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Kuo H.-C.,Immunology and Rheumatology | 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. Source

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. Source

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. Source

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 3 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. Source

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. Source

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