West China Second Hospital

Chengdu, China

West China Second Hospital

Chengdu, China
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Yang C.,West China Second Hospital | Zhang L.,West China Second Hospital | Guo Q.,University of Sichuan
Medicine (United States) | Year: 2016

Background: Tic disorders (TD) are common neuropsychiatric disorders among children and adolescents. Still, there is great uncertainty regarding their epidemiology in China. We aim to depict the prevalence of TD for children in China and explore the influence of sex, age, geographic distribution, and diagnostic criteria on the prevalence rates. Methods: We searched PubMed, EMBASE, four Chinese electronic databases, and relevant lists. Two reviewers independently selected trials, assessed trial quality, and extracted the data. Results: We included 13 studies investigating 269,571 participants. The sample size ranged from 563 to 216,005 participants. The age of participants ranged from 3 to 16 years. The meta-analysis of the prevalence of TD was 6.1% [95% CI: 0.036-0.100, I 2 = 49.7%]. The prevalence of transient tic disorder (TTD), chronic tic disorder (CTD), and Tourette syndrome (TS) was 1.7% [95% CI = 0.009-0.031, I 2 = 49%], 1.2% [95% CI = 0.007-0.022, I 2 = 48.3%], and 0.3% [95% CI = 0.001-0.008, I 2 = 49.5%], respectively. The prevalence of TD in boys [5.1%, 95% CI = 0.026-0.098, I 2 = 49.3%] was higher than that in girls [2.4%, 95% CI = 0.009-0.065, I 2 = 49.4%]. The prevalence of TD in urban area [2.6%, 95% CI = 0.019-0.034, I 2 = 35.5%] was higher than that in rural area [2.2%, 95% CI = 0.016-0.030, I 2 = 33.9%]. The prevalence of TD in central China [10.7%, 95% CI = 0.043-0.242, I 2 = 49.2%] was higher than that in North China [7.8%, 95% CI = 0.007-0.522, I 2 = 49.9%] and East China [4.4%, 95% CI = 0.015-0.120, I 2 = 49.8%]. Conclusion: TD is a common disease in China, with prevalence differing based on sex, age, and region. Copyright © 2016 the Author(s). Published by Wolters Kluwer Health, Inc. All rights reserved.


Yu Y.,West China Second Hospital | Yu Y.,University of Texas Southwestern Medical Center | Chen Y.,University of Texas Southwestern Medical Center | Kim B.,University of Texas Southwestern Medical Center | And 14 more authors.
Cell | Year: 2013

Establishment of oligodendrocyte identity is crucial for subsequent events of myelination in the CNS. Here, we demonstrate that activation of ATP-dependent SWI/SNF chromatin-remodeling enzyme Smarca4/Brg1 at the differentiation onset is necessary and sufficient to initiate and promote oligodendrocyte lineage progression and maturation. Genome-wide multistage studies by ChIP-seq reveal that oligodendrocyte-lineage determination factor Olig2 functions as a prepatterning factor to direct Smarca4/Brg1 to oligodendrocyte-specific enhancers. Recruitment of Smarca4/Brg1 to distinct subsets of myelination regulatory genes is developmentally regulated. Functional analyses of Smarca4/Brg1 and Olig2 co-occupancy relative to chromatin epigenetic marking uncover stage-specific cis-regulatory elements that predict sets of transcriptional regulators controlling oligodendrocyte differentiation. Together, our results demonstrate that regulation of the functional specificity and activity of a Smarca4/Brg1-dependent chromatin-remodeling complex by Olig2, coupled with transcriptionally linked chromatin modifications, is critical to precisely initiate and establish the transcriptional program that promotes oligodendrocyte differentiation and subsequent myelination of the CNS. © 2013 Elsevier Inc.


Zhao L.,West China Second Hospital | Zhao L.,University of Sichuan | Yang H.,West China Second Hospital | Yang H.,University of Sichuan | And 12 more authors.
European Journal of Obstetrics Gynecology and Reproductive Biology | Year: 2015

Objective(s) This study aims to identify a critical molecule that potentially participates in endometriosis pathogenesis and characterize its correlation with dysmenorrhea and recurrence. Study design We utilized a bioinformatics-based strategy to screen for candidate genes and fibroblast growth factor receptor 1(FGFR1) was chosen for further validation. FGFR1 expression was examined in specimens of ectopic and eutopic endometrium obtained from 48 patients with endometriosis and specimens of eutopic endometrium from 26 healthy control subjects using immunohistochemistry and Western blotting. In addition, FGFR shRNA treatment was applied in a nude mice endometriosis model to examine the functional role of FGFR1 in endometriosis formation in vivo. Results FGFR1 was found commonly overexpressed in ectopic endometrium of endometriosis compared with either its eutopic counterpart or endometrium from normal patients (P < 0.05). FGFR shRNA treatment impaired endometriosis formation and alleviated endometriosis-related symptoms in vivo. FGFR1 expression in ectopic endometrium was correlated with dysmenorrhea severity (P < 0.05) and recurrence in endometriosis patients (P < 0.05). Conclusion(s) FGFR1 might be involved in endometriosis development, which could possibly serve as a novel therapeutic target and prognostic marker for this disease. © 2014 Published by Elsevier Ireland Ltd.


PubMed | Thomas Jefferson University, University of Sichuan, Sichuan University, West China Second Hospital and Kaiser Permanente
Type: Journal Article | Journal: Oncotarget | Year: 2016

Ovarian cancer constitutes one of the most lethal gynaecological malignancies worldwide and currently no satisfactory therapeutic approaches have been established. Therefore, elucidation of molecular mechanisms to develop targeted therapy of ovarian cancer is crucial. PDLIM2 is critical to promote ubiquitination of nuclear p65 and thus its role in inflammation has been highlighted recently. We demonstrate that PDLIM2 is decreased in both ovarian high-grade serous carcinoma and in various human ovarian cancer cell lines compared with normal ovary tissues and human ovarian surface epithelial cells (HOSE). Further functional analysis revealed that PDLIM2 is epigenetically repressed in ovarian cancer development and inhibition of PDLIM2 promoted ovarian cancer growth both in vivo and in vitro via NOS2-derived nitric oxide signaling, leading to recruitment of M2 type macrophages. These results suggest that PDLIM2 might be involved in ovarian cancer pathogenesis, which could serve as a promising therapeutic target for ovarian cancer patients.


Zhao L.,West China Second Hospital | Zhao L.,Chengdu University of Technology | Zhou S.,West China Second Hospital | Zou L.,Chengdu University of Technology | Zhao X.,West China Second Hospital
Human Reproduction | Year: 2013

Study Questio: NWhat is the expression pattern and functionality of caveolin 1 (CAV1) in the endometrium of patients with adenomyosis? Summary Answer: The stromal CAV1 expression is down-regulated that leads to the release of a variety of molecules that either enhance the metastatic capacity of endometrial cells or contribute to adenomyosis-associated dysmenorrhea. What Is Known Already: Adenomyosis is characterized by invasion of endometrium into the uterine myometrium. CAV1 has been linked to tumor progression and clinical outcome in a variety of human malignancies; however, its role in adenomyosis development and adenomyosis-associated dysmenorrhea is still poorly recognized.STUDY Design: , SIZE, DURATIONWe retrospectively analyzed the expression levels of CAV1 and RANTES protein using immunohistochemistry in 65 patients who were pathologically diagnosed with adenomyosis and 12 control women without related pathology, who were subjected to surgery between 2009 and 2010. Endometrial tissues from six additional normal females without related pathology were collected from 2011 to 2012; these tissues were subjected to subsequent primary cell culture experiments. Participants/Materials, Setting, Methods: The expression of CAV1 and RANTES was examined by immunohistochemistry in ectopic endometrium and paired eutopic endometrium of 65 adenomyosis patients and 12 control patients. Primary endometrial stromal cells (ESCs) and endometrial epithelial cells (EECs) were isolated from 6 additional control females without related pathology. The expression of CAV1 in ESCs was either (i) inhibited by siRNA transfection and methyl-β-cyclodextrin (MβCD) treatment or (ii) increased by pcDNA3.1/CAV1 transfection. The impact of each treatment on the proliferation, migration and invasion of both ESCs and EECs was evaluated by methylthiazolydiphenyl-tetrazolium assay, colony formation assay, Transwell migration and invasion assay. Furthermore, ESC treatment with MβCD and siCAV1 was assessed for the effect on the expression of a panel of inflammatory cytokines. The levels of two pain mediators, nitric oxide (NO) and prostaglandin E2 (PGE2), were assessed in CAV-1-depleted and control ESCs, whereas immunoblotting was performed to characterize signaling pathways downstream to loss of stromal CAV1 in endometrium. The correlation between dysmenorrhea severity and stromal CAV1 and RANTES expression was further examined using 'Pearson's' correlation analysis.MAIN RESULTSStromal CAV1 expression in ectopic endometrium of adenomyosis patients was significantly lower than that of paired eutopic endometrium or normal controls as analyzed by immunohistochemistry (P < 0.001). Although no significant difference was observed in the proliferation of CAV1-depleted ESCs when compared with control group, EECs cultured with conditioned media from CAV1-depleted ESCs demonstrated a significantly elevated proliferation rate when compared with those treated with control ESC-conditioned media. Moreover, both CAV1-depleted ESCs and EECs cultured with conditioned media from CAV1-depleted ESCs showed enhanced migration and invasion capacity when compared with control group (P < 0.05). In contrast, incubation with conditioned media of ESCs with enforced CAV1 expression led to decreased proliferation capacity of EECs. Furthermore, the expression of RANTES in ESCs treated with MβCD and siCAV1 was significantly increased. Stromal RANTES expression in the ectopic endometrium of adenomyosis patients was significantly higher than that of paired eutopic endometrium or normal controls as analyzed by immunohistochemistry (P = 0.0026). Stromal CAV1 expression in eutopic endometrium was significantly lower in women with more severe dysmenorrhea (P < 0.05) and was negatively correlated with dysmenorrhea severity in adenomyosis patients (r2 = 0.1549; P = 0.012, 'Pearson's' χ2 test), whereas stromal RANTES expression in eutopic endometrium was significantly higher in women with more severe dysmenorrhea (P < 0.05) and was positively correlated with dysmenorrhea severity in adenomyosis patients (r2 = 0.1646; P = 0.0094, 'Pearson's' χ2 test). Silencing of CAV1 in ESCs led to increased release of NO and PGE2 when compared with control and was associated with enhanced activity of ERK-FAK signaling pathway.LIMITATIONS, REASONS FOR CAUTIONThis study assessed the functional role of stromal CAV1 and RANTES in a small number of human adenomyosis samples by immunohistochemistry and in primary human ESCs by functional studies. In future investigations, a larger sample size should be adopted and the functional role of stromal CAV1 should be further characterized in animal models. Wider Implications of the Findings: Loss of stromal CAV1 expression may play a critical role in the pathogenesis of adenomyosis and is correlated with adenomyosis-related dysmenorrhea. Study Funding National Basic Research Program of China and Ph.D. Programs Foundation of Ministry of Education of China. Competing Interestnone. © 2013 The Author.


Zhang L.L.,University of Sichuan | Liu C.T.,University of Sichuan | Gong J.,West China Second Hospital
Genetics and Molecular Research | Year: 2014

Vitamin D deficiency and insufficiency are increasingly being recognized in the general population over the last few decades. However, a number of other disorders have now been linked to vitamin D deficiency and insufficiency, including asthma and COPD. The aim of this study was to evaluate the evidence on the effect of vitamin D on asthma and COPD. We searched electronic databases including SCI, EMBASE, Ovid, and PubMed. Reviewers working independently and in duplicate extracted study characteristics, quality, and the outcomes. The weighted mean differences across trials and random-effect meta-analysis were used to pool the relative risks (RR). This is the first meta-analysis about the risk of vitamin D deficiency for asthma and COPD. Ten studies were available for this meta-analysis and systematic review. The prevalence of vitamin D deficiency was significantly greater among cases than control subjects [RR = 1.59, 95%CI = 1.07-2.36, 488/812 (60%) vs 278/875 (32%)] for asthma. However, vitamin D insufficiency was not significantly associated with asthma [RR = 1.09, 95%CI = 0.91-1.30, 702/996 (70%) vs 665/1016 (65%)]. Moreover, studies failed to demonstrate that COPD patients had an increased risk for vitamin D deficiency or insufficiency compared to controls (RR = 0.89, 95%CI = 0.63-1.25). Vitamin D deficiency was associated with a significant decrease in lung function in asthmatic children. Vitamin D deficiency was highly prevalent in asthma patients, and vitamin D status was associated with lung function. COPD cannot be considered as completely free of vitamin D deficiency. © FUNPEC-RP.


Feng Y.,West China Second Hospital | Zhao X.,West China Second Hospital | Zhou C.,University of Sichuan | Yang L.,West China Second Hospital | And 6 more authors.
Gene | Year: 2013

The Val158Met polymorphism of the COMT gene has been implicated in susceptibility to uterine leiomyoma (ULM), but the reported results were inconclusive. The aim of the study was to evaluate the Val158Met polymorphism of the COMT gene and the risk of ULM by meta-analysis. A comprehensive electronic search for relevant articles was conducted in Pubmed, Embase, CNKI, Wanfang, and Weipu databases. Statistical analysis was performed by using the Revman4.2 software and Stata10.0 software. A total of 7 articles including 12 case-control studies were identified in this meta-analysis. The results showed that the polymorphism was associated with decreased risk of ULM (Met/Met. +. Val/Met vs. Met/Met: OR=0.84, 95% CI=0.70-0.99, Z=2.07, p=0.04). In the subgroup analyses by ethnicity, significant decreased risk was found among the black populations (OR=0.68, 95% CI=0.48-0.97, Z=2.15, p=0.03). The current meta-analysis suggested that the Val158Met polymorphism in the COMT gene was associated with decreased risk of ULM, especially in the black population. Future studies are needed to validate our conclusions. © 2013 Elsevier B.V.


PubMed | West China Second Hospital
Type: Journal Article | Journal: Gene | Year: 2013

The Val158Met polymorphism of the COMT gene has been implicated in susceptibility to uterine leiomyoma (ULM), but the reported results were inconclusive. The aim of the study was to evaluate the Val158Met polymorphism of the COMT gene and the risk of ULM by meta-analysis. A comprehensive electronic search for relevant articles was conducted in Pubmed, Embase, CNKI, Wanfang, and Weipu databases. Statistical analysis was performed by using the Revman4.2 software and Stata10.0 software. A total of 7 articles including 12 case-control studies were identified in this meta-analysis. The results showed that the polymorphism was associated with decreased risk of ULM (Met/Met+Val/Met vs. Met/Met: OR=0.84, 95% CI=0.70-0.99, Z=2.07, p=0.04). In the subgroup analyses by ethnicity, significant decreased risk was found among the black populations (OR=0.68, 95% CI=0.48-0.97, Z=2.15, p=0.03). The current meta-analysis suggested that the Val158Met polymorphism in the COMT gene was associated with decreased risk of ULM, especially in the black population. Future studies are needed to validate our conclusions.


PubMed | West China Second Hospital
Type: Journal Article | Journal: Pediatrics international : official journal of the Japan Pediatric Society | Year: 2015

Congenital heart disease (CHD) is one of the most common birth defects in newborns. The etiology of CHD has remained largely unknown, but it is assumed to result from the combined effects of genetic and environmental factors. Recent investigations have detected potentially pathogenic copy number variations (CNV) in a proportion of patients with CHD. The present case-control study evaluated whether CNV in the GATA4 and NKX2-5 genes contribute to the pathogenesis of CHD in Chinese fetuses (n = 117), by comparing them with non-CHD control subjects (n = 100).Multiplex ligation-dependent probe amplification with the P311A probe mixture was used to detect CNV.The normalized signals were within the normal range for all exons in all CHD patients and non-CHD control subjects. Of the 117 CHD patients, three had a deletion of 22q11, and two had a duplication of 22q11.There was no evidence of a role for NKX2-5 and GATA4CNV in fetal CHD; therefore, these CNV may not be common in fetal CHD in China.


PubMed | West China Second Hospital
Type: Journal Article | Journal: Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition | Year: 2012

To observe the influence of ciclosporin A (CsA) or/and FK506 on vascular endothelium of hyperlipidemic rats.Hyperlipidemic rat model was established as previously described. The injury of vascular endothelium of these rats was observed after stimulation with FK506 or/and CsA. The mRNA transcription and protein expression of the vascular endothelium growth factor (VEGF), decay-accelerating factor (DAF) and C reactive protein (CRP) in vascular endothelium of rats were measured. The serum reactive oxygen species (ROS) was detected.Compared with FK506, CsA was more likely to cause injury of vascular endothelium, damaging the integrity of endothelium of hyperlipidemic rats. CsA inhibited the expression of VEGF and the complement inhibitor DAF and increased the expression of CRP of vascular endothelial cells. CsA also up-regulated the serum level of ROS. FK506 showed no such impacts.CsA can damage vascular endothelium of hyperlipidemic rats by activating the complement system induced by VEGF/DAF and ROS/CRP pathway. FK506 has no influence on the VEGF/DAF pathway and the expression of ROS/CRP.

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