The Third Peoples Hospital of Chengdu

Chengdu, China

The Third Peoples Hospital of Chengdu

Chengdu, China
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Liu H.,Sichuan Provincial Peoples Hospital | Yang Z.,Sichuan Provincial Peoples Hospital | Zhang J.,The Third Peoples Hospital Of Chengdu | Zhu X.,Sichuan Provincial Peoples Hospital
International Journal of Clinical and Experimental Medicine | Year: 2017

Mounting studies indicated that aberrant circulating microRNA expression was associated to gastric cancer (GC). In the present study, we aimed to explore plasma miR-217 expression in GC patients and evaluated its diagnostic value as a promising biomarker for GC screening. The plasma samples were collected from 137 patients with GC and 145 healthy controls. Plasma miR-217 expression was determined through qRT-PCR and further correlated with patients’ clinicopathological parameters and follow-up data. Receiver-operating characteristic (ROC) curve analysis was carried out to assess the diagnostic value of plasma miR-217 in GC, and COX regression analysis was performed to find independent risk factors for overall survival (OS) and disease-free survival (DFS) of GC patients. Compared with healthy controls, expression of plasma miR-217 was remarkably lower in GC patients (P<0.001). ROC curve analysis showed that the area under the curve (AUC) of plasma miR-217 was 0.893, and its specificity and sensitivity were 0.832 and 0.813 at a diagnostic threshold of 0.021. Down-regulation of plasma miR-217 was closely associated with larger tumor size (P=0.040), present distant metastasis (P=0.038), poor differentiation status (P=0.016) and advanced TNM stage (P=0.005). GC patients with low plasma miR-217 expression had relatively lower overall survival (OS) rate and disease-free survival (DFS) rate after surgery than those with high plasma miR-217 expression. Moreover, multivariate COX regression analysis demonstrated that plasma miR-217 expression was an independent risk factor for OS and DFS of GC patients. Plasma miR-217 levels were significantly down-regulated in GC patients and it could be considered as a promising non-invasive biomarker for GC. © 2017, E-Century Publishing Corporation. All rights reserved.


Zhu X.,Sichuan Provincial Peoples Hospital | Yang Z.,Sichuan Provincial Peoples Hospital | Zhang J.,The Third Peoples Hospital Of Chengdu | Liu H.,Sichuan Provincial Peoples Hospital
International Journal of Clinical and Experimental Medicine | Year: 2017

Background: Despite advances in technology, human gastric cancer (GC) remains a diagnostic challenge mainly because of its variable features and lack of reliable diagnostic method. MicroRNAs (miRNAs) are reported to regulate gene expression through modulating a wide range of pathophysiologic processes. Serum miRNAs are promising biomarkers in various human cancers, including GC. In the present study, we aimed to indentify microRNA-145 (miR-145) as a serum biomarker for GC screening in clinical. Methods: Serum miR-145 expression of 114 GC patients, 68 patients with precancerous lesion (PL) and 95 healthy donors was detected through qRT-PCR. Receiver operator characteristic (ROC) curve analysis was performed to evaluate the diagnostic value of serum miR-145 characterized as the alternative biomarker. Serum miR-145 levels were correlated with the clinicopathological characteristics and follow-up information of the GC patients. Multivariate regression analysis was finally conducted to confirm if serum miR-145 expression could be regarded as an independent risk factor for GC patients’ prognosis. Results: Serum miR-145 levels were dramatically lower in the GC patients than in healthy controls and PL patients (all P<0.001). ROC curve analysis showed that serum miR-145 was a specific diagnostic biomarker for distinguishing GC patients from healthy individuals and PL patients. Low expression of serum miR-145 was significantly correlated to tumor size (P=0.018), distant metastasis (P=0.039), histologic differentiation (P=0.016) and TNM stage (P=0.012). GC patients with relatively lower serum miR-145 levels had remarkably decreased disease-free survival (DFS) rate and overall survival (OS) rate after surgery (all P<0.01). Multivariate regression analysis revealed that serum miR-145 level (P=0.035) was an independent risk factor for OS in GC. Conclusions: Our findings revealed that serum miR-145 level could be considered as a promising biomarker for GC diagnosis in the future. © 2017, E-Century Publishing Corporation. All rights reserved.


Tang Y.,The Third Peoples Hospital of Chengdu | Shi W.,The Third Peoples Hospital of Chengdu | Sun X.,The Third Peoples Hospital of Chengdu | Xi W.,The Third Peoples Hospital of Chengdu
Diseases of the Esophagus | Year: 2017

Definite diagnosis of esophageal tuberculosis (ET) requires isolation of tubercle bacilli, which is challenging in clinical practice. Difficulty in differentiating ET from other esophageal diseases may well result in a delay in diagnosis. The literature on utility of endoscopic ultrasound (EUS) in diagnosis of ET is insufficient. This study aims to evaluate the role of EUS morphology combined with EUS-guided tissue acquisition in the diagnosis of ET. Data of the 35 patients diagnosed with ET from January 2006 to October 2015 were retrospectively analyzed. After miniprobe and linear echoendoscopic visualization, either linear EUS-guided deep biopsy or EUS-guided fine needle aspiration was performed for tissue acquisition. Histocytopathological results showing caseous necrosis or acid fast bacilli (AFB) or epithelioid granuloma were considered diagnostic. Esophageal wall thickening or mass formation with disruption of the adventitia due to infiltration by adjacent mediastinal lymphadenopathy was typically observed under EUS. Tissue acquisition revealed epithelioid granuloma in 33 patients, caseous necrosis in 13, a positive AFB stain in 14, and nonspecific chronic inflammation in 2. Of the 35 patients, 33 (94.3%) with both characteristic EUS morphology and diagnostic histocytopathology were considered to have an EUS established diagnosis. The remaining two with only nonspecific chronic inflammation received empirical antitubercular chemotherapy based solely on EUS morphology. The two-year follow-up confirmed diagnosis of ET in all patients. While the final diagnosis of ET was based upon two-year follow-up of treatment response to antitubercular medication in addition to caseous necrosis/granuloma/positive-AFB stain revealed by EUS-guided tissue acquisition, an EUS-established diagnosis of ET and medical treatment with long-term follow-up is rational and practical compared with surgery or untreated follow-up. © 2017, © The Authors 2017. Published by Oxford University Press on behalf of International Society for Diseases of the Esophagus. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.


Zhang J.,The third peoples hospital of Chengdu | Fan J.,The third peoples hospital of Chengdu | Zhou C.,The third peoples hospital of Chengdu | Qi Y.,The third peoples hospital of Chengdu
BMC Gastroenterology | Year: 2017

Background: This study aimed to investigate potential miRNAs and genes associated with the prognosis of hepatocellular carcinoma (HCC). Methods: Weighted co-expression network analysis was utilized to analyze the mRNA and miRNA sequencing data of HCC from TCGA (The Cancer Genome Atlas) database. Significant network modules were identified, and then functions of genes in the gene network modules and target genes of miRNAs in the miRNA network modules were explored. Additionally, correlations between network modules and prognostic factors of HCC were analyzed. Results: In total, 10 mRNA network modules were identified, three of which were significantly related to tumor stage, NAFLD (non-alcoholic fatty liver disease) and patient age. Four miRNA network modules were identified, of which one was associated with tumor stage. Targets of hsa-miR-363-5p were found distributed in the gene network modules, such as RGPD5, RGPD6, ZNF445 and ZNF780B. Kaplan-Meier test revealed that low expression of hsa-miR-363-5p was associated with better overall survival of HCC patients. Conclusion: hsa-miR-363-5p may be a potential prognostic marker for HCC. © 2017 The Author(s).


Zhou H.,Sichuan Cancer Hospital | Zeng C.,The Third Peoples Hospital of Chengdu | Wei Y.,Sichuan Cancer Hospital | Zhou J.,Sichuan Cancer Hospital | Yao W.,Sichuan Cancer Hospital
PLoS ONE | Year: 2013

Background:Maintenance chemotherapy is widely provided to patients with small cell lung cancer (SCLC). However, the benefits of maintenance chemotherapy compared with observation are a subject of debate.Methodology and Principal Findings:To identify relevant literature, we systematically searched the Medline, Embase, and Cochrane Central Register of Controlled Trials databases. Eligible trials included patients with SCLC who either received maintenance chemotherapy (administered according to a continuous or switch strategy) or underwent observation. The primary outcome was 1-year mortality, and secondary outcomes were 2-year mortality, overall survival (OS), and progression-free survival (PFS). Of the 665 studies found in our search, we identified 14 relevant trials, which together reported data on 1806 patients with SCLC. When compared with observation, maintenance chemotherapy had no effect on 1-year mortality (odds ratio [OR]: 0.88; 95% confidence interval [CI]: 0.66-1.19; P = 0.414), 2-year mortality (OR: 0.82; 95% CI: 0.57-1.19; P = 0.302), OS (hazard ratio [HR]: 0.87; 95% CI: 0.71-1.06; P = 0.172), or PFS (HR: 0.87; 95% CI: 0.62-1.22; P = 0.432). However, subgroup analyses indicated that maintenance chemotherapy was associated with significantly longer PFS than observation in patients with extensive SCLC (HR, 0.72; 95% CI: 0.58-0.89; P = 0.003). Additionally, patients who were managed using the continuous strategy of maintenance chemotherapy appeared to be at a disadvantage in terms of PFS compared with patients who only underwent observation (HR, 1.27; 95% CI: 1.04-1.54; P = 0.018).Conclusions/Significance:Maintenance chemotherapy failed to improve survival outcomes in patients with SCLC. However, a significant advantage in terms of PFS was observed for maintenance chemotherapy in patients with extensive disease. Additionally, our results suggest that the continuous strategy is inferior to observation; its clinical value needs to be investigated in additional trials. © 2013 Zhou et al.


Shan J.,Hyogo College of Medicine | Shan J.,The Third Peoples Hospital of Chengdu | Oshima T.,Hyogo College of Medicine | Farre R.,Catholic University of Leuven | And 3 more authors.
American Journal of Physiology - Gastrointestinal and Liver Physiology | Year: 2014

Barrett's esophagus is characterized by a distinct Th2-predominant cytokine profile (IL-4) from in vivo or ex vivo evidence. The detailed role of cytokines in Barrett's esophagus, particularly whether Th2 cytokines are causative factors driving metaplastic processes, remains unknown. In this study, air-liquid interface-cultured human esophageal epithelial cells were stimulated by a Th2 cytokine, IL-4, and Th1 cytokines, TNF-α and IL-1β, continuously for 10 days. Barrier function was determined by transepithelial electrical resistance. Morphological changes were investigated by hematoxylin and eosin staining. Keratin profile (keratin 7, 8, 13, and 14) and squamous differentiation markers (involucrin) were investigated by RT-quantitative PCR, Western blotting, and immunohistochemical staining. Pharmacological inhibitors were used to identify the underlying cellular signaling. We report that IL-4, TNF-α, and IL-1β decrease barrier function, but only IL-4 significantly increases cell layers and changes cell morphology. IL-4 time dependently downregulates the expression levels of the squamous cell markers involucrin and keratin 13 and upregulates the expression levels of the columnar cell markers keratin 7 and 8. Neither TNF-α nor IL-1β shows any effect on these indexes. JAK inhibitor I and PI3K inhibitors significantly block the IL-4-induced changes in the levels of keratin 8 and 13. In conclusion, IL-4 inhibits squamous differentiation program of esophageal epithelial cells and induces differentiation toward columnar cells through the JAK/PI3K pathway. Thus IL-4 may be involved in the early stages of Barrett's esophagus development. © 2014 the American Physiological Society.


Shan J.,Hyogo College of Medicine | Shan J.,The Third Peoples Hospital Of Chengdu | Oshima T.,Hyogo College of Medicine | Muto T.,Hyogo College of Medicine | And 5 more authors.
Journal of Gastroenterology | Year: 2015

Background: IL-33 is a new tissue-derived cytokine constitutively expressed in epithelial cells and plays a role in sensing damage caused by inflammatory diseases. The function of IL-33 in the esophageal mucosa has not been previously described. Accordingly, we examined the expression of IL-33 and its role in the pathogenesis of reflux esophagitis (RE). Methods: IL-33 in the esophageal mucosa of RE patients and in an in vitro stratified normal esophageal squamous epithelial model was examined at the messenger RNA and protein levels. The correlation of the level of IL-33 and IL-8 or IL-6 was examined. Cell layers were stimulated with bile acids and cytokines. IL-33 was knocked down by small interfering RNA (siRNA). Pharmacological inhibitors and signal transducer and activator of transcription 1 (STAT1) siRNA were used. Results: IL-33 was significantly upregulated in RE patients, and was located in the nuclei of basal and suprabasal layers. Upregulated IL-33 messenger RNA expression was correlated with IL-8 and IL-6 expression. In vitro, IL-33 was upregulated in the nuclei of basal and suprabasal layers by interferon-γ (IFNγ), and the upregulation was aggravated by the combination of deoxycholic acid (DCA) and IFNγ. IL-33 knockdown dampened IFNγ- and DCA-induced IL-8 and IL-6 production. IFNγ-induced IL-33 was inhibited by a Janus kinase inhibitor, a p38 mitogen-activated protein kinase inhibitor, and STAT1 siRNA. Conclusions: Nuclear IL-33 is upregulated in erosive mucosa of RE patients and is correlated with IL-8 and IL-6 levels. The normal esophageal epithelial model enables us to show for the first time that epithelial-cell-derived nuclear but not exogenous IL-33 is located upstream of the production of inflammatory cytokines and can aggravate the inflammation. © 2014, Springer Japan.


Tan Y.,Dujiangyan Maternal and Child Health Care Hospital | Yang P.,The Third Peoples Hospital of Chengdu | Deng X.,The Third Peoples Hospital of Chengdu | Tang Y.,The Third Peoples Hospital of Chengdu
Oncology Letters | Year: 2015

A 44-year-old male presented with progressing cough, dyspnea and hemoptysis due to a tracheal tumor involving the posterior wall of the lower trachea, with severe airway obstruction and coagulopathy. Consequently the patient underwent segmental resection of the trachea with an end-to-end anastomosis. Twenty months after treatment there remained no evidence of endobronchial recurrence at bronchoscopy or imaging studies. The diagnosis was benign tracheal glomus tumor (GT) which is an exceedingly rare mass lesion in the trachea. There are three subtypes: GT proper, glomangioma and glomangiomyoma. The present study describes the clinical and pathological features of glomangioma through a case report and literature review. To the best of our knowledge, this is the fifth report of glomangioma subtype arising from the trachea. © 2014, Spandidos Publications. All rights received.


Xie J.,Chongqing Medical University | Xie J.,The Third Peoples Hospital of Chengdu | Xiang D.-B.,Jiangjin Central Hospital | Wang H.,Chongqing Medical University | And 5 more authors.
PLoS ONE | Year: 2012

Aberrant activation of β-catenin/Tcf-4 signaling has been implicated in human carcinogenesis, including colorectal cancer. In this study, we compared the effects of Tcf-4 knockdown with β-catenin knockdown on cell proliferation, apoptosis, and chemosensitivity in SW480 and HCT116 colon cancer cells using adenoviral vector-mediated short hairpin RNA (shRNA). Our results show that, compared to β-catenin knockdown, Tcf-4 knockdown more effectively inhibited colony formation, induced apoptosis, and increased 5-FU and oxaliplatin-mediated cytotoxicity in colon cancer cells. We further investigated the mechanisms involved in the different efficacies observed with β-catenin and Tcf-4 knockdown in colon cancer cells. FOXO4 is a member of the subfamily of mammalian FOXO forkhead transcription factors and plays a major role in controlling cellular proliferation, apoptosis, and DNA repair. Our data showed that the protein level of FOXO4 did not change after treatment with both β-catenin and Tcf-4 shRNA. However, β-catenin shRNA was found to increase the accumulation of phosphorylated FOXO4 S193 and decrease the expression of FOXO target genes p27Kip1 and MnSOD, whereas Tcf-4 shRNA showed the opposite effect. Therefore, compared to β-catenin knockdown, Tcf-4 knockdown shows better efficacy for inhibiting proliferation and inducing apoptosis of colorectal cancer cells, which may be related to increased FOXO4 transcriptional activity. These results suggest that Tcf-4 is an attractive potential therapeutic target for colorectal cancer therapy. © 2012 Xie et al.


Zhuo G.-Y.,Chongqing Medical University | Zhuo G.-Y.,University of Sichuan | He Q.,The Third Peoples Hospital of Chengdu | Xiang-Lian L.,University of Sichuan | And 2 more authors.
Pulmonary Pharmacology and Therapeutics | Year: 2014

Background: Infection, resulting in chronic airway inflammation, forms the basis of bronchiectasis pathogenesis. Macrolides possess antibacterial, anti-inflammatory and immunomodulatory properties, and are used to treat patients with non-cystic fibrosis bronchiectasis (NCFB). However, the efficacy and safety of long-term treatment with macrolides in patients with bronchiectasis have been controversial. We performed a meta-analysis to assess the efficacy and safety of macrolides in adults with NCFB. Methods: We performed electronic search of several databases, including: Pubmed, EMBASE, EBSCO, SCI, and CENTRAL, and also searched references from identified articles for further consideration. Only randomized controlled trials (RCTs) comparing prolonged macrolide treatment with placebo for adult bronchiectasis were included. Data were extracted independently by two reviewers and combined using a fixed-effects model or random-effects with effect size expressed as OR or MD or SMD and 95% CIs for different situations. Results: 834 studies were identified. Four RCTs met the inclusion criteria. Macrolide treatment significantly reduced pulmonary exacerbation (OR=0.39, 95% CI 0.25-0.63) and improved lung function (SMD=0.37, 95% CI 0.16-0.58) as compared to the placebo group. However, macrolide treatment did not significantly improve quality of life (MD=-1.90, 95% CI-7.01 to 3.20). With respect to the total numbers of participants who developed adverse events, there was no significant difference between the macrolides and placebo groups (OR=0.83, 95% CI 0.50-1.39). Macrolides therapy could have increased the rate of macrolide resistance in adults with NCFB. Conclusions: Macrolide maintenance therapy was effective in reducing pulmonary exacerbations, and improving lung function in adults with NCFB. However, it did not improve quality of life, and could have led to macrolide resistance. © 2014 Elsevier Ltd.

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