MicroRNA-885-3p alleviates bronchial epithelial cell injury induced by lipopolysaccharide via toll-like receptor 4.

Airway inflammation is one of the typical pathological characteristics of asthma. MicroRNAs (miRNAs) play important roles in regulating inflammation. Nevertheless, miRNA-885-3p (miR-885-3p)'s role in asthmatic inflammation and the underlying mechanism need to be explained. In this work, miR-885-3p expression and toll-like receptor 4 (TLR4) expression in asthma patients' plasma and lipopolysaccharide (LPS)-treated 16HBE cells were detected through quantitative real-time PCR. The interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels in 16HBE cell supernatant were examined via enzyme-linked immunosorbent assay. Cell counting kit-8 (CCK-8) assay and flow cytometry were employed to examine 16HBE cell viability and apoptosis, respectively. Western blotting was performed to examine the expression of TLR4, cleaved caspase-3, B-cell lymphoma-2 (Bcl-2), nuclear factor-kappa B (NF-κB) p65, Bcl-2-related X protein (Bax), phosphorylated (p)-NF-κB p65 and myeloid differentiation primitive-response protein 88 (MyD88) in 16HBE cells. Furthermore, the targeted relationship between TLR4 and miR-885-3p in 16HBE cells was determined through dual-luciferase reporter gene assay. Compared with healthy volunteers, miR-885-3p expression in acute asthma patients' plasma was significantly downregulated. In 16HBE cells, the stimulation of LPS reduced miR-885-3p expression. MiR-885-3p overexpression reduced LPS-stimulated 16HBE cell injury by enhancing cell viability, and suppressing the levels of inflammatory factors and apoptosis. Furthermore, TLR4 was identified as miR-885-3p's target gene. TLR4 overexpression weakened the impacts of miR-885-3p on LPS-stimulated cell injury and NF-κB-MyD88 signaling. In conclusion, miR-885-3p can reduce LPS-induced 16HBE cell damage, via targeting TLR4 to suppress the NF-κB-MyD88 pathway.

Expression and clinical significance of AURKB gene in lung adenocarcinoma: Analysis based on the data-mining of bioinformatic database.

ABSTRACT: This study aimed to investigate the expression and clinical significance of aurora B kinase (AURKB) gene in lung adenocarcinoma (LUAD) by collecting relevant data in Oncomine database.Firstly, mRNA expression level of AURKB in LUAD was systematically analyzed using the ONCOMINE and the cancer genome atlas databases. Then, the association between AURKB expression and clinical parameters was investigated by UALCAN. The Kaplan-Meier Plotter was used to assess the prognostic significance of AURKB.Pooled analysis showed that AURKB was frequently up-regulated expression in LUAD. In addition, immunohistochemistry showed that AURKB was highly expressed in lung adenocarcinoma tissues, while it was weakly expressed in normal tissues. Subsequently, AURKB expression was identified to be negatively associated with Overall survival (P < 1e-16), post-progression survival (P = .017), first progression (P = 9.8e-09).This study confirms that increased expression of AURKB in LUAD is associated with poor prognosis, suggesting that AURKB might be used as a promising prognostic biomarker and novel therapeutic target for LUAD.

Implantation of 125I radioactive seeds via c-TBNA combined with chemotherapy in an advanced non-small-cell lung carcinoma patient.

BACKGROUND: The critical management of advanced non-small-cell lung carcinoma (NSCLC), especially when complicated by severe airway stenosis, is difficult and often leads to high clinical risks and medical costs. CASE PRESENTATION: A 51-year-old previously healthy male was admitted to the Department of Respiratory and Critical Care Medicine, Taizhou People's Hospital, in November 2018 for haemoptysis and difficulty breathing during a 15-d period. Following admission, chest computed tomography (CT) showed a large mass in the left hilum with atelectasis in the left upper lobe and obstructive pneumonia in the left lower lobe. Bronchoscopy revealed that the lesions occurred in the distal segment of the left main trachea, with occlusion of the left upper bronchus and significant narrowing of the lower bronchus. A basal mucosal biopsy of the lump tissue was performed after haemostasis treatment with sub-plasma coagulation (APC), and squamous lung carcinoma was confirmed. Following the final diagnosis, the patient was successfully treated with implantation of 125I radioactive seeds via transbronchial needle aspiration (c-TBNA) combined with chemotherapy. CONCLUSION: We believe that implantation of 125I radioactive seeds via c-TBNA is an effective treatment for patients with advanced lung cancer and those presenting with severe and mixed main bronchus stenosis.

The Risk Factors of Postoperative Pressure Ulcer After Liver Resection With Long Surgical Duration: A Retrospective Study.

OBJECTIVE: The aim of this study is to investigate the risk factors of postoperative pressure ulcer (PU) development after liver resection with a long surgical duration. MATERIALS AND METHODS: A retrospective analysis was performed of patients who underwent a liver resection with a surgical duration greater than 2 hours between January 2015 and December 2016 at a tertiary referral hospital in eastern China. Univariate analysis and multivariate logistic regression were used to analyze the independent risk factors for postoperative PUs. RESULTS: Of the 128 patients included in the study, 11 (8.6%; 95% confidence interval [CI], 4.4%-14.9%) developed a stage 1 PU. Univariate analysis showed albumin on admission, diabetes mellitus complication, length of surgery, and intraoperative blood loss were all significantly different between the developed PU group (n = 11) and no PU group (n = 117; P ⟨ .05). However, multivariate logistic regression showed length of surgery (odds ratio [OR] = 1.026; 95% CI, 1.008-1.146) and intraoperative blood loss (OR = 1.014; 95% CI, 1.009-1.124) as only the independent risk factors for PU development after liver resection with a long surgical duration. CONCLUSIONS: These results showed length of surgery and intraoperative blood loss were independent risk factors for PU after liver resection with a long surgical duration. Use of PU prevention strategies are recommended for patients who undergo liver resection with massive intraoperative blood loss and long surgical duration.

MerTK Downregulates Lipopolysaccharide-Induced Inflammation Through SOCS1 Protein but Does Not Affect Phagocytosis of Escherichia coli in Macrophages.

Bacterial lipopolysaccharide (LPS) induces inflammatory response via toll-like receptor 4 (TLR4). However, this response must be strictly regulated because unbalanced overproduction of pro-inflammatory cytokines can lead to tissue damage and even be fatal. Herein, we explore whether Mer receptor tyrosine kinase (MerTK) regulates Escherichia coli (E. coli) LPS-induced inflammation and mediates phagocytosis of E. coli by macrophages. The results showed that LPS activated TLR4 signaling pathway and induced MerTK pathway in RAW264.7 macrophages, including suppressor of cytokine signaling1 (SOCS1). Preincubation with MerTK-specific blocking antibody (MerTK-Ab) markedly suppressed LPS-induced expression of phosphorylated MerTK, while further promoted LPS-induced production of TNF-α, IL-6, and IL-1ß as well as phosphorylation of IκB-α and p65. Likewise, MerTK-Ab prevented LPS-induced SOCS1 expression. Furthermore, LPS-induced production of pro-inflammatory cytokines and activation of NF-κB were increased by transfection with SOCS1 siRNA. Additionally, we demonstrated that MerTK was dispensable in phagocytosis of E. coli by RAW264.7 or peritoneal macrophages. Collectively, these results indicate that MerTK downregulates LPS-induced inflammation through SOCS1 protein without affecting phagocytosis of E. coli in macrophages.

Long non-coding RNA EPIC1 promotes human lung cancer cell growth.

Long non-coding RNA (LncRNA) EPIC1 (Lnc-EPIC1) is a MYC-interacting LncRNA. In the present study, the expression and potential function of Lnc-EPIC1 in human lung cancer cells are tested. We show that Lnc-EPIC1 expression is significantly higher in established/primary human lung cancer cells than that in human lung epithelial cells. Lnc-EPIC1 is also elevated in human lung cancer tissues. Silencing of Lnc-EPIC1 by targeted siRNA significantly inhibited human lung cancer cell growth, survival and proliferation, whiling inducing G1-S cell cycle arrest and cell apoptosis. MYC targets, including Cyclin A1, CDC20 and CDC45, were downregulated by Lnc-EPIC1 siRNA. MYC knockout by CRISPR/Cas-9 gene-editing method mimicked actions by Lnc-EPIC1 siRNA in A549 cells. Conversely, forced overexpression of Lnc-EPIC1 by a lentiviral construct increased expression of MYC targets to promote A549 cell growth. Lnc-EPIC1 directly associated with MYC protein in the nuclei of A549 cells. Significantly MYC knockout abolished Lnc-EPIC1 silencing- or overexpression-induced actions in human lung cancer cells. Together, our results show that Lnc-EPIC1 promotes human lung cancer cell growth possibly by targeting MYC.

k-RAS mutations in non-small cell lung cancer patients treated with TKIs among smokers and non-smokers: a meta-analysis.

AIM OF THE STUDY: Recent studies have suggested that k-RAS mutations are related to the response to epidermal growth factor receptor (EGFR) tyrosine-kinase inhibitions (TKIs) in advanced non-small cell lung cancer (NSCLC) treatment. The aim of this meta-analysis was to assess the relationship between smoking history and k-RAS mutations in NSCLC treated with TKIs. MATERIAL AND METHODS: We searched MEDLINE and Web of Science up to 15 March 2014. The pooled relative risk (RR) was estimated by using fixed effect model or random effect model, according to heterogeneity between studies. We also carried out power analyses. RESULTS: We identified 12 studies with 1193 patients, including 196 patients (16.4%) with k-RAS mutations. The pooled k-RAS mutations incidence was 22.8% (174/764) in patients with smoke expose vs. 5.4% (23/429) in those with no smoke exposure. The pooled RR was 2.991 (95% CI: 1.884-4.746; Z = 4.65, p = 0.000). No publication bias was found (Begg's test: z = 1.09, p = 0.274 and Egger's test: t = 1.38, p = 0.201). In subgroup analyses, the pooled RR was 3.336 (95% CI: 1.925-5.779; Z = 4.30, p = 0.000) in the Caucasian subgroup, while in the Asian subgroup the pooled RR was 2.093 (95% CI: 0.909-4.822; Z = 1.73, p = 0.083), but the sample size was underpowered (0.465). CONCLUSIONS: The current meta-analysis found that smoking was related to increased incidence of k-RAS mutations in non-small cell lung cancer treated with TKIs. This may be further evidence that smoking will lead to a worse prognosis in NSCLC patients treated with TKIs.

Primary pulmonary synovial sarcoma presenting with a large lump mass in the left upper mediastinum: A case report.

Primary pulmonary synovial sarcoma is a rare lesion that occurs in 0.5% cases of lung malignancies. Chest computed tomography (CT) reveals a heterogeneously enhancing mass in the lobe or hilum of the lungs, frequently calcified and with pleural invasion. Involvement of the mediastinum in the course of primary pulmonary synovial sarcoma, in particular detection of a large mass in the mediastinum as the sole initial imaging manifestation, is extremely rare, which may contribute to a delayed diagnosis or misdiagnosis. The present case report describes an extremely rare case of a patient with primary pulmonary synovial sarcoma presenting with a large mass in the left upper mediastinum. A 59-year-old patient was admitted to the Department of Respiratory Medicine of Taizhou People's Hospital in May 2014, complaining of a persistent cough and blood sputum for 2 weeks. Following admission, a chest CT showed a large mass in the left upper mediastinum. Thoracoscopy was performed and revealed that the left pulmonary artery was engulfed by the mass, and thus surgical resection of the tumor was abandoned. The patient was definitively diagnosed with primary pulmonary synovial sarcoma following the histopathological and immunohistochemical analysis of biopsy specimens obtained via thoracoscopy. Following the final diagnosis, the patient was transferred to the Department of Oncology for chemotherapy treatments with ifosfamide and doxorubicin. Unfortunately, no partial regression was achieved after two rounds of chemotherapy, and the patient was lost to follow-up 3 months after the diagnosis was confirmed. The present case may promote the consideration of primary pulmonary synovial sarcoma in the differential diagnosis of patients who present with a large mass in the mediastinum.

siRNA targeting of Trop2 suppresses the proliferation and invasion of lung adenocarcinoma H460 cells.

The aim of the present study was to investigate the effect of the small interfering RNA (siRNA)-induced inhibition of the Trop2 gene on the proliferation and invasion of lung adenocarcinoma H460 cells. A recombinant adenovirus expression vector, which contained siRNA targeting open reading frames for Trop2 (rAd5-siTrop2), was transfected into lung adenocarcinoma H460 cells. Three groups were included in the study, namely the Ctrl (non-transfected control), rAd5-siCtrl (native control) and rAd5-siTrop2 (knockdown Trop2 gene) groups. The mRNA and protein expression levels of Trop2 were detected using quantitative polymerase chain reaction and western blot analysis, respectively. In addition, the expression levels of cyclin Dl and phospho-extracellular signal regulated kinase (p-ERK)-1 were detected using western blot analysis. The effects of Trop2 inhibition on the proliferation and invasion of lung adenocarcinoma H460 cells were investigated using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and Transwell assay. Trop2-targeted siRNA recombinant plasmids were successfully constructed. The recombinant adenovirus vector, rAd5-siTrop2, significantly downregulated the mRNA and protein expression levels of Trop2 in the lung adenocarcinoma H460 cells, with cyclin D1 and p-ERK-1 expression downregulated simultaneously. In addition, following the silencing of Trop2, the proliferation and invasion rates of the lung adenocarcinoma H460 cells were reduced. Therefore, the results indicated that Trop2 serves a key function in the proliferation and invasion of lung adenocarcinoma H460 cells in vitro.

The relationship between Glasgow Prognostic Score and serum tumor markers in patients with advanced non-small cell lung cancer.

BACKGROUND: Glasgow Prognostic Score (GPS) has been reported as a powerful prognostic tool for patients with advanced non-small cell lung cancer (NSCLC). The aim of this study was to assess the relationship between GPS and prognosis related tumor markers in patients with advanced NSCLC. METHODS: We included 138 advanced NSCLC patients and twenty healthy controls in the study. GPS was calculated by combined serum C-reactive protein (CRP) and albumin. Three serum tumor markers, which included cytokeratin 19 fragment antigen 21-1 (CYFRA21-1), carcinoembryonic antigen (CEA) and tissue polypeptide specific antigen (TPS), were detected by enzyme-linked immunosorbent assay (ELISA). GPS and tumor markers were all assessed before chemotherapy. All patients received at least 2 courses of cisplatin-based chemotherapy. After that, 2 to 5 years follow-up was conducted. RESULTS: Median levels of CYFRA21-1 were 1.5 ng/ml (0.1-3.1 ng/ml) in healthy controls, and 4.6 ng/ml (0.7-35.2 ng/ml) in GPS 0 advanced NSCLC, 11.2 ng/ml (0.4-89.2) ng/ml in GPS 1 advanced NSCLC, and 15.7 ng/ml (2.9-134.6 ng/ml) in GPS 2 advanced NSCLC, respectively. Median levels of CYFRA21-1 were higher in NSCLC patients than in healthy controls, and CYFRA21-1 increased gradually according to GPS category in NSCLC patients (P< 0.05). Similar results were found for median levels of CEA and TPS in healthy controls and NSCLC patients (P < 0.05). In NSCLC patients, positive correlations were found between CYFRA21-1 and GPS, CEA and GPS, TPS and GPS. The Spearman's rank correlation coefficient were 0.67 (P < 0.05), 0.61 (P < 0.05) and 0.55 (P < 0.05), respectively. Survival analyses showed GPS was an independent prognostic factor for advanced NSCLC. CYFRA21-1(>3.3 ng/ml) and TPS (>80 U/l) were related with the prognosis of advanced NSCLC by univariate analyses, but multivariate analyses showed CYFRA21-1, TPS and CEA were not the independent prognostic factors for advanced NSCLC. CONCLUSIONS: Our results showed GPS were positive correlated with CYFRA21-1, CEA and TPS in patients with advanced NSCLC. However, GPS was more efficient in predicting prognosis of advanced NSCLC than these three single prognosis related tumor markers.

Short hairpin RNA targeting AKT1 and PI3K/p85 suppresses the proliferation and self-renewal of lung cancer stem cells.

The aim of the present study was to investigate the effect of short hairpin (sh)RNA targeting AKT1 and phosphatidylinositol 3-kinase (PI3K)/p85 on the proliferation and self-renewal of lung cancer stem cells (LCSCs). The recombinant adenovirus expression vector, which contained shRNA targeting open reading frames of AKT1 and PI3K/p85, was transfected into LCSCs. It was found that AKT1 and PI3K/p85 expression was upregulated in LCSCs compared with that in the primary lung cancer cells. Recombinant adenovirus vector rAd5-siAKT1-siPI3K/p85 significantly downregulated AKT1 and PI3K/p85 mRNA and protein expression in LCSCs. The downstream factors, proliferating cell nuclear antigen (PCNA) and cyclin D1 were also downregulated, while p53 was upregulated. Following silencing of AKT1 and PI3K/p85, cell proliferation, tumor sphere formation and tumor formation in NOD/SCID mice were also reduced. According to the present results, it was hypothesized that the PI3K/Akt signaling pathway is important in the self­renewal and proliferation of LCSCs, and that targeting the PI3K/Akt signaling pathway decreases the rate of tumor formation in vivo.

Bilateral pleural effusion as an initial manifestation of multiple myeloma: A case report and literature review.

Multiple myeloma (MM) is a rare type of malignant hematological neoplasm. Although primarily involving the bone marrow, MM has a significant risk of metastasizing to other organs and may present with various clinical symptoms. However, the involvement of the respiratory system in the course of MM is extremely uncommon, particularly presenting with bilateral pleural effusion as the sole initial manifestation, which may result in a delayed diagnosis of MM. The present study describes the extremely rare case of a patient with MM presenting with myelomatous pleural effusion (MPE). The 78-year-old patient was admitted to the Department of Respiratory Medicine, Taizhou People's Hospital (Taizhou, China) in March 2014, complaining of persistent dyspnea. Following admission, chest computed tomography scans revealed bilateral pleural effusion and a small amount of pericardial effusion, but no evident mass lesion. Thoracentesis was performed and the resulting pleural effusion was exudative and slightly bloody. In the following cytological examination, myeloma cells were identified in the pleural effusion. The patient was diagnosed definitively with MM following a histopathological study of the bone marrow aspiration. Therefore, the observations of the present case report may promote the consideration of MM in the differential diagnosis of patients with unexplained and refractory pleural effusion. The present study also reviewed the literature with regard to the association between MM and pleural effusion.

Comparison of Glasgow prognostic score and prognostic index in patients with advanced non-small cell lung cancer.

OBJECTIVES: Previous studies have shown that Glasgow prognostic score (GPS) and prognostic index (PI) are also powerful prognostic tool for patients with advanced non-small cell lung cancer (NSCLC). The aim of this study was to compare the prognostic value between GPS and PI. METHODS: We enrolled consecutive patients with advanced NSCLC in this prospective cohort. GPS and PI were calculated before the onset of chemotherapy. The prognosis outcomes included 1-, 3-, and 5-year progression-free survival and overall survival (OS). The performance of two scores in predicting prognosis was analyzed regarding discrimination and calibration. RESULTS: 138 patients were included in the study. The area under the receiver operating characteristic curve for GPS predicting 1-year DFS was 0.62 (95 % confidence interval (CI) 0.56-0.68, P < 0.05), and the area under curve for PI predicting 1-year DFS was 0.57 (95 % CI 0.52-0.63). Delong's test showed that GPS was more accurate than PI in predicting 1-year DFS (P < 0.05). Similar results of discriminatory power were found for predicting 3-year DFS, 1-year OS, and 3-year OS. The predicted 1-year DFS by GPS 0, GPS 1, and GPS 2 were 62.5, 42.1, and 23.1 %, respectively, while actual 1-year DFS by GPS 0, GPS 1, and GPS 2 were 61.1, 43.8, and 27.2 %, respectively. Calibration of the Hosmer and Lemeshow statistic showed good fit of the predicted 1-year DFS to the actual 1-year DFS by GPS (χ(2) = 4.326, P = 0.462), while no fit was found between the predicted 1-year DFS and the actual 1-year DFS by PI (χ(2) = 15.234, P = 0.091). Similar results of calibration power were found for predicting 3-year DFS, 5-year DFS, 1-year OS, 3-year OS, and 5-year OS by GPS and PI. CONCLUSIONS: GPS is more accurate than PI in predicting prognosis for patients with advanced NSCLC. GPS can be used as a useful and simple tool for predicting prognosis in patients with NSCLC. However, GPS only can be used for preliminary assessment because of low predicting accuracy.

Isolation, cultivation and identification of human lung adenocarcinoma stem cells.

Recently, an increasing number of studies have demonstrated that lung cancer is a stem cell disease. However, ideal cell surface markers for isolating stem cells in lung cancer are yet to be identified. In the present study, a cell population with a cluster of differentiation (CD)133+ phenotype was successfully isolated from a single cell suspension of lung adenocarcinoma tissue using magnetic-activated cell sorting (MACS) and enriched in a serum-free culture. In comparison to CD133- cells, the CD133+ cells exhibited an enhanced capacity for self-renewal and differentiation, and a greater potential for in vivo tumor formation, in non-obese diabetic/severe combined immunodeficient (NOD/SCID) mice. Tumors could be induced in NOD/SCID mice by the transplantation of 102 stem-like cells per mouse. The results of the present study demonstrated that CD133 may serve as a specific cell surface marker for lung adenocarcinoma stem cells, and that MACS combined with serum-free culture is an effective method for isolating and enriching lung cancer stem cells.

The Glasgow prognostic score as a prognostic factor in patients with advanced non-small cell lung cancer treated with cisplatin-based first-line chemotherapy.

OBJECTIVES: The aim of this study was to assess the predictive value of survival in patients with advanced non-small cell lung cancer (NSCLC) treated with cisplatin-based first-line chemotherapy. METHODS: In this study, 138 consecutive patients with advanced NSCLC were included in this study. Glasgow prognostic score (GPS) was calculated before the onset of treatment. The outcome indicators were progression free survival (PFS) and overall survival (OS). RESULTS: Univariate log-rank test showed that GPS was significantly associated with both PFS (P  =  0.01) and OS (P  =  0.02). Multivariate Cox model revealed that the hazard ratios (HRs) for PFS were 0.8(0.5-0.9) for GPS 1 versus GPS 0 and 0.5(0.3-0.8) for GPS 2 versus GPS 0, respectively. The HRs for OS were 0.8(0.4-0.9) for GPS 1 versus GPS 0 and 0.5(0.2-0.8) for GPS 2 versus GPS 0, respectively. CONCLUSIONS: The GPS can be used as an independent predictor for survival in patients with advanced NSCLC.

Diagnosis and management of a patient with primary pulmonary diffuse large B-cell lymphoma: A case report and review of the literature.

Primary pulmonary lymphoma (PPL) is an uncommon type of non-Hodgkin's lymphoma. The majority of PPLs are of low-grade, mucosa-associated lymphoid tissue type. Primary pulmonary diffuse large B-cell lymphoma (DLBCL) is extremely rare, and prompt diagnosis may be challenging since its clinical symptoms and signs are nonspecific. Although the clinical features, diagnostic procedures, optimal management and prognostic factors of this disease have not yet been well defined, open thoracotomy and chest computed tomography (CT)-guided percutaneous biopsy are the preferred methods used in previous studies. In the present case report, the diagnosis and management of a patient with primary pulmonary DLBCL is reported. A 68-year-old patient was admitted to hospital in May 2013, with complaints of shortness of breath and intermittent wheezing and a cough associated with the production of small amounts of phlegm. Following admission, chest CT scans revealed a mass in the right middle lobe with ground-glass opacities at the lesion margins, as well as air bronchograms in the areas of consolidation. Bronchoscopy was performed and revealed an endobronchial lesion and partial stenosis in the distal end of the middle segment bronchus. Transbronchial needle aspiration (TBNA) of the right hilar lymph node, as well as endobronchial biopsy, was performed. The patient was diagnosed with primary pulmonary DLBCL by subsequent histopathological and immunohistochemical analysis of biopsy specimens collected via TBNA. Following the final diagnosis, standard treatment with CHOP chemotherapy resulted in significant clinical and radiological response and the patient remained in remission 8 months later. These results indicate that TBNA may be an effective method for the diagnosis of primary pulmonary DLBCL.

Expression and clinical significance of the phosphatidylinositol 3-kinase/protein kinase B signal transduction pathway in non-small cell lung carcinoma.

The overactivation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signal transduction pathway has been examined in various carcinomas and is reported to be significantly correlated with prognosis. However, little is known with regard to the PI3K/Akt signal transduction pathway in advanced non-small cell lung carcinoma (NSCLC). The present study investigated the expression of PI3K and phosphorylated (p)-Akt protein and its clinical significance in NSCLC. The clinical records of 157 patients with NSCLC (70 stage I-IIIA and 87 stage IIIB-IV cases), consisting of 75 cases of squamous cell carcinoma and 82 cases of adenocarcinoma, together with 30 resected lung cancer tumor-adjacent tissue samples, were retrospectively evaluated. PI3K and p-Akt expression in the NSCLC and tumor-adjacent tissues were measured using an immunohistochemical method, and its correlation with the clinicopathological data and prognosis in advanced NSCLC was evaluated. PI3K and p-Akt expression was significantly higher in the cancer tissues (χ2=14.8455; P=0.001) than in the tumor-adjacent tissues (χ2=14.2615; P=0.001). The overexpression of p-Akt in stage I-IIIA NSCLC was associated with lymph node metastasis (χ2=6.1189; P=0.013) and tumor-node-metastasis (TNM) stage (χ2=8.9752; P=0.011), however, no correlation was observed with gender, age, pathological type and histological grade. The overexpression of p-Akt in stage IIIB-IV NSCLC was only associated with TNM stage (χ2=5.7501; P=0.016), and no correlation was observed with gender, age, pathological type, histological grade and Eastern Cooperative Oncology Group (ECOG) performance status (PS). The overexpression of PI3K was not found to correlate with the aforementioned clinicopathological variables in all patients. Survival was significantly improved in advanced NSCLC with PI3K- and p-Akt-negative expression compared with PI3K- and p-Akt-positive expression [P13K: 17.70 months (95% confidence interval (CI), 15.11-20.28 months) vs. 13.43 months (95% CI, 11.83-15.02 months); P=0.004; and p-Akt: 17.13 months (95% CI, 14.93-19.34 months) vs. 13.07 months (95% CI, 11.32-14.82 months); P=0.007]. Multivariate analysis showed that PI3K [hazard ratio (HR)=2.143; 95% CI, 1.211-3.790; P=0.009], p-Akt (HR=1.991; 95% CI, 1.009-3.927; P=0.047), TNM stage (HR=4.788; 95% CI, 2.591-8.848; P=0.001) and ECOG-PS (HR=3.272; 95% CI, 1.701-6.296; P=0.001) were independent predictors for survival in stage IIIB-IV NSCLC. These results indicated that p-Akt overexpression closely correlates with factors of an unfavorable prognosis in NSCLC. PI3K and p-Akt overexpression are independent markers of a poor prognosis in advanced NSCLC.

Diagnosis and management of an elderly patient with severe tracheomalacia: A case report and review of the literature.

Severe adult tracheomalacia is a dangerous disease that is difficult to manage, particularly at the time of airway infection, and has a high mortality rate. The present study reports the diagnosis and treatment of an elderly patient with severe adult tracheomalacia. In March 2012, the 59-year-old patient presented with progressive dyspnea to the Department of Respiratory Medicine, Taizhou People's Hospital (Jiangsu, China). Following admission, chest radiography revealed symptoms consistent with chronic obstructive pulmonary disease (COPD) and chest computed tomography (CT) demonstrated an evident stenosis of the tracheal lumen at the end of expiration. Bronchoscopy revealed a 91% reduction in the cross-sectional area of the tracheal lumen at the end of expiration. Following the final diagnosis, the patient was successfully treated with nasal continuous positive airway pressure (CPAP) combined with implantation of a temporary Chinese Li's metallic stent. These treatment methods appeared to be temporarily effective in alleviating the symptoms of the disease.

Expression and clinical significance of the Trop-2 gene in advanced non-small cell lung carcinoma.

The Trop-2 gene has been examined in various carcinomas and is reported to be significantly associated with prognosis. Little is known with regard to Trop-2 gene expression in advanced non-small cell lung carcinoma (NSCLC). The present study investigated the expression of Trop-2 and its association with the prognosis of advanced NSCLC. The clinical records of 87 patients with advanced NSCLC, consisting of 37 cases of squamous cell carcinoma (SCC) and 50 cases of adenocarcinoma (AdC), together with 17 tumor-adjacent normal tissues, were retrospectively evaluated. Trop-2 expression was measured using an immunohistochemical method and its association with clinicopathological data and prognosis was also evaluated. The expression of Trop-2 was significantly higher in the cancer tissues compared with the tumor-adjacent normal tissues, and significantly higher in SCC compared with AdC (P=0.018). In SCC, the overexpression of Trop-2 was only correlated with the histological grade of the tumor (P= 0.035) and no correlation was observed with gender, age, lymph node metastasis, TNM stage or Eastern Cooperative Oncology Group (ECOG) performance status (PS). In AdC, the over-expression of Trop-2 was correlated with the histological grade, lymph node metastasis and TNM stage (P= 0.01, 0.024 and 0.015, respectively), while no correlation with gender, age or ECOG-PS was observed. The survival frequency was significantly higher in the Trop-2-negative patients compared with the Trop-2-positive patients [17.25 months (95% CI, 14.922-19.577) vs. 13.274 months (95% CI, 11.507-15.041); P= 0.008]. The survival time was significantly longer in the Trop-2-negative AdC patients [17.275 months (95% CI, 14.575-19.975) vs. 11.469 months (95% CI, 11.507-15.041); P= 0.002], but not in the SCC patients [17.167 months (95% CI, 12.428-21.906) vs. 14.647 months (95% CI, 12.062-17.232); P= 0.276]. The multivariate analysis revealed that Trop-2 expression [hazard ratio (HR) 2.381; P= 0.038], TNM stage (HR, 2.193; P= 0.03) and ECOG-PS (HR, 2.696; P= 0.007) were independent predictors for the survival outcome of patients with AdC. These results suggest that Trop-2 overexpression is closely correlated with an unfavorable prognosis in advanced NSCLC. Trop-2 is an independent prognostic marker and a potential new therapeutic target in advanced AdC.