Browsing by Author "Lin, Yu-Sheng"

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Circulating miR-148b-3p and miR-409-3p as biomarkers for heart failure in patients with mitral regurgitation
(2016-11-01)
Chen, Mien-Cheng
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Chang, Tzu-Hao
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Chang, Jen-Ping
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Huang, Hsien-Da
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Ho, Wan-Chun
Background: MicroRNAs (miRs) regulate gene expression in heart failure. Circulating miRs as biomarkers for heart failure in mitral regurgitation patients (MR) remain unexplored. Methods: This case-control study enrolled 32 MR patients with heart failure, 16 asymptomatic MR patients, and 12 control subjects without heart failure. We used next generation sequencing to study the gene expression profiles in the sera, and quantitative RT-PCR to study serum and tissue miRs in the left atria. Results: Next generation sequencing analysis and enrichment analysis showed that 25 miRs were differentially expressed in the sera of MR patients with heart failure compared to control subjects. The circulating miR-148b-3p (p = 0.002) and miR-409-3p (p = 0.010) were significantly down-regulated in the MR patients with heart failure compared to control subjects. However, only circulation miR-148b-3p was significantly down-regulated in the MR patients without heart failure compared to control subjects (p = 0.009). The tissue miR-409-3p was significantly down-regulated in the MR patients with heart failure compared to 3 purchased normal controls (p = 0.041). Notably, the tissue RASGRP3 mRNA, target gene of miR-409-3p, was significantly upregulated in the MR patients with heart failure compared to normal controls (p = 0.010). The tissue FRY (p = 0.010) and GADD45A (p = 0.010) mRNAs, target genes of miR-148b-3p, were significantly up-regulated in the MR patients with heart failure compared to normal controls. Conclusions: Circulating miR-148b-3p might serve as biomarker for future development of heart failure and miR-409-3p might serve as biomarker for incident heart failure in MR patients. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
Exploring Regulatory Mechanisms of Atrial Myocyte Hypertrophy of Mitral Regurgitation through Gene Expression Profiling Analysis: Role of NFAT in Cardiac Hypertrophy
(2016-12-01)
Chang, Tzu-Hao
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Chen, Mien-Cheng
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Chang, Jen-Ping
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Huang, Hsien-Da
;
Ho, Wan-Chun
Background Left atrial enlargement in mitral regurgitation (MR) predicts a poor prognosis. The regulatory mechanisms of atrial myocyte hypertrophy of MR patients remain unknown. Methods and Results This study comprised 14 patients with MR, 7 patients with aortic valve disease (AVD), and 6 purchased samples from normal subjects (NC). We used microarrays, enrichment analysis and quantitative RT-PCR to study the gene expression profiles in the left atria. Microarray results showed that 112 genes were differentially up-regulated and 132 genes were differentially down-regulated in the left atria between MR patients and NC. Enrichment analysis of differentially expressed genes demonstrated that "NFAT in cardiac hypertrophy" pathway was not only one of the significant associated canonical pathways, but also the only one predicted with a non-zero score of 1.34 (i.e. activated) through Ingenuity Pathway Analysis molecule activity predictor. Ingenuity Pathway Analysis Global Molecular Network analysis exhibited that the highest score network also showed high association with cardiac related pathways and functions. Therefore, 5 NFAT associated genes (PPP3R1, PPP3CB, CAMK1, MEF2C, PLCE1) were studies for validation. The mRNA expressions of PPP3CB and MEF2C were significantly up-regulated, and CAMK1 and PPP3R1 were significantly down-regulated in MR patients compared to NC. Moreover, MR patients had significantly increased mRNA levels of PPP3CB, MEF2C and PLCE1 compared to AVD patients. The atrial myocyte size of MR patients significantly exceeded that of the AVD patients and NC. Conclusions Differentially expressed genes in the "NFAT in cardiac hypertrophy" pathway may play a critical role in the atrial myocyte hypertrophy of MR patients.
Fixed-dose combination of amlodipine and atorvastatin improves clinical outcomes in patients with concomitant hypertension and dyslipidemia
(1970-01-01)
Lin, Chia-Pin
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Tung, Ying-Chang
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Hsiao, Fu-Chih
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Yang, Chia-Hung
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Kao, Yi-Wei
Hypertension and dyslipidemia are important risk factors for cardiovascular disease. However, the clinical outcomes of fixed-dose combination (FDC) versus free-equivalent combination (FEC) of amlodipine and atorvastatin in the treatment of concurrent hypertension and dyslipidemia remain unknown. In this study, we included patients with newly diagnosed hypertension and dyslipidemia, without previously established cardiovascular disease, and treated with either FDC or FEC of amlodipine and atorvastatin were identified from the National Health Insurance Research Database of Taiwan and follow-up for 5 years. By using 1:1 propensity score matching, a total of 1756 patients were enrolled in this study. The composite of major adverse cardiovascular events, including all-cause mortality, myocardial infarction (MI), stroke, and coronary revascularization, occurred more frequently in the FEC group than in the FDC group (hazard ratio, 1.88; 95% confidence interval [CI], 1.42 to 2.5). Although the all-cause mortality did not differ (hazard ratio, 0.46; 95% CI, 0.36 to 1.59), the FEC group developed increased MI, stroke, and coronary revascularization (hazard ratio, 2.87; 95% CI, 1.07 to 7.68; hazard ratio, 1.97; 95% CI, 1.41 to 2.74; and hazard ratio, 2.44; 95% CI, 1.26 to 4.69, respectively). Furthermore, as an unexpected result, a higher risk to develop new-onset diabetes mellitus was observed with FEC regimens (hazard ratio, 2.19; 95% CI, 1.6 to 3.0). In conclusion, although the all-cause mortality did not differ between the two groups, the FDC regimen of amlodipine and atorvastatin improved clinical outcomes when compared to FEC in patients with newly diagnosed hypertension and dyslipidemia.
Idi1 and Hmgcs2 Are Affected by Stretch in HL-1 Atrial Myocytes
(2018-12-01)
Fang, Chih-Yuan
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Chen, Mien-Cheng
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Chang, Tzu-Hao
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Wu, Chia-Chen
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Chang, Jen-Ping
Background: Lipid expression is increased in the atrial myocytes of mitral regurgitation (MR) patients. This study aimed to investigate key regulatory genes and mechanisms of atrial lipotoxic myopathy in MR. Methods: The HL-1 atrial myocytes were subjected to uniaxial cyclic stretching for eight hours. Fatty acid metabolism, lipoprotein signaling, and cholesterol metabolism were analyzed by PCR assay (168 genes). Results: The stretched myocytes had significantly larger cell size and higher lipid expression than non-stretched myocytes (all p < 0.001). Fatty acid metabolism, lipoprotein signaling, and cholesterol metabolism in the myocytes were analyzed by PCR assay (168 genes). In comparison with their counterparts in non-stretched myocytes, seven genes in stretched monocytes (Idi1, Olr1, Nr1h4, Fabp2, Prkag3, Slc27a5, Fabp6) revealed differential upregulation with an altered fold change >1.5. Nine genes in stretched monocytes (Apoa4, Hmgcs2, Apol8, Srebf1, Acsm4, Fabp1, Acox2, Acsl6, Gk) revealed differential downregulation with an altered fold change <0.67. Canonical pathway analysis, using Ingenuity Pathway Analysis software, revealed that the only genes in the superpathway of cholesterol biosynthesis were Idi1 (upregulated) and Hmgcs2 (downregulated). The fraction of stretched myocytes expressing Nile red was significantly decreased by RNA interference of Idi1 (p < 0.05) and was significantly decreased by plasmid transfection of Hmgcs2 (p = 0.004). Conclusions: The Idi1 and Hmgcs2 genes have regulatory roles in atrial lipotoxic myopathy associated with atrial enlargement.
Improvement of perovskite photoluminescence characteristics by using a lithography-free metasurface
(2018-01-01)
Chen, Wenjun
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Sha, Jun
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Yan, Kanghong
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Luo, Ji
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Xu, Ruijia
Organic-inorganic metal halid perovskite is an emerging field of promising semiconductive material in optoelectronic devices applications. It has been a research topic of interest for scientists. To date, photoluminescence (PL) efficiency of perovskite is low and does not have any literature to report the solution. Here, we proposed and demonstrated an effective approach for the improvement of perovskite PL characteristics. The PL intensity and spectra bandwidth could be enhanced significantly by using Al-disk metasurface formed on perovskite surface. Such strategy can be exploited to enhance perovskite PL characteristics for developing high efficient light emitting diodes, solar cells, and photodetectors, etc.
Interface and thickness tuning for blade coated small-molecule organic light-emitting diodes with high power efficiency
(2013-09-28)
Chang, Yu-Fan
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Chiu, Yu-Chian
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Chang, Hao-Wen
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Wang, Yi-Siang
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Shih, Yi-Lun
We developed a general method based on fluorescence microscopy to characterize the interface dissolution in multi-layer organic light-emitting diodes (OLEDs) by blade coating. A sharp bi-layer edge was created before blade coating, with the bottom layer being insoluble and top layer soluble. After blade coating, fluorescence images showed that the edge of the top layer shifted when the layer dissolved completely, whereas the bottom layer's edge remained in place as a positioning mark. The dissolution depth was determined to be 15-20 nm when the emissive-layer host of 2,6-bis (3-(9H-carbazol-9-yl) phenyl) pyridine (26DCzPPy) was coated on the hole-transport layer of N, N'-bis(naphthalen-1-yl)-N, N'-bis(phenyl)-benzidine(NPB), which was consistent with a sudden drop in efficiency of orange OLEDs with layer thickness below 20 nm. Thus, the layer thickness of OLEDs was optimized to stay more than 20 nm for blade coating. For a two-color white OLED with the structure TCTA/26DCzPPy:PO-01-TB:FIrpic/TPBI, efficiency was 24 cd/A and 8.5 lm/W at 1000 cd/m(2). For a three-color white OLED with Os(fptz)(2)(dhpm) added as the emitter, the efficiency was 12.3 cd/A and 3.7 lm/W at 1000 cd/m(2). For a green device with the structure TCTA/26DCzPPy: Ir(mppy)(3)/TPBI, the efficiency was 41.9 cd/A and 23.4 lm/W at 1000 cd/m(2). VC 2013 AIP Publishing LLC.
Liver X Receptor/Retinoid X Receptor Pathway Plays a Regulatory Role in Pacing-Induced Cardiomyopathy
(2019-01-08)
Lin, Yu-Sheng
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Chang, Tzu-Hao
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Shi, Chung-Sheng
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Wang, Yi-Zhen
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Ho, Wan-Chun
Background-The molecular mechanisms through which high-demand pacing induce myocardial dysfunction remain unclear. Methods and Results-We created atrioventricular block in pigs using dependent right ventricular septal pacing for 6 months. Echocardiography was performed to evaluate dyssynchrony between pacing (n=6) and sham control (n=6) groups. Microarray and enrichment analyses were used to identify differentially expressed genes (DEGs) in the left ventricular (LV) myocardium between pacing and sham control groups. Histopathological and protein changes were also analyzed and an A cell pacing model was also performed. Pacing significantly increased mechanical dyssynchrony. Enrichment analysis using Ingenuity Pathway Analysis and the activation z-score analysis method demonstrated that there were 5 DEGs (ABCA1, APOD, CLU, LY96, and SERPINF1) in the LV septum (z-score=- 0.447) and 5 DEGs (APOD, CLU, LY96, MSR1, and SERPINF1) in the LV free wall (z-score=- 1.000) inhibited the liver X receptor/retinoid X receptor (LXR/RXR) pathway, and 4 DEGs (ACTA2, MYL1, PPP2R3A, and SNAI2) activated the integrin-linked kinase (ILK) pathway in the LV septum (z-score=1.000). The pacing group had a larger cell size, higher degree of myolysis and fibrosis, and increased expression of intracellular lipid, inflammatory cytokines, and apoptotic markers than the sham control group. The causal relationships between pacing and DEGs related to LXR/RXR and ILK pathways, apoptosis, fibrosis, and lipid expression after pacing were confirmed in the cell pacing model. Luciferase reporter assay in the cell pacing model also supported inhibition of the LXR pathway by pacing. Conclusions-Right ventricular septal-dependent pacing was associated with persistent LV dyssynchrony-induced cardiomyopathy through inhibition of the LXR/RXR pathway.
Quasi-Pushout Cell Discarding
(1997-09-01)
Lin, Yu-Sheng
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Shung, C. Bernard
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電子工程學系及電子研究所
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Department of Electronics Engineering and Institute of Electronics
Cell discarding takes place when the buffer space of a network node is used up. Though Pushout cell discarding was found to achieve fair buffer utilization and good cell loss performance, it is difficult to implement because of the large number of queue length comparisons. In this letter, we propose Quasi-Pushout cell discarding which reduces the number of queue length comparisons by employing the concept of quasi-longest queue. Simulation results under bursty and imbalanced traffic conditions show that Quasi-Pushout can achieve comparable cell loss performance as Pushout at a much lower complexity.
Self-carbonized lamellar nano/micro hierarchical structure C/TiO2 and its Li-ion intercalation performance
(2012)
Chen, Po-Chin
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Tsai, Min-Chiao
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Chen, Huang-Chin
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Lin, I-Nan
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Sheu, Hwo-Shuenn
In this study, two new layered titanates, fibrillar TiO2 center dot(CH3COOH)(1.4) and chrysanthemum-like TiO2 center dot(CH3COOH)(0.9) (named as FT and CT) with acetic acid and acetate intercalation have been synthesized by reacting titanium isopropoxide (TTIP) with acetic acid at different temperatures. Furthermore, nano/micro hierarchical structure TiO2 with high TiO2-B/anatse ratio was obtained by annealing the titanate (CT). For use as an anode for lithium ion batteries, uniform carbon coated titanium dioxide with high TiO2-B content was obtained by "self-carbonizing'' CT under argon atmosphere at 350 degrees C, and the compound was named SC-CT350. The capacity of the anode made from SC-CT350 can reach 144 mA h g(-1) under a high charging/discharging rate (10 C) and showed excellent retention ability.
Structural properties of pressure-induced structural phase transition of Si-doped GaAs by angular-dispersive X-ray diffraction
(2016-02)
Lin, Kung-Liang
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Lin, Chih-Ming
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Lin, Yu-Sheng
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Jian, Sheng-Rui
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Liao, Yen-Fa
Pressure-induced phase transitions in n-type silicon-doped gallium arsenide (GaAs: Si) at ambient temperature were investigated by using angular-dispersive X-ray diffraction (ADXRD) under high pressure up to around 18.6 (1) GPa, with a 4:1 (in volume ratio) methanol-ethanol mixture as the pressure-transmitting medium. In situ ADXRD measurements revealed that n-type GaAs: Si starts to transform from zinc-blende structure to an orthorhombic structure [GaAs-II phase], space group Pmm2, at 16.4 (1) GPa. In contrast to previous studies of pure GaAs under pressure, our results show no evidence of structural transition to Fmmm or Cmcm phase. The fitting of volume compression data to the third-order Birch-Murnaghan equation of state yielded that the zero-pressure isothermal bulk moduli and the first-pressure derivatives were 75 (3) GPa and 6.4 (9) for the B3 phase, respectively. After decompressing to the ambient pressure, the GaAs: Si appears to revert to the B3 phase completely. By fitting to the empirical relations, the Knoop microhardness numbers are between H-PK = 6.21 and H-A = 5.85, respectively, which are substantially smaller than the values of 7-7.5 for pure GaAs reported previously. A discontinuous drop in the pressure-dependent lattice parameter, N-N distances, and V/V-0 was observed at a pressure of 11.5 (1) GPa, which was tentatively attributed to the pressure-induced dislocation activities in the crystal grown by vertical gradient freeze method.