Shin Kong Memorial Hospital

Taipei, Taiwan

Shin Kong Memorial Hospital

Taipei, Taiwan
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Wang K.A.,Shin Kong Memorial Hospital | Wang K.A.,Fu Jen Catholic University | Wang J.-C.,Taipei Veterans General Hospital | Lin C.-L.,China Medical University at Taichung | Tseng C.-H.,China Medical University at Taichung
PLoS ONE | Year: 2017

Purpose The correlation of fibromyalgia syndrome (FMS) with peptic ulcer disease (PUD) is unclear. We therefore conducted a cohort study to investigate whether FMS is correlated with an increased risk of PUD. Methods In this study, we established an FMS cohort comprising 26068 patients aged more than 20 years who were diagnosed with FMS from 2000 to 2011. Furthermore, we established a control cohort by randomly choosing 104269 people without FMS who were matched to the FMS patients by gender, age, and index year. All patients were free of PUD at the baseline. Cox proportional hazard regressions were performed to compute the hazard ratio of PUD after adjustment for demographic characteristics and comorbidities. Results The prevalence of comorbidities was significantly higher in the FMS patients than in the controls. The incidence of PUD was 29.8 and 19.4 per 1000 person-years in the FMS and control cohorts, respectively. In addition, the FMS cohort exhibited a 1.40-fold higher risk of PUD (95% confidence interval = 1.35-1.45) compared with the control cohort. After control for confounding factors, the medications (selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, and antidepressants) taken by the FMS patients did not increase the risk of PUD. Conclusion FMS patients exhibit a higher risk of PUD than that of patients without FMS. © 2017 Wang 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.

Liao C.-C.,Taipei Medical University Hospital | Liao C.-C.,Taipei Medical University | Shen W.W.,Taipei Medical University | Chang C.-C.,Taipei Medical University Hospital | And 5 more authors.
Annals of Surgery | Year: 2013

Objective:: To validate the global features of postoperative adverse outcomes for surgical patients with schizophrenia. Background:: Patients with schizophrenia were known to have a higher risk of complications during hospitalization. Quality of care has become the key factor in reducing their potential mortality afterwards. METHODS:: We present a population-based study of 8967 schizophrenic patients receiving major surgery from the Taiwan National Health Insurance Research Database within the years 2004 and 2007 compared with 35,868 surgical patients without mental disorders. Eight major postoperative complications and mortality after complications were evaluated among schizophrenic patients with different severity. RESULTS:: Schizophrenic patients had significantly higher risk for postoperative complications, including acute renal failure, pneumonia, bleeding, septicemia, stroke, and 30-day postoperative mortality (adjusted OR = 2.70; 95% CI: 2.08-3.49), than surgical patients without mental disorders. Among surgical patients with 1 to 2, 3 to 18, 19 to 48, and more than 49 schizophrenia-related outpatient visits within 24-month period preoperatively, the adjusted ORs of 30-day mortality ranged from 1.95 (95% CI: 1.25-3.02) to 3.97 (95% CI: 2.66-5.92) in a frequency-dependent pattern when compared with controls. When compared with surgical patients with schizophrenia-related outpatient services only, OR of 30-day postoperative mortality increased from 2.54 (95% CI: 1.93-3.34) to 3.69 (95% CI: 2.25-6.03) in surgical patients with preoperative hospitalization or emergency visit because of schizophrenia. CONCLUSIONS:: Surgical patients with schizophrenia showed significantly higher postoperative adverse outcome rates with risk of 30-day mortality nearly threefold when compared with patients without mental disorders. Our findings suggest the urgency revising the protocol of postoperative care for this specific population. © 2013 by Lippincott Williams & Wilkins.

Chao J.-K.,Yuli Veterans Hospital | Chao J.-K.,Shu-Te University | Hwang T.I.-S.,Shin Kong Memorial Hospital | Hwang T.I.-S.,Fu Jen Catholic University | And 5 more authors.
Journal of Sexual Medicine | Year: 2011

Introduction. Obesity is receiving growing research attention. However, investigations concerning the potential impact of obesity and testosterone on erectile dysfunction (ED) in young men have not been completely clarified. Aim. To identify the relationship between ED, serum testosterone level, and obesity in draftees in Taiwan. Methods. Data were obtained from a baseline survey of 364 young adult military conscripts (19-24years old). Their demographic data, body mass index (BMI), serum testosterone, and ED status were assessed. Sixty-four subjects had ED, and 300 comprised the normal control group. Main Outcome Measures. The International Index of Erectile Function-5 (IIEF-5), Sexual Desire Inventory, and Sexual Behavior Scale were used to assess ED, sexual desire, and sexual function. Results. Three hundred sixty-four men were available for analysis. The mean age of the sample was 21.66±0.92years (19-24years). The IIEF total score had a mean of 21.99±2.34 and median of 23; 64 (17.6%) subjects had ED, although mild. The results showed an increased risk of ED among obese men and subjects with lower serum testosterone. Among the predictors of ED, obesity (odds ratio=83.97, 95% CI=16.17-436.03, degrees of freedom [d.f.]=1, P<0.001) and lower serum testosterone (odds ratio=679.84, 95% CI=108.48-4,260.58, d.f.=1, P<0.001) were significantly independent factors. Testosterone levels were lower in subjects with obesity (P<0.001). Conclusion. This study supports the idea that BMI and serum testosterone may provide warning signs of ED and, at the same time, an opportunity for early intervention in young men. © 2011 International Society for Sexual Medicine.

Lee C.-C.,Shin Kong Memorial Hospital | Lee C.-C.,Taipei Medical University | Lee C.-C.,Fu Jen Catholic University | Jan H.-J.,Taipei Medical University | And 9 more authors.
Oncogene | Year: 2010

Uncontrolled growth and diffused invasion are major causes of mortality in patients with malignant gliomas. Nodal has been shown to have a central role in the tumorigenic signaling pathways of malignant melanoma. In this study, we show that grade IV human glioma cell lines expressed different levels of Nodal, paralleled to the potential for cell invasiveness. Treatment of glioma cell lines with recombinant Nodal (rNodal) increased matrix metalloproteinase 2 (MMP-2) secretion and cell invasiveness. The ectopic expression of Nodal in GBM glioma cells that expressed Nodal at low level resulted in increased MMP-2 secretion, enhanced cell invasiveness, raised cell proliferation rates in vitro, increased tumor growth in vivo, and was associated with poor survival in a mice xenograft model. In contrast, the knockdown of Nodal expression in U87MG glioma cells with high Nodal expression level had reduced MMP-2 secretion, less cell invasiveness, lower tumor growth in vivo and longer lifespan in mice with U87MG/shNodal cell xenografts. In addition, Nodal knockdown promoted the reversion of malignant glioma cells toward a differentiated astrocytic phenotype. Furthermore, our data support the notion that Nodal may regulate glioma progression through the induction of the leukemia inhibitory factor (LIF) and Cripto-1 through activated Smad. © 2010 Macmillan Publishers Limited All rights reserved.

Lee C.-C.,Shin Kong Memorial Hospital | Lee C.-C.,Taipei Medical University | Lee C.-C.,Yuanpei University | Lai J.-H.,Tri Service General Hospital | And 7 more authors.
Cancer Cell International | Year: 2013

Background: Glioblastoma stem-like cells (GSC) have been shown to promote tumor growth, tumor-associated neovascularization, therapeutic resistance, and metastasis. CXCR4 receptors have been found involved in the proliferation, metastasis, angiogenesis, and drug-resistant characteristics of glioblastoma. However, the role of CXCR4 in modulating the stem-like cell properties of rat glioblastoma remains ambiguous.Methods: To explore the role of the CXCL12/CXCR4 axis in maintaining rat GSC properties, we disrupted the CXCR4 signaling by using small hairpin interfering RNA (shRNA). To investigate the role of the CXCL12/CXCR4 axis in maintaining rat GSC properties, we used a spheroid formation assay to assess the stem cell self-renewal properties. A western blot analysis and PCR arrays were used to examine the genes involved in proliferation, self-renewal, and cancer drug resistance. Finally, DNA content and flow cytometry, an immunohistochemical analysis, and methylcellulose colony formation, in vitro invasive and intracranial injection xenograft assays were employed to examine the disruptive effect of CXCR4 on the characteristics of GSCs of the RG2 cell line.Results: Disrupting CXCR4 inhibited the proliferation of RG2 cells both in vitro and in vivo. The spheroid formation assay indicated that CXCR4 was vital for the self-renewal of RG2 GSCs. Disrupting the CXCL12/CXCR4 pathway also reduced the expression of GSC cell markers, including Nestin, ABCG2, and musashi (Msi), and the expression of genes involved in regulating stem cell properties, including Oct4, Nanog, maternal embryonic leucine zipper kinase (MELK), MGMT, VEGF, MMP2, and MMP9.Conclusion: The chemokine receptor CXCR4 is crucial for maintaining the self-renewal, proliferation, therapeutic resistance, and angiogenesis of GSCs of rat RG2 glioblastoma. © 2013 Lee et al.; licensee BioMed Central Ltd.

PubMed | Shin Kong Memorial Hospital, Fu Jen Catholic University, Chi Mei Medical Center, Cheng Ching General Hospital and Cathay General Hospital
Type: | Journal: Brain, behavior, and immunity | Year: 2015

Colitis is a group of inflammatory and auto-immune disorders that affect the tissue lining of the gastrointestinal (GI) system. Studies of chemically-induced animal models of colitis have indicated that nociceptive afferents or neuropeptides have differing effects on GI inflammation. However, the molecular mechanisms involved in visceral pain and the role of visceral sensory afferents involved in the modulation of colitis remains unclear. A previous study demonstrated that Runx1, a Runt domain transcription factor, is restricted to nociceptors. In these neurons, Runx1 regulates the expression of numerous ion channels and receptors, controlling the lamina-specific innervation patterns of nociceptive afferents in the spinal cord. Moreover, mice that lack Runx1 exhibit specific defects in thermal and neuropathic pain. To examine the function of Runx1 in visceral nociception, we employed double-transgenic mice (WntCre: Runx1(F/F)), in which the expression of Runx1 was specifically disrupted in the sensory neurons. To determine the role of Runx1 in visceral pain sensation, the WntCre: Runx1(F/F) mice and their control littermates (Runx1(F/F)) were treated using dextran sodium sulfate (DSS) to induce colitis. The results indicated that disrupted Runx1 in the sensory afferents resulted in: (1) impairment of the visceral pain sensation in murine DSS-induced colitis; (2) exacerbating the phenotypes in murine DSS-induced colitis; (3) a differential effect on the production of pro- and anti-inflammatory cytokines in the colon tissues isolated from mice treated using DSS and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis; and (4) alteration of the distribution of lymphocytes and mast cells in mucosa. These results show that the function of Runx1 in sensory afferents is vital for modulating visceral pain and the neuro-immune axis.

Lai J.-H.,A-Life Medical | Jan H.-J.,Taipei Medical University | Liu L.-W.,Taipei Medical University | Lee C.-C.,Shin Kong Memorial Hospital | And 7 more authors.
Neuro-Oncology | Year: 2013

BackgroundA shift in glucose metabolism from oxidative phosphorylation to anaerobic glycolysis is the biochemical hallmark of malignant cancer cells.MethodsIn the present study, we demonstrated that Nodal stimulated the expression of glycolytic enzymes and decreased reliance on mitochondrial oxidative phosphorylation in human glioma cancer cells. The shift in glucose metabolism was mediated by induction of the hypoxia-inducible factor (HIF).ResultsNodal protein expression was shown to be correlated with expression levels of glucose transporter (Glut)-1, hexokinase (HK)-II, pyruvate dehydrogenase kinase (PDK)-1, the phosphorylation level of pyruvate dehydrogenase (PDH), glucose uptake, and lactate accumulation in human glioma cells. These effects were inversely correlated with mitochondrial oxygen consumption and ATP production. Knockdown of Nodal expression with specific small hairpin RNA reduced Glut-1, HK-II, and PDK-1 expressions and PDH phosphorylation. Nodal knockdown also reduced glucose uptake and lactate generation, which in turn increased mitochondrial membrane potential (Ψ), O2 utilization, and ATP synthesis. The ectopic expression of Nodal in low-expressing Nodal glioma cells resulted in the opposite results compared with those of Nodal knockdown glioma cells. Treatment of cells with recombinant Nodal increased HIF-1 expression, and this effect was regulated at the transcriptional level. Blockage of the Nodal receptor by a pharmacological inhibitor or Nodal knockdown in U87MG cells decreased HIF-1 expression. Furthermore, HIF-1 knockdown in U87MG cells decreased Glut-1, HK-II, and PDK-1 expressions and PDH phosphorylation, which were similar to results in Nodal knockdown cells.ConclusionTaken together, these results suggest that Nodal affects energy metabolism through HIF-1. © 2013 © The Author(s) 2013. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. All rights reserved. For permissions, please e-mail:

Background: Using microarray analysis, this study showed up-regulation of toll-like receptors 1, 2, 4, 7, 8, NF-κB, TNF, p38-MAPK, and MHC molecules in human peripheral blood mononuclear cells following infection with Plasmodium falciparum. Methods. This analysis reports herein further studies based on time-course microarray analysis with focus on malaria-induced host immune response. Results: The results show that in early malaria, selected immune response-related genes were up-regulated including α β and γ interferon-related genes, as well as genes of IL-15, CD36, chemokines (CXCL10, CCL2, S100A8/9, CXCL9, and CXCL11), TRAIL and IgG Fc receptors. During acute febrile malaria, up-regulated genes included α β and γ interferon-related genes, IL-8, IL-1b IL-10 downstream genes, TGFB1, oncostatin-M, chemokines, IgG Fc receptors, ADCC signalling, complement-related genes, granzymes, NK cell killer/inhibitory receptors and Fas antigen. During recovery, genes for NK receptorsand granzymes/perforin were up-regulated. When viewed in terms of immune response type, malaria infection appeared to induce a mixed TH1 response, in which α and β interferon-driven responses appear to predominate over the more classic IL-12 driven pathway. In addition, TH17 pathway also appears to play a significant role in the immune response to P. falciparum. Gene markers of TH17 (neutrophil-related genes, TGFB1 and IL-6 family (oncostatin-M)) and THαβ (IFN-γ and NK cytotoxicity and ADCC gene) immune response were up-regulated. Initiation of THαβ immune response was associated with an IFN-αβ response, which ultimately resulted in moderate-mild IFN-γ achieved via a pathway different from the more classic IL-12 TH1 pattern. Conclusions: Based on these observations, this study speculates that in P. falciparum infection, THαβ/TH17 immune response may predominate over ideal TH1 response. © 2013 Hu; licensee BioMed Central Ltd.

Chi K.-H.,Shin Kong Memorial Hospital | Chi K.-H.,National Yang Ming University | Liao C.-S.,Shin Kong Memorial Hospital | Chang C.-C.,Shin Kong Memorial Hospital | And 4 more authors.
International Journal of Radiation Oncology Biology Physics | Year: 2010

Purpose: We report our preliminary experience of combining sunitinib and helical tomotherapy in patients with advanced HCC. Methods and Materials: Records of patients with advanced hepatocellular carcinoma (HCC) treated with helical tomotherapy and sunitinib after radiation therapy (RT) from March 2007 to August 2008 were retrospectively reviewed. We report acute toxicities, radiologic response, serial α-fetoprotein (AFP) kinetics, and survival. Results: Of 23 evaluable patients, 60% had ≥2 hepatic lesions, extrahepatic disease was present in 5 (21.7%), and all received 2 tablets (25 mg) of sunitinib at least 1 week before, during, and 2 weeks after RT. Thirteen patients continued maintenance sunitinib after RT until disease progression. Hypofractionated RT with a median target dose of 52.5 Gy/15 fractions was delivered. An objective response was achieved in 74% of patients. The 1-year survival rate was 70%, with median survival of 16 months. Multivariate analysis showed that maintenance sunitinib was the most significant factor for survival. The time to progression was 10 months in the maintenance group compared with 4 months in the control group. Eighteen out of 21 patients with elevated AFP (85.7%) had ≧50% decline of AFP within 2 months after RT. There were three episodes of upper gastrointestinal bleeding and one episode of pancreatitis; 10 patients had ≥Grade 2 elevation of liver enzymes, and 15 had ≥Grade 2 thrombocytopenia. Conclusions: These preliminary results suggest that sunitinib and helical tomotherapy yield high Response Evaluation Criteria in Solid Tumors (RECIST) and AFP response rates in advanced HCC with an acceptable safety profile. Maintenance sunitinib after RT potentially prolongs survival. A randomized trial is warranted. © 2010 Elsevier Inc.

Jan H.-J.,Taipei Medical University | Lee C.-C.,Shin Kong Memorial Hospital | Shih Y.-L.,Shin Kong Memorial Hospital | Hueng D.-Y.,Tri services General Hospital | And 5 more authors.
Neuro-Oncology | Year: 2010

Human malignant glioma cells are characterized by local invasion. In the present study, we investigated the role of osteopontin (OPN) in the invasiveness of human glioma cells isolated from grade IV tumors. We found that the expression levels of OPN in these cell lines paralleled matrix metalloproteinase-2 (MMP-2) expression and cell invasiveness potential. When U87MG glioma cells (with a high-OPN expression level) were stably transformed with specific small hairpin RNA to knock down OPN expression, MMP-2 secretion, cell invasiveness, and tumor growth in implanted brains were dramatically reduced. Conversely, forced expression of OPN in GBM-SKH glioma cells (which expressed OPN at a low level) increased MMP-2 secretion, enhanced cell invasiveness, and increased tumor growth in a rodent xenograft model. Expression of OPN was associated with increased expression of vimentin and decreased expression of glial fibrillary acidic protein. Treatment of glioma cells with 5-aza-2'-deoxycytidine (5-aza-dC) suppressed OPN expression in a concentration-dependent manner. Suppression of OPN expression by 5-aza-dC was associated with reductions in MMP-2 secretion, vimentin expression, cell invasion, intravasation, and tumor growth. These data suggest that OPN may play important roles in regulating cell invasion in glioma cells and that 5-aza-dC may serve as a therapeutic agent for human gliomas. © The Author(s) 2009.

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