Hsin Chu General Hospital

Taipei, Taiwan

Hsin Chu General Hospital

Taipei, Taiwan
SEARCH FILTERS
Time filter
Source Type

Chang M.-C.,Chang Gung Institute of Technology | Chen L.-I.,National Taiwan University Hospital | Chan C.-P.,Chang Gung Memorial Hospital | Lee J.-J.,National Taiwan University Hospital | And 6 more authors.
Biomaterials | Year: 2010

Biocompatibility of dentin bonding agents (DBAs) and resin composite is important to preserve the pulp vitality after operative restoration. Bisphenol-glycidyl-methacrylate (BisGMA) is one common monomer adding into DBAs and resin. In this study, we found that exposure of human dental pulp cells to BisGMA (>0.1 m. m) led to cytotoxicity, G2/M cell cycle arrest and apoptosis as analyzed by propidium iodide (PI) and PI/annexin V dual fluorescent flow cytometry. These events were associated with a decline of cdc2, cdc25C and cyclinB1 expression at both mRNA and protein levels. BisGMA also induced the expression of hemeoxygenase-1 (HO-1), an oxidative stress responsive gene, in pulp cells. Catalase could prevent the BisGMA-induced alteration of cell cycle-related genes (cdc2, cdc25C, cyclinB1) and HO-1 expression in dental pulp cells. Interestingly, Zn-protoporphyrin (2.5-5 μ m), a HO inhibitor, enhanced the BisGMA-induced reactive oxygen species (ROS) production and cytotoxicity. These results suggest that exposure to higher concentrations of BisGMA may stimulate ROS production, cell cycle arrest, apoptosis and cell death. Inducing the expression of HO-1 in dental pulp cells by BisGMA is mediated by ROS production and important to protect dental pulp against the toxicity by monomers present in composite resin and DBAs. © 2010 Elsevier Ltd.


Chen C.-H.,National Taiwan University Hospital | Wu T.,National Taiwan University Hospital | Sun J.-S.,National Taiwan University Hospital | Sun J.-S.,Hsin Chu General Hospital | And 2 more authors.
Journal of Hand Surgery: European Volume | Year: 2012

Space occupying lesions found at surgery caused or contributed to carpal tunnel syndrome in 23 of 779 patients operated for carpal tunnel syndrome from January 1999 to December 2008. The mean age of these 23 patients was 52.9 years, and in patients who had a local swelling or palpable mass, ultrasonography or magnetic resonance imaging (MRI) was done. All had open release of the transverse carpal ligament and lesions were removed. Histopathology showed tophaceous gout in 10 men, tenosynovitis in seven patients and tumors in eight. The tumors included ganglion cysts in two, lipoma in three and fibroma of the tendon sheath in one. The neurological symptoms subsided after surgery in all. In patients with gout, one had an infected wound and another had recurrence of symptoms 1 year after later. Carpal tunnel syndrome caused by a space occupying lesion is rare and more complicated than idiopathic carpal tunnel syndrome. © The Author(s) 2011.


Chen P.-Y.,National Taiwan University | Sun J.-S.,Taipei Medical University | Sun J.-S.,Hsin Chu General Hospital | Tsuang Y.-H.,Taipei Medical University Hospital | And 3 more authors.
Nutrition Research | Year: 2010

Statins inhibit 3-hydroxy-3-methylglutaryl-coenzyme A reductase, which catalyzes the conversion of 3-hydroxy-3-methylglutaryl-coenzyme A to mevalonate, a rate-limiting step in cholesterol synthesis. Statins are able to reduce cardiovascular risk in hypercholesterolemic patients. In recent years, the possible effect of statins on bone tissue has received particular attention. The present study was undertaken to understand the events of osteoblast differentiation induced by statins. Our hypothesis is that simvastatin promotes osteoblast viability and differentiation via Ras/Smad/Erk/bone morphogenic protein (BMP)-2 signaling pathway. The viability and differentiation of osteoblasts were examined by mitochondrial activity assay, alkaline phosphatase (ALP) activity, and gene expression. The associated signaling pathways were analyzed by cytoplasmic and membrane proteins manifestation. After administration of 10-6 M simvastatin, the ALP activity was significantly enhanced, and the expression of BMP-2, ALP, sialoprotein, and type I collagen genes were up-regulated. After simvastatin treatment, both the RasGRF1 and phospho-RasGRF1 in the cytoplasm decreased significantly, whereas those on the plasma membrane increased. A marked increase in membranous GAP-associated protein (P190) and the activated form of both phospho-extracellular signal-regulated kinase1/2 and phospho-Smad1 were also noted. In conclusion, this study shows that statins pose a positive effect on the metabolism of osteoblasts. Simvastatin can promote osteoblast viability and differentiation via membrane-bound Ras/Smad/Erk/BMP-2 pathway. Statins stimulate osteoblast differentiation in vitro and may be a promising drug for the treatment of osteoporosis in the future. © 2010 Elsevier Inc.


Lin K.-C.,National Taiwan University | Fu T.,National Taiwan University | Wu C.-Y.,Chang Gung University | Wang Y.-H.,National Taiwan University | And 5 more authors.
Neurorehabilitation and Neural Repair | Year: 2010

Objectives. The purpose of this study was to establish the minimal detectable change (MDC) and clinically important differences (CIDs) of the physical domains of the Stroke Impact Scale (SIS) and to assess the proportions of patients' change scores exceeding the MDC and CIDs after stroke rehabilitation. Methods. Seventy-four patients received 1 of 3 treatments for 3 weeks and underwent clinical assessment before and after treatment. The MDC was calculated from the standard error of measurement to indicate a real change with 95% confidence for individual patients (MDC95). Anchor-based and distribution-based approaches were adopted to triangulate the ranges of minimal CIDs. The percentage of patients exceeding MDC95 and minimal CIDs were also calculated. Results. The MDC95 of the strength, activities of daily living/instrumental activities of daily living, mobility, and hand function subscales were 24.0, 17.3, 15.1, and 25.9, respectively. The respective minimal CIDs for these 4 subscales were 9.2, 5.9, 4.5, and 17.8 points, respectively, and the MDC95 and CID proportions were 14% to 43%, 16% to 49%, 10% to 50%, and 23% to 64%, respectively. Conclusions. The change score of an individual patient has to reach 24.0, 17.3, 15.1, and 25.9 on the 4 subscales to indicate a true change. The mean change scores of a stroke group on the 4 subscales should reach 9.2, 5.9, 4.5, and 17.8 points to be regarded as clinically important changes. Future research with larger sample sizes is warranted to validate these estimates. © 2010 The Author(s).


Hung H.-F.,Hsin Chu General Hospital | Chen H.-H.,National Taiwan University
PharmacoEconomics | Year: 2011

Background: As neonates born to mothers with positive hepatitis B e antigen may not be completely protected by hepatitis B vaccination, prophylactic lamivudine use in mothers with high viraemia has been proposed. However, the overall effectiveness and the balance between cost and benefit for such a prophylactic strategy have rarely been addressed. Objective: Using a review of recent literature, we aimed to assess the cost effectiveness, from the Taiwanese societal perspective, of administering prophylactic lamivudine to mothers to reduce vertical transmission of hepatitis B virus and its long-term sequelae in neonates. Methods: A meta-analysis of three randomized controlled trials was conducted to evaluate the efficacy of lamivudine versus placebo. A Markov decision model was constructed in which in both treatment arms infants received active and passive immunoprophylaxis. An economic evaluation was performed to calculate costs, acute infections averted, and QALYs gained. Probabilistic sensitivity analyses were conducted and a cost-effectiveness acceptability curve drawn. All these analyses were from the societal perspective. Costs (£US) were valued in year 2008 prices. Result: Supplemental lamivudine use gained an additional 0.0024 QALYs and averted 0.23 acute infections per birth compared with the routine activepassive immunization without lamivudine. The cost-effectiveness analysis suggested that the use of additional prophylactic lamivudine dominated the routine strategy. The acceptability curve suggested that the probability of being cost effective under the willingness-to-pay threshold of £US20 000 was 94%. Conclusion: This analysis suggests that supplemental use of lamivudine in mothers with high hepatitis B viraemia is effective in reducing vertical transmission and may be cost effective, from a Taiwanese societal perspective, compared with the routine active-passive immunization without lamivudine. © 2011 Adis Data Information BV. All rights reserved.


Lin G.-J.,National Defense Medical Center | Huang S.-H.,Tri Service General Hospital | Chen Y.-W.,Tri Service General Hospital | Hueng D.-Y.,Tri Service General Hospital | And 5 more authors.
Diabetologia | Year: 2011

Aims/hypothesis: Autoimmune diabetes results from a progressive destruction of insulin-producing beta cells in the pancreatic islets by chemokine-attracted lymphocytes. Because islet cells in NOD mice produce chemokines during the development of autoimmune diabetes, we investigated the role of inflammatory CC chemokines in disease progression in these mice. Methods: We generated a transgenic NOD mouse model that overproduces the inflammatory CC chemokine decoy receptor D6 in pancreatic islets. Results: The frequency of diabetes and insulitis scores of transgenic mice were decreased significantly, compared with non-transgenic control littermates. Transgenic expression of D6 (also known as Ccbp2) did not affect systemic lymphocyte development or alter: (1) the T cell subsets such as T helper (Th)1, Th2 and T regulatory cells; or (2) antigen-presenting cells such as dendritic cells or macrophages. The percentages and numbers of T and B lymphocytes were decreased significantly in the pancreas. Activation status, autoantigen-specific proliferation and diabetogenicity of lymphocytes were also markedly reduced. Conclusions/ interpretation: Inflammatory CC chemokines play a critical role in the development of autoimmune diabetes. Transgenic expression of D6 in pancreatic islets of NOD mice reduced this pathogenic process by suppressing activation of autoreactive lymphocytes and by reducing migration of lymphocytes to the pancreas. © 2011 Springer-Verlag.


Liu H.-H.,Kaohsiung Veterans General Hospital | Chou Y.-J.,Kaohsiung Veterans General Hospital | Chen C.-H.,Kaohsiung Veterans General Hospital | Chia W.-T.,Hsin Chu General Hospital | Wong C.-Y.,Kaohsiung Veterans General Hospital
Orthopedics | Year: 2010

Various surgical procedures have been described for the treatment of complete acromioclavicular joint dislocation, but no consensus exists on the optimal therapy. The aim of each type of procedure is to stabilize the clavicle by substitution of the ruptured coracoclavicular ligaments. Treatment modalities have changed with increasing understanding of the nature of the problem and the biomechanics of the joint. This article presents a method consisting of a modified Weaver-Dunn procedure and a clavicular hook plate for the operative management of acute acromioclavicular joint injuries. We performed a retrospective study of 46 patients who had undergone a modified Weaver-Dunn procedure with a clavicular hook plate for acute acromioclavicular joint injuries between July 2002 and December 2006. Average follow-up was 36.6 months (range, 24-46 months). There was 1 skin-deep infection, 1 dislocation of the hook, and 2 redislocations of the acromioclavicular joint. Thirteen patients had some calcification between the clavicle and the coracoid process, which did not cause loss of motion or other symptoms. All but 1 patient returned to work, and all but 1 returned to their preoperative activity level. The mean Constant score was 88.2 points. The mean Disabilities of the Arm, Shoulder, and Hand (DASH) score was 12.2 points. Treatment of acute acromioclavicular joint injuries using a modified Weaver-Dunn procedure and a clavicular hook plate showed good short-term clinical results with a low complication rate. Further investigation and long-term results are needed to confirm these preliminary findings.


Hsieh T.-P.,Taipei Medical University | Sheu S.-Y.,Taipei Medical University | Sun J.-S.,Taipei Medical University | Sun J.-S.,Hsin Chu General Hospital | Chen M.-H.,National Yang Ming University
Phytomedicine | Year: 2011

Icariin has been reported to enhance bone healing and treat osteoporosis. In this study, we examined the detail molecular mechanisms of icariin on lipopolysaccharide (LPS)-induced osteolysis. Our hypothesis is that icariin can inhibit osteoclast differentiation and bone resorption by suppressing MAPKs/NF-κB regulated HIF-1α and PGE2 synthesis. After treatment with icariin, the activity of osteoclasts differentiation maker, tatrate resistances acid phosphatease (TRAP), significantly decreased at the concentration of 10-8 M. Icariin (10-8 M) reduced the size of LPS-induced osteoclasts formation, and diminished their TRAP and acid phosphatease (ACP) activity without inhibition of cell viability. Icariin also inhibited LPS-induced bone resorption and interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) expression. The gene expression of osteoprotegerin (OPG) was up-regulated, while receptor activator of NF-κB ligand (RANKL) was down-regulated. Icariin also inhibited the synthesis of cyclo-oxygenase type-2 (COX-2) and prostaglandin E2 (PGE 2). In addition, icariin had a dominant repression effect on LPS-induced hypoxia inducible factor-1α (HIF-1α) expression of osteoclasts. On osteoclasts, icariin suppresses LPS-mediated activation of the p38 and JNK; while on the osteoblasts, icariin reduced the LPS-induced activation of ERK1/2 and I-kappa-B-alpha (IκBα), but increased the activation of p38. In conclusion, we demonstrated that icariin has an in vitro inhibitory effects on osteoclasts differentiation that can prevent inflammatory bone loss. Icariin inhibited LPS-induced osteoclastogenesis program by suppressing activation of the p38 and JNK pathway. © 2010 Elsevier GmbH.


Kuo H.-Y.,Hsin Chu General Hospital | Yang C.-M.,Hsin Chu General Hospital | Lin M.-F.,Chutung Hospital | Cheng W.-L.,Yuanpei University | And 2 more authors.
Diagnostic Microbiology and Infectious Disease | Year: 2010

We investigated the molecular epidemiology and OXA-type carbapenemase genes of 83 imipenem-resistant Acinetobacter spp. collected from 2 university hospitals (hospitals A and B) and a regional hospital (hospital C) during 2007 in Taiwan. Genotyping by pulsed-field gel electrophoresis identified 51 pulsotypes. None of the pulsotypes established predominance throughout the 3 hospitals. Multiplex polymerase chain reaction of blaOXA genes showed that 100% (18/18), 91%(31/34), and 100% (31/31) of the Acinetobacter spp. collected from hospital A, B, and C, respectively, possessed blaOXA-51-like genes. None of the strains carrying blaOXA-23-like and blaOXA-24-like genes were found in hospital A. The coexistences of blaOXA-51-like/blaOXA-23-like and blaOXA-51-like/blaOXA-24-like genes detected in hospitals B and C were 26% (9/34) and 12% (4/34) and 58% (18/31) and 3% (1/31), respectively. Among blaOXA-23-like gene-carrying isolates collected from hospitals, clonal spread of strains carrying the blaOXA-23 gene was detected in the regional hospital but not the other 2 university hospitals. The results suggest that interhospital dissemination of imipenem-resistant Acinetobacter spp. was not found in these hospitals. The increasing percentage of OXA-23 in OXA-type carbapenemases in Acinetobacter spp. from the regional hospitals to medical centers deserves further attention in Taiwan. © 2010 Elsevier Inc. All rights reserved.


Hsu C.P.,Yuanpei University | Kao T.Y.,Tri Service General Hospital | Chang W.L.,Yuanpei University | Chang W.L.,Tri Service General Hospital | And 4 more authors.
European Journal of Surgical Oncology | Year: 2011

Background: It has been demonstrated that the deletion, mutation, hypermethylation and subcellular location of the tumor suppressor phosphatase and tensin homologue (PTEN) are closely correlated with carcinogenesis, progression and prognosis of malignancy. Both mutation and the microsatellite instability of the PTEN gene influence regulation of the PI3K/Akt signaling pathway. This study investigated whether loss of nuclear PTEN is correlated with chemosensitivity, clinicopathological parameters and survival. Methods: Intracellular levels of PTEN of multiple cell lines of colorectal carcinoma (CRC) were evaluated by Western blotting and immunocytochemistry. The chemosensitivity of cell lines with various expression levels of PTEN was evaluated using 5-flurouracil (5-FU), oxaliplatin and irinotecan (CPT), and clinical significance was evaluated by immunohistochemical analysis of 133 CRC specimens. Results: Colon cancer cell lines HT-29, LoVo and SW480 differed in expression of PTEN, with high, moderate and low levels, respectively. HT-29 and LoVo PTEN expression was suppressed by a low concentration of 5-FU and oxaliplatin; however, SW480 was insensitive to these chemotherapeutic agents. Nuclear PTEN was overexpressed in most (>80%) normal colon mucosa samples, but the incidence significantly decreased (89.2% → 53.4%) in the CRC group. PTEN in the nucleus was negatively correlated with tumor size and vascular invasion in CRC, and CRC patients with negative PTEN expression in the nucleus exhibited poor survival. Conclusion: Cell lines with a high expression of PTEN are sensitive to chemotherapy with 5-FU and oxaliplatin. Nuclear PTEN expression gradually decreases after malignant transformation, and loss of PTEN expression in the nucleus is associated with tumor progression and poor clinical outcome in CRC. © 2010 Elsevier Ltd. All rights reserved.

Loading Hsin Chu General Hospital collaborators
Loading Hsin Chu General Hospital collaborators