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Chao C.M.,Chi Mei Medical Center Liouying | Lai C.C.,Chi Mei Medical Center Liouying | Tsai H.Y.,Far Eastern Memorial Hospital | Wu C.J.,National Cheng Kung University | And 4 more authors.
European Journal of Clinical Microbiology and Infectious Diseases | Year: 2013

We investigated the clinical characteristics of patients with pneumonia caused by Aeromonas species. Patients with pneumonia caused by Aeromonas species during the period 2004 to 2011 were identified from a computerized database of a regional hospital in southern Taiwan. The medical records of these patients were retrospectively reviewed. Of the 84 patients with pneumonia due to Aeromonas species, possible Aeromonas pneumonia was diagnosed in 58 patients, probable Aeromonas pneumonia was diagnosed in 18 patients, and pneumonia due to Aeromonas was conclusively diagnosed in 8 patients. Most of the cases of Aeromonas pneumonia developed in men and in patients of advanced age. A. hydrophila (n = 50, 59.5 %) was the most common pathogen, followed by A. caviae (n = 24, 28.6 %), A. veronii biovar sobria (n = 7, 8.3 %), and A. veronii biovar veronii (n = 3, 3.6 %). Cancer (n = 37, 44.0 %) was the most common underlying disease, followed by diabetes mellitus (n = 27, 32.1 %). Drowning-associated pneumonia developed in 6 (7.1 %) patients. Of 47 patients who were admitted to the intensive care ward, 42 patients developed acute respiratory failure and 24 of those patients died. The overall in-hospital mortality rate was significantly associated with liver cirrhosis, cancer, initial presentation of shock, and usage of mechanical ventilation. In conclusion, Aeromonas species should be considered as one of the causative pathogens of severe pneumonia, especially in immunocompromised patients, and should be recognized as a cause of drowning-associated pneumonia. Cirrhosis, cancer, and shock as the initial presenting symptom are associated with poor outcome. © 2013 Springer-Verlag Berlin Heidelberg.


Chen C.-H.,Buddhist Tzu Chi General Hospital | Chen C.-H.,Taipei Veterans General Hospital | Chen H.-A.,Chi Mei Medical Center Liouying | Lu C.-L.,Chi Mei Medical Center Liouying | And 4 more authors.
Clinical Rheumatology | Year: 2013

We investigated the association between smoking and the disease activity, functional ability, physical mobility, and systemic inflammation in Chinese ankylosing spondylitis (AS) patients. Seventy five male Chinese AS patients in Taiwan were enrolled in the cross-sectional study. These patients fulfilled the 1984 modified New York criteria. Patients completed the questionnaires, containing the demographic data, disease activity, functional ability (BASFI), and patient's global assessment. Meanwhile, physical examinations were performed to determine the patient's physical mobility. Acute-phase reactants, erythrocyte sedimentation rate (ESR), and C-reactive protein levels were also measured in the AS patients. Smoking habits with smoking duration and smoking intensity (pack-years of smoking) were recorded. Among these physical mobility parameters, modified Schober's index (p < 0.001), cervical rotation (p = 0.034), later lumbar flexion (p = 0.002), chest expansion (p = 0.016), and occiput-to-wall distances (p = 0.003) were significantly impaired in smoking AS patients (n = 35) as compared to non-smoking (n = 40). Systemic inflammation parameter, ESR was significantly higher in smoking AS patients than non-smoking (p = 0.03). The odds ratio of advanced modified Schober's index, lateral lumbar flexion, fingertip-to-floor distance, chest expansion, and occiput-to-wall were significantly elevated in smoking AS patients as compared to non-smoking. Moreover, the smoking intensity correlated significantly with BASFI (r = 0.481, p = 0.005), cervical rotation (r = -0.401, p = 0.031), fingertip-to-floor distance (r = 0.485, p = 0.004), and occiput-to-wall distance (r = 0.473, p = 0.005) in the 35 smoking AS patients. The cigarette smokers in the Chinese AS patients have increased systemic inflammation and poor physical mobility. In addition, the higher smoking intensity in the AS smokers is associated with poor disease outcome, including functional ability and physical mobility. Thus, it is quite important for the physician to emphasize the association of smoking with poor disease prognosis in AS, and patients should be strongly recommended to avoid smoking cigarette. © 2013 Clinical Rheumatology.


Chiu C.-T.,Chang Gung Memorial Hospital | Chiang W.-F.,Chi Mei Medical Center Liouying | Chuang C.-Y.,Sin Lau Christian Hospital | Chang S.-W.,Chang Gung Memorial Hospital
Journal of Oral and Maxillofacial Surgery | Year: 2010

Purpose: To offer recommendations of risk factors, prevention, and treatment of oral bisphosphonate and steroid-related osteonecrosis of the jaw (BSRONJ) in Taiwan. Materials and Methods: Twelve patients were clinicopathologically proved to have bisphosphonate-related osteonecrosis of the jaw (BRONJ). All of the patients were taking oral bisphosphonates and were concurrently administered long-term steroids. Of the 12 patients, 3 patients were assigned to the first stage of BRONJ; 5 patients were assigned to the second stage, and 4 patients were assigned to the third stage. The patients' symptoms, localization of necrosis, presence of a fistula, and association with possible triggering factors for onset of the lesion were recorded. Results: The radiologic investigations revealed osteolytic areas and scintigraphy demonstrated increased bone metabolism. Microbiologic analysis showed pathogenic actinomycosis organisms in a majority of patients (91.6%). Antibiotic therapy, minor debridement surgery, and combined hyperbaric oxygen therapy were useful in obtaining short-term symptomatic relief. Conclusions: Comorbidities of steroid use along with bisphosphonates may cause osteonecrosis of the jaw to occur sooner, be more severe, and respond more slowly to a drug discontinuation. The clinical disease of BSRONJ is more severe and more unpredictable to treat than BRONJ. From the data gained from other published studies of BRONJ and our clinical experience with the series of cases of BSRONJ, we offer recommendations of risk factors, prevention, and treatment of BSRONJ in southern Taiwan. © 2010 American Association of Oral and Maxillofacial Surgeons.


PubMed | National Taiwan University Hospital, China Medical University at Taichung, Sin Ren Hospital, Mackay Memorial Hospital and 22 more.
Type: Journal Article | Journal: Nephrology (Carlton, Vic.) | Year: 2016

Acute kidney injury (AKI) carries an increasing incidence rate worldwide and increases the risk of developing end-stage renal disease (ESRD) as well as the medical expenses during the post-AKI course. The Taiwan Consortium for Acute Kidney Injury and Renal Diseases (CAKs) has thus launched a nationwide epidemiology and prognosis of dialysis-requiring acute kidney injury (NEP-AKI-D) study, which prospectively enrols critically ill patients with AKI. Through thoroughly evaluating the risk and prognostic factors of AKI, we hope to lower the incidence of AKI and ESRD from the perspective of AKI-ESRD interaction.The CAKs includes 30 hospitals which distribute widely through the four geographical regions (north, middle, south, and east) of Taiwan, and have a 1:1 ratio of medical centres to regional hospitals in each region. The NEP-AKI-D study enrols intensive care unit-based AKI patients who receive dialysis in the four seasonal sampled months (October 2014, along with January, April, and July 2015) in the included hospitals. The collected data include demographic information, pertaining laboratory results, dialysis settings and patient outcomes. The data are uploaded in a centre website and will be audited by on-site principal investigators, computer logic gates, and the CAKs staffs. The outcomes of interest are in-hospital mortality, dialysis-dependency and readmission rate within 90 days after discharge.The NEP-AKI-D study enrols a large number of representative AKI patients throughout Taiwan. The results of the current study are expected to provide more insight into the risk and prognostic factors of AKI and further attenuated further chronic kidney disease transition.


Lan J.,Chang Gung University | Huang H.-Y.,Chang Gung University | Lee S.-W.,Chi Mei Medical Center Liouying | Chen T.-J.,Chi Mei Medical Center | And 8 more authors.
Tumor Biology | Year: 2014

Despite the advances in diagnostic imaging and treatment modalities, the risk stratification and final outcomes in patients with nasopharyngeal carcinomas (NPC) still remain suboptimal. Through data mining from published transcriptomic database, topoisomerase IIα (TOP2A) was first identified as a differentially upregulated gene in NPC tissues, which implicates cell division via selective cleavage, rearrangement, and re-ligation of DNA strands. Given the roles of TOP2A in prognostication and in the frontline therapeutic regimen of common carcinomas, such as breast cancer, we explored TOP2A immunoexpression status and its associations with clinicopathological variables and survival in a well-defined cohort of NPC patients. TOP2A immunohistochemistry was retrospectively performed and analyzed using H-score method for biopsy specimens from 124 NPC patients who received standard treatment without distant metastasis at initial diagnosis. Those cases with H-score larger than the median value were construed as featuring TOP2A overexpression. The findings were correlated with the clinicopathological variables, disease-specific survival (DSS) and distant metastasis-free survival (DMFS). TOP2A overexpression was significantly associated with American Joint of Cancer Committee (AJCC) stages III-IV (p = 0.019) and univariately predictive of adverse outcomes for DSS (p = 0.0078) and DMFS (p = 0.0003). In the multivariate comparison, TOP2A overexpression remained prognostically independent to portend worse DSS (p = 0.047, hazard ratio = 1.732) and DMFS (p = 0.003, hazard ratio = 2.569), together with advanced AJCC stages III-IV. TOP2A expression is upregulated in a subset of NPCs and its increased immunoexpression significantly correlated with advanced stages and tumor aggressiveness, justifying the potentiality of TOP2A as a prognostic biomarker and a novel therapeutic target of NPC. © 2013 International Society of Oncology and BioMarkers (ISOBM).


PubMed | Sin Lau Christian Hospital Tainan, Chung Shan Medical University, Taipei Medical University, Guangxi Medical University and 7 more.
Type: Journal Article | Journal: International journal of clinical and experimental pathology | Year: 2014

Angioimmunoblastic T-cell lymphoma (AITL) is an aggressive peripheral T-cell lymphoma (PTCL) of follicular helper T-cell origin and is rare in Taiwan. There are overlapping features of AITL and peripheral T-cell lymphoma with a follicular growth pattern (PTCL-F). Around one fifth of PTCL-F exhibits t(5;9)(q33;q22)/ITK-SYK chromosomal translocation, which is essentially absent in AITL. We retrospectively investigated 35 cases of AITL from Taiwan with histopathology review, immunohistochemistry, in situ hybridization for Epstein-Barr virus (EBV) and fluorescence in situ hybridization (FISH) for t(5;9)(q33;q22)/ITK-SYK and correlated the results with overall survival. Twenty-six cases of not otherwise specified PTCL (PTCL-NOS) were also examined by FISH for comparison. Most AITL patients were male (69%) and elderly (median age at 67 years) with frequent bone marrow involvement (53%), high Ann Arbor stages (77%), and elevated serum lactate dehydrogenase (68%). Most cases (80%) showed a typical CD4+/CD8- phenotype and in 90% cases there were scattered EBV-positive B-cells (less than 10% cells). None of these cases showed t(5;9)(q33;q22)/ITK-SYK translocation by FISH. Gain of ITK and SYK gene was identified in 38% and 14% tumors, respectively, but both were not associated with overall survival. Performance status < 2 was associated with a better outcome but not the other clinicopathological factors. All PTCL-NOS cases were negative for ITK-SYK translocation with similar rates (38% and 12%, respectively) of gains at ITK and SYK loci as that of AITL. In this so far the largest series of AITL from Taiwan, we reported the clinicopathological features and FISH findings on ITK and SYK genes. We confirmed the absence of t(5;9)(q33;q22)/ITK-SYK translocation, which may serve as an additional differential diagnostic tool from PTCL-F when present. PTCL-NOS shared a similar pattern of ITK and SYK gains with AITL. More studies are warranted to elucidate the roles of SYK and ITK and other genes in the lymphomagenesis of AITL in Taiwan.


PubMed | Chang Gung University, Southern Taiwan University of Science and Technology, Chi Mei Medical Center Tainan, National Sun Yat - sen University and 2 more.
Type: Journal Article | Journal: American journal of translational research | Year: 2016

Neoadjuvant concurrent chemoradiotherapy (CCRT) followed by surgery is the mainstay of treatment for locally advanced rectal cancer. Several heparin-binding associated proteins have been reported to play a critical role in cancer progression. However, the clinical relevancies of such proteins and their associations with CCRT response in rectal cancer have not yet to be fully elucidated.The analysis of a public transcriptome of rectal cancer indicated that thrombospondin 2 (THBS2) is a predictive factor for CCRT response. Immunohistochemical analyses were conducted to evaluate the expression of THBS2 in pretreatment biopsy specimens from rectal cancer patients without distant metastasis. Furthermore, the relationships between THBS2 expression and various clinicopathological factors or survival were analyzed.Low expression of THBS2 was significantly associated with advanced pretreatment tumor (P<0.001) and nodal status (P=0.004), post-treatment tumor (P<0.001) and nodal status (P<0.001), increased vascular invasion (P=0.003), increased perineural invasion (P=0.023) and inferior tumor regression grade (P=0.015). In univariate analysis, low THBS2 expression predicted worse outcomes for disease-free survival, local recurrence-free survival and metastasis-free survival (all P<0.001). In multivariate analysis, low expression of THBS2 still served as a negative prognostic factor for disease-free survival (Hazard ratio=3.057, P=0.002) and metastasis-free survival (Hazard ratio=3.362, P=0.012).Low THBS2 expression was correlated with advanced disease status and low tumor regression after preoperative CCRT and that it acted as an independent negative prognostic factor in rectal cancer. THBS2 may represent a predictive biomarker for CCRT response in rectal cancer.


Lee L.-M.,Taipei Medical University | Tsai T.-C.,Chi Mei Medical Center Liouying | Chung H.-H.,National Cheng Kung University | Tong Y.-C.,National Cheng Kung University | And 2 more authors.
BJU International | Year: 2012

OBJECTIVES To compare agmatine-induced prostatic relaxation in hypertensive and control rats. To investigate the responsible mechanism(s) and the role of the ATP-sensitive potassium channel. Methods Prostate strips were isolated from male spontaneously hypertensive (SH) rats and normal Wistar-Kyoto (WKY) rats for measurement of isometric tension. The strips were precontracted with 1 Âμmol/L phenylephrine or 50 mmol/L KCl. Dose-dependent relaxation of the prostatic strips was studied by cumulative administration of agmatine, 1 to 100 Âμmol/L, into the organ bath. Effects of specific antagonists on agmatine-induced relaxation were studied. Western blotting analysis was used to measure the gene expression of the ATP-sensitive potassium channel in the rat prostate. Results Prostatic relaxation induced by agmatine was markedly reduced in SH rats compared with WKY rats. The relaxation caused by agmatine was abolished by BU224, a selective imidazoline I2-receptor antagonist, but was not modified by efaroxan at a dose sufficient to block imidazoline I1-receptors. The relaxation induced by diazoxide at a concentration sufficient to activate ATP-sensitive potassium channels was markedly reduced in the SH rat prostate. Expressions of ATP-sensitive potassium channel sulphonylurea receptor and inwardly rectifying potassium channel (Kir) 6.2 subunits were both decreased in the prostate of SH rats. CONCLUSION The decrease of agmatine-induced prostatic relaxation in SH rats is related to the change in ATP-sensitive potassium channels. © 2012 THE AUTHORS. BJU INTERNATIONAL © 2012 BJU INTERNATIONAL.


Lee L.-M.,Taipei Medical University | Lin C.-S.,Chi Mei Medical Center Liouying | Chung H.-H.,National Cheng Kung University | Lin K.-C.,Chi Mei Medical Center | And 3 more authors.
Experimental and Clinical Endocrinology and Diabetes | Year: 2012

The role of opioid μ-receptor activation in the improvement of overactive bladder (OAB) remains obscure. Thus, we used loperamide to activate opioid μ-receptors for urinary bladder relaxation and compared the differences between normal and diabetic rats. Urinary bladder strips were isolated from Wistar rats that did or did not receive streptozotocin (STZ) injection for analysis of isometric tension. Samples were contracted with either acetylcholine (ACh) or KCl, and decrease of muscle tone (relaxation) was characterized after treatment with loperamide. Specific antagonists were used for pretreatment to compare the changes in loperamide-induced relaxation. As compared with normal rats, loperamide produced a more marked relaxation in bladder strips of STZ-diabetic rats in a dose-dependent manner. This relaxation by loperamide was attenuated by glibenclamide at a dose sufficient to block ATP-sensitive K + (K ATP) channels. In addition, this action of loperamide was abolished by protein kinase A (PKA) inhibitor and enhanced by the inhibitor of phosphodiesterase for cyclic AMP (cAMP). However, treatment with forskolin, an activator of adenylate cyclase, resulted in no difference in relaxation in normal and diabetic rats. The action of loperamide was abolished by cyprodime and naloxone, but was not modified by naloxonazine at a dose sufficient to block opioid μ-1 receptors. A higher expression of opioid μ-receptors in diabetic rats was observed. Our results suggest that the increase in urinary bladder relaxation in STZ-diabetic rats by loperamide is mainly induced through activation of opioid μ-receptors linked to the cAMP-PKA pathway to open K ATP channels. © J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart New York.


PubMed | University of Auckland, Chi Mei Medical Center, Deakin University, National Cheng Kung University and 2 more.
Type: | Journal: Frontiers in pharmacology | Year: 2016

SAHA is a class I HDAC/HDAC6 co-inhibitor and an autophagy inducer currently undergoing clinical investigations in breast cancer patients. However, the molecular mechanism of action of SAHA in breast cancer cells remains unclear. In this study, we found that SAHA is equally effective in targeting cells of different breast cancer subtypes and tamoxifen sensitivity. Importantly, we found that down-regulation of survivin plays an important role in SAHA-induced autophagy and cell viability reduction in human breast cancer cells. SAHA decreased survivin and XIAP gene transcription, induced survivin protein acetylation and early nuclear translocation in MCF7 and MDA-MB-231 breast cancer cells. It also reduced survivin and XIAP protein stability in part through modulating the expression and activation of the 26S proteasome and heat-shock protein 90. Interestingly, targeting HDAC3 and HDAC6, but not other HDAC isoforms, by siRNA/pharmacological inhibitors mimicked the effects of SAHA in modulating the acetylation, expression, and nuclear translocation of survivin and induced autophagy in MCF7 and MDA-MB-231 cancer cells. Targeting HDAC3 also mimicked the effect of SAHA in up-regulating the expression and activity of proteasome, which might lead to the reduced protein stability of survivin in breast cancer cells. In conclusion, this study provides new insights into SAHAs molecular mechanism of actions in breast cancer cells. Our findings emphasize the complexity of the regulatory roles in different HDAC isoforms and potentially assist in predicting the mechanism of novel HDAC inhibitors in targeted or combinational therapies in the future.

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