Third Peoples Hospital of Chengdu

of Chengdu, China

Third Peoples Hospital of Chengdu

of Chengdu, China
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Wang B.,University of Sichuan | Wang B.,Second Peoples Hospital of Chengdu | He P.,Third Peoples Hospital of Chengdu | Dong B.,University of Sichuan
Archives of Gerontology and Geriatrics | Year: 2015

Objective: To explore the associations between social networks, social contacts, and cognitive impairment in the very elderly aged 90-108 years. Methods: Data were from subjects of the Project of Longevity and Ageing in Dujiangyan, China. The socio-demographic, social networks, and social contacts data were collected and cognitive function was assessed in all subjects using the Mini-Mental State Examination (MMSE). Results: 764 Chinese nonagenarians and centenarians (67.41% women, mean age 93.47 years) were included. The mean MMSE score was 14.99. ±. 5.93). The prevalence of cognitive impairment was 64.53%. The mean social contact score was 4.37. ±. 1.86. There were significantly different cognitive function scores among individuals with different marital status, number of close friends, and different social contact levels (all P<. 0.05). Spearman rank correlation analysis showed that number of close friends and social contact scores were significantly positively but single status was significantly negatively correlated with the MMSE scores (all P<. 0.05). Multiple logistic regression analysis showed that there were associations between single status, no close friend, and low level of social contact with cognitive impairment (all P<. 0.05), but not other social network variables. Conclusion: Single status, no close friend, and low level of social contact were associated with increased risk of cognitive impairment in Chinese nonagenarians and centenarians. Our finding might add new information for social networks, social contacts, and cognitive research in the elderly. © 2015 Elsevier Ireland Ltd.


Wang B.,University of Sichuan | Wang B.,Second Peoples Hospital of Chengdu | He P.,Third Peoples Hospital of Chengdu | Dong B.,University of Sichuan
Geriatrics and Gerontology International | Year: 2015

Aim: We explored the association between family functioning and cognitive impairment in the very elderly aged 90-108years. Methods: The present study comprised data from subjects included in the 2005 Project of Longevity and Aging in Dujiangyan, China. Sociodemographic and family functioning data were collected, and cognitive function was assessed in all subjects using the Mini-Mental State Examination. Results: Data from 699 Chinese nonagenarians and centenarians were included. The prevalence of cognitive impairment was 62.8%. The prevalence of family dysfunction was 52.2%, including 8.6% severe and 43.6% moderate dysfunction. There were significant differences among individuals with different family functioning level with regard to cognitive function scores (P=0.005) or cognitive impairment prevalence (P=0.012). Subjects with cognitive impairment had lower family functioning scores than those without cognitive impairment (P=0.004). Pearson's correlation analysis showed that family functioning scores were correlated with Mini-Mental State Examination scores (r=0.13, P=0.001). Multiple logistic regressions showed that severe family dysfunction was a risk factor for cognitive impairment. The effect remained after adjusting for sociodemographic status, life habits and metabolic indicators. Conclusions: Family functioning was related to cognitive impairment among Chinese nonagenarians and centenarians. We found that the higher the family functioning scores, the higher the Mini-Mental State Examination scores. Severe family dysfunction was associated with increased risk of cognitive impairment. © 2015 Japan Geriatrics Society.


Lei W.,Peoples Hospital Of Mianzhu | Liu Y.-E.,The PLA Second Artillery General Hospital | Zheng Y.,Third Peoples Hospital Of Chengdu | Qu L.,Design Institute of Chengdu Military Region
Medical Science Monitor | Year: 2015

Background: Oral squamous cell carcinoma (OSCC) is the sixth most common human malignancy worldwide. To develop new therapeutics requires elucidation of the underlying mechanism of OSCC pathogenesis. The role of miR-429 in OSCC remains unknown.Material/Methods: The level of miR-429 and ZEB1 in OSCC tissues and cell lines was measured by qRT-PCR. MiR-429 was downregulated by miRNAs antisense oligonucleotides (ASO) transfection and up-regulated by miRNAs mimics. Cell proliferation was analyzed by MTT assay. Cell apoptosis was revealed by FACS analysis. Targeted genes were predicted by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay.Results: MiR-429 was down-regulated in OSCC tissues, and miR-429 overexpression inhibited OSCC cell lines growth and vice versa. Further, we found that miR-429 could inhibit zinc finger E-boxbinding homeobox 1 (ZEB1) expression, and that miR-429 and ZEB1 expression in OSCC tissues were negatively correlated.Conclusions: Our data demonstrate the tumor suppressor role of miR-429 in OSCC, and may provide a potential therapeutic target that warrants further investigation. © Med Sci Monit.


Zhang Y.,Third Peoples Hospital of Chengdu | Yan L.,Chongqing Medical University | Zhao Y.,Chongqing Medical University | Ou L.,Chongqing Medical University | And 2 more authors.
Cancer Biotherapy and Radiopharmaceuticals | Year: 2013

Transitional cell carcinoma of bladder (TCCB) is a common malignancy worldwide, and outcomes for patients with advanced bladder cancer remain poor. To study the pathogenesis of TCCB, we investigated roles of Phospholipase C (PLC)Eε, an effector of Ras and Rap small GTPases. RNA interference was used to knockdown PLCEε expression in human bladder cancer cell lines (BIU-87 and T24). The expression levels of PLCEε mRNA and protein were detected by reverse transcriptase-polymerase chain reaction and Western blot, respectively. Flow cytometry (FCM) was used to detect distribution of cell cycle. Cellular apoptosis was reflected by transmission electron microscopy and the expression of bcl-2 and bax. We found that PLCEε could be efficiently knocked down by shRNA. FCM assay showed that the pGenesil-PLCEε-transfected cells were arrested at the G0/G1 phase. Silence of PLCEε might induce apoptosis via modulation of bcl-2 and bax. In conclusion, our results suggest that PLCEε plays an important role in the pathogenesis of human bladder cancer cells. PLCEε may be used as a potential target of gene therapy for bladder cancer in future. © Mary Ann Liebert, Inc.


Yu H.,University of Sichuan | Yu H.,Third Peoples Hospital of Chengdu | Qing H.,University of Sichuan | Qing H.,Third Peoples Hospital of Chengdu | Lei Z.,University of Sichuan
American Journal of Emergency Medicine | Year: 2013

Objectives Cytidine diphosphate choline (CDP-choline) is a cholinergic agent that can both stimulate the cholinergic pathway and increase blood pressure. We aimed to investigate the effects of CDP-choline on the outcome of cardiac arrest in comparison with epinephrine. Methods This was a randomized prospective animal study. Cardiac arrest was induced by asphyxia in 45 rats. After 7 minutes of asphyxia, resuscitation was attempted. The rats were allocated to different groups treated with 2 mL/kg saline, 100 μg/kg epinephrine, or 250 mg/kg CDP-choline. The hemodynamic parameters were monitored for 2 hours after resuscitation, and cardiac function was evaluated by echocardiography 2 hours after resuscitation. The hearts were harvested at the end of monitoring for histologic evaluation. Results Epinephrine and CDP-choline improved the rate of return of spontaneous circulation and blood pressure during cardiopulmonary resuscitation; however, postresuscitation cardiac function in the CDP-choline and placebo groups was better than in the epinephrine group. Compared with the epinephrine group, less myocardial and mitochondrial injury was observed by electron microscopy in the CDP-choline and placebo groups; the level of superoxide dismutase and malondialdehyde indicated less peroxidative injury in the CDP-choline and placebo groups. Cytidine diphosphate choline and placebo also preserved connexin 43 when compared with epinephrine. Conclusion When administered during resuscitation, CDP-choline increased the rate of return of spontaneous circulation similarly to epinephrine. In addition, it did not increase the severity of myocardial injury and postresuscitation myocardial dysfunction, whereas epinephrine appeared to be harmful. © 2013 Elsevier Inc.


Shan J.,Hyogo College of Medicine | Shan J.,Third Peoples Hospital of Chengdu | Oshima T.,Hyogo College of Medicine | Wu L.,Hyogo College of Medicine | And 4 more authors.
PLoS ONE | Year: 2016

Background: Esophageal epithelial cells are an initiating cell type in esophageal inflammation, playing an essential role in the pathogenesis of gastroesophageal reflux disease (GERD). A new tissue-derived cytokine, interleukin-33 (IL-33), has been shown to be upregulated in esophageal epithelial cell nuclei in GERD, taking part in mucosal inflammation. Here, inflammatory cytokines secreted by esophageal epithelial cells, and their regulation by IL-33, were investigated. Methods: In an in vitro stratified squamous epithelial model, IL-33 expression was examined using quantitative RT-PCR, western blot, ELISA, and immunofluorescence. Epithelial cell secreted inflammatory cytokines were examined using multiplex flow immunoassay. IL-33 was knocked down with small interfering RNA (siRNA) in normal human esophageal epithelial cells (HEECs). Pharmacological inhibitors and signal transducers and activators of transcription 1 (STAT1) siRNA were used to explore the signaling pathways. Results: Interferon (IFN)γ treatment upregulated nuclear IL-33 in HEECs. Furthermore, HEECs can produce various inflammatory cytokines, such as IL-6, IL-8, monocyte chemoattractant protein 1 (MCP-1), regulated on activation normal T-cell expressed and presumably secreted (RANTES), and granulocyte-macrophage colony-stimulating factor (GM-CSF) in response to IFNγ. Nuclear, but not exogenous IL-33, amplified IFN induction of these cytokines. P38 mitogen-activated protein kinase (MAPK) and janus protein tyrosine kinases (JAK)/STAT1 were the common signaling pathways of IFNγ-mediated induction of IL-33 and other cytokines. Conclusions: Esophageal epithelial cells can actively participate in GERD pathogenesis through the production of various cytokines, and epithelial-derived IL-33 might play a central role in the production of these cytokines. © 2016 Shan et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Wang J.,Third Peoples Hospital of Chengdu
Chinese Journal of Evidence-Based Medicine | Year: 2010

Objective: To discuss the safety and effectiveness of removing esophageal foreign bodies in children by using Foley catheter. Method: Retrospective analysis on the effect, operation method, complication and the types of foreign bodies of 138 cases of removing esophageal foreign bodies in children by using Foley catheter, which happened from January 1998 to January 2008 in Department of Otorhinolaryngology, the Third People's Hospital of Chengdu. Result: Among these 138 cases with esophageal foreign bodies, 126 cases (91.3%) were successfully taken out by using Foley catheter without anaesthesia, 7 cases were applied esophagoscopy under general anaesthesia, and 5 cases were cured owing to the slipping of foreign body into stomach. The operating time for Foley catheter was 5.1 minutes in average, and there's no complicating disease in any case. The hard esophagoscope operation lasted for 15 minutes in average and one case was accompanied by dyspnea. The foreign bodies in 138 cases were coin (98 cases), button (14 cases), chess and I-go piece (13 cases), key-ring (4 cases), plastic bottle cap (3 cases), oblate battery (3 cases) and ring (3 cases), respectively. Conclusion: Foley catheter is safe and effective for removing esophageal obtuse-rounded foreign bodies in children. © 2010 Editorial Board of Chin J Evid-based Med.


Yang Y.,China Pharmaceutical University | Yang Y.,Third Peoples Hospital of Chengdu | Wu X.,China Pharmaceutical University | Wei Z.,China Pharmaceutical University | And 7 more authors.
Pharmacological Research | Year: 2015

Curcumin (CUR) has been proven to be clinically effective in rheumatoid arthritis (RA) therapy, but its low oral bioavailability eclipses existent evidence that attempts to explain the underlying mechanism. Small intestine, the only organ exposed to a relatively high concentration of CUR, is the main site that generates gut hormones which are involved in the pathogenesis of RA. This study aims at addressing the hypothesis that one or more gut hormones serve as an intermediary agent for the anti-arthritic action of CUR. The protein and mRNA levels of gut hormones in CUR-treated rats were analyzed by ELISA and RT-PCR. Somatostatin (SOM) depletor and receptor antagonist were used to verify the key role of SOM in CUR-mediated anti-arthritic effect. The mechanisms underlying CUR-induced upregulation of SOM levels were explored by cellular experiments and immunohistochemical staining. The data showed that oral administration of CUR (100 mg/kg) for consecutive two weeks in adjuvant-induced arthritis rats still exhibited an extremely low plasma exposure despite of a dramatic amelioration of arthritis symptoms. When injected intraperitoneally, CUR lost anti-arthritic effect in rats, suggesting that it functions in an intestine-dependent manner. CUR elevated SOM levels in intestines and sera, and SOM depletor and non-selective SOM receptor antagonist could abolish the inhibitory effect of CUR on arthritis. Immunohistochemical assay demonstrated that CUR markedly increased the number of SOM-positive cells in both duodenum and jejunum. In vitro experiments demonstrated that CUR could augment SOM secretion from intestinal endocrine cells, and this effect could be hampered by either MEK1/2 or Ca2+/calmodulin-dependent kinase II (CAMKII) inhibitor. In summary, oral administration of CUR exhibits anti-arthritic effect through augmenting SOM secretion from the endocrine cells in small intestines via cAMP/PKA and Ca2+/CaMKII signaling pathways. © 2015 Elsevier Ltd. All rights reserved.


Shan J.,Hyogo College of Medicine | Shan J.,Third Peoples Hospital of Chengdu | Oshima T.,Hyogo College of Medicine | Chen X.,Hyogo College of Medicine | And 3 more authors.
American Journal of Physiology - Gastrointestinal and Liver Physiology | Year: 2012

Immune- mediated injury by the protease-activated receptor-2-interleukin- 8 (PAR-2-IL8) pathway may underlie the development of gastroesophageal reflux disease (GERD). However, the localization of PAR-2 and the mechanism of PAR-2 activation remain unclear. This study aimed to address these questions on an esophageal stratified squamous epithelial model and in the human esophageal mucosa of GERD patients. Normal human esophageal epithelial cells were cultured with the air-liquid interface system to establish the model. SLIGKV-NH2 (PAR-2 synthetic agonist), trypsin (PAR-2 natural activator), and weak acid (pH 4, 5, and 6) were added to either the apical or basolateral compartment to evaluate their effects on transepithelial electrical resistance (TEER) and IL-8 production. PAR-2 localization was examined both in the cell model and biopsies from GERD patients by immunohistochemistry. Apical trypsin stimulation induced IL-8 accompanied by decreased TEER in vitro, whereas the effective concentration from the basolateral side was 10 times lower. SLIGKV-NH2 from basolateral but not apical stimulation induced IL-8 production. Apical weak acid stimulation did not influence TEER or IL-8 production. Immunohistochemistry showed intense reactivity of PAR-2 in the basal and suprabasal layers after stimulation with trypsin. A similar PAR-2 reactivity that was mainly located at the basal and suprabasal layers was detected in GERD patients. In conclusion, the activation of the PAR-2-IL-8 pathway probably occurred at the basal and suprabasal layers, while the esophageal epithelial barrier may influence the activation of PAR-2. Under proton pump inhibitor therapy, refluxed trypsin may remain active and be a potential agent in the pathogenesis of refractory GERD. © 2012 the American Physiological Society.


Guo J.,Chongqing Medical University | Cheng C.,Chongqing Medical University | Yan W.,Chongqing Medical University | Xu G.,Third Peoples Hospital of Chengdu | And 4 more authors.
PLoS ONE | Year: 2014

Background: High quality clinical practice guidelines (CPGs) can provide clinicians with explicit recommendations on how to manage health conditions and bridge the gap between research and clinical practice. Unfortunately, the quality of CPGs for multiple sclerosis (MS) has not been evaluated. Objective: To evaluate the methodological quality of CPGs on MS using the AGREE II instrument. Methods: According to the inclusion and exclusion criteria, we searched four databases and two websites related to CPGs, including the Cochrane library, PubMed, EMBASE, DynaMed, the National Guideline Clearinghouse (NGC), and Chinese Biomedical Literature database (CBM). The searches were performed on September 20th 2013. All CPGs on MS were evaluated by the AGREE II instrument. The software used for analysis was SPSS 17.0. Results: A total of 27 CPGs on MS met inclusion criteria. The overall agreement among reviews was good or substantial (ICC was above 0.70). The mean scores for each of all six domains were presented as follows: scope and purpose (mean ± SD: 59.05±16.13), stakeholder involvement (mean ± SD: 29.53±17.67), rigor of development (mean ± SD: 31.52±21.50), clarity of presentation (mean ± SD: 60.39±13.73), applicability (mean ± SD: 27.08±17.66), editorial independence (mean ± SD: 28.70±22.03). Conclusions: The methodological quality of CPGs for MS was acceptable for scope, purpose and clarity of presentation. The developers of CPGs need to pay more attention to editorial independence, applicability, rigor of development and stakeholder involvement during the development process. The AGREE II instrument should be adopted by guideline developers. © 2014 Guo et al.

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