic signature in LUSC (lung squamous cell carcinoma). We constructed an optimized prognostic risk model consisting of five PIR-lncRNAs (AC107884.1, LCMT1-AS1, AL163051.1, AC005730.3 and LINC02635). To evaluate and verify the prognostic value of the model, we subsequently conducted independent prognostic and mortality analysis on the prognostic risk model. Additionally, we conducted a distinct study of immune cell infiltration in the model among high- and low individuals. By using co-expression network analysis, we were able to identify 654 immune-related lncRNAs (IR-lncRNAs) and 18 prognostic IR-lncRNAs (PIR-lncRNAs) and derive 546 differently expressed genes and 21 immune-related genes. We proved that the impact of immunotherapy in individuals in the high-risk category may be lessened through the study of immune escape and immunotherapy. Our findings elucidate the intrinsic molecular biological link between the pathogenic genes of LUSC and immune cells, which has important exploration and reference significance for the precise and potential immunotherapy of LUSC patients, especially for high-risk patients.

Leucine-rich repeat kinase 2 (LRRK2) plays an important role in a variety of inflammatory diseases, as well as peripheral and central immune responses. At present, there are few reports about the role of LRRK2 in lung cancer, and need to be further explored. The main purpose of this study is to explore the role and mechanism of LRRK2 in lung cancer. The results revealed that the expression of LRRK2 was increased in the tissues of lung cancer patient and lung cancer cells. Further studies found that interference with LRRK2 expression significantly induced the apoptosis, and promoted the expression of caspase-3, caspase-9, and Bax. More importantly, si-LRRK2 inhibited the expression of VEGF and P-gp, indicating inhibition of cell proliferation and drug resistance. What's more, LRRK2 regulated TLR4/NF-κB signaling pathways and NLRP3 inflammasome, and TLR4/NF-κB pathways was involved in the molecular mechanism of LRRK2 on lung cancer cells. In conclusion, this study suggested that the mechanism of si-LRRK2 inhibiting the progression of lung cancer is to regulate the TLR4/NF-κB signaling pathways and NLRP3 inflammasome.

目的 探讨和厚朴酚对慢性哮喘模型大鼠气道炎症和气道重塑的影响及其可能机制.方法 24 只雄性SD大鼠随机分为4 组(每组各6 只):对照组、卵清蛋白(ovalbumin,OVA)模型组、和厚朴酚组以及地塞米松组.OVA模型组第 1,7,14天腹腔注射新鲜配制OVA混悬液致敏,第21 天起接受 1%OVA溶液雾化吸入30 min/次,隔日 1 次,共雾化8 周.对照组PBS代替OVA腹腔注射及雾化吸入;和厚朴酚组和地塞米松组每次OVA雾化前 1h分别腹腔注射和厚朴酚溶液(5 mg/kg)和地塞米松(0.5 mg/kg).末次激发后 24h处死大鼠,观察各组大鼠肺组织病理变化;收集支气管肺泡灌洗液(bronchoalveolar lavage fluid,BALF)进行炎性细胞计数及分类;ELISA法检测血清及BALF中IL-4、IL-6、IL-17 含量;免疫印迹法检测肺组织Yes相关蛋白(Yes-associated protein,YAP)水平变化.结果 与对照组相比,OVA模型组支气管管壁、平滑肌层增厚,气道及血管周围大量炎性细胞浸润;BALF炎性细胞总数、嗜酸性粒细胞及中性粒细胞数显著增加(P＜0.01),BALF中IL-4、IL-6、IL-17 水平显著增高(P＜0.01),大鼠肺组织内YAP表达增多(P＜0.01).与OVA模型组相比,和厚朴酚组及地塞米松组大鼠肺组织病理改变明显减轻,BAFL中炎性细胞总数、嗜酸性粒细胞及中性粒细胞数显著减少(P＜0.01),IL-4、IL-6、IL-17 水平降低(P＜0.01),而和厚朴酚组与地塞米松组间上述改变相似;与OVA模型组相比,和厚朴酚组大鼠肺组织内YAP表达减少(P＜0.01).结论 和厚朴酚可以抑制慢性哮喘模型大鼠气道炎症和气道重塑,推测其作用机制可能与和厚朴酚下调YAP表达有关.

The aims of the present study were to examine the signaling mechanisms for transforming growth factor-β1 (TGF-β1)-induced rat airway smooth muscle cells (ASMCs) proliferation and migration and to determine the effect of lipoxin A4 (LXA4) on TGF-β1-induced rat ASMCs proliferation and migration and its underlying mechanisms. TGF-β1 upregulated transcriptional coactivator Yes-associated protein (YAP) expression by activating Smad2/3 and then upregulated cyclin D1, leading to rat ASMCs proliferation and migration. This effect was reversed after treatment with the TGF-β1 receptor inhibitor SB431542. YAP is a critical mediator of TGF-β1-induced ASMCs proliferation and migration. Knockdown of YAP disrupted the pro-airway remodeling function of TGF-β1. Preincubation of rat ASMCs with LXA4 blocked TGF-β1-induced activation of Smad2/3 and changed its downstream targets, YAP and cyclin D1, resulting in the inhibition of rat ASMCs proliferation and migration. Our study suggests that LXA4 suppresses Smad/YAP signaling to inhibit rat ASMCs proliferation and migration and therefore has potential value in the prevention and treatment of asthma by negatively modulating airway remodeling.

目的 探讨肺腺癌(lung adenocarcinoma,LUAD)组织中微小染色体维持蛋白 4(minichromosome mainte-nance proteins 4,MCM4)的表达及其与预后、免疫微环境的相关性.方法 选取 2021 年 1～7 月陕西省人民医院收治的LUAD患者 4 例,应用转录组测序检测LUAD患者癌组织和癌旁组织MCM4 表达水平.癌症基因组图谱肺腺癌(the cancer genome atla-LUAD,TCGA-LUAD)数据用于验证LUAD中 MCM4 表达并探究其与生存期的相关性.采用LinkedOmics分析LUAD中MCM4 共表达基因、功能富集及调控因子靶向富集情况.STRING用于构建蛋白质-蛋白质互作网络.采用TIMER分析MCM4与LUAD肿瘤免疫微环境的相关性.COX回归分析LUAD患者预后的影响因素.结果 与癌旁组织比较,LUAD癌组织中MCM4表达水平(6.50±0.86 vs 4.22±0.66)升高,差异有统计学意义(U=16,P=0.029).TCGA-LUAD发现相似结果(癌组织 3.63±0.92 vs癌旁组织 1.90±0.28),差异有统计学意义(U = 30355,P＜0.001).生存分析显示,MCM4 高表达LUAD患者总生存期和无病生存期200个月的累积生存率(8.79%和 19.25%)均低于MCM4 低表达患者(28.87%和 36.82%),差异有统计学意义(风险比=1.7,1.4,均P＜0.05).共表达分析显示,LUAD中与MCM4正相关的基因主要参与P53信号通路、DNA复制、错配修复等通路.肿瘤免疫微环境分析显示,MCM4与中性粒细胞浸润呈正相关(partial.cor=0.14,P=0.002),与B细胞浸润呈负相关(partial.cor =-0.152,P＜0.001).COX回归分析显示,MCM4是影响LUAD患者预后的独立因子.结论 LUAD癌组织中MCM4表达升高,与预后及免疫微环境显著相关,可作为LUAD患者不良预后评估的分子标志物.

ObjectiveEarly life bronchiolitis has been hypothesised to be associated with the subsequent risk of persistent wheezing or asthma. However, the link remains controversial. The objective of our study was to evaluate the association between bronchiolitis before 2 years of age and the late-onset wheezing/asthma.DesignSystematic review and meta-analysis.MethodsPubMed, Embase and Web of Science databases were systematically searched for studies published between 1955 and January 2020. Meanwhile, we also checked through the reference lists of relevant articles to see whether these references included reports of other studies that might be eligible for the review. Cohort and case–control studies assessing the association between early-life bronchiolitis and late-onset wheezing/asthma were included in this meta-analysis. Data were extracted by two independent reviewers. Results were pooled using a random-effects model or fixed-effects model according to the heterogeneity among studies.Results32 original articles with 292 844 participants, which met the criteria, were included in this meta-analysis. Bronchiolitis before 2 years of age was associated with an increased risk of subsequent wheezing/asthma (relative risk=2.46, 95% CI 2.14 to 2.82, p<0.001). After categorising studies into different groups based on age at the end of follow-up, geographical region and study quality, the association still remained significant.ConclusionsThe meta-analysis indicates an association between bronchiolitis before 2 years of age and the wheezing/asthma in later life. Well-designed and highly standardised prospective studies that better address bias due to potential confounding factors are needed to validate the risk identified in our meta-analysis.PROSPERO registration numberCRD42018089453.

Lung cancer is the leading cause of cancer-related mortality worldwide and cigarette smoking is reported to contribute to the lung cancer-related mortality. The present study aimed to investigate the molecular mechanism underlying nicotine-induced chemoresistance in lung cancer. The expression of microRNA (miR)-21-3p and its predicted target FOXO3a in lung cancer cells was detected via reverse transcription-quantitative PCR, in the presence or absence of nicotine. The regulatory effect of miR-21-3p and FOXO3a on lung cancer cell proliferation and apoptosis induced by docetaxel or cisplatin treatment was evaluated by performing Cell Counting Kit-8 and Annexin V/PI staining assays, respectively. The interaction between miR-21-3p and FOXO3a was analyzed by performing luciferase reporter assays and western blotting. FOXO3a overexpression rescue experiments were conducted in vitro and in vivo using a xenograft mouse model to assess the function of miR-21-3p/FOXO3a in lung cancer. Nicotine induced miR-21-3p expression in lung cancer cells in a dose-dependent manner. miR-21-3p downregulated FOXO3a expression by directly binding to the 3'-untranslated region of FOXO3a. Moreover, miR-21-3p knockdown sensitized lung cancer cells to docetaxel or cisplatin treatment. Mechanistically, FOXO3a was predicted as a direct target of miR-21-3p. FOXO3a overexpression promoted the chemosensitivity of lung cancer cells to docetaxel or cisplatin treatment. Furthermore, FOXO3a overexpression antagonized the regulatory function of miR-21-3p on docetaxel- or cisplatin-treated lung cancer cells. In the docetaxel- or cisplatin-treated lung cancer xenograft mouse model, miR-21-3p promoted chemoresistance via negatively regulating FOXO3a. Therefore, the present study demonstrated that nicotine-induced miR-21-3p promoted chemoresistance to docetaxel or cisplatin treatment via negatively regulating FOXO3a, which may serve as a novel therapeutic strategy for the treatment of patients with chemoresistant lung cancer.

肺脏具有丰富的结缔组织和微血管循环,故易受到高血糖的影响.目前,肺功能降低与糖尿病的关系尚未完全明确.笔者分析国内外相关文献发现,糖尿病致肺损伤的可能病理生理机制包括胰岛素抵抗、低级别炎症、微血管病变、累及呼吸肌的神经病变及蛋白质非酶糖基化;此外,除胰岛素之外的大多数降糖药被证实可以通过减轻炎症、降低气道高反应性、促进癌细胞凋亡等机制而对肺疾病产生积极影响,而胰岛素可能对肺疾病产生消极影响,这对糖尿病合并肺疾病患者的治疗具有一定参考价值.

Background: About 50% of patients with initially diagnosed lung cancer have developed distant metastasis. The probability of occurrence of digestive tract metastases found by autopsy is rarely. This report presents a rare clinical case of small intestinal metastasis from primary squamous cell carcinoma of the lung. Case presentation: An 82-year-old male with aggravated cough and more acute shortness of breath than usual was diagnosed with primary squamous cell carcinoma of the lung Stage IV,because of the advanced age, underlying diseases, and poor cardiopulmonary function,the family refused the chemoradiotherapy. One month later, the patient gradually developed right lower quadrant pain. An upright abdominal X-ray suggested small intestinal obstruction and partial resection and anastomosis of the small intestine were performed. Postoperative pathology revealed poorly differentiated squamous-cell carcinoma of the small intestine. The patient died of sudden cardio-respiratory arrest one month later. Conclusions:We conclude that the real incidence of digestive tract metastases from lung cancer may be higher than the reported because of the symptoms of those patients are not obvious. Clinicians should select the appropriate examination methods (such as positron emission tomography) and pay attention to the assessment of abdominal hollow organs

Abstract Aim: The purpose of the present study was to explore the function and mechanism of tensin 1 (TNS1) in non-small cell lung cancer (NSCLC) progression. Methods: The expression of TNS1 in NSCLC cells and tissues was assessed by RT-PCR and Western blot. Besides, Kaplan–Meier survival analysis was recruited to explore the association between TNS1 and NSCLC. Cell growth was analyzed by MTT and flow cytometry assay, while cell metastasis was determined by wound healing and transwell assays. The targeting relationship between TNS1 and miR-152 was assessed by luciferase activity assays. And Western blot was employed to determine the expression of related proteins of Akt/mTOR/RhoA pathway. Results: TNS1 level was boosted in NSCLC cells and tissues, related to the prognosis of NSCLC patients. Furthermore, it was proved that TNS1 promoted the growth and metastasis of NSCLC cells via Akt/mTOR/RhoA pathway. And miR-152 targeted TNS1 to affect the progression of NSCLC. Conclusion: miR-152/TNS1 axis inhibits the progression of NSCLC by Akt/mTOR/RhoA pathway.

新型冠状病毒肺炎(COVID-19)已引起全球关注,通过采取一系列防控及医疗救治措施,国内疫情已经得到显著的遏制,境外输入的发病人数不断上升,疫情仍严峻.目前研究发现COVID-19的发病机制可能与病毒直接侵害肺组织、细胞免疫功能下降、炎症风暴、细胞凋亡级联反应有关.现就COVID-19可能的发病机制以及治疗研究进展进行综述,以期为其治疗提供更多的理论依据.

目的 探究microRNA-223(miR-223)对甲型流感病毒(IAV)诱导的肺上皮细胞(human bronchial epithelial cells,BEAS-2B)炎症反应、氧化应激和凋亡的作用机制.方法 RT-qPCR检测流感患者和正常受试者血清中miR-223和NOD样受体蛋白3(NLRP3)mRNA的表达量,并检测不同时间的IAV处理对miR-223和NLRP3表达量的影响;CCK-8实验检测肺上皮细胞BEAS-2B的细胞活力;Annexin V-FITC/PI凋亡检测试剂盒检测BEAS-2B细胞的凋亡水平;Western blot 实验检测凋亡相关蛋白 Caspase-3、Caspase-9、Bax和Bcl-2的表达水平;活性氧(ROS)指示剂DCFH-DA检测ROS的水平.结果 miR-223在流感患者血清中的表达量低于正常受试者;IAV抑制miR-223并促进NLRP3 mRNA的表达,且具有时间依赖性(P＜0.05);过表达miR-223可有效降低IAV诱导的BEAS-2B的细胞凋亡率和炎症因子的水平(P＜0.05);此外,过表达miR-223还可以缓解IAV诱导的BEAS-2B的氧化应激(P＜0.05);进一步的实验提示,miR-223抑制TLR4和p65的表达,并抑制NLRP3炎症小体的表达(P＜0.05).结论 miR-223能够缓解IAV诱导的肺上皮细胞的氧化应激和凋亡,减轻细胞损伤,其作用机制是通过抑制TLR4/NF-κB信号通路并抑制NLRP3炎症小体的活化来实现的.

慢性阻塞性肺疾病(COPD)被认为是以中性粒细胞为主的气道炎症,但近年的研究发现部分COPD患者存在嗜酸性粒细胞增多的现象,这类患者具有其特殊的临床特征,即具有部分支气管哮喘样症状,这提示了嗜酸性粒细胞参与了部分COPD患者的发病环节.大量研究发现,嗜酸性粒细胞可作为生物标志物预测COPD急性加重并指导临床治疗.鉴于嗜酸性粒细胞在COPD气道炎症中发病的重要性,现对嗜酸性粒细胞的特点与调控因素、嗜酸性表型COPD的发生机制及嗜酸性粒细胞作为生物标志物在COPD中的应用价值、存在问题及靶向治疗的研究进展做一综述.

目的 探讨异甘草素对LPS诱导小鼠急性肺损伤的保护作用及其可能机制.方法 6-8周的BALB/c雄性小鼠18只随机分成:对照组(Con组)、LPS组和异甘草素组(ISL+LPS组).Con组小鼠气管内滴注无菌PBS 60μl作用24 h;LPS组小鼠气管内滴注1 mg/ml LPS 60μl,作用24 h;ISL+LPS组小鼠在LPS给药前1 h给予5％DMSO溶解异甘草素(200 mg/kg)腹腔注射,再气管内滴注1 mg/ml LPS 60μl造模24 h.观察各组小鼠肺组织病理学变化,肺泡灌洗液中炎症细胞总数及中性粒细胞计数,ELISA法检测肺泡灌洗液中TNF-α的浓度,测定肺组织内髓过氧化物酶(MPO)活性、丙二醛(MDA)含量和超氧化物歧化酶(SOD)活力.Western blotting方法检测Nrf2的细胞核易位变化.结果 与对照组相比,LPS组病理学显示大量的炎性细胞浸润,肺组织结构明显被破坏.与对照组相比,LPS组支气管肺泡灌洗液中细胞总数、中性粒细胞数明显增加(P<0.01),TNF-α的浓度显著升高(P<0.01),肺组织匀浆MPO活性显著升高(P<0.01),SOD活力显著下降(P<0.01),两组间细胞核内的Nrf2蛋白水平差异没有统计学意义(P>0.05).与LPS组比较,异甘草素干预组小鼠肺组织结构破坏明显减轻,支气管肺泡灌洗液中炎症细胞显著减少(P<0.01),TNF-α的浓度显著下降(P<0.01),肺组织内MPO活性显著下降(P<0.01),SOD活力有所升高(P<0.05),而肺组织内核蛋白Nrf2水平显著增加(P<0.01),为LPS组的1.37倍.结论 异甘草素对LPS诱导小鼠急性肺损伤具有一定的保护作用,这种保护作用可能与激活并增加Nrf2核易位有关.

AIMS:Influenza A virus (IAV) infection accelerates the inflammatory injury of lung epithelial cells that contributes to pulmonary lesion. Recently, stromal interaction molecule 1 (STIM1) was found to mediate cellular immune response and participated in lung tumorigenesis. Our study aimed to illustrate the function and mechanism of STIM1 in IAV-induced inflammation injury and oxidative stress of lung epithelial cells.MAIN METHODS:We evaluated the levels of STIM1 in IAV-infected patients' serum and BEAS-2B cells using RT-qPCR, Elisa and western blotting methods. MTT and Elisa were performed to measure cell viability and cytokine contents. Besides, ROS intensity, SOD contents and cell apoptosis were detected based on DCFH-DA probe, colorimetry and cell death kits. A luciferase assay and Pearson's correlation analysis evaluated the associations between target genes.KEY FINDINGS:STIM1 was dramatically up-regulated in IAV-infected patients' serum and BEAS-2B cells. Silencing STIM1 in vitro inhibited oxidative stress and inflammatory responses induced by IAV, and reversed cell viability and suppressed apoptosis. Moreover, miR-223 and NLRP3 were negatively and positively correlated with STIM1. STIM1 was found to regulate NLRP3 expression by binding the AACUGAC motif in miR-223. STIM1/miR-223/NLRP3 axis modulated IAV-induced inflammation injury of lung epithelial cells.SIGNIFICANCE:Our evidence indicated that silencing STIM1 alleviated IAV-induced inflammation injury of lung epithelial cells by inactivating NLRP3 and inflammasome via promoting miR-223 expression. These findings may contribute to understand the mechanism of IAV-induced lung injury and help for therapy of IAV infection.

高流量湿化氧疗(HFNC)是一种新型的供氧装置,能够以最大流量60 L/min输送100％的加湿、加热氧气,与传统的氧气输送装置相比其存在诸多优势.越来越多的证据表明HFNC是成人早期呼吸衰竭的有效治疗方法.但也有研究指出,不适当使用HFNC可能会延迟气管插管并增加病死率,还有报道HFNC造成严重漏气事件,尽管缺乏一套指导HFNC使用的指南,但将其应用于不同疾病及临床环境已成为惯例.本文从HFNC的生理效应及其在临床中的一系列应用等方面进行综述,为HFNC的临床应用提供依据和参考.

Objective To investigate the prognostic value of microRNA-210 (miR-210) in patients with non-small cell lung cancer (NSCLC).Methods In this study,the expression of miR-210 in fresh tissue samples from NSCLC patients undergoing surgery in our hospital from January 2011 to March 2012 was detected by reverse transcriptase polymerase chain reaction (RT PCR).The relationship between miR-210 expression and clinical factors in the whole group of patients,lung adenocarcinoma and squamous cell carcinoma.Analysis of miR-210 expression differences and relationship between diseases-free and overall survival in all patients and those of lung adenocarcinoma.Results In NSCLC,patients with lower miR-210 expression had lower disease-free survival (x2 =8.119,P ＜ 0.01) and lower overall survival (x 2 =7.914,P ＜ 0.01) than patients with low miR-210 expression.In the miR-210 high expression group,the disease-free survival rate was lower in the low-expression group than in the miR-210 group (P ＜0.01),and the overall survival rate was shorter (P ＜0.01);miR-210 expression and pathological stage,lymph node metastasis and disease relapse (RR =2.181,P ＜0.01) were significantly related.Cox multivariate analysis showed that miR-210 expression was an independent prognostic factor for overall survival (RR =1.978,P ＜ 0.05).Conclusions High expression of miR-210 is significantly associated with the prognostic of NSCLC patients,especially those with adenocarcinoma.MiR-210 may be a biomarker for prognosis of lung adenocarcinoma patients.

Objective To investigate the changes of serum cytokines,coagulation parameters,serum cholinesterase (SchE) levels and their significance in patients with severe pulmonary infection.Methods To detect the changes and significance of serum inflammatory factors,coagulation function indexs and SchE levels in patients with severe pulmonary infection.Results The levels of serum IL-6,IL-8,IL-10,TNF-a,and SchE in the severe group were significantly higher than those in the normal group (P ＜0.05);The serum SchE level in the severe group was lower than in normal group.The difference was statistically significant (P ＜0.05),and the activated partial thrombin time (APTT),prothrombin time (PT),thrombin time (TT),D-Ⅱ Polymers (DD),and fibrinogen (Fib) levels were significantly higher in the severe group than in the normal group (P ＜0.05).The R value and K value of the patients were significantly higher than that of the normal group (P ＜0.05).The maximum amplitide value and the α angle of the severe group were significantly lower than the normal group,and the difference showed significant (P ＜ 0.05).Conclusions The inflammatory response is further enhanced in patients with severe pulmonary infection,coagulation disorders,serum SchE activity decreased.