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Jiayi Shi, Taiwan

Yeh S.-B.,Changhua Christian Hospital | Yeh P.-Y.,St. Martin de Porres Hospital | Schenck C.H.,University of Minnesota
Journal of Clinical Sleep Medicine | Year: 2010

We report the case of an 88-year-old man with Alzheimer's disease (AD) of 8 years duration (emerging shortly after the de novo onset of sleeptalking) who developed REM sleep behavior disorder (RBD) after increasing the nightly dose of rivastigmine, an acetylcholinesterase inhibitor, from 1.5 mg to 3 mg (total daily dose, 4.5 mg), as therapy for his dementia. His family then became aware of recurrent nocturnal episodes arising from sleep of his leaving bed, and he sustained multiple abrasion injuries from falling down. Polysomnography (PSG), utilizing a seizure montage with fast paper speed, conducted with the patient taking rivastigmine 3 mg at bedtime, documented 3 abrupt episodes of bilateral arm-waving with moaning and shouting that emerged exclusively during each of the 3 REM sleep periods, with the duration of the episodes lasting 8 to 25 seconds. No epileptiform discharge appeared with the onset of these REM sleep behaviors. Therapy with clonazepam, 0.5 mg at bedtime (with ongoing 3 mg bedtime and 4.5 mg total daily rivastigmine therapy), fully suppressed the sleep-related events, with prompt relapse whenever clonazepam was not taken. This is the second reported case (both males with AD) of rivastigmine-induced RBD, and the oldest reported case of RBD; and it represents reversible, medication-induced, acute RBD.

Tseng L.-M.,Taipei Veterans General Hospital | Tseng L.-M.,National Yang Ming University | Liu C.-Y.,National Yang Ming University | Liu C.-Y.,Taipei Veterans General Hospital | And 5 more authors.
Breast Cancer Research | Year: 2012

Introduction: Triple negative breast cancer (TNBC) is very aggressive and currently has no specific therapeutic targets, such as hormone receptors or human epidermal growth factor receptor type 2 (HER2); therefore, prognosis is poor. Bortezomib, a proteasome inhibitor, may exert efficacy in TNBC through its multiple cellular effects. Here, we tested the efficacy of bortezomib and examined the drug mechanism in breast cancer cells.Methods: Five breast cancer cell lines: TNBC HCC-1937, MDA-MB-231, and MDA-MB-468; HER2-overexpressing MDA-MB-453; and estrogen receptor positive MCF-7 were used for in vitro studies. Apoptosis was examined by both flow cytometry and Western Blot. Signal transduction pathways in cells were assessed by Western Blot. Gene silencing was done by small interfering RNA (siRNA). In vivo efficacy of bortezomib was tested in nude mice with breast cancer xenografts. Immunohistochemical study was performed on tumor tissues from patients with TNBC.Results: Bortezomib induced significant apoptosis, which was independent of its proteasome inhibition, in the three TNBC cell lines, but not in MDA-MB-453 or MCF-7 cells. Furthermore, cancerous inhibitor of protein phosphatase 2A (CIP2A), a cellular inhibitor of protein phosphatase 2A (PP2A), mediated the apoptotic effect of bortezomib. We showed that bortezomib inhibited CIP2A in association with p-Akt downregulation in a dose- and time-dependent manner in all sensitive TNBC cells, whereas no alterations in CIP2A expression and p-Akt were noted in bortezomib-resistant cells. Overexpression of CIP2A upregulated p-Akt and protected MDA-MB-231 and MDA-MB-468 cells from bortezomib-induced apoptosis, whereas silencing CIP2A by siRNA overcame the resistance to bortezomib-induced apoptosis in MCF-7 cells. In addition, bortezomib downregulated CIP2A mRNA but did not affect the degradation of CIP2A protein. Furthermore, bortezomib exerted in vivo antitumor activity in HCC-1937 xenografted tumors, but not in MCF-7 tumors. Bortezomib downregulated CIP2A expression in the HCC-1937 tumors but not in the MCF-7 tumors. Importantly, CIP2A expression is readily detectable in tumor samples from TNBC patients.Conclusions: CIP2A is a major determinant mediating bortezomib-induced apoptosis in TNBC cells. CIP2A may thus be a potential therapeutic target in TNBC. © 2012 Tseng et al.; licensee BioMed Central Ltd.

Hsu N.C.,Kaohsiung Medical University | Huang Y.-F.,Kaohsiung Medical University | Yokoyama K.K.,Kaohsiung Medical University | Chu P.-Y.,St. Martin de Porres Hospital | And 3 more authors.
PLoS ONE | Year: 2013

BRCA1-associated breast cancers are associated with particular features such as early onset, poor histological differentiation, and hormone receptor negativity. Previous studies conducted in Taiwanese population showed that the mutation of BRCA1 gene does not play a significant role in the occurrence of breast cancer. The present study explored methylation of BRCA1 promoter and its relationship to clinical features and outcome in Taiwanese breast cancer patients. Tumor specimens from a cohort of 139 early-stage breast cancer patients were obtained during surgery before adjuvant treatment for DNA extraction. Methylation of BRCA1 promoter region was determined by methylation-specific PCR and the results were related to clinical features and outcome of patients using statistical analysis. Methylation of the BRCA1 promoter was detected in 78 (56%) of the 139 tumors. Chi-square analysis indicated that BRCA1 promoter methylation correlated significantly with triple-negative (ER-/PR-/HER2-) status of breast cancer patients (p = 0.041). The Kaplan-Meier method showed that BRCA1 promoter methylation was significantly associated with poor overall survival (p = 0.026) and disease-free survival (p = 0.001). Multivariate analysis which incorporated variables of patients' age, tumor size, grade, and lymph node metastasis revealed that BRCA1 promoter methylation was associated with overall survival (p = 0.27; hazard ratio, 16.38) and disease-free survival (p = 0.003; hazard ratio, 12.19). Our findings underscore the clinical relevance of the methylation of BRCA1 promoter in Taiwanese patients with early-stage breast cancer. © 2013 Hsu et al.

Chen C.-C.,St. Martin de Porres Hospital | Chen C.-C.,National Cheng Kung University | Chang H.-C.,National Cheng Kung University
Journal of Infection | Year: 2013

Objectives: The prediction of dengue outbreaks is a critical concern in many countries. However, the setup of an ideal prediction system requires establishing numerous monitoring stations and performing data analysis, which are costly, time-consuming, and may not achieve the desired results. In this study, we developed a novel method for predicting impending dengue fever outbreaks several weeks prior to their occurrence. Methods: By reversing moving approximate entropy algorithm and pattern recognition on time series compiled from the weekly case registry of the Center for Disease Control, Taiwan, 1998-2010, we compared the efficiencies of two patterns for predicting the outbreaks of dengue fever. Results: The sensitivity of this method is 0.68, and the specificity is 0.54 using Pattern A to make predictions. Pattern B had a sensitivity of 0.90 and a specificity of 0.46. Patterns A and B make predictions 3.1±2.2 weeks and 2.9±2.4 weeks before outbreaks, respectively. Conclusions: Combined with pattern recognition, reversed moving approximate entropy algorithm on the time series built from weekly case registry is a promising tool for predicting the outbreaks of dengue fever. © 2013.

Luh S.-P.,St. Martin de Porres Hospital
Journal of Zhejiang University: Science B | Year: 2010

Primary spontaneous pneumothorax (PSP) commonly occurs in tall, thin, adolescent men. Though the pathogenesis of PSP has been gradually uncovered, there is still a lack of consensus in the diagnostic approach and treatment strategies for this disorder. Herein, the literature is reviewed concerning mechanisms and personal clinical experience with PSP. The chest computed tomography (CT) has been more commonly used than before to help understand the pathogenesis of PSP and plan further management strategies. The development of video-assisted thoracoscopic surgery (VATS) has changed the profiles of management strategies of PSP due to its minimal invasiveness and high effectiveness for patients with these diseases. © 2010 Zhejiang University and Springer-Verlag Berlin Heidelberg.

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