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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.


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.


Wu L.,Hyogo College of Medicine | Wu L.,The Third Peoples Hospital Of Chengdu | Oshima T.,Hyogo College of Medicine | Tomita T.,Hyogo College of Medicine | And 4 more authors.
Journal of Gastroenterology | Year: 2016

Background: Serotonin regulates gastrointestinal function, and mast cells are a potential nonneuronal source of serotonin in the esophagus. Tight junction (TJ) proteins in the esophageal epithelium contribute to the barrier function, and the serotonin signaling pathway may contribute to epithelial leakage in gastroesophageal reflux disease. Therefore, the aim of this study was to investigate the role of serotonin on barrier function, TJ proteins, and related signaling pathways. Methods: Normal primary human esophageal epithelial cells were cultured with use of an air–liquid interface system. Serotonin was added to the basolateral compartment, and transepithelial electrical resistance (TEER) was measured. The expression of TJ proteins and serotonin receptor 7 (5-HT7) was assessed by Western blotting. The involvement of 5-HT7 was assessed with use of an antagonist and an agonist. The underlying cellular signaling pathways were examined with use of specific blockers. Results: Serotonin decreased TEER and reduced the expression of TJ proteins ZO-1, occludin, and claudin 1, but not claudin 4. A 5-HT7 antagonist blocked the serotonin-induced decrease in TEER, and a 5-HT7 agonist decreased TEER. Inhibition of p38 mitogen-activated protein kinase (MAPK) reduced the serotonin-induced decrease in TEER. Inhibition of p38 MAPK blocked the decrease of ZO-1 levels, whereas extracellular-signal-regulated kinase (ERK) inhibition blocked the decrease in occludin levels. Cell signaling pathway inhibitors had no effect on serotonin-induced alterations in claudin 1 and claudin 4 levels. Serotonin induced phosphorylation of p38 MAPK and ERK, and a 5-HT7 antagonist partially blocked serotonin-induced phosphorylation of p38 MAPK but not that of ERK. Conclusions: Serotonin disrupted esophageal squamous epithelial barrier function by modulating the levels of TJ proteins. Serotonin signaling pathways may mediate the pathogenesis of gastroesophageal reflux disease. © 2016 Japanese Society of Gastroenterology


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.


Shan J.,Hyogo College of Medicine | Shan J.,The Third Peoples Hospital of Chengdu | Oshima T.,Hyogo College of Medicine | Fukui H.,Hyogo College of Medicine | And 2 more authors.
Journal of Gastroenterology and Hepatology (Australia) | Year: 2013

Background and Aim: Immune-mediated mucosal inflammation characterized by the production of interleukin (IL)-8 is associated with the development of gastroesophageal reflux disease. The effects of bile acids, which are major components of reflux fluid, on the production of IL-8 and related mechanisms remain unclear. This study aimed to address these questions using an esophageal stratified squamous epithelial model. Methods: Normal human esophageal epithelial cells were seeded on the Transwell inserts and cultured with the air-liquid interface system to establish the model. Bile acids under different pH conditions were added to the apical compartment to examine their effects on IL-8 production and the underlying cellular signaling. Results: Conjugated bile acids under a neutral or acidic condition did not induce IL-8 production, and unconjugated bile acids, deoxycholic acid (DCA), and chenodeoxycholic acid (CDCA) all significantly induced IL-8 production, dose- and time-dependently, only under weakly acid conditions. Inhibition of p38 mitogen-activated protein kinase (p38 MAPK) and protein kinase A (PKA) attenuated the production of IL-8 induced by acidic DCA and CDCA. Inhibition of PKA did not block the bile acid-induced p38 MAPK activation. Conclusions: Compared with conjugated bile acids, the unconjugated bile acids DCA and CDCA are more likely to induce IL-8 production in vivo, especially under weakly acid conditions. This process involves two independent signaling pathways, p38 MAPK and PKA. © 2013 Journal of Gastroenterology and Hepatology Foundation and Wiley Publishing Asia Pty Ltd.


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.


Zhong D.-K.,University of Sichuan | Tang D.,Chengdu University of Traditional Chinese Medicine | Xue L.,The Third Peoples Hospital Of Chengdu | Wen J.,University of Sichuan | Li Y.-P.,University of Sichuan
Chinese Journal of Integrative Medicine | Year: 2016

Objective: To review and assess the effect of single moxibustion for exercise-induced fatigue: (EIF). Methods: Computer-search for 8 medical databases and 5 clinical trail registries were conducted for: randomized controlled trials (RCTs), added with hand-search for 10 Chinese acupuncture-moxibustion journals and additional references. Data from included RCTs were pooled by RevMan5.1. Methodology quality of RCTs was judged by Cochrane Collaboration assessment tool while quality of primary outcomes was evaluated by GRADE3.2. Results: Five RCTs were finally included, all reported in small sample size with high risk of: bias. Comparisons on single moxibustion and rest relief (without treatment) were studied. Six outcomes were reported, all favored moxibustion to rest relief for EIF. Primary outcomes showed as rating of perceived exertion (RPE) with mean difference (MD)=−0.49, 95% confidence interval (CI) [−0.80, −0.19], 800-m race performance with MD=−2.21, 95% CI [−3.57, −0.85], and Harvard Step Index (HSI) with MD=14.75, 95% CI [8.35, 21.15]. Moreover, all primary outcomes as RPE, 800-m race performance and HSI were rated low quality. Conclusions: Single moxibustion might be considered effective for EIF. However, due to small samples of included RCTs, high risk of bias among studies and poor quality of primary outcomes and subjects restricted to Chinese athletes only, these results present limitation, and should be taken with caution for practice. More large-size studies with rigorous design are warranted to further test effectiveness of moxibustion for EIF. © 2014, Chinese Association of the Integration of Traditional and Western Medicine and Springer-Verlag Berlin Heidelberg.

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