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Search Results: 1 - 10 of 10137 matches for " Yung-Ho Hsu "
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Biomarkers in Acute Kidney Injury  [PDF]
Cai-Mei Zheng, Min-Tser Liao, Mei-Yu Lin, Lan Lo, Chia-Chao Wu, Yung-Ho Hsu, Yuh-Feng Lin, Kuo-Cheng Lu
Open Journal of Nephrology (OJNeph) , 2013, DOI: 10.4236/ojneph.2013.31009
Abstract: Acute kidney injury (AKI) is one of the popular topics of discussions due to increasing development of biomarkers recently. The disease progression and prognosis may be determined by these biomarkers detected in blood and urine specimens. Since acute kidney injury is associated with a broad spectrum of disease conditions, prevention and early detection of AKI becomes very important in those clinical settings. Early measurements of AKI biomarkers predict subsequent development of intrinsic AKI, dialysis requirement, duration of intensive care unit stay and finally affect mortality. We, here, discuss the acute kidney injury in different clinical situations and associated natures of biomarkers, which may help us guide to prevent and treat AKI more effectively.
Association of Serum Phosphate and Related Factors in ESRD-Related Vascular Calcification
Cai-Mei Zheng,Kuo-Cheng Lu,Chia-Chao Wu,Yung-Ho Hsu,Yuh-Feng Lin
International Journal of Nephrology , 2011, DOI: 10.4061/2011/939613
Abstract: Vascular calcification is common in ESRD patients and is important in increasing mortality from cardiovascular complications in these patients. Hyperphosphatemia related to chronic kidney disease is increasingly known as major stimulus for vascular calcification. Hyperphosphatemia and vascular calcification become popular discussion among nephrologist environment more than five decades, and many researches have been evolved. Risk factors for calcification are nowadays focused for the therapeutic prevention of vascular calcification with the hope of reducing cardiovascular complications. 1. Introduction Vascular calcification is a kind of extraosseous calcification and is associated with aging physiologically, and a number of disorders including ESRD, diabetes mellitus, and cardiovascular disease pathologically. Multifactorial processes contribute to VC in which derangements in calcium and phosphorus homeostasis plays an important role and becomes popular therapeutic target nowadays. In ESRD patients with vascular calcification, a mixture of intimal and medial calcification has been observed in the effected vessels with dominant medial involvement. The risk of CVD mortality in ESRD patients with vascular calcification is 20 to 30 times higher than that of the general population [1–5]. Although phosphate is important for diverse cellular and physiological functions, impaired renal function with resultant phosphate accumulation with consequent bone and mineral disorders and vascular calcification are major problems among nephrologists. The increased risk of CVD mortality by hyperphosphatemia was partially explained by the predisposition of this population to vascular calcification [6–8]. (Figure 1) Even in early stage CKD, serum phosphorus level disturbances are proved to promote vascular calcification, hypertension, myocardial hypertrophy, and heart failure [9–11]. Current understanding of relationship between phosphorus and those disorders becomes popular in medical field, with the hope of halting or retarding the vascular calcification from the very early status in those patients. Figure 1: Mechanisms of VSMC osteogenesis during vascular calcification in chronic kidney disease. VSMC upregulate expression of transcription factors Osf2/Cbfa1 which were enhanced by ROS, leptin, vitamin D, increased CaxP product, or high PO 4 (Pi) levels induced by Pit-1. VSMC activation occurs in part as a result of the phenotypic switch of VSMCs into osteoblast-like cells. VSMCs that have acquired an osteogenic phenotype express ALP and produce hydroxyapatite crystals.
Far-Infrared Therapy Induces the Nuclear Translocation of PLZF Which Inhibits VEGF-Induced Proliferation in Human Umbilical Vein Endothelial Cells
Yung-Ho Hsu, Yen-Cheng Chen, Tso-Hsiao Chen, Yuh-Mou Sue, Tzu-Hurng Cheng, Jia-Rung Chen, Cheng-Hsien Chen
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0030674
Abstract: Many studies suggest that far-infrared (FIR) therapy can reduce the frequency of some vascular-related diseases. The non-thermal effect of FIR was recently found to play a role in the long-term protective effect on vascular function, but its molecular mechanism is still unknown. In the present study, we evaluated the biological effect of FIR on vascular endothelial growth factor (VEGF)-induced proliferation in human umbilical vein endothelial cells (HUVECs). We found that FIR ranging 3~10 μm significantly inhibited VEGF-induced proliferation in HUVECs. According to intensity and time course analyses, the inhibitory effect of FIR peaked at an effective intensity of 0.13 mW/cm2 at 30 min. On the other hand, a thermal effect did not inhibit VEGF-induced proliferation in HUVECs. FIR exposure also inhibited the VEGF-induced phosphorylation of extracellular signal-regulated kinases in HUVECs. FIR exposure further induced the phosphorylation of endothelial nitric oxide (NO) synthase (eNOS) and NO generation in VEGF-treated HUVECs. Both VEGF-induced NO and reactive oxygen species generation was involved in the inhibitory effect of FIR. Nitrotyrosine formation significantly increased in HUVECs treated with VEGF and FIR together. Inhibition of phosphoinositide 3-kinase (PI3K) by wortmannin abolished the FIR-induced phosphorylation of eNOS and Akt in HUVECs. FIR exposure upregulated the expression of PI3K p85 at the transcriptional level. We further found that FIR exposure induced the nuclear translocation of promyelocytic leukemia zinc finger protein (PLZF) in HUVECs. This induction was independent of a thermal effect. The small interfering RNA transfection of PLZF blocked FIR-increased PI3K levels and the inhibitory effect of FIR. These data suggest that FIR induces the nuclear translocation of PLZF which inhibits VEGF-induced proliferation in HUVECs.
A Comparison of Three-Stage DEA and Artificial Neural Network on the Operational Efficiency of Semi-Conductor Firms in Taiwan  [PDF]
Hsiang-Hsi Liu, Tser-Yieth Chen, Yung-Ho Chiu, Fu-Hsiang Kuo
Modern Economy (ME) , 2013, DOI: 10.4236/me.2013.41003
Abstract:

In this study, the data envelopment analysis (DEA), three-stage DEA (3SDEA) and artificial neural network (ANN) are employed to measure the technical efficiency of 29 semi-conductor firms in Taiwan. Estimated results show that there are significant differences in efficiency scores among DEA, 3SDEA and ANN analysis. The advanced setting of the three stages mechanism of DEA does show some changes in the efficiency scores between DEA and ANN approaches. We further find that the environmental factor is still a significant variable to explain technical efficiency inTaiwan, irrespective of whether a DEA, 3SDEA or ANN approach is used.

MicroRNA-328 Inhibits Renal Tubular Cell Epithelial-to-Mesenchymal Transition by Targeting the CD44 in Pressure-Induced Renal Fibrosis
Cheng-Hsien Chen, Chung-Yi Cheng, Yen-Cheng Chen, Yuh-Mou Sue, Chung-Te Liu, Tzu-Hurng Cheng, Yung-Ho Hsu, Tso-Hsiao Chen
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0099802
Abstract: Epithelial-mesenchymal transition (EMT) occurs in stressed tubular epithelial cells, contributing to renal fibrosis. Initial mechanisms promoting EMT are unknown. Pressure force is an important mechanism contributing to the induction and progression of renal fibrogenesis in ureteric obstruction. In our study of cultured rat renal tubular cells (NRK-52E) under 60 mmHg of pressure, we found that the epithelial marker E-cadherin decreased and mesenchymal markers, e.g., α-smooth muscle actin, fibronectin and Snail, increased. Pressure also induced the expression of connective tissue growth factor and transforming growth factor-β. MicroRNA array assays showed that pressure reduced miR-328 at the initial stage of pressurization. We identified a potential target sequence of miR-328 in rat CD44 3′-untranslated regions. In contrast with the miR-328 expression, CD44 expression was up-regulated at the initial pressurization stage. We also found that miR-328 expression decreased and CD44 increased in ureteric obstruction kidneys in the animal study. CD44 siRNA transfection significantly increased E-cadherin expression and inhibited pressure-induced EMT. Both hyaluronan binding peptide pep-1 and osteopontin neutralizing antibody inhibited pressure-induced EMT. Our results suggest that miR-328-mediated CD44 transient upregulation is an important trigger of the pressure-induced EMT in renal fibrosis.
Technical Analysis of the Taiwanese Stock Market
Massoud Metghalchi,Yung-Ho Chang,Xavier Garza-Gomez
International Journal of Economics and Finance , 2011, DOI: 10.5539/ijef.v4n1p90
Abstract: We study the profitability of technical trading rules based on 9 popular technical indicators. To further examine whether investors can design technical trading strategies that can beat the buy-and-hold strategy, we establish 13 trading models based on one indicator, 25 models based on two indicators, and 28 models based on three indicators. The empirical results show that 58 out of 66 models reject the null hypothesis of equality of the mean returns between buy days and sell days. Our findings provide support for the predictive power of technical trading rules. Finally we employ Hansen’s (2005) Superior Predictive Ability to investigate data snooping problem. Overall we observe an inverse association between the number of technical indicator combinations and trading profitability.
Anticoccidial Effects of Magnolia officinalis Extract on Eimeria tenella in Chicken
Hyun-A Lee,Sunhwa Hong,Yung-Ho Chung,Okjin Kim
Journal of Animal and Veterinary Advances , 2012, DOI: 10.3923/javaa.2012.4156.4160
Abstract: Anticoccidial effects of Magnoliae officinalis Extract (MOE) were evaluated in chickens following oral infection with Eimeria (E.) tenella. This study was conducted on the 3 days old chickens (n = 30). Those animals were divided with 3 groups; MOE 0.5% treated/infected (n = 10), MOE untreated/infected (n = 10) and non-infected control (n = 10). Chickens were fed a standard diet supplemented with or without MOE for 1 week prior to infection with E. tenella (10,000 sporulated oocysts per chicken). The effects of MOE on E. tenella infection were assessed by two parameters, fecal oocyst shedding and body weight gain. The MOE-fed chickens produced significantly reduced fecal oocysts (p<0.05) when compared to the E. tenella-infected group fed standard diet. Also, MOE-based diet, improved body weight loss caused by E. tenella infection. The data demonstrated that MOE had remarkable anticoccidial activities against E. tenella. This finding might have implications for the development of anticoccidial drug.
Endothelin Type A Receptor Genotype is a Determinant of Quantitative Traits of Metabolic Syndrome in Asian Hypertensive Families: A SAPPHIRe Study
Low-Tone Ho,Yung-Pei Hsu,Lee-Ming Chuang
Frontiers in Endocrinology , 2013, DOI: 10.3389/fendo.2013.00172
Abstract: Co-heritability of hypertension and insulin resistance (IR) within families not only implies genetic susceptibility may be responsible for these complex traits but also suggests a rational that biological candidate genes for hypertension may serve as markers for features of the metabolic syndrome (MetS). Thus we determined whether the T323C polymorphism (rs5333) of endothelin type A (ETA) receptor, a predominant receptor evoking potent vasoconstrictive action of endothelin-1, contributes to susceptibility to IR-associated hypertension in 1694 subjects of Chinese and Japanese origins. Blood pressures (BPs) and biochemistries were measured. Fasting insulin level, insulin-resistance homeostasis model assessment (HOMAIR) score, and area under curve of insulin concentration (AUCINS) were selected for assessing insulin sensitivity. Genotypes were obtained by methods of polymerase chain reaction-restriction fragment length polymorphism. Foremost findings were that minor allele frequency of the T323C polymorphism was noticeable lower in our overall Asian subjects compared to multi-national population reported in gene database; moreover both the genotypic and allelic frequencies of the polymorphism were significantly different between the two ethnic groups we studied. The genotype distributions at TT/TC/CC were 65, 31, 4% in Chinese and 51, 41, 8% in Japanese, respectively (p < 0.0001). Additionally, carriers of the C homozygote revealed characteristics of IR, namely significantly higher levels of fasting insulin, HOMAIR score, and AUCINS at 29.3, 35.3, and 39.3%, respectively, when compared to their counterparts with TT/TC genotypes in Chinese. Meanwhile, the CC genotype was associated with a higher level of high density lipoprotein cholesterol in Japanese. No association of the polymorphism with BP was observed. This study demonstrated for the first time that T323C polymorphism of ETA receptor gene was associated with an adverse insulin response in Chinese and a favorite atherogenic index in Japanese.
The Welfare Effects of Pension Reforms in an Aging Economy  [PDF]
Yuan-Ho Hsu
American Journal of Industrial and Business Management (AJIBM) , 2017, DOI: 10.4236/ajibm.2017.75049
Abstract: This paper develops a multigenerational overlapping (OLG) model to investigate the welfare effects of pension reforms in an aging economy. Given the declining trend in the proportion of young people to the old aged, it is feared that existing pay-as-you-go pension system may not be sustainable and it necessitates higher tax or premium contributions to maintain the sustainability of the fiscal and pension system. This paper investigates the effects of four reform programs aiming to enhance the sustainability of the pension system. The programs are: (a) an increase in pension contribution, (b) a reduction in pension benefit, (c) an extension of mandatory retirement age, and (d) a combination of program (b) and (c). Policy simulation results from this paper indicate that extending mandatory retirement age harms only little of the current generations’ lifetime utility whereas it gradually improves future generations’ life time utility. On the contrary, increase in pension contribution reduces lifetime utility of the current generation without benefitting future generation. Alternately increase in contribution ratio improves future GDP growth whereas reducing replacement ratio cannot. Finally, an increase in pension contribution worsens government budgetary condition whereas reducing replacement ratio does not.
Evidence for predilection of macrophage infiltration patterns in the deeper midline and mesial temporal structures of the brain uniquely in patients with HIV-associated dementia
Li Zhou, Rejane Rua, Thomas Ng, Valentina Vongrad, Yung S Ho, Carolyn Geczy, Kenneth Hsu, Bruce J Brew, Nitin K Saksena
BMC Infectious Diseases , 2009, DOI: 10.1186/1471-2334-9-192
Abstract: To study activation and infiltration patterns of macrophages, CD8+ T cells in relation to HIV in diverse CNS areas of patients with and without dementia. 46 brain regions from two rapidly progressing severely demented patients and 53 regions from 4 HIV+ non-dementia patients were analyzed. Macrophage and CD8+ T cell infiltration of the CNS in relation to HIV was assessed using immuno-histochemical analysis with anti-HIV (P24), anti-CD8 and anti-CD68, anti-S-100A8 and granzyme B antibodies (cellular activation). Statistical analysis was performed with SPSS 12.0 with Student's t test and ANOVA.Overall, the patterns of infiltration of macrophages and CD8+ T cells were indiscernible between patients with and without dementia, but the co-localization of macrophages and CD8+ T cells along with HIV P24 antigen in the deeper midline and mesial temporal structures of the brain segregated the two groups. This predilection of infected macrophages and CD8+ T cells to the middle part of the brain was unique to both HAD patients, along with unique nature of provirus gag gene sequences derived from macrophages in the midline and mesial temporal structures.Strong predilection of infected macrophages and CD8+ T cells was typical of the deeper midline and mesial temporal structures uniquely in HAD patients, which has some influence on neurocognitive impairment during HIV infection.Human immunodeficiency virus type 1 (HIV-1) is associated with the development of neurological complications in many infected individuals, most especially a broad spectrum of motor impairments and cognitive deficits. Approximately 80-90% of autopsied cases of HIV-1-infected people demonstrated neuropathological changes [1-4]. The histopathology of HIV-associated dementia (HAD) is characterized by brain infiltration of mononuclear cells, formation of multinucleated giant cells, astrogliosis, and neuronal damage sometimes with neuronal loss [5,6]. The underlying mechanisms of HAD leading to neurological disor
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