Shanghai Respiratory Research Institute

Shanghai, China

Shanghai Respiratory Research Institute

Shanghai, China
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Zhu H.-X.,Shanghai JiaoTong University | Zhu H.-X.,Shanghai Respiratory Research Institute | Shi L.,Fudan University | Zhang Y.,Fudan University | And 7 more authors.
Journal of Translational Medicine | Year: 2017

Background: Lung cancer is the leading cause of cancer-related morbidity and mortality worldwide. Patients with chronic respiratory diseases, such as chronic obstructive pulmonary disease (COPD), are exposed to a higher risk of developing lung cancer. Chronic inflammation may play an important role in the lung carcinogenesis among those patients. The present study aimed at identifying candidate biomarker predicting lung cancer risk among patients with chronic respiratory diseases. Methods: We applied clinical bioinformatics tools to analyze different gene profile datasets with a special focus on screening the potential biomarker during chronic inflammation-lung cancer transition. Then we adopted an in vitro model based on LPS-challenged A549 cells to validate the biomarker through RNA-sequencing, quantitative real time polymerase chain reaction, and western blot analysis. Results: Bioinformatics analyses of the 16 enrolled GSE datasets from Gene Expression Omnibus online database showed myocyte enhancer factor 2D (MEF2D) level significantly increased in COPD patients coexisting non-small-cell lung carcinoma (NSCLC). Inflammation challenge increased MEF2D expression in NSCLC cell line A549, associated with the severity of inflammation. Extracellular signal-regulated protein kinase inhibition could reverse the up-regulation of MEF2D in inflammation-activated A549. MEF2D played a critical role in NSCLC cell bio-behaviors, including proliferation, differentiation, and movement. Conclusions: Inflammatory conditions led to increased MEF2D expression, which might further contribute to the development of lung cancer through influencing cancer microenvironment and cell bio-behaviors. MEF2D might be a potential biomarker during chronic inflammation-lung cancer transition, predicting the risk of lung cancer among patients with chronic respiratory diseases. © 2017 The Author(s).


Yan X.,Second Hospital Affiliated to Hebei Medical UniversityHebei | Song Y.,Fudan University | Song Y.,Shanghai Respiratory Research Institute | Shen C.,Shanghai JiaoTong University | And 11 more authors.
International Journal of COPD | Year: 2017

Airway mucus hypersecretion is a frequent symptom associated with acute and chronic airway disease. Inhibition of mucus production or promotion of mucolysis not only relieved symptoms but also improved disease outcomes. There are numerous available mucoactive medicines for prescription, and how to select them properly for different diseases is important for clinical practice. So far, there is no one consensus or guideline reported. A group of Chinese pulmonary physicians worked together to complete this consensus based on literature review, summarized mechanism and usage of each classical mucoactive medicine. In general, antioxidant mucoactive medicines play an important role in chronic airway disease, including but not limited to airway mucus clearance, reduced acute exacerbation and improved pulmonary function. © 2017 Yan et al.


Zhang D.,Wenzhou University | Li C.,Wenzhou University | Song Y.,Fudan University | Song Y.,Shanghai Respiratory Research Institute | And 8 more authors.
American Journal of Physiology - Lung Cellular and Molecular Physiology | Year: 2017

Integrin αvβ5 mediates pulmonary endothelial barrier function and acute lung injury (LI), but its roles in cell apoptosis and autophagy are unclear. Thus, the aims of this study were to investigate the significance of αvβ5 in ischemia-reperfusion (I/R)-induced apoptosis and LI and to explore the relationship between αvβ5 and autophagy. Human pulmonary microvascular endothelial cells (HPMVECs) were pretreated with an αvβ5-blocking antibody (ALULA) and challenged with oxygen-glucose deprivation/ oxygen-glucose restoration, which mimics I/R; then, cellular autophagy and apoptosis were detected, and cell permeability was assessed. In vivo, mice were pretreated with the autophagy inhibitor chloroquine (CLQ), followed by treatment with ALULA. The mice then underwent operative lung I/R. LI was assessed by performing a pathological examination, calculating the wet/dry lung weight ratio and detecting the bronchial alveolar lavage fluid (BALF) protein concentration. αvβ5 inhibition promoted HPMVEC autophagy under I/R in vitro, alleviated cell permeability, decreased the apoptosis ratio, and activated caspase-3 expression. These outcomes were significantly diminished when autophagy was inhibited with a small-inter-fering RNA construct targeting autophagy-related gene 7 (siATG7). Moreover, ALULA pretreatment alleviated I/R-induced LI (I/R-LI), which manifested as a decreased wet/dry lung weight ratio, an altered BALF protein concentration, and lung edema. Preinhibiting autophagy with CLQ, however, eliminated the protective effects of ALULA on I/R-LI. Therefore, inhibiting αvβ5 effectively ameliorated I/R-induced endothelial cell apoptosis and I/R-LI. This process was dependent on improved autophagy and its inhibitory effects on activated caspase-3. © 2017 the American Physiological Society.


Chavannes N.H.,Leiden University | Du Puy R.S.,Leiden University | Bai C.-X.,Sun Yat Sen University | Bai C.-X.,Shanghai Respiratory Research Institute | And 2 more authors.
Fudan University Journal of Medical Sciences | Year: 2017

Health information technology (HIT) is sometimes seen as a silver bullet for human resource, medical and economic challenges facing health systems.The evidence supporting widespread use of HIT is, however, still patchy and inconsistent.In this perspective piece, we seek to interpret and draw key lessons from a selection of illustrative trials in developed countries with robust health-care settings in respiratory medicine that failed to demonstrate effectiveness, and offer suggestions to maximise the chances of success in subsequent HIT deployments.Particularly low- and middle-income countries, with relatively weak health infrastructures and limited health care, propose considerable room for improvement.Early experiences of studying HIT thus far in high-income country settings suggest that this process should preferably begin with trials of low-cost, well-established technologies in patient groups with a moderate burden of disease while carefully evaluating patient safety. © 2017, Editorial Department of Fudan University Journal of Medical Sciences. All right reserved.


Yang D.,Fudan University | Yang D.,Shanghai Respiratory Research Institute | Zhou J.,Fudan University | Zhou J.,Shanghai Respiratory Research Institute | And 12 more authors.
Cancer Letters | Year: 2015

Objective: Inflammation plays an important role in the microenvironment of lung cancer. The present study aimed to evaluate the association of inflammatory biomarker networks with chemotherapies for patients with non-small cell lung cancer (NSCLC). Methods: The sera of healthy non-smokers (n = 14) and patients with NSCLC (n = 50), 36 with adenocarcinoma and 14 with squamous cell carcinoma, were collected. Healthy patients were untreated, while those with NSCLC were either chemotherapy-naïve or had received one and two courses of chemotherapy. The cytokine concentrations were measured using multiplexed cytokine immunoassays. The clinical informatics was scored with a Digital Evaluation Score System (DESS) to assess the severity of the patients. All patients completed follow-up for up to 2 years. Results: Among the 40 mediators measured, 13 significantly differed between patients with lung cancer and healthy controls, while 18 differed between untreated patients and those with stage IV adenocarcinoma who had undergone the first and second chemotherapy courses. The protein network of cytokines in NSCLC after multiple courses of chemotherapy was similar to that of normal persons. MIP-3α is the most crucial biomarker for predicting survival rates in NSCLC patients. Conclusions: Our data identify an NSCLC-specific profile of inflammatory mediators that may be useful for cancer sub-classification, as well as the evaluation of therapeutic effects and overall survival. © 2015 Elsevier Ireland Ltd.


Wu X.,Fudan University | Wu X.,Shanghai Respiratory Research Institute | Yuan B.,Harbin Medical University | Lopez E.,Hospital Universitario Nino Jesus | And 4 more authors.
Journal of Cellular and Molecular Medicine | Year: 2014

The genetic component was suggested to contribute to the development of chronic obstructive pulmonary disease (COPD), a major and growing public health burden. The present review aims to characterize the evidence that gene polymorphisms contribute to the aetiology of COPD and related traits, and explore the potential relationship between certain gene polymorphisms and COPD susceptibility, severity, lung function, phenotypes, or drug effects, even though limited results from related studies lacked consistency. Most of these studies were association studies, rather than confirmatory studies. More large-sized and strictly controlled studies are needed to prove the relationship between gene polymorphisms and the reviewed traits. More importantly, prospective confirmatory studies beyond initial association studies will be necessary to evaluate true relationships between gene polymorphisms and COPD and help individualized treatment for patients with COPD. © 2013 The Authors.


Yang D.-W.,Fudan University | Yang D.-W.,Shanghai Respiratory Research Institute | Zhang Y.,Fudan University | Zhang Y.,Shanghai Respiratory Research Institute | And 18 more authors.
Cancer | Year: 2015

BACKGROUND This study applied a combined cancer biomarker panel to clinically identify small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC) in a high-risk population. METHODS The serum levels of 4 biomarkers (progastrin-releasing peptide [ProGRP], carcinoembryonic antigen [CEA], squamous cell carcinoma antigen [SCC], and cytokeratin 19 fragment [CYFRA21-1]) were determined in 153 patients with a high risk of lung cancer (12 with a new diagnosis of SCLC, 52 with NSCLC, and 89 without lung cancer). Information about diagnosis delays was collected through interviews of all participants. RESULTS Significantly higher serum levels of ProGRP (P < .0001) were found among the SCLC patients versus the rest of the population. A receiver operating characteristic curve analysis established the cutoff values of ProGRP, CEA, SCC, and CYFRA21-1 as 300 pg/mL, 7.3 ng/mL, 3 ng/mL, and 6.5 ng/mL, respectively. The sensitivity and specificity of ProGRP in diagnosing SCLC were 75% and 100%, respectively. Among the 14 lung cancer patients with a false-negative computed tomography (CT) result, the diagnostic panel detected 8 additional cancers. CONCLUSIONS This panel increased the diagnostic specificity for high-risk subjects (those with renal failure being excluded), and auxiliary to a CT scan, it increased the sensitivity for patients with lung cancer. These results might be applied to shorten the diagnosis delay at health care institutions in China. © 2015 American Cancer Society.


Zhu H.-X.,Fudan University | Zhou J.-B.,Fudan University | Zhu X.-D.,Fudan University | Zhou J.,Fudan University | And 7 more authors.
Respiratory Physiology and Neurobiology | Year: 2016

In this study, we utilized AQP3-knockout mice as the in vivo model and AQP3-knockdown human bronchial epithelial cells (HBECs) as the in vitro model. Airway injury was experimentally induced by intra-tracheal injection of naphthalene. HE staining, transmission and scanning electron microscope were performed to evaluate self-healing capacity in vivo. Transwell and wound-healing assays were performed to evaluate epithelial cell migration in vitro. We found that both the airway epithelial cells of AQP3-knockout mice and AQP3-knockdown HBECs exhibited an obviously impaired self-healing capacity with defective epithelial cell migration through AQP3-facilitated glycerol transport. In addition, glycerol supplementation could largely correct defective injury healing and epithelial cell migration. For the first time, we found evidence for distinct defects in AQP3-deficient airway epithelial cell migration. Mechanistic analysis showed AQP3-facillitated glycerol transport plays a role in airway epithelial self-healing after injury. © 2016 Elsevier B.V.


Zhou J.,Fudan University | Zhu Z.,Liaoning Medical University | Bai C.,Fudan University | Bai C.,Shanghai Respiratory Research Institute | And 3 more authors.
Journal of Translational Medicine | Year: 2014

Lymphocytes play important roles in the balance between body defense and noxious agents involved in a number of diseases, e.g. autoimmune diseases, allergic inflammation and cancer. The proteomic analyses have been applied to identify and validate disease-associated and disease-specific biomarkers for therapeutic strategies of diseases. The proteomic profiles of lymphocytes may provide more information to understand their functions and roles in the development of diseases, although proteomic approaches in lymphocytes are still limited. The present review overviewed the proteomics-based studies on lymphocytes to headlight the proteomic profiles of lymphocytes in diseases, such as autoimmune diseases, allergic inflammation and cancer, with a special focus on lung diseases. We will explore the potential significance of diagnostic biomarkers and therapeutic targets from the current status in proteomic studies of lymphocytes and discuss the value of the currently available proteomic methodologies in the lymphocytes research. © 2014 Zhou et al.; licensee BioMed Central Ltd.


Huang P.,Fudan University | Xu X.,Fudan University | Wang L.,Fudan University | Zhu B.,Fudan University | And 3 more authors.
Journal of Cellular and Molecular Medicine | Year: 2014

Epidermal growth factor (EGF) and their receptor (EGFR) play an important role in the development of cancer proliferation, and metastasis, although the mechanism remains unclear. The present study aimed at investigating the role of EGF-EGFR signalling pathway in the development of human hepatocellular carcinoma (HCC) inflammatory environment. Gene profiles of inflammatory cytokines from HCC were measured. Cell bio-behaviours of HCC with low or high metastasis were detected by the live cell monitoring system. Cell proliferation was measured by CCK8. The protein level of CXCL5 and CXCL8 was measured by ELISA. The phosphorylation of PI3K, ERK, MAPK was measured by western blot. EGF significantly induced cell proliferation in HepG2 cells, but not in HCCLM3 cells. EGF prompted the cell movement in both HepG2 and HCCLM3 and regulated the production of CXCL5 and CXCL8 from HCC, which were inhibited by EGFR inhibitor, Erk inhibitor (U0126), or PI3K inhibitors (BEZ-235 and SHBM1009). HCC proliferation, metastasis and production of inflammatory cytokines were regulated via EGF-EGFR signal pathways. CXCL5 could interact with CXCL8, possibly by CXCR2 or the cross-talk between CXCR2 and EGFR. EGF-EGFR signaling pathway can be the potential target of therapies for HCC. © 2013 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

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