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Wu H.-S.,Centers for Disease Control | Wu H.-S.,Taipei Medical University | Yang J.-R.,Centers for Disease Control | Liu M.-T.,Centers for Disease Control | And 4 more authors.
Emerging Infectious Diseases | Year: 2014

Six persons in Taiwan who had contact with poultry infected with influenza A(H5N2) showed seroconversion for the virus by hemagglutinin inhibition or microneutralization testing. We developed an ELISA based on nonstructural protein 1 of the virus to differentiate natural infection from cross-reactivity after vaccination; 2 persons also showed seroconversion by this test. Source


Hsieh D.-S.,National Taiwan Ocean University | Hsieh D.-S.,National Defence Medical Center | Wang H.,National Taiwan Ocean University | Tan S.-W.,National Taiwan Ocean University | And 4 more authors.
Biomaterials | Year: 2011

(-)-Epigallocatechin-3-gallate (EGCG), an active ingredient in green tea, was known to effectively inhibit formation and development of tumors. However, excessive uptake of EGCG was also known to cause cytotoxicity to normal cells. In this study, EGCGs that were physically attached onto the surface of nanogold particles (pNG) was confirmed by scanning electron microscopy. The anticancer activity of the EGCG-adsorbed pNG was investigated in C3H/HeN mice subcutaneously implanted with MBT-2 murine bladder tumor cells. EGCG-pNG was confirmed to inhibit tumor cell growing by means of cell apoptosis. The mechanism that EGCG-pNG mediates tumor apoptosis was uncovered to activate the caspase cascade through the Bcl-family proteins in the mitochondrial pathway. Additionally, the mechanism that tumors were suppressed by injecting EGCG-pNG directly into the tumor site was determined to be through downregulation of VEGF, whereas that by oral administration of EGCG was through reversing immune suppression upon cancer progression. In this assessment, the prepared EGCG-pNG was confirmed to be more effective than free EGCG in inhibiting bladder tumor in model mice. © 2011 Elsevier Ltd. Source


Lai C.-H.,Department of National Defence | Jaakkola J.J.K.,University of Oulu | Chuang C.-Y.,Department of National Defence | Liou S.-H.,Department of National Defence | And 4 more authors.
Journal of Exposure Science and Environmental Epidemiology | Year: 2013

Cooking oil fumes (COF) contain polycyclic aromatic hydrocarbons (PAHs), heterocyclic aromatic amines, benzene, and formaldehyde, which may cause oxidative damages to DNA and lipids. We assessed the relations between exposure to COF and subsequent oxidative DNA damage and lipid peroxidation among military cooks and office-based soldiers. The study population, including 61 Taiwanese male military cooks and a reference group of 37 office soldiers, collected urine samples pre-shift of the first weekday and post-shift of the fifth workday. We measured airborne particulate PAHs in military kitchens and offices and concentrations of urinary 1-OHP, a biomarker of PAH exposure, urinary 8-hydroxydeoxyguanosine (8-OHdG), a biomarkers of oxidative DNA damage, and urinary isoprostane (Isop). Airborne particulate PAHs levels in kitchens significantly exceeded those in office areas. The concentrations of urinary 1-OHP among military cooks increased significantly after 5 days of exposure to COF. Using generalized estimating equation analysis adjusting for confounding, a change in log(8-OHdG) and log(Isop) were statistically significantly related to a unit change in log(1-OHP) (regression coefficient (β), β0.06, 95% CI 0.001-0.12) and (β0.07, 95% CI 0.001-0.13), respectively. Exposure to PAHs, or other compounds in cooking oil fumes, may cause both oxidative DNA damage and lipid peroxidation. © 2013 Nature America, Inc. All rights reserved. Source


Chen S.-F.,China Medical University at Taichung | Chen S.-F.,Department of National Defence | Nieh S.,Department of National Defence | Jao S.-W.,National Defence Medical Center | And 4 more authors.
Journal of Pathology | Year: 2013

Head and neck squamous cell carcinoma (HNSCC) is one of the leading causes of cancer-related death worldwide. The prognosis of HNSCC is usually poor because of its propensity for extensive invasion, local recurrence and frequent regional lymph node metastasis, even at initial diagnosis. Carcinoma-associated fibroblasts (CAFs), a major type of tumour-surrounding stromal cell, generate mediators through which they interact with tumours and contribute to cancer progression. The orchestration between CAFs and cancer cells is complex. Despite recent studies demonstrating the paracrine effect of stromal cells in the tumour microenvironment on initiation and progression of cancer cells, the major mediator related to CAFs and its underlying mechanism remain unknown. In the present study, we used organotypic culture to investigate CAFs that promote aggressive behaviour of HNSCC cells. Using microarray analysis, we detected abundant expression of interleukin-33 (IL-33) in CAFs and identified IL-33 as a critical mediator in CAF-induced invasiveness. Counteracting IL-33 activity diminished the aggressive phenotype of cancer cells induced by CAFs. Administration of IL-33 promoted cancer cell migration and invasion through induction of epithelial-to-mesenchymal transdifferentiation and increased IL-33 gene expression in cancer cells. In 40 patients with HNSCC, IL-33 expression in CAFs correlated with IL-33 expression in cancer cells. Most cases with a low invasion pattern grading score (IPGS) showed low or no expression of IL-33, whereas most HNSCC cases with high IPGS displayed over-expression of IL-33 in CAFs and cancer cells. High IL-33 expression associated with poor prognosis in terms of nodal metastasis-free survival. These results indicate that CAFs promote cancer invasiveness via paracrine and autocrine effects on microenvironmental IL-33 signalling, and suggest that IL-33 is a potential prognostic biomarker that could be considered in therapeutic strategies for the treatment of patients with HNSCC. Copyright © 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. Copyright © 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. Source


Chen C.-C.,National Taiwan Ocean University | Wu C.-J.,National Taiwan Ocean University | Yeh M.-K.,National Defence Medical Center
International Journal of Nanotechnology | Year: 2013

Cancer is a major cause of deaths. More recently, drug delivery systems (DDSs) using gold nanoparticles (GNPs) have been widely developed in cancer therapy for their easily synthesised, functionalised, better biocompatible, and low toxicity properties. Gold nanoparticle-based platforms as cancer-targeted molecules delivery to tumour tissues have been proposed as an effective strategy by overcoming various biological barriers and increasing retention effect. Coupled with the active targeting on the specific sites during cancer process they can facilitate anticancer effects. This review is focused on the current applications of GNPs as improving cancer-targeted delivery platforms. © 2013 Inderscience Enterprises Ltd. Source

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