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Search Results: 1 - 10 of 43052 matches for " Yee-Shin Lin "
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Dengue Vaccines: Challenge and Confrontation  [PDF]
Guey Chuen Perng, Huan-Yao Lei, Yee-Shin Lin, Kulkanya Chokephaibulkit
World Journal of Vaccines (WJV) , 2011, DOI: 10.4236/wjv.2011.14012
Abstract: Dengue has been recognized as one of the most important vector-borne human diseases. The disease is induced by dengue virus infection resulting from the bite of an infected Aedes spp. mosquito after imbibing the tainted blood from animals or patients. Dynamic clinical spectrums ranging from asymptomatic, undifferentiated fever, typical dengue fever (DF), dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS) have been well documented. Initially, the disease was mainly restricted in tropical and subtropical zones. However, with factors such as ineffective vector control, frequency of human migration, unplanned urbanization, and changing climate temperature, the disease has been spotted at almost every territory of the earth. Dengue has been associated with human disease for more than two centuries. Although classic DF is viewed as a self-limited illness, subjects normally resolve within two weeks and recover without any noticeable complications or sequelae, some of these infected individuals may progress to life-threatening DHF/DSS, characterized with plasma leakage due to an increase in capillary permeability. The significantly increased public health threat and the burden of morbidity and mortality of dengue globally has caught the attention of public officials and prompted an action to find a way to contain and prevent the disease. The lack of specific dengue therapeutics has led to an emphasis on vaccine development, one of the best and effective strategies to reduce and prevent the illness. Making a dengue vaccine has been attempted more than six decades; although some of these products are in clinical trials, vaccine development for the prevention of dengue disease is still at its infancy. So far no dengue vaccine is available for the public. Dengue vaccine development may be hindered by the complexity of the clinical presentations, which implicates that multiple pathogenic mechanisms are involved in dengue disease. Some of these elements will be discussed in the current review. Opening up discussion on these pros and cons and engaging in more research to understand these features would not only improve the understanding of the pathogenesis of the dengue virus infection but also pave a new tactic to develop a safer and effective dengue vaccine.
Apoptotic Sphingolipid Ceramide in Cancer Therapy
Wei-Ching Huang,Chia-Ling Chen,Yee-Shin Lin,Chiou-Feng Lin
Journal of Lipids , 2011, DOI: 10.1155/2011/565316
Abstract: Apoptosis, also called programmed cell death, is physiologically and pathologically involved in cellular homeostasis. Escape of apoptotic signaling is a critical strategy commonly used for cancer tumorigenesis. Ceramide, a derivative of sphingolipid breakdown products, acts as second messenger for multiple extracellular stimuli including growth factors, chemical agents, and environmental stresses, such as hypoxia, and heat stress as well as irradiation. Also, ceramide acts as tumor-suppressor lipid because a variety of stress stimuli cause apoptosis by increasing intracellular ceramide to initiate apoptotic signaling. Defects on ceramide generation and sphingolipid metabolism are developed for cancer cell survival and cancer therapy resistance. Alternatively, targeting ceramide metabolism to correct these defects might provide opportunities to overcome cancer therapy resistance. 1. Introduction Apoptosis, also named programmed cell death, is a normal component for cellular homeostasis involving embryonic/organ development and health in human. For tumorigenesis, oncogenic factors are generally involved in activation of antiapoptotic signaling pathways, whereas tumor suppressor factors are normally proapoptotic [1]. During the past two decades, studies of sphingolipids reveal the important role of bioactive sphingolipids, such as ceramide, in regulation of multiple biological functions especially in apoptosis [2–6]. The cytopathic effects of ceramide are proapoptotic as well as necroticlike, depending on the cell types and the dosages of stimulation. Thus, apoptotic signaling caused by ceramide is diverse because several intracellular organelles are generally involved [7]. Inhibiting cell death by interference on ceramide signaling is a key strategy for tumorigenesis escape from apoptotic stimuli. Therefore, for the development of cancer therapy, ceramide metabolic pathways become candidate target currently [8–11]. The antiproliferative activities of ceramide for cancer therapy depend on the induction of various apoptotic pathways as demonstrated previously [12–14]. Most of these studies are based on the exogenous administration of ceramide analogue, particularly C2- and C6-ceramide. Endogenous generation of ceramide through the newly de novo synthesis or the hydrolysis of sphingomyelin is also reported to trigger signaling pathways after apoptotic stimulation. However, it remains controversial for verifying the different molecular mechanisms between these two experimental approaches. In this article, we briefly discussed the link of ceramide and
Plasma kallistatin levels in patients with severe community-acquired pneumonia
Wei-Chieh Lin, Shiou-Ling Lu, Chiou-Feng Lin, Chang-Wen Chen, Lee Chao, Julie Chao, Yee-Shin Lin
Critical Care , 2013, DOI: 10.1186/cc12507
Abstract: Plasma samples and clinical data were prospectively collected from 54 patients with severe CAP requiring ICU admission. Seventeen healthy control subjects were included for comparison. Plasma kallistatin, kallikrein, and other biomarkers of inflammation (tumor necrosis factor-alpha [TNF-alpha], interleukin [IL]-1beta, IL-6, IL-8, C-reactive protein [CRP]) and anti-coagulation (protein C, anti-thrombin III) were measured on days 1 and 4 of ICU admission. Comparison between survivors (n = 41) and non-survivors (n = 13) was performed.Plasma kallistatin was significantly consumed in severe CAP patients compared with healthy individuals. Lower day 1 kallistatin levels showed a strong trend toward increased mortality (P = 0.018) and higher day 1 CURB-65 scores (P = 0.004). Plasma kallistatin levels on day 1 of ICU admission were significantly decreased in patients who developed septic shock (P = 0.017) and who had acute respiratory distress syndrome (P = 0.044). In addition, kallistatin levels were positively correlated with anti-thrombin III and protein C and inversely correlated with IL-1beta, IL-6 and CRP levels. In a multivariate logistic regression analysis, higher day 1 CURB-65 scores were independent predictors of mortality (odds ratio = 29.9; P = 0.009). Also, higher day 1 kallistatin levels were independently associated with a decreased risk of death (odds ratio = 0.1) with a nearly significant statistical difference (P = 0.056). Furthermore, we found that a cutoff level of 6.5 mug/mL of day 1 kallistatin determined by receiver operating characteristic curves could be used to distinguish between patients who survived in 60 days and those who did not.These results suggest that kallistatin may serve as a novel marker for severe CAP prognosis, and may be involved in the pathogenesis of CAP through anti-inflammatory and anti-coagulation effects.
Macrophage Migration Inhibitory Factor Induces Autophagy via Reactive Oxygen Species Generation
Yung-Chun Chuang, Wen-Hong Su, Huan-Yao Lei, Yee-Shin Lin, Hsiao-Sheng Liu, Chih-Peng Chang, Trai-Ming Yeh
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0037613
Abstract: Autophagy is an evolutionarily conserved catabolic process that maintains cellular homeostasis under stress conditions such as starvation and pathogen infection. Macrophage migration inhibitory factor (MIF) is a multifunctional cytokine that plays important roles in inflammation and tumorigenesis. Cytokines such as IL-1β and TNF-α that are induced by MIF have been shown to be involved in the induction of autophagy. However, the actual role of MIF in autophagy remains unclear. Here, we have demonstrated that incubation of human hepatoma cell line HuH-7 cells with recombinant MIF (rMIF) induced reactive oxygen species (ROS) production and autophagy formation, including LC3-II expression, LC3 punctae formation, autophagic flux, and mitochondria membrane potential loss. The autophagy induced by rMIF was inhibited in the presence of MIF inhibitor, ISO-1 as well as ROS scavenger N-acetyl-L-cysteine (NAC). In addition, serum starvation-induced MIF release and autophagy of HuH-7 cells were partly blocked in the presence of NAC. Moreover, diminished MIF expression by shRNA transfection or inhibition of MIF by ISO-1 decreased serum starvation-induced autophagy of HuH-7 cells. Taken together, these data suggest that cell autophagy was induced by MIF under stress conditions such as inflammation and starvation through ROS generation.
Structure and Photoluminescence Properties of Pr3+ Ion-Doped BaY2ZnO5 Phosphor Prepared Using a Sol-Gel Method?  [PDF]
Hung-Rung Shih, Mu-Tsun Tsai, Lay-Gaik Teoh, Yee-Shin Chang
Journal of Modern Physics (JMP) , 2019, DOI: 10.4236/jmp.2019.102008
Abstract: The Pr3+ ion-doped BaY2ZnO5 phosphor with the orthorhombic structure was synthesized successfully using a sol-gel method in this study. The SEM images show that the BaY2ZnO5:Pr3+ phosphor particles are aggregational but have an isotropic distribution for 2 mol% Pr3+ ions doped. Under an excitation wavelength of 311 nm, the emission bands that appear in the emission spectra are due to the 3P03H4,5,6, 1D23H4 and 3P03F2 electron transition of Pr3+ ion, and it is the same as that for solid state reaction preparation. Comparing to the solid state reaction preparation, the intensities of the 3P03H4 transition were increased by about 6.5 times for sol-gel method. The enhancement in emission intensity is because the activators have more homogeneous contribution in host for the sol-gel method preparation. In addition, the color tone did not change very obviously, which located around the green light region for Pr3+ ion concentrations increasing. The color stability is better for sol-gel method than that for the solid state reaction preparation.
Antibody-Dependent Enhancement Infection Facilitates Dengue Virus-Regulated Signaling of IL-10 Production in Monocytes
Tsung-Ting Tsai,Yi-Jui Chuang,Yee-Shin Lin,Chih-Peng Chang,Shu-Wen Wan,Sheng-Hsiang Lin,Chia-Ling Chen,Chiou-Feng Lin
PLOS Neglected Tropical Diseases , 2014, DOI: 10.1371/journal.pntd.0003320
Abstract: Background Interleukin (IL)-10 levels are increased in dengue virus (DENV)-infected patients with severe disorders. A hypothetical intrinsic pathway has been proposed for the IL-10 response during antibody-dependent enhancement (ADE) of DENV infection; however, the mechanisms of IL-10 regulation remain unclear. Principle Finding We found that DENV infection and/or attachment was sufficient to induce increased expression of IL-10 and its downstream regulator suppressor of cytokine signaling 3 in human monocytic THP-1 cells and human peripheral blood monocytes. IL-10 production was controlled by activation of cyclic adenosine monophosphate response element-binding (CREB), primarily through protein kinase A (PKA)- and phosphoinositide 3-kinase (PI3K)/PKB-regulated pathways, with PKA activation acting upstream of PI3K/PKB. DENV infection also caused glycogen synthase kinase (GSK)-3β inactivation in a PKA/PI3K/PKB-regulated manner, and inhibition of GSK-3β significantly increased DENV-induced IL-10 production following CREB activation. Pharmacological inhibition of spleen tyrosine kinase (Syk) activity significantly decreased DENV-induced IL-10 production, whereas silencing Syk-associated C-type lectin domain family 5 member A caused a partial inhibition. ADE of DENV infection greatly increased IL-10 expression by enhancing Syk-regulated PI3K/PKB/GSK-3β/CREB signaling. We also found that viral load, but not serotype, affected the IL-10 response. Finally, modulation of IL-10 expression could affect DENV replication. Significance These results demonstrate that, in monocytes, IL-10 production is regulated by ADE through both an extrinsic and an intrinsic pathway, all involving a Syk-regulated PI3K/PKB/GSK-3β/CREB pathway, and both of which impact viral replication.
Protection against Dengue Virus Infection in Mice by Administration of Antibodies against Modified Nonstructural Protein 1
Shu-Wen Wan, Yi-Tien Lu, Chia-Hui Huang, Chiou-Feng Lin, Robert Anderson, Hsiao-Sheng Liu, Trai-Ming Yeh, Yu-Ting Yen, Betty A. Wu-Hsieh, Yee-Shin Lin
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0092495
Abstract: Background Infection with dengue virus (DENV) may cause life-threatening disease with thrombocytopenia and vascular leakage which are related to dysfunction of platelets and endothelial cells. We previously showed that antibodies (Abs) against DENV nonstructural protein 1 (NS1) cross-react with human platelets and endothelial cells, leading to functional disturbances. Based on sequence homology analysis, the C-terminal region of DENV NS1 protein contains cross-reactive epitopes. For safety in vaccine development, the cross-reactive epitopes of DENV NS1 protein should be deleted or modified. Methodology/Principal Findings We tested the protective effects of Abs against full-length DENV NS1, NS1 lacking the C-terminal amino acids (a.a.) 271-352 (designated ΔC NS1), and chimeric DJ NS1 consisting of N-terminal DENV NS1 (a.a. 1-270) and C-terminal Japanese encephalitis virus NS1 (a.a. 271-352). The anti-ΔC NS1 and anti-DJ NS1 Abs showed a lower binding activity to endothelial cells and platelets than that of anti-DENV NS1 Abs. Passive immunization with anti-ΔC NS1 and anti-DJ NS1 Abs reduced DENV-induced prolonged mouse tail bleeding time. Treatment with anti-DENV NS1, anti-ΔC NS1 and anti-DJ NS1 Abs reduced local skin hemorrhage, controlled the viral load of DENV infection in vivo, synergized with complement to inhibit viral replication in vitro, as well as abolished DENV-induced macrophage infiltration to the site of skin inoculation. Moreover, active immunization with modified NS1 protein, but not with unmodified DENV NS1 protein, reduced DENV-induced prolonged bleeding time, local skin hemorrhage, and viral load. Conclusions/Significance These results support the idea that modified NS1 proteins may represent an improved strategy for safe and effective vaccine development against DENV infection.
Distinct Structural Features of the Peroxide Response Regulator from Group A Streptococcus Drive DNA Binding
Chang Sheng-Huei Lin, Shi-Yu Chao, Michal Hammel, Jay C. Nix, Hsiao-Ling Tseng, Chih-Cheng Tsou, Chun-Hsien Fei, Huo-Sheng Chiou, U-Ser Jeng, Yee-Shin Lin, Woei-Jer Chuang, Jiunn-Jong Wu, Shuying Wang
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0089027
Abstract: Group A streptococcus (GAS, Streptococcus pyogenes) is a strict human pathogen that causes severe, invasive diseases. GAS does not produce catalase, but has an ability to resist killing by reactive oxygen species (ROS) through novel mechanisms. The peroxide response regulator (PerR), a member of ferric uptake regulator (Fur) family, plays a key role for GAS to cope with oxidative stress by regulating the expression of multiple genes. Our previous studies have found that expression of an iron-binding protein, Dpr, is under the direct control of PerR. To elucidate the molecular interactions of PerR with its cognate promoter, we have carried out structural studies on PerR and PerR-DNA complex. By combining crystallography and small-angle X-ray scattering (SAXS), we confirmed that the determined PerR crystal structure reflects its conformation in solution. Through mutagenesis and biochemical analysis, we have identified DNA-binding residues suggesting that PerR binds to the dpr promoter at the per box through a winged-helix motif. Furthermore, we have performed SAXS analysis and resolved the molecular architecture of PerR-DNA complex, in which two 30 bp DNA fragments wrap around two PerR homodimers by interacting with the adjacent positively-charged winged-helix motifs. Overall, we provide structural insights into molecular recognition of DNA by PerR and define the hollow structural arrangement of PerR-30bpDNA complex, which displays a unique topology distinct from currently proposed DNA-binding models for Fur family regulators.
Peroxide Responsive Regulator PerR of group A Streptococcus Is Required for the Expression of Phage-Associated DNase Sda1 under Oxidative Stress
Chih-Hung Wang, Chuan Chiang-Ni, Hsin-Tzu Kuo, Po-Xing Zheng, Chih-Cheng Tsou, Shuying Wang, Pei-Jane Tsai, Woei-Jer Chuang, Yee-Shin Lin, Ching-Chuan Liu, Jiunn-Jong Wu
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0081882
Abstract: The peroxide regulator (PerR) is a ferric uptake repressor-like protein, which is involved in adaptation to oxidative stress and iron homeostasis in group A streptococcus. A perR mutant is attenuated in surviving in human blood, colonization of the pharynx, and resistance to phagocytic clearance, indicating that the PerR regulon affects both host environment adaptation and immune escape. Sda1 is a phage-associated DNase which promotes M1T1 group A streptococcus escaping from phagocytic cells by degrading DNA-based neutrophil extracellular traps. In the present study, we found that the expression of sda1 is up-regulated under oxidative conditions in the wild-type strain but not in the perR mutant. A gel mobility shift assay showed that the recombinant PerR protein binds the sda1 promoter. In addition, mutation of the conserved histidine residue in the metal binding site of PerR abolished sda1 expression under hydrogen peroxide treatment conditions, suggesting that PerR is directly responsible for the sda1 expression under oxidative stress. Our results reveal PerR-dependent sda1 expression under oxidative stress, which may aid innate immune escape of group A streptococcus.
Hepatoprotective Effects of Panus giganteus (Berk.) Corner against Thioacetamide- (TAA-) Induced Liver Injury in Rats
Wei-Lun Wong,Mahmood Ameen Abdulla,Kek-Heng Chua,Umah Rani Kuppusamy,Yee-Shin Tan,Vikineswary Sabaratnam
Evidence-Based Complementary and Alternative Medicine , 2012, DOI: 10.1155/2012/170303
Abstract: Panus giganteus, a culinary and medicinal mushroom consumed by selected indigenous communities in Malaysia, is currently being considered for large scale cultivation. This study was undertaken to investigate the hepatoprotective effects of P. giganteus against thioacetamide- (TAA-) induced liver injury in Sprague-Dawley rats. The rats were injected intraperitoneally with TAA thrice weekly and were orally administered freeze-dried fruiting bodies of P. giganteus (0.5 or 1 g/kg) daily for two months, while control rats were given vehicle or P. giganteus only. After 60 days, rats administered with P. giganteus showed lower liver body weight ratio, restored levels of serum liver biomarkers and oxidative stress parameters comparable to treatment with the standard drug silymarin. Gross necropsy and histopathological examination further confirmed the hepatoprotective effects of P. giganteus. This is the first report on hepatoprotective effects of P. giganteus. The present study showed that P. giganteus was able to prevent or reduce the severity of TAA-induced liver injury.
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