Show Chwan Memorial Hospital in Chang Bing

Changhua, Taiwan

Show Chwan Memorial Hospital in Chang Bing

Changhua, Taiwan
Time filter
Source Type

Kuo H.-C.,Chang Gung University | Chang W.-C.,Taipei Medical University | Yang K.D.,Show Chwan Memorial Hospital in Chang Bing | Yang K.D.,National Yang Ming University | And 4 more authors.
BMC Pediatrics | Year: 2013

Background: The risk of allergic diseases among Kawasaki disease (KD) patients relative to the general population is not known. The aim of this study was to perform a population-based cohort study to investigate the risk of allergic diseases among children after KD in Taiwan- a country with the third highest incidence of KD in the world.Methods: Data were obtained from the Taiwan National Health Insurance Research Database. In total, 253 patients who were 5 years of age or younger and had a first-time hospitalization with a diagnosis of KD between 1997 and 2005 were included as the study cohort and 1,012 non-KD patients matched for age and sex were included as comparison cohort. Multivariate Cox proportional hazard regression model was used to adjust for confounding and to compare the 6-year allergic-free survival rate between these two cohorts.Results: The incidence rate of allergic diseases (184.66 per 1000 person-year) was significantly higher in the KD cohort than in the control cohort (124.99 per 1000 person-years). After adjusting for potential confounders, the adjusted hazard ratios of asthma and allergic rhinitis were 1.51 (95% confidence interval = 1.17-1.95) and 1.30 (95% confidence interval = 1.04-1.62), respectively.Conclusion: We conclude that KD patients were at an increased risk for allergic diseases compared with the comparison cohort. © 2013 Kuo et al.; licensee BioMed Central Ltd.

Kuo H.-C.,Kaohsiung Chang Gung Memorial Hospital | Kuo H.-C.,Chang Gung University | Yang K.D.,Show Chwan Memorial Hospital in Chang Bing | Chang W.-C.,Kaohsiung Medical University | And 3 more authors.
Pediatrics and Neonatology | Year: 2012

Kawasaki disease (KD) is an acute multi-system vasculitis syndrome of unknown etiology occurring mostly in infants and children younger than 5 years of age. In developed countries, it is the leading cause of acquired heart disease in children. However, KD remains a mysterious disease. Some viruses potentially causing the condition have been isolated, but the results have not been able to be reproduced. This article reviews and summarizes different aspects of KD and provides updated information on diagnosis and treatment. The supplementary criteria for incomplete presentation of KD patients suggested by the American Heart Association, treatment (including tumor necrosis factor-alpha antagonist, methylprednisolone pulse therapy, statins, plasma exchange, and cytotoxic agents) for those with intravenous immunoglobulin treatment failure, and other experiences are also included in this review. © 2012, Taiwan Pediatric Association. Published by Elsevier Taiwan LLC. All rights reserved.

Chen R.-F.,Show Chwan Memorial Hospital in Chang Bing | Yang K.D.,Show Chwan Memorial Hospital in Chang Bing | Lee I.-K.,Chang Gung University | Liu J.-W.,Chang Gung University | And 5 more authors.
Journal of Infection | Year: 2014

Objective: Suppressors of cytokine signalling (SOCS) proteins regulate cytokine responses and control immune balance. The objective of our study was to determine whether the expression of SOCS1 and its potential regulatory microRNAs (miRNAs) in leukocytes is correlated to the development of dengue haemorrhagic fever (DHF). Methods: We performed a case-control study to investigate the SOCS1 and miRNA expression in leukocytes for patients with DF and DHF in a DENV-2 outbreak that occurred in Taiwan between 2002 and 2003. We performed reverse transcription polymerase chain reaction to evaluate the expression of SOCS1 and its regulatory miRNAs in mononuclear leukocytes obtained from patients with or without DHF. The reciprocal relationship between SOCS1 and miR-150 expression was validated in DENV-2-infected peripheral mononuclear cells (PBMCs). Results: SOCS1 expression and lower IFN-γ level were significantly reduced in DHF patients, but not in patients with DF. Elevated SOCS1 and reduced miR-150 levels were detected 24h after DENV-2 infection in PBMCs. Transfection of a miR-150 mimic into CD14+ cells infected with DENV-2 suppressed the induction of SOCS1 expression in a dose-dependent manner. Conclusion: We demonstrate for the first time that augmented miR-150 expression with depressed SOCS1 expression in CD14+ cells are associated with the pathogenesis of DHF. © 2014 The Authors.

Chou C.-K.,Chang Gung Memorial Hospital Kaohsiung Medical Center | Yang K.D.,Show Chwan Memorial Hospital in Chang Bing | Chou F.-F.,Chang Gung Memorial Hospital Kaohsiung Medical Center | Huang C.-C.,Chang Gung Memorial Hospital Kaohsiung Medical Center | And 5 more authors.
Journal of Clinical Endocrinology and Metabolism | Year: 2013

Context: Recent studies suggest that miR-146b deregulation in papillary thyroid carcinoma (PTC) was associated with advanced tumor characteristics. However, the influence of miR-146b expression on the prognosis of PTC remains unknown. We sought to correlate tumor expression levels of miR-146b with the prognosis of a previously reported PTC cohort and reveal the underlying mechanisms via a PTC cell line model. Methodology: Expression levels of miR-146b were assessed via quantitative real-time PCR in 71 cases of PTC with distinct clinico-pathogenetic characteristics. All patients were classified into the disease-free or active disease group, based on their medical records at the end of the follow-up period. In vitro gain-of-function experiments were performed in a BCPAP human papillary thyroid cancer cell line model, which harbored the homozygous mutation of BRAF. BCPAP cells were transfected with a mimic-miR-146b and nonspecific microRNA (miRNA) control to determine whether miR-146b overexpression promotes cell migration and invasion. Proliferation assay, colony formation assay, and chemotherapy-induced apoptosis were also determined. Results: Multivariate logistic regression analysis demonstrated advanced tumor stage, presence of cervical lymph node metastasis, and miR-146b expression were independent risk factors for poor prognosis in PTC. Patients with higher miR-146b expression levels had significantly poorer overall survival compared with those with lower miR-146b levels. The associated hazard ratio was 3.92 (95% confidence interval, 1.73-8.86, log-rank P < .05). Overexpression of miR-146b significantly increased cell migration and invasiveness. Furthermore, miR-146b also increased resistance to chemotherapy-induced apoptosis. Conclusions: Our results suggest that miR-146b is a novel prognostic factor of PTC. Furthermore, in vitro functional studies provided the mechanistic explanation for miR-146b in tumor aggressiveness. These results enhance understanding of the molecular mechanisms involved in tumor aggressiveness in PTC, provide new prognostic biomarkers, and ultimately offer new leads for developing therapies for PTC. Copyright © 2013 by The Endocrine Society.

Wang L.,Chang Gung University | Chang L.-S.,Chang Gung University | Lee I.-K.,Chang Gung University | Tang K.-S.,Chang Gung University | And 4 more authors.
Influenza and other Respiratory Viruses | Year: 2014

Background: The sensitivity of rapid influenza diagnostic test (RIDT) of children with influenza-like illness (ILI) remains low. Objective: We compare the parameters between pandemic A(H1N1) 2009 influenza with negative RIDT and ILI not H1N1 for improving the low sensitivity of RIDT for children with ILI. Methods: In a cohort of consecutive laboratory-confirmed H1N1 influenza, we identified 150 H1N1 children with positive RIDT, 152 H1N1 children with negative RIDT, and 75 children with ILI not H1N1. Viral load in throat, complete blood count (CBC), and C-reactive protein (CRP) levels between H1N1 children with negative RIDT and children with ILI not H1N1 were assessed. Results: The diagnostic sensitivity of the RIDT was 45·5%. An analysis of CBC and CRP levels indicated that H1N1 children with negative RIDT had lower total leukocyte, neutrophil, lymphocyte, and basophil counts, and serum CRP levels (P < 0·01). Lymphocyte counts less than 1500 cells/mm3 and CRP levels <15 mg/l, determined by a receiver operating characteristic curve, showed a diagnostic sensitivity of 52·5% and 80·7%, respectively. Combining the lymphocyte counts and CRP levels provided a diagnostic sensitivity of 91·5%. Moreover, H1N1 children with negative RIDT had a lower viral load than those with positive RIDT (3·33 versus 4·48 log10 copies/ml, P < 0·001); the viral load was negatively correlated to the lymphocyte count (P < 0·001). Conclusions: A combination of a low lymphocyte count and a low CRP level could, in the early disease phase, provide a useful screening for H1N1 children with false-negative RIDT, potentially facilitating differential diagnoses. © 2013 The Authors.

Chen C.-H.,Chang Gung University | Lin L.-Y.,Chang Gung University | Yang K.D.,Show Chwan Memorial Hospital in Chang Bing | Hsieh K.-S.,Kaohsiung Veterans General Hospital | Kuo H.-C.,Chang Gung University
Journal of Microbiology, Immunology and Infection | Year: 2014

Kawasaki disease (KD) is a systemic vasculitis primarily affecting children who are younger than 5 years. The most serious complications are coronary artery aneurysms and sequelae of vasculitis with the subsequent development of coronary artery aneurysm. According to the literature, intravenous immunoglobulin (IVIG) plus high-dose aspirin (acetylsalicylic acid) were standard treatment for KD, whereas low-dose aspirin (3-5 mg/kg/day) was used for thrombocytosis in KD via antiplatelet effect. However, aspirin has been reported to have hemolytic potential in individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency. We report a child with G6PD-deficiency who has KD, and review the literature. © 2012.

Lin I.-C.,Chang Gung University | Kuo H.-C.,Chang Gung University | Lin Y.-J.,Chang Gung University | Wang F.-S.,Chang Gung University | And 8 more authors.
PLoS ONE | Year: 2012

Background: Kawasaki disease (KD) of unknown immunopathogenesis is an acute febrile systemic vasculitis and the leading cause of acquired heart diseases in childhood. To search for a better strategy for the prevention and treatment of KD, this study compared and validated human KD immunopathogenesis in a mouse model of Lactobacillus casei cell wall extract (LCWE)-induced coronary arteritis. Methods: Recruited subjects fulfilled the criteria of KD and were admitted for intravenous gamma globulin (IVIG) treatment at the Kaohsiung Chang Gung Memorial Hospital from 2001 to 2009. Blood samples from KD patients were collected before and after IVIG treatment, and cardiovascular abnormalities were examined by transthoracic echocardiography. Wild-type male BALB/c mice (4-week-old) were intraperitoneally injected with LCWE (1 mg/mL) to induce coronary arteritis. The induced immune response in mice was examined on days 1, 3, 7, and 14 post injections, and histopathology studies were performed on days 7 and 14. Results: Both human KD patients and LCWE-treated mice developed coronary arteritis, myocarditis, valvulitis, and pericarditis, as well as elevated plasma levels of interleukin (IL)-2, IL-6, IL-10, monocyte chemoattractant protein (MCP)-1, and tumor necrosis factor (TNF)-α in acute phase. Most of these proinflammatory cytokines declined to normal levels in mice, whereas normal levels were achieved in patients only after IVIG treatment, with a few exceptions. Toll-like receptor (TLR)-2, but not TLR4 surface enhancement on circulating CD14+ monocytes, was augmented in KD patients before IVIG treatment and in LCWE-treated mice, which declined in patients after IVIG treatment. Conclusion: This result suggests that that not only TLR2 augmentation on CD14+ monocytes might be an inflammatory marker for both human KD patients and LCWE-induced CAL mouse model but also this model is feasible for studying therapeutic strategies of coronary arteritis in human KD by modulating TLR2-mediated immune activation on CD14+ monocytes. © 2012 Lin et al.

Guo M.M.-H.,Chang Gung University | Tseng W.-N.,Chang Gung University | Ou C.-Y.,Chang Gung University | Hsu T.-Y.,Chang Gung University | And 4 more authors.
Allergy: European Journal of Allergy and Clinical Immunology | Year: 2015

Background Atopic dermatitis affects 15-30% of children worldwide. Onset of disease usually occurs within the first year of life, over half of which regress by 6 years of age. The aim of this study was to investigate the risk factors related to the persistence of infantile atopic dermatitis. Methods In this birth cohort study, patients were enrolled prenatally and followed until 6 years of age; 246 patients had infantile atopic dermatitis at 6 months of age. Family history, maternal and paternal total and specific Immunoglobulin E (IgE) levels, and cord blood IgE were recorded. Clinical examination, questionnaire survey, and blood samples for total and specific IgE of the children were collected at each follow-up visit. Results Of the 246 patients with infantile atopic dermatitis at 6 months of age, 48 patients had persisted atopic dermatitis at 6 years of age (19.5%). Risk factors associated with persistent infantile atopic dermatitis included egg white sensitization (odds ratio: 3.801, P = 0.020), and atopic dermatitis involving two or more areas at 6 months old (odds ratio: 2.921, P = 0.018) after multivariate analysis with logistic regression. Patients with persistent infantile atopic dermatitis had a higher risk of asthma before 6 years old (39.6% vs 24.2%, P = 0.032). Conclusion Egg white sensitization and the initial involvement of two or more areas at 6 months of age were associated with the persistent infantile atopic dermatitis. Patients with persistent infantile atopic dermatitis are more likely to develop asthma by 6 years of age. © 2015 John Wiley and Sons A/S. Published by John Wiley and Sons Ltd.

Yu H.-R.,Chang Gung University | Kuo H.-C.,Chang Gung University | Huang L.-T.,Chang Gung University | Chen C.-C.,Chang Gung University | And 7 more authors.
Immunology | Year: 2014

Summary: In cases of arginine depletion, lymphocyte proliferation, cytokine production and CD3ζ chain expression are all diminished. In addition to myeloid suppressor cells, polymorphonuclear cells (PMN) also exert T-cell immune suppressive effects through arginase-induced l-arginine depletion, especially during pregnancy. In this study, we investigated how arginase/l-arginine modulates neonatal lymphocyte proliferation. Results showed that the neonatal plasma l-arginine level was lower than in adults (48·1 ± 11·3 versus 86·5 ± 14·6 μm; P = 0·003). Neonatal PMN had a greater abundance of arginase I protein than adult PMN. Both transcriptional regulation and post-transcriptional regulation were responsible for the higher arginase I expression of neonatal PMN. Exogenous l-arginine enhanced neonate lymphocyte proliferation but not that of adult cells. The RNA-binding protein HuR was important but was not the only modulation factor in l-arginine-regulated neonatal T-cell proliferation. l-Arginine-mediated neonatal lymphocyte proliferation could not be blocked by interleukin-2 receptor blocking antibodies. These results suggest that the altered arginase/l-arginine cascade may be one of the mechanisms that contribute to altered neonatal immune responses. Exogenous l-arginine could enhance neonate lymphocyte proliferation through an interleukin-2-independent pathway. © 2014 John Wiley & Sons Ltd.

Yang B.,University of North Carolina at Chapel Hill | Chuang H.,Kaohsiung Chang Gung Memorial Hospital | Chen R.-F.,Show Chwan Memorial Hospital in Chang Bing
Open Glycoscience | Year: 2012

Sugar-lectin interactions play an important role in viral infections. Many viruses, such as human immunodefi-ciency virus (HIV), Ebola, dengue, cytomegalovirus, and hepatitis C, possess glycans that recognize C-type lectins, espe-cially CD209 (DC-SIGN), for infection. Other viruses possess lectins on their surfaces that recognize glycan epitopes on human epithelial cells for infection. Human and avian influenza viruses recognize different glycan epitopes, sialic acid-α2,6 galactose (SA-α2,6Gal) and SA- α 2,3Gal, respectively, as their receptors, resulting in different host ranges for these two viruses. We and others have shown that sialogalactosides and fucosyllactoses are receptors for enterovirus 71 and no-rovirus infections, respectively; human milk oligosaccharides (HMOs) could block enterovirus 71 and norovirus infec-tions. Several lines of evidence also suggest that HMOs cannot only mimic viral receptors and block viral infections, but also raise immune responses through sugar/lectin (galactosides/galactins and sialylglycans/Siglecs) interactions and im-prove gut ecology by nurturing intestinal cells and/or intestinal microbiota. This review article summarizes how and why HMOs directly or indirectly protect humans from viral infections. © Yang et al.

Loading Show Chwan Memorial Hospital in Chang Bing collaborators
Loading Show Chwan Memorial Hospital in Chang Bing collaborators