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Pleural fibrosis is an irreversible pathological process occurred in the development of several lung diseases. TMEM88 is a member of transmembrane (TMEM) family and has been found to be involved in the regulation of fibrogenesis. However, the role of TMEM88 in pleural fibrosis remains unknown. In this study, we aimed to explore the role of TMEM88 in pleural fibrosis

Background Female pelvic floor dysfunction (PFD), a common disease affecting women, has attracted a significant amount of attention in the field of obstetrics and gynecology in recent years. Pelvic floor disorders can induce urinary incontinence, vaginal prolapse and other dysfunction, which seriously affect the quality of life of patients. This study aimed to analyze the current status of PFD in urban women in Xi'an City. Methods A total of 1300 women in the urban area of Xi'an City were selected based on a multi-stage sampling method. A face-to-face questionnaire survey and gynecological examination were carried out, and the prevalence rates of stress urinary incontinence (SUI) and pelvic organ prolapse (POP) and PFD were calculated, Multivariate logistic regression analysis was performed to analyze the risk factors of PFD in urban women in Xi'an City. Results The effective questionnaire recovery rate was 76.69% (997/1,300). The number of patients with SUI, POP, and SUI combined POP were 124 (55.11%), 64 (28.44%) and 37 (16.44%), respectively, and the prevalence of PFD was 22.57% (225/997). Multivariate logistic regression analysis showed that the risk of PFD in women with vaginal delivery, delivery times ≥2, menopause or prolonged labor was higher than that in women with cesarean section, delivery times of 1, no menopause, or no prolonged labor (P Conclusions The prevalence rate of PFD in urban women in Xi'an City cannot be ignored, especially women who have experienced vaginal delivery, delivered ≥2 children, menopause, or prolonged labor. It may be necessary to prioritize these women so as to actively prevent and control PFD.

Abnormal proliferation and migration of airway smooth muscle cells (ASMCs) have been found to be important for the airway remodeling during the pathogenesis of asthma. Salidroside a bioactive glucoside that exerts antitumor activity via inhibiting the cell proliferation and migration of cancer cells. The aim of the current study was to evaluate the effects of salidroside on the proliferation and migration of ASMCs. Our results showed that salidroside inhibited the proliferation and migration of ASMCs in response to platelet-derived growth factor (PDGF) stimulation. Salidroside markedly attenuated the PDGF-induced production of matrix metalloproteinase 2 (MMP-2) and MMP-9 in ASMCs. The levels of contractile phenotype markers including smooth muscle α-actin and calponin were reduced in response to PDGF stimulation, which was attenuated by salidroside pretreatment. Salidroside diminished the increase in the expression levels of type I collagen and fibronectin in PDGF-stimulated ASMCs. Furthermore, salidroside blocked the PDGF-induced activation of the nuclear factor-κB (NF-κB) pathway in ASMCs. The results suggested that salidroside functionally regulated the proliferation, migration, phenotype plasticity, and extracellular matrix deposition in PDGF-induced ASMCs and the NF-κB pathway might be implicated in the effects of salidroside on ASMCs induced by PDGF.

BACKGROUND Chronic obstructive pulmonary disease (COPD) is a leading cause of hospital admissions, which can result in a significant financial burden. OBJECTIVE To determine hospitalisation costs and factors associated with higher costs in patients with acute exacerbations of COPD (AE-COPD). DESIGN Patients hospitalised for a whole year formed the study cohort. Demographic features, clinical data and hospitalisation bills were evaluated retrospectively. Student's t-test or the Mann-Whitney U-test were used to compare the mean values of variables between high-cost and low-cost groups. Logistic regression analysis was used to study the relationship between hospitalisation costs with clinical factors. RESULTS A total of 188 patients were evaluated. The mean length of stay in hospital (LOSH) was 8.5 days. The mean cost of AE-COPD was US$1722.0. Costs were significantly associated with LOSH and the per cent predicted value of forced expiratory volume in one second. Age, sex, smoking index, partial oxygen pressure, partial carbon dioxide pressure, haemoglobin concentration and white blood cell counts were not associated with hospitalisation costs. CONCLUSION Medications and laboratory services are the main drivers of hospitalisation costs in AE-COPD. Longer LOSH and reduced pulmonary function determine the high costs in hospitalised patients with AE-COPD admitted to a general ward. To reduce hospitalisation costs, more emphasis should be placed on shortening LOSH and preventing the worsening of pulmonary function.

Lung cancer is the leading cause of cancer deaths worldwide, many miRNAs play critical role in lung cancer initiation and progression. Here, we demonstrated that miR-1254 was upregulated in lung cancer tissues and cells. miR-1254 overexpression promoted lung cancer cell proliferation determined by MTT assay, colony formation assay, soft agar growth ability assay and BrdU incorporation assay, miR-1254 knockdown suppressed lung cancer cell proliferation. Mechanism analysis revealed that Wnt/β-catenin pathway antagonist secreted frizzled related protein 1 (SFRP1) was its target, its expression was opposite to SFRP1 level, and directly bound to the 3'UTR of SFRP1. Double knockdown of miR-1254 and SFRP1 promoted lung cancer cell proliferation, suggesting miR-1254 promoted lung cancer cell proliferation by targeting SFRP1.

In this study, we investigated the utility of pentraxin 3 (PTX-3) in bronchoalveolar lavage fluid (BALF) as lung cancer (LCa) diagnostic. A total of 89 LCa patients and 84 non-LCa patients who received bronchoscopy in the First Affiliated Hospital of Xi’an Jiaotong University from December 2014 to February 2015 were enrolled. LCa was subdivided according to pathological type (scale, gland, and small cell lung cancer). BALF samples were obtained during bronchoscopy and PTX-3 levels assayed by ELISA. t-tests, Mann-Whitney, and Kruskal-Wallis tests were performed for the comparison of PTX-3 levels between the different groups. Correlation analysis and receiver operating characteristic (ROC) analysis were used to analyze clinical data. The levels of PTX-3 increased in the LCa groups. PTX-3 levels were higher in the small cell lung cancer (SCLC) compared to non-small-cell lung cancer (NSCLC) groups. In LCa patients, obstructive pneumonia could upregulate the expression of PTX-3 in BALF. The area under the ROC curve of PTX-3 in BALF during LCa diagnosis, SCLC, and LCa with obstructive pneumonia was 0.949 (p≤0.001), 0.672 (p<0.05), and 0.838 (p<0.01), respectively. In conclusion, PTX-3 in BALF has a potential value as an LCa biomarker, particularly in cases of SCLC and LCa with obstructive pneumonia.

Objective: To conduct survey on cognition of clinical nurses on knowledge of high-alert medication and propose relevant strategies for effective improvement. Methods: One hundred twenty clinical nurses were randomly selected from medical staff in our hospital from July 2016 to February 2017, and the results were analyzed and evaluated by questionnaires. Results: The results showed that, the total score of clinical nurses on knowledge of high-alert medication was 14-37 points, averaging 26.8 ± 3.32 points. The cognition of high-alert medication knowledge was significantly different among nursing staff with different age, service age, technical title and educational level (P

Four new xenicanes, namely 4a-hydroxyisodictyohemiacetal (1), 4a-hydroxyisodictyoacetal (2), 13,18-diacetoxy-4-hydroxyisodictyo-19-al (3), and 4a-hydroxypachylactone (8), were isolated from a Chinese collection of the brown alga Dictyota plectens, along with four known analogues (4-7). The structures of the new diterpenes were determined by extensive spectroscopic data analysis. All compounds were evaluated for their antiviral activities against human immunodeficiency virus type 1 (HIV-1) and the highly pathogenic avian influenza A (H5N1) virus, and inhibitory effects on lipopolysaccharide (LPS)-induced nitric oxide (NO) production in mouse peritoneal macrophages (PEM Phi).

Pleural fibrosis can dramatically lower the quality of life. Numerous studies have reported that epithelial-mesenchymal transition (EMT) regulated by transforming growth factor-β (TGF-β) is involved in fibrosis. However, the molecular mechanism is inadequately understood. Fibroblast-specific protein-1 (S100A4) is a target of TGF-β signaling. In our previous study, we have reported that S100A4 is highly expressed in pleural fibrosis. Thus, we suggest that S100A4 took part in the TGF-β-induced EMT in pleural fibrosis. In this study, we determined the expression of S100A4 and EMT-related markers in Met-5A cells (pleural mesothelial cells) treated with TGF-β or TGF-β inhibitor by real-time PCR and western blot. In order to explore the role of S100A4, we used siRNA to knock down the expression of S100A4 in cell model. We found that the expression of epithelial cell marker was decreased and the mesenchymal cell marker increased with S100A4 upregulation after treatment with TGF-β. Moreover, the changes of EMT-related event were restricted when the expression of S100A4 was knocked down. Conversely, S100A4 can partially rescue the EMT-related expression changes induced by TGF-β inhibitor. These findings suggest that S100A4 expression is induced by the TGF-β pathway, and silencing S100A4 expression can inhibit the process of TGF-β-induced EMT.

This article has been withdrawn at the request of the Editor-in-Chief. Following peer-review and acceptance of the above referenced paper for publication in Lung Cancer, the Editor-in-Chief was contacted by the Editor-in-Chief of the journal, Gene Therapy, with information that the manuscript had simultaneously been submitted to both Lung Cancer and Gene Therapy. A referee selected to review the manuscript for Gene Therapy was also contacted by the Editor-in-Chief of the journal, Respiratory Research, with a request to review the same manuscript for that journal. The three journals ascertained that the manuscript had been simultaneously submitted to all three journals. In addition, as part of their investigation of potential simultaneous submission, the Editors of Lung Cancer compared the manuscript submitted to Gene Therapy with that accepted for publication in Lung Cancer, and this has raised concerns related to the data presented in the paper. The paper accepted for publication in Lung Cancer examines A549 and H810 cells. The paper submitted to Gene Therapy examines A549 and H510A cells. However, the data presented in both papers, including the figures, are identical. The Editors of Lung Cancer have asked the authors for an explanation, but the corresponding author has not responded. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at https://www.elsevier.com/about/our-business/policies/article-withdrawal.

Background: Emodin is the main active component of rhubarb, which has demonstrated many beneficial effects against inflammation. Nanosilver is an effective antimicrobial agent. The present study was designed to observe the effects of Emodin combined with silver nanoparticles (E/S) on sepsis protection and related mechanism. Methods: E/S was prepared by loading different concentrations of Emodin on nanosilver and cytotoxicity of E/S were determined by suphorhodamine B assays. Anti-microbial activities of E/S were assayed by direct interaction with various common pathogens and anti-adhesive activites of E/S on leukocytes with endothelial cells were assayed by biochemical analysis. Next, inflammatory cell enumeration, inflammatory mediators in bronchoalveolar lavage fluid (BALF) and endothelial cell function were analyzed on a clinically relevant model of sepsis induced by cecal ligation and puncture (CLP) after E/S administration. The effects of E/S on NF-κB and p38 were also examined by western blot. Results: E/S exhibited little cytotoxicity action on endothelial cells and significant inhibitory activities against all tested common microorganisms and adherence between leukocyte and endothelial cells. E/S induced anti-sepsis protection mainly mediated by inhibition of inflammatory cells infiltration, down-regulation of TNF-alpha, IL-8 and lactic dehydrogenase (LDH), and inhibition of NF-κB and p38 pathways in mice 24 h post-CLP. Conclusion: Our data suggest that E/S has strong anti-sepsis effects, which was related with anti-inflammatory protection and thereby promote survival following sepsis challenge.

Introduction: Endoplasmic reticulum (ER) stress has been considered to be an important regulator of airway inflammation in the pathogenesis of bronchial asthma, but the mechanism of ER stress involved in neutrophilic asthma remain not fully understood. Methods: Tunicamycin is a mixture of homologous nucleoside antibiotics, which is used to induce ER stress. In the present study, Tunicamycin was administered to mouse bronchial epithelial cells and a neutrophilic asthma model (OVALPS-OVA mice), and ER stress indicators and inflammatory cytokines were measured by Western blotting and Elisa. Results: Tunicamycin not only induced ER stress in mouse bronchial epithelial cells, but also increased expression of inflammation indicators such as IL-6, IL-8, and TNF-α via PERK-ATF4-CHOP signaling. Additionally, the phosphorylation of PERK and the expression levels of ATF4 and CHOP proteins and inflammatory cytokines (IL-6, IL-8 and TNF-α) were elevated in the lung tissue of OVALPS-OVA mice. Administering tuni...

Background/Aims: The study was designed to explore the potential relationship of TLR4 and endothelial PAS domain-containing protein 1 (EPAS1) in vivo and vitro experiments. Methods: Bronchoalveolar lavage fluid (BALF) samples were collected from 55 chronic obstructive pulmonary disease (COPD) patients and 25 healthy subjects. The differential cell count was performed using Wright-Giemsa staining. The expression levels of TLR4 and TLR5 were detected by RT-qPCR. The levels of methylation and mRNA expression of EPAS1 were assayed by bisulfite sequencing PCR and real-time PCR. The correlation of TLR4 and EPAS1 was also analyzed in TLR 4-overexpressing endothelial cells. Results: The results showed that the number of neutrophils, lymphocytes and macrophages and expression of TLR 4 were significantly increased in lower respiratory tract of COPD patients. Moreover, decreased EPAS1 mRNA and increased EPAS1 promoter methylation were detected in COPD, which were closely associated with increased TLR4 expression. According to in vitro experiments, TLR 4 inhibited EPAS1 mRNA expression and promoted promoter methylation in endothelial cells. Conclusion: These findings suggest that TLR4 over-expression decreased EPAS1expression which contributes to the progress of COPD.

Background Fibroblast specific protein-1 (S100A4) is related with many fibrotic diseases, but its role in the pathogenesis of pleural fibrosis has not been fully elucidated. Then we aim to investigate the expression and effect of fibroblast specific protein-1 (S100A4) in pleural tuberculosis and, subsequently, pleural fibrosis. Methods The expression of S100A4 in pleura was examined in 30 patients with pleural tuberculosis and 5 control (disease-free) patients by immunohistochemistry using the streptavidin-peroxidase (S-P) conjugated method. Results The expression of S100A4 in pleura was mainly distributed in the nucleus and cytoplasm of fibroblasts and vascular endothelial cells, and the positive rate was 90.0% (27 out of 30 patients with pleural tuberculosis). There were no expressions of S100A4 in the control group. In the pleura of all 30 patients with pleural tuberculosis, S100A4 had a higher expression in the two- to eight-week duration of the disease. Conclusions S100A4 plays an important role in the phenotypic transformation of pleural mesothelial cells and the development of pleural fibrosis.