Yuli Veterans Hospital

Hualian, Taiwan

Yuli Veterans Hospital

Hualian, Taiwan

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Liao S.-C.,National Taiwan University | Liao S.-C.,National Taiwan University Hospital | Chen W.J.,National Taiwan University | Chen W.J.,National Taiwan University Hospital | And 8 more authors.
Psychological Medicine | Year: 2012

Background This study examined the prevalence of major depressive disorder (MDD), and the correlations and co-morbid conditions associated with MDD, in the adult Taiwanese population, which a previous estimate in the 1980s had found to be at the lower end of the spectrum worldwide. Possible explanations for the reported low prevalence of MDD were evaluated.Method As part of a survey of common psychiatric disorders in a nationally representative sample of individuals aged ≥18 years who were non-institutionalized civilians in Taiwan, a face-to-face interview using the paper version of the World Mental Health Survey of the World Health Organization (WHO) Composite International Diagnostic Interview (WMH-CIDI) was conducted between 2003 and 2005. Functional impairment and help-seeking behaviors were compared between Taiwanese subjects with MDD and their counterparts in the USA.Results Among the 10 135 respondents, the lifetime prevalence of MDD was 1.20% [standard error (s.e.)=0.2%]. Individuals who were divorced or widowed, aged ≤40 years, and female were at increased risk, whereas rural residents were at lower risk for MDD. The proportion of MDD cases co-morbid with other psychiatric disorders in this study was much lower than in the US study. Only one-third of Taiwanese individuals with MDD sought help despite having twice the number of lost workdays compared with the US sample.Conclusions Despite the low prevalence of MDD in Taiwanese adults, the pattern of low help-seeking behavior and profound functional impairment indicates much room for improvement in the early detection of and intervention in major depression in this population. © 2012 Cambridge University Press.


Shi M.-D.,Kaohsiung Veterans General Hospital Tainan Branch | Chao J.-K.,Yuli Veterans Hospital | Ma M.-C.,National Cheng Kung University | Hao L.-J.,Kaohsiung Veterans General Hospital Tainan Branch | Chao I.-C.,Chinese Institute of Clinical Medicine
Journal of Sexual Medicine | Year: 2014

Introduction: Obesity has been receiving an increasing amount of attention recently, but investigations regarding the potential impact of obesity, sexual behaviors, and sex hormones on erectile dysfunction (ED) in men have not completely clarified the association. Aim: To identify the relationship between ED, sexual behavior, sexual satisfaction, sex hormones, and obesity in older adult males in Taiwan. Methods: Data were obtained from a baseline survey of 476 older adult males (≧40 years old). Their demographic data, body mass index (BMI), sex hormones, sexual desire, sexual satisfaction, and ED status were assessed. Main Outcome Measures: The International Index of Erectile Function-5 (IIEF-5), Sexual Desire Inventory (SDI), and Sexual Satisfaction Scale (SSS) were used to assess ED, sexual desire, and sexual satisfaction. Results: In all, 476 men were available for analysis. The mean age of the sample was 51.34±7.84 years (range 40 to 70 years). The IIEF total score had a mean of 19.44±4.98; 264 (55.5%) subjects had ED, 250 (52.9%) were currently obese (BMI≧27), and 297 (62.4%) had metabolic syndrome. The results showed an increased risk of ED among obese men and subjects with lower levels of sex hormones and lower sexual desire. Testosterone levels were lower in subjects with obesity (P<0.001). Among the predictors of ED, obesity (odds ratio [OR]=1.62, 95% CI=1.07-2.44, P=0.021), abnormal high sensitivity C-reactive protein (hs-CRP) (OR=10.59, 95% CI=4.70-23.87, P<0.001), and lower serum full testosterone (OR=3.27, 95% CI=2.16-4.93, P<0.001) were significantly independent factors. Conclusions: This study supports the idea of a close relationship between low levels of sex hormones, sexual desire, sexual satisfaction, obesity, and ED, and also shows that low free testosterone and hs-CRP may predict ED, even in obese populations. © 2013 International Society for Sexual Medicine.


Liang K.-Y.,Yuli Veterans Hospital | Meg Tseng M.-C.,National Taiwan University Hospital | Meg Tseng M.-C.,National Taiwan University
Journal of the Formosan Medical Association | Year: 2011

Eating disorders (EDs) are often associated with various impulsive behaviors. This study investigated the prevalence of impulsive behaviors in ED patients in Taiwan. Three hundred sixteen female outpatients with ED and 142 psychiatric controls were recruited. All participants completed self-administered questionnaires assessing lifetime presence of impulsive behaviors, including suicide, self-injury, stealing, alcohol use, illicit drug use, excessive spending, sexual promiscuity, and general psychopathology. More than 60% of the ED patients had at least one impulsive behavior. The most common impulsive behaviors among ED patients were excessive spending (34.9%), deliberate self-harm (32.7%), and stealing (26.3%). However, there were no significant differences in prevalences of any impulsive behaviors between ED patients and psychiatric controls. Clinicians should routinely assess and treat impulsive behaviors in female psychiatric patients with negative affectivity, regardless of the presence of ED, to help prevent potential adverse outcomes related to impulsive behaviors. © 2011, Elsevier Taiwan LLC & Formosan Medical Association.


Bai Y.M.,Taipei Veterans General Hospital | Bai Y.M.,National Yang Ming University | Chen T.-T.,Yuli Veterans Hospital | Liou Y.-J.,Taipei Veterans General Hospital | And 5 more authors.
Schizophrenia Research | Year: 2011

Background: Previous research indicates that common single-nucleotide polymorphisms (SNPs) in the serotonin 5-HT2C receptor gene (HTR2C) are associated with metabolic syndrome (MetS) related to antipsychotic treatment. This study analyzes a large sample of patients with schizophrenia treated with atypical antipsychotics to determine whether variation in the HTR2C is associated with MetS. Methods: Six tag SNPs, capturing all common genetic variations in the HTR2C gene in the Han population, were genotyped in 456 Chinese schizophrenic inpatients treated with atypical antipsychotics (clozapine: 171, olanzapine: 91, and risperidone: 194). Results: Single-marker based analysis shows that of the six HTR2C SNPs, the rs498177 SNP showed a significant association with MetS in female patients, and the C allele was associated with an increased risk of MetS (for genotype TT/TC/CC: MetS vs. non-MetS. = 50%/27%/23% vs. 69%/28%/3%, and for allele T/C: MetS vs. non-MetS. = 63%/37% vs. 83%/17%, p. = 0.0007). Haplotype analysis shows that the A-C type of rs521018-rs498177 in the HTR2C gene significantly decreased the risk of MetS (corrected p. = 0.0108) in female patients. Conclusions: The results of this study support the role of HTR2C genetic variants in susceptibility to MetS in patients treated with atypical antipsychotics. However, this association is gender-dependent. © 2010 Elsevier B.V.


Cheng M.-C.,Yuli Veterans Hospital | Lu C.-L.,Hualien Armed Forces General Hospital | Luu S.-U.,Taoyuan Armed Forces General Hospital | Tsai H.-M.,National Health Research Institute | And 5 more authors.
PLoS ONE | Year: 2010

Hypofunction of N-methyl-D-aspartate (NMDA) receptor-mediated signal transduction has been implicated in the pathophysiology of schizophrenia. Post-synaptic density protein 95 (PSD95) plays a critical role in regulating the trafficking and activity of the NMDA receptor and altered expression of the PSD95 has been detected in the post-mortem brain of patients with schizophrenia. The study aimed to examine whether the DLG4 gene that encodes the PSD95 may confer genetic susceptibility to schizophrenia. We re-sequenced the core promoter, all the exons, and 3' untranslated regions (UTR) of the DLG4 gene in 588 Taiwanese schizophrenic patients and conducted an association study with 53' non-psychotic subjects. We did not detect any rare mutations at the protein-coding sequences of the DLG4 gene associated with schizophrenia. Nevertheless, we identified four polymorphic markers at the core promoter and 5' UTR and one single nucleotide polymorphism (SNP) at the 39UTR of the DLG4 gene in this sample. Genetic analysis showed an association of a haplotype (C-D) derived from 2 polymorphic markers at the core promoter (odds ratio = 1.26, 95% confidence interval = 1.06-1.51, p = 0.01), and a borderline association of the T allele of the rs13331 at 39UTR with schizophrenia (odds ratio = 1.19, 95% confidence interval = 0.99-1.43, p = 0.06). Further reporter gene assay showed that the C-D-C-C and the T allele of the rs13331 had significant lower activity than their counter parts. Our data indicate that the expression of the DLG4 gene is subject to regulation by the polymorphic markers at the core promoter region, 5' and 3'UTR of the gene, and is associated with the susceptibility of schizophrenia. © 2010 Cheng et al.


Li J.-M.,Taoyuan Armed Forces General Hospital | Lu C.-L.,Hualien Armed Forces General Hospital | Cheng M.-C.,Yuli Veterans Hospital | Luu S.-U.,Taoyuan Armed Forces General Hospital | And 4 more authors.
Psychiatry Research | Year: 2013

Schizophrenia is a severe chronic mental disorder with high genetic components in its etiology. Several studies indicated that synaptic dysfunction is involved in the pathophysiology of schizophrenia. Postsynaptic synapse-associated protein 90/postsynaptic density 95-associated proteins (SAPAPs) constitute a part of the N-methyl-d-aspartate receptor-associated postsynaptic density proteins, and are involved in synapse formation. We hypothesized that genetic variants of the SAPAPs might be associated with schizophrenia. Thus, we systemically sequenced all the exons of the discs, large (Drosophila) homolog-associated protein 1 (DLGAP1) gene that encodes SAPAP1 in a sample of 121 schizophrenic patients and 120 controls from Taiwan. We totally identified six genetic variants, including five known SNPs (rs145691437, rs3786431, rs201567254, rs3745051 and rs11662259) and one rare missense mutation (c.1922A>G) in this sample. SNP- and haplotype-based analyses showed no association of these SNPs with schizophrenia. The c.1922A>G mutation that changes the amino acid lysine to arginine at codon 641 was found in one out of 121 patients, but not in 275 control subjects, suggesting it might be a patient-specific mutation. Nevertheless, bioinformatic analysis showed this mutation does not affect the function of the DLGAP1 gene and appears to be a benign variant. Hence, its relationship with the pathogenesis remains to be investigated. © 2012 Elsevier Ireland Ltd.


Shen Y.-C.,Tzu Chi General Hospital | Shen Y.-C.,Tzu Chi University | Tsai H.-M.,National Health Research Institute | Cheng M.-C.,Yuli Veterans Hospital | And 4 more authors.
Schizophrenia Research | Year: 2012

Objectives: Schizophrenia is a highly heritable disorder, but many aspects of its etiology and pathophysiology remain poorly understood. Recently, a SNP rs12807809 located upstream of the neurogranin (NRGN) gene achieved genome-wide significance in this disorder. Methods: In order to find the causal variants of NRGN gene in schizophrenia, we searched for genetic variants in the promoter region and all the exons (including both UTR ends and rs12807809) using direct sequencing in a sample of patients with schizophrenia (n. =. 346) and non-psychotic controls (n. =. 345), both being Han Chinese from Taiwan, and conducted an association and functional study. Results: We identified 7 common polymorphisms in the NRGN gene. SNP and haplotype-based analyses displayed no associations with schizophrenia. Additionally, we identified 5 rare variants in 6 out of 346 patients, including 3 rare variants located at the promoter region (g.-620A>G, g.-578C>G, and g.-344G>A) and 2 rare variants located at 5' UTR (c.-74C>G, and c.-41G>A). No rare variants were found in the control subjects. The results of the reporter gene assay demonstrated that the regulatory activity of construct containing g.-620G, g.-578G, g.-344A, c.-74G, and c.-41A was significantly lower as compared to the wild type construct (P. <. 0.01 for g.-578G; P. <. 0.001 for the other constructs). . In silico analysis also demonstrated their influences on the regulatory function of NRGN gene. Conclusions: Our study lends support to the hypothesis of multiple rare mutations in schizophrenia, and provides genetic clues that indicate the involvement of NRGN in this disorder. © 2011 Elsevier B.V.


Liao H.-M.,National Tsing Hua University | Chao Y.-L.,Tzu Chi University | Huang A.-L.,Yuli Veterans Hospital | Cheng M.-C.,Yuli Veterans Hospital | And 7 more authors.
Schizophrenia Research | Year: 2012

Schizophrenia is a complex mental disorder with high degree of genetic influence in its etiology. Several recent studies revealed that copy number variations (CNVs) of genomic DNA contributed significantly to the genetic architecture of sporadic schizophrenia. This study aimed to investigate whether CNVs also contribute to the familial forms of schizophrenia. Using array-based comparative genomic hybridization technology, we searched for pathogenic CNV associated with schizophrenia in a sample of 60 index cases from multiplex schizophrenia families. We detected three inherited CNVs that were associated with schizophrenia in three families, including a microdeletion of ~. 4.4. Mb at chromosome 6q12-q13, a microduplication of ~. 1. Mb at chromosome 18q12.3, and an interstitial duplication of ~. 5. Mb at chromosome 15q11.2-q13.1. Our data indicate that CNVs contribute to the genetic underpinnings of the familial forms of schizophrenia as well as of the sporadic form. As 15q11-13 duplication is a well-known recurrent CNV associated with autism in the literature, the detection of the 15q11.2-q13.1 duplication in our schizophrenia patients provides additional support to other studies reporting that schizophrenia is part of the clinical spectrum of 15q11-q13 duplication syndrome. © 2012 Elsevier B.V.


Sun C.,Pennsylvania State University | Cheng M.,Yuli Veterans Hospital | Qin R.,Pennsylvania State University | Liao D.,Bali Psychiatric Center | And 6 more authors.
Human Molecular Genetics | Year: 2011

Schizophrenia is a severe chronic mental disorder with a high genetic component in its etiology. Several lines of study have suggested that synaptic dysfunction may underlie the pathogenesis of schizophrenia. Neuroligin proteins function as cell-adhesion molecules at post-synaptic membrane and play critical roles in synaptogenesis and synaptic maturation. In this study, we systemically sequenced all the exons and promoter region of neuroligin-2 (NLGN2) gene in a sample of 584 schizophrenia patients and 549 control subjects from Taiwan. In total, we identified 19 genetic variants, including six rare missense mutations such as R215H (one patient), V510M (two patients), R621H (one patient), A637T (two patients), P800L (one patient and one control) and A819S (one patient and one control). In silico analysis predicted that two patient-specific missense mutations, R215H and R621H, had damaging effect, whereas the other missense mutations were benign. Importantly, functional analysis with immunocytochemistry and electrophysiological recordings identified the R215H mutant as a loss-of-function mutant in inducing GABAergic synaptogenesis. Mechanistically, the synaptogenic deficiency of R215H mutant was due to its retention inside the endoplasmic reticulum and inability to be transported to cell membrane. Our study suggests that defects in GABAergic synapse formation in the brain may be an important contributing factor for the onset of schizophrenia. In the family study of this mutation, we found his elder brother also carried this mutation but did not have psychiatric symptoms, indicating that this mutation has incomplete penetrance, and thus the clinical relevance of this mutation should be interpreted with caution. © The Author 2011. Published by Oxford University Press. All rights reserved.


Lee T.-C.,Tzu Chi University | Lee T.-C.,Yuli Veterans Hospital | Ho H.-C.,Tzu Chi University
Fertility and Sterility | Year: 2011

Significantly higher levels of prostaglandin E2 and vascular endothelial growth factor were associated with the severity of endometriosis. In this study, pathologic concentrations of prostaglandin E2 and vascular endothelial growth factor found in endometriotic women significantly inhibited sperm motility, acrosome reaction, and sperm-oocyte interaction, which might result in endometriosis-associated subfertility/infertility. © 2011 American Society for Reproductive Medicine, Published by Elsevier Inc.

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