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Search Results: 1 - 10 of 38243 matches for " Hsiao-Han Chang "
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Hypokalemia, Its Contributing Factors and Renal Outcomes in Patients with Chronic Kidney Disease
Hsiao-Han Wang, Chi-Chih Hung, Daw-Yang Hwang, Mei-Chuan Kuo, Yi-Wen Chiu, Jer-Ming Chang, Jer-Chia Tsai, Shang-Jyh Hwang, Julian L. Seifter, Hung-Chun Chen
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0067140
Abstract: Background In the chronic kidney disease (CKD) population, the impact of serum potassium (sK) on renal outcomes has been controversial. Moreover, the reasons for the potential prognostic value of hypokalemia have not been elucidated. Design, Participants & Measurements 2500 participants with CKD stage 1–4 in the Integrated CKD care program Kaohsiung for delaying Dialysis (ICKD) prospective observational study were analyzed and followed up for 2.7 years. Generalized additive model was fitted to determine the cutpoints and the U-shape association between sK and end-stage renal disease (ESRD). sK was classified into five groups with the cutpoints of 3.5, 4, 4.5 and 5 mEq/L. Cox proportional hazard regression models predicting the outcomes were used. Results The mean age was 62.4 years, mean sK level was 4.2±0.5 mEq/L and average eGFR was 40.6 ml/min per 1.73 m2. Female vs male, diuretic use vs. non-use, hypertension, higher eGFR, bicarbonate, CRP and hemoglobin levels significantly correlated with hypokalemia. In patients with lower sK, nephrotic range proteinuria, and hypoalbuminemia were more prevalent but the use of RAS (renin-angiotensin system) inhibitors was less frequent. Hypokalemia was significantly associated with ESRD with hazard ratios (HRs) of 1.82 (95% CI, 1.03–3.22) in sK <3.5mEq/L and 1.67 (95% CI,1.19–2.35) in sK = 3.5–4 mEq/L, respectively, compared with sK = 4.5–5 mEq/L. Hyperkalemia defined as sK >5 mEq/L conferred 1.6-fold (95% CI,1.09–2.34) increased risk of ESRD compared with sK = 4.5–5 mEq/L. Hypokalemia was also associated with rapid decline of renal function defined as eGFR slope below 20% of the distribution range. Conclusion In conclusion, both hypokalemia and hyperkalemia are associated with increased risk of ESRD in CKD population. Hypokalemia is related to increased use of diuretics, decreased use of RAS blockade and malnutrition, all of which may impose additive deleterious effects on renal outcomes.
Amino Acids Transitioning of 2009 H1N1pdm in Taiwan from 2009 to 2011
Guang-Wu Chen, Kuo-Chien Tsao, Chung-Guei Huang, Yu-Nong Gong, Shih-Cheng Chang, Yi-Chun Liu, Hsiao-Han Wu, Shu-Li Yang, Tzou-Yien Lin, Yhu-Chering Huang, Shin-Ru Shih
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0045946
Abstract: A swine-origin influenza A was detected in April 2009 and soon became the 2009 H1N1 pandemic strain (H1N1pdm). The current study revealed the genetic diversity of H1N1pdm, based on 77 and 70 isolates which we collected, respectively, during the 2009/2010 and 2010/2011 influenza seasons in Taiwan. We focused on tracking the amino acid transitioning of hemagglutinin (HA) and neuraminidase (NA) genes in the early diversification of the virus and compared them with H1N1pdm strains reported worldwide. We identified newly emerged mutation markers based on A/California/04/2009, described how these markers shifted from the first H1N1pdm season to the one that immediately followed, and discussed how these observations may relate to antigenicity, receptor-binding, and drug susceptibility. It was found that the amino acid mutation rates of H1N1pdm were elevated, from 9.29×10?3 substitutions per site in the first season to 1.46×10?2 in the second season in HA, and from 5.23×10?3 to 1.10×10?2 in NA. Many mutation markers were newly detected in the second season, including 11 in HA and 8 in NA, and some were found having statistical correlation to disease severity. There were five noticeable HA mutations made to antigenic sites. No significant titer changes, however, were detected based on hemagglutination inhibition tests. Only one isolate with H275Y mutation known to reduce susceptibility to NA inhibitors was detected. As limited Taiwanese H1N1pdm viruses were isolated after our sampling period, we gathered 8,876 HA and 6,017 NA H1N1pdm sequences up to April 2012 from NCBI to follow up the dynamics of mentioned HA mutations. While some mutations described in this study seemed to either settle in or die out in the 2011–2012 season, a number of them still showed signs of transitioning, prompting the importance of continuous monitoring of this virus for more seasons to come.
Genetic Surveillance Detects Both Clonal and Epidemic Transmission of Malaria following Enhanced Intervention in Senegal
Rachel Daniels, Hsiao-Han Chang, Papa Diogoye Séne, Danny C. Park, Daniel E. Neafsey, Stephen F. Schaffner, Elizabeth J. Hamilton, Amanda K. Lukens, Daria Van Tyne, Souleymane Mboup, Pardis C. Sabeti, Daouda Ndiaye, Dyann F. Wirth, Daniel L. Hartl, Sarah K. Volkman
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0060780
Abstract: Using parasite genotyping tools, we screened patients with mild uncomplicated malaria seeking treatment at a clinic in Thiès, Senegal, from 2006 to 2011. We identified a growing frequency of infections caused by genetically identical parasite strains, coincident with increased deployment of malaria control interventions and decreased malaria deaths. Parasite genotypes in some cases persisted clonally across dry seasons. The increase in frequency of genetically identical parasite strains corresponded with decrease in the probability of multiple infections. Further, these observations support evidence of both clonal and epidemic population structures. These data provide the first evidence of a temporal correlation between the appearance of identical parasite types and increased malaria control efforts in Africa, which here included distribution of insecticide treated nets (ITNs), use of rapid diagnostic tests (RDTs) for malaria detection, and deployment of artemisinin combination therapy (ACT). Our results imply that genetic surveillance can be used to evaluate the effectiveness of disease control strategies and assist a rational global malaria eradication campaign.
Increased Toll-Like Receptor 2 Expression in Peptidoglycan-Treated Blood Monocytes Is Associated with Insulin Resistance in Patients with Nondiabetic Rheumatoid Arthritis
Shih-Wei Wang,Tsun-Mei Lin,Chiou-Huey Wang,Hsiao-Han Liu,Jer-Yiing Houng
Mediators of Inflammation , 2012, DOI: 10.1155/2012/690525
Abstract: The close relationship between increased TLR-2 expression in blood monocytes and insulin resistance in RA patients is shown in this study. Traditional risk factors for metabolic disorders, including the waist circumstance, body mass index (BMI), triglyceride (TG), and ratio of TG to high density lipoprotein (HDL) cholesterol, were closely correlated with HOMA (homoeostasis model assessment) index in patients with nondiabetic RA. Expressions of TLR2 in peripheral blood monocytes, following stimulation with peptidoglycan which is known as a TLR2 agonist, were closely correlated with the HOMA index, TNF-α, and IL-6 concentrations. Accordingly, TLR-2 receptor and its related inflammatory cytokines could be potential therapeutic targets in managing insulin resistance in RA patients. 1. Introduction Rheumatoid arthritis (RA) is a complex disease whose pathogenesis remains unknown. Patients with RA have systemic inflammation, as well as increased morbidity and mortality from cardiovascular disease [1, 2]. Various risk factors have been identified that contribute to atherosclerosis in RA patients [3, 4]. Insulin resistance is the most important of these risk factors. Recent years have seen increased attention devoted to inflammation associated insulin resistance [5]. Increasing numbers of research studies illuminate several possible mechanisms, including activation of innate system. Toll-like receptors (TLRs), as key molecular components of the innate immune system, are of a central interest in innate system associated insulin resistance. Twelve members of TLRs have been identified in mammals [6]. The predominant site of TLRs expression is on cells of the innate system, particularly on monocytes [7]. Monocytes are involved in inflammation and the development of insulin resistance [8–10]. The TLRs recognize numerous ligands; for example, TLR2 and TLR4 were hypothesized to recognize components of the bacterial cell wall such as peptidoglycan and lipopolysaccharide, respectively, and to interact with lipid-containing molecules [11]. TLRs participate in the pathogenesis of insulin resistance in animal models [12, 13] and mediate vascular inflammation and insulin resistance in diet-induced obesity [14]. Additionally, TLRs can link innate immunity and fatty acid-induced insulin resistance [12]. Activation of TLRs in adipocyte has been implicated in the onset of insulin resistance in obesity and type-2 diabetes [15]. Raised TLR expression and signaling were also observed in muscles of insulin resistant individuals [16]. High glucose can induce TLR2 and TLR4
Integrin α PAT-2/CDC-42 Signaling Is Required for Muscle-Mediated Clearance of Apoptotic Cells in Caenorhabditis elegans
Hsiao-Han Hsieh equal contributor,Tsung-Yuan Hsu equal contributor,Hang-Shiang Jiang,Yi-Chun Wu
PLOS Genetics , 2012, DOI: 10.1371/journal.pgen.1002663
Abstract: Clearance of apoptotic cells by engulfment plays an important role in the homeostasis and development of multicellular organisms. Despite the fact that the recognition of apoptotic cells by engulfment receptors is critical in inducing the engulfment process, the molecular mechanisms are still poorly understood. Here, we characterize a novel cell corpse engulfment pathway mediated by the integrin α subunit PAT-2 in Caenorhabditis elegans and show that it specifically functions in muscle-mediated engulfment during embryogenesis. Inactivation of pat-2 results in a defect in apoptotic cell internalization. The PAT-2 extracellular region binds to the surface of apoptotic cells in vivo, and the intracellular region may mediate signaling for engulfment. We identify essential roles of small GTPase CDC-42 and its activator UIG-1, a guanine-nucleotide exchange factor, in PAT-2–mediated cell corpse removal. PAT-2 and CDC-42 both function in muscle cells for apoptotic cell removal and are co-localized in growing muscle pseudopods around apoptotic cells. Our data suggest that PAT-2 functions through UIG-1 for CDC-42 activation, which in turn leads to cytoskeletal rearrangement and apoptotic cell internalization by muscle cells. Moreover, in contrast to PAT-2, the other integrin α subunit INA-1 and the engulfment receptor CED-1, which signal through the conserved signaling molecules CED-5 (DOCK180)/CED-12 (ELMO) or CED-6 (GULP) respectively, preferentially act in epithelial cells to mediate cell corpse removal during mid-embryogenesis. Our results show that different engulfing cells utilize distinct repertoires of receptors for engulfment at the whole organism level.
Dengue Type Four Viruses with E-Glu345Lys Adaptive Mutation from MRC-5 Cells Induce Low Viremia but Elicit Potent Neutralizing Antibodies in Rhesus Monkeys
Hsiao-Han Lin, Hsiang-Chi Lee, Xiao-Feng Li, Meng-Ju Tsai, Hung-Ju Hsiao, Jia-Guan Peng, Shih-Che Sue, Cheng-Feng Qin, Suh-Chin Wu
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0100130
Abstract: Knowledge of virulence and immunogenicity is important for development of live-attenuated dengue vaccines. We previously reported that an infectious clone-derived dengue type 4 virus (DENV-4) passaged in MRC-5 cells acquired a Glu345Lys (E-E345K) substitution in the E protein domain III (E-DIII). The same cloned DENV-4 was found to yield a single E-Glu327Gly (E-E327G) mutation after passage in FRhL cells and cause the loss of immunogenicity in rhesus monkeys. Here, we used site-directed mutagenesis to generate the E-E345K and E-E327G mutants from DENV-4 and DENV-4Δ30 infectious clones and propagated in Vero or MRC-5 cells. The E-E345K mutations were consistently presented in viruses recovered from MRC-5 cells, but not Vero cells. Recombinant E-DIII proteins of E345K and E327G increased heparin binding correlated with the reduced infectivity by heparin treatment in cell cultures. Different from the E-E327G mutant viruses to lose the immunogencity in rhesus monkeys, the E-E345K mutant viruses were able to induce neutralizing antibodies in rhesus monkeys with an almost a 10-fold lower level of viremia as compared to the wild type virus. Monkeys immunized with the E-E345K mutant virus were completely protected with no detectable viremia after live virus challenges with the wild type DENV-4. These results suggest that the E-E345K mutant virus propagated in MRC-5 cells may have potential for the use in live-attenuated DENV vaccine development.
Role of the CCAAT-Binding Protein NFY in SCA17 Pathogenesis
Li-Ching Lee, Chiung-Mei Chen, Hao-Chun Wang, Hsiao-Han Hsieh, I-Sheng Chiu, Ming-Tsan Su, Hsiu-Mei Hsieh-Li, Chung-Hsin Wu, Guan-Chiun Lee, Guey-Jen Lee-Chen, Jung-Yaw Lin
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035302
Abstract: Spinocerebellar ataxia 17 (SCA17) is caused by expansion of the polyglutamine (polyQ) tract in human TATA-box binding protein (TBP) that is ubiquitously expressed in both central nervous system and peripheral tissues. The spectrum of SCA17 clinical presentation is broad. The precise pathogenic mechanism in SCA17 remains unclear. Previously proteomics study using a cellular model of SCA17 has revealed reduced expression of heat shock 70 kDa protein 5 (HSPA5) and heat shock 70 kDa protein 8 (HSPA8), suggesting that impaired protein folding may contribute to the cell dysfunction of SCA17 (Lee et al., 2009). In lymphoblastoid cells, HSPA5 and HSPA8 expression levels in cells with mutant TBP were also significantly lower than that of the control cells (Chen et al., 2010). As nuclear transcription factor Y (NFY) has been reported to regulate HSPA5 transcription, we focused on if NFY activity and HSPA5 expression in SCA17 cells are altered. Here, we show that TBP interacts with NFY subunit A (NFYA) in HEK-293 cells and NFYA incorporated into mutant TBP aggregates. In both HEK-293 and SH-SY5Y cells expressing TBP/Q61~79, the level of soluble NFYA was significantly reduced. In vitro binding assay revealed that the interaction between TBP and NFYA is direct. HSPA5 luciferase reporter assay and endogenous HSPA5 expression analysis in NFYA cDNA and siRNA transfection cells further clarified the important role of NFYA in regulating HSPA5 transcription. In SCA17 cells, HSPA5 promoter activity was activated as a compensatory response before aggregate formation. NFYA dysfunction was indicated in SCA17 cells as HSPA5 promoter activity reduced along with TBP aggregate formation. Because essential roles of HSPA5 in protection from neuronal apoptosis have been shown in a mouse model, NFYA could be a target of mutant TBP in SCA17.
An Analysis of Video Navigation Behavior for Web Leisure
Hsiao-Tieh Pu,Ying-Han Chang
Journal of Library and Information Studies , 2012,
Abstract: People nowadays put much emphasis on leisure activities, and web video has gradually become one of the main sources for popular leisure. This article introduces the related concepts of leisure and navigation behavior as well as some recent research topics. Moreover, using YouTube as an experimental setting, the authors invited some experienced web video users and conducted an empirical study on their navigating the web videos for leisure purpose. The study used questionnaires, navigation logs, diaries, and interviews to collect data. Major results show: the subjects watched a variety of video content on the web either from traditional media or user-generated video; these videos can meet their leisure needs of both the broad and personal interests; during the navigation process, each subject quite focuses on video leisure, and is willingly to explore unknown videos; however, within a limited amount of time for leisure, a balance between leisure and rest becomes an issue of achieving real relaxation, which is worth of further attention. [Article content in Chinese]
Determination of Fragmentation Schemes and Metabolites of Fluorinated Histone Deacetylase Inhibitors for Use as Positron Emission Tomography Imaging Agents Using HPLC-MS/MS  [PDF]
Wei-Hsi Chen, Yu-Chieh Hsiao, Ming-Hsin Li, Mu-Chen Tsai, Chun-Fang Feng, Han-Chih Chang, Hung-Wen Yu, Chyng-Yann Shiue
International Journal of Analytical Mass Spectrometry and Chromatography (IJAMSC) , 2018, DOI: 10.4236/ijamsc.2018.61001
Abstract: High performance liquid chromatography coupled with tandem mass spectrometry was developed and validated as a method for the analysis of fluorinated histone deacetylase inhibitors (F-HDACi), and then employed to study their metabolism in biosystems. Four HDACi analogs labeled with the positron emission nuclide 18F constitute a group of potential positron emission tomography imaging agents, which were developed by the Institute of Nuclear Energy Research (INER) and coded as INER-1577 #1, #2, #3, and #4 during animal studies for the diagnosis of dementia. The performance of the method was found to be suitable for the determination of analog #3, and it was employed to determine the structures and fragmentation mechanisms of all four analogs and to study the biotransformations of analogs #3 and #4. The results indicated that the method used for the determination of analog #3 was suitable for determining the abundance of the analogs in chemical and biochemical tests with high precision, accuracy, reproducibility, and recovery. Weaknesses in the chemical bonding of the analogs were found to involve the fluoro, dimethylamino, and benzamide groups in a fragmentation mechanism deduced via tandem mass spectrometry. The metabolites of analogs #3 and #4 in rat liver microsomes and rat plasma were also identified to clarify their characteristic behaviors in biosystems. The major product of analogs #3 in liver microsomes was produced by hydroxylation of the benzylic carbon atom, but in rat plasma the metabolites of analog #3 were produced by hydrolysis of the benzamide group to give a diaminobiphenyl compound with the simultaneous replacement of a fluorine atom by a hydroxyl group. The metabolites of analog #4 in liver microsomes were produced by hydroxylation of the benzylic carbon atom and hydrolysis of the benzamide bond. The results of the studies characterized the chemical and biochemical behaviors of the series F-HADCi analogs.
Utilizing Joint Routing and Capacity Assignment Algorithms to Achieve Inter- and Intra-Group Delay Fairness in Multi-Rate Multicast Wireless Sensor Networks
Frank Yeong-Sung Lin,Chiu-Han Hsiao,Leo Shih-Chang Lin,Yean-Fu Wen
Sensors , 2013, DOI: 10.3390/s130303588
Abstract: Recent advance in wireless sensor network (WSN) applications such as the Internet of Things (IoT) have attracted a lot of attention. Sensor nodes have to monitor and cooperatively pass their data, such as temperature, sound, pressure, etc. through the network under constrained physical or environmental conditions. The Quality of Service (QoS) is very sensitive to network delays. When resources are constrained and when the number of receivers increases rapidly, how the sensor network can provide good QoS (measured as end-to-end delay) becomes a very critical problem. In this paper; a solution to the wireless sensor network multicasting problem is proposed in which a mathematical model that provides services to accommodate delay fairness for each subscriber is constructed. Granting equal consideration to both network link capacity assignment and routing strategies for each multicast group guarantees the intra-group and inter-group delay fairness of end-to-end delay. Minimizing delay and achieving fairness is ultimately achieved through the Lagrangean Relaxation method and Subgradient Optimization Technique. Test results indicate that the new system runs with greater effectiveness and efficiency.
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