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Search Results: 1 - 10 of 516257 matches for " Thomas M. Chiang and V. Woo-Rasberry "
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The Toxicity of a Chemically Synthesized Peptide Derived from Non-Integrin Platelet Collagen Receptors
Thomas M. Chiang and V. Woo-Rasberry
Drug Target Insights , 2012,
Abstract: A chemically synthesized peptide derived from platelet non-integrin collagen receptor has been shown to be an effective agent for inhibiting collagen-induced platelet aggregation and adhesion of washed radiolabeled platelets onto natural matrices and collagen coated microtiter plates. In order to be a therapeutic agent, we have used a cell culturing system and an animal model to test its cytotoxicities. In cell culture experiments, the peptide is not toxic to MEG-01, a megakaryoblastic cell line. Prior to performing experiments in rats, the existence of both platelet type I and type III collagen receptors and its functional roles in rat platelets had to be established. In this investigation, we report that rat platelets contain both receptors and the cHyB peptide inhibits both type I and type III collagen-induced rat platelet aggregation. In addition, analysis of the rat sera collected at various time intervals following an injection of cHyB into the rat-tail vein, did not show an increase in the activity of key enzymes which indicate tissue and/or organ damage. These results suggest that the cHyB peptide is safe and its development into a potential therapeutic agent for inhibiting thrombi formation is possible.
The Toxicity of a Chemically Synthesized Peptide Derived from Non-Integrin Platelet Collagen Receptors
Thomas M. Chiang,V. Woo-Rasberry
Drug Target Insights , 2008,
Abstract: A chemically synthesized peptide derived from platelet non-integrin collagen receptor has been shown to be an effective agent for inhibiting collagen-induced platelet aggregation and adhesion of washed radiolabeled platelets onto natural matrices and collagen coated microtiter plates. In order to be a therapeutic agent, we have used a cell culturing system and an animal model to test its cytotoxicities. In cell culture experiments, the peptide is not toxic to MEG-01, a megakaryoblastic cell line. Prior to performing experiments in rats, the existence of both platelet type I and type III collagen receptors and its functional roles in rat platelets had to be established. In this investigation, we report that rat platelets contain both receptors and the cHyB peptide inhibits both type I and type III collagen-induced rat platelet aggregation. In addition, analysis of the rat sera collected at various time intervals following an injection of cHyB into the rat-tail vein, did not show an increase in the activity of key enzymes which indicate tissue and/or organ damage. These results suggest that the cHyB peptide is safe and its development into a potential therapeutic agent for inhibiting thrombi formation is possible.
The Toxicity of a Chemically Synthesized Peptide Derived from Non-Integrin Platelet Collagen Receptors
Thomas M. Chiang,V. Woo-Rasberry
Drug Target Insights , 2008,
Abstract: A chemically synthesized peptide derived from platelet non-integrin collagen receptor has been shown to be an effective agent for inhibiting collagen-induced platelet aggregation and adhesion of washed radiolabeled platelets onto natural matrices and collagen coated microtiter plates. In order to be a therapeutic agent, we have used a cell culturing system and an animal model to test its cytotoxicities. In cell culture experiments, the peptide is not toxic to MEG-01, a megakaryoblastic cell line. Prior to performing experiments in rats, the existence of both platelet type I and type III collagen receptors and its functional roles in rat platelets had to be established. In this investigation, we report that rat platelets contain both receptors and the cHyB peptide inhibits both type I and type III collagen-induced rat platelet aggregation. In addition, analysis of the rat sera collected at various time intervals following an injection of cHyB into the rat-tail vein, did not show an increase in the activity of key enzymes which indicate tissue and/or organ damage. These results suggest that the cHyB peptide is safe and its development into a potential therapeutic agent for inhibiting thrombi formation is possible.
The Beta3 499–513 Peptide Region is Required for AlphaIIb/ Beta3 Active Complex Formation and Fibrinogen Binding
Virginia Woo-Rasberry and Thomas M. Chiang
Drug Target Insights , 2012,
Abstract: Background: AlphaIIb/beta3 (αIIb/β3) complex is an important integrin that is involved in the nal step of platelet aggregation. Peptides derived from either αIIb or β3 have demonstrated to have an effect on the activation of the complex and its ability to bind brinogen. We have previously de ned a peptide from β3, which inhibits agonists-induced platelet aggregation. Methods: We used standard methodologies for construction of clones and expression of cDNAs, establishment of stable cell lines that contained these cDNAs. Expression of proteins was detected with immunoblots. Flow cytometric analyses were used to verify the presence of the active and inactive complexes with different antibodies. In addition, a brinogen- binding assay was used to determine the inhibition of the active complex by the peptide. Results and discussion: A stable cell line of the co-transfected cDNAs of αIIb, β3 wild type and mutants of β3 (scrambled sequence of the peptide region, replacement of C499A and C512A), expressing the inactive complex on CHO cells, has allowed us to examine the important role of the peptide sequence and the cysteine residues within the peptide. The peptide inhibits the active complex formation and thereby inhibits the binding of FITC-PAC-1 in a dose dependent manner by ow cytometric analyses, as well as binding of [3H]- brinogen. In addition, creation of a second stable cell line containing wild type αIIb and the mutated region of β3 (residues 499–513) shows that the binding of FITC-PAC-1 and [3H]- brinogen on the mutant activated complex was much lower than the wild type activated complex. Our results indicate that the region 499–513 in β3 is one of the important sites for αIIb/β3 active complex formation and the cysteines play an important role in the process.
The Beta3 499–513 Peptide Region is Required for AlphaIIb/ Beta3 Active Complex Formation and Fibrinogen Binding
Virginia Woo-Rasberry,Thomas M. Chiang
Drug Target Insights , 2008,
Abstract: Background: AlphaIIb/beta3 (αIIb/β3) complex is an important integrin that is involved in the nal step of platelet aggregation. Peptides derived from either αIIb or β3 have demonstrated to have an effect on the activation of the complex and its ability to bind brinogen. We have previously de ned a peptide from β3, which inhibits agonists-induced platelet aggregation.Methods: We used standard methodologies for construction of clones and expression of cDNAs, establishment of stable cell lines that contained these cDNAs. Expression of proteins was detected with immunoblots. Flow cytometric analyses were used to verify the presence of the active and inactive complexes with different antibodies. In addition, a brinogen- binding assay was used to determine the inhibition of the active complex by the peptide.Results and discussion: A stable cell line of the co-transfected cDNAs of αIIb, β3 wild type and mutants of β3 (scrambled sequence of the peptide region, replacement of C499A and C512A), expressing the inactive complex on CHO cells, has allowed us to examine the important role of the peptide sequence and the cysteine residues within the peptide. The peptide inhibits the active complex formation and thereby inhibits the binding of FITC-PAC-1 in a dose dependent manner by ow cytometric analyses, as well as binding of [3H]- brinogen. In addition, creation of a second stable cell line containing wild type αIIb and the mutated region of β3 (residues 499–513) shows that the binding of FITC-PAC-1 and [3H]- brinogen on the mutant activated complex was much lower than the wild type activated complex. Our results indicate that the region 499–513 in β3 is one of the important sites for αIIb/β3 active complex formation and the cysteines play an important role in the process.
Directed Evaluation of Enterotoxigenic Escherichia coli Autotransporter Proteins as Putative Vaccine Candidates
Jessica A. Harris equal contributor,Koushik Roy equal contributor,Virginia Woo-Rasberry,David J. Hamilton,Rita Kansal,Firdausi Qadri,James M. Fleckenstein
PLOS Neglected Tropical Diseases , 2011, DOI: 10.1371/journal.pntd.0001428
Abstract: Background Enterotoxigenic Escherichia coli (ETEC) is a major diarrheal pathogen in developing countries, where it accounts for millions of infections and hundreds of thousands of deaths annually. While vaccine development to prevent diarrheal illness due to ETEC is feasible, extensive effort is needed to identify conserved antigenic targets. Pathogenic Escherichia coli, including ETEC, use the autotransporter (AT) secretion mechanism to export virulence factors. AT proteins are comprised of a highly conserved carboxy terminal outer membrane beta barrel and a surface-exposed amino terminal passenger domain. Recent immunoproteomic studies suggesting that multiple autotransporter passenger domains are recognized during ETEC infection prompted the present studies. Methodology Available ETEC genomes were examined to identify AT coding sequences present in pathogenic isolates, but not in the commensal E. coli HS strain. Passenger domains of the corresponding autotransporters were cloned and expressed as recombinant antigens, and the immune response to these proteins was then examined using convalescent sera from patients and experimentally infected mice. Principal Findings Potential AT genes shared by ETEC strains, but absent in the E. coli commensal HS strain were identified. Recombinant passenger domains derived from autotransporters, including Ag43 and an AT designated pAT, were recognized by antibodies from mice following intestinal challenge with H10407, and both Ag43 and pAT were identified on the surface of ETEC by flow cytometry. Likewise, convalescent sera from patients with ETEC diarrhea recognized Ag43 and pAT, suggesting that these proteins are expressed during both experimental and naturally occurring ETEC infections and that they are immunogenic. Vaccination of mice with recombinant passenger domains from either pAT or Ag43 afforded protection against intestinal colonization with ETEC. Conclusions Passenger domains of conserved autotransporter proteins could contribute to protective immune responses that develop following infection with ETEC, and these antigens consequently represent potential targets to explore in vaccine development.
Pathways Involved in the Synergistic Activation of Macrophages by Lipoteichoic Acid and Hemoglobin
Kathleen H. Cox, Michelle E. Cox, Virginia Woo-Rasberry, David L. Hasty
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0047333
Abstract: Lipoteichoic acid (LTA) is a Gram-positive cell surface molecule that is found in both a cell-bound form and cell-free form in the host during an infection. Hemoglobin (Hb) can synergize with LTA, a TLR2 ligand, to potently activate macrophage innate immune responses in a TLR2- and TLR4-dependent way. At low levels of LTA, the presence of Hb can result in a 200-fold increase in the secretion of IL-6 following macrophage activation. Six hours after activation, the macrophage genes that are most highly up-regulated by LTA plus Hb activation compared to LTA alone are cytokines, chemokines, receptors and interferon-regulated genes. Several of these genes exhibit a unique TLR4-dependent increase in mRNA levels that continued to rise more than eight hours after stimulation. This prolonged increase in mRNA levels could be the result of an extended period of NF-κB nuclear localization and the concurrent absence of the NF-κB inhibitor, IκBα, after stimulation with LTA plus Hb. Dynasore inhibition experiments indicate that an endocytosis-dependent pathway is required for the TLR4-dependent up-regulation of IL-6 secretion following activation with LTA plus Hb. In addition, interferon-β mRNA is present after activation with LTA plus Hb, suggesting that the TRIF/TRAM-dependent pathway may be involved. Hb alone can elicit the TLR4-dependent secretion of TNF-α from macrophages, so it may be the TLR4 ligand. Hb also led to secretion of high mobility group box 1 protein (HMGB1), which synergized with LTA to increase secretion of IL-6. The activation of both the TLR2 and TLR4 pathways by LTA plus Hb leads to an enhanced innate immune response.
Structural and electronic origin of the magnetic structures in hexagonal LuFeO$_3$
Hongwei Wang,Igor V. Solovyev,Wenbin Wang,Xiao Wang,Phillip Ryan,David J. Keavney,Jong-Woo Kim,Thomas Z. Ward,Leyi Zhu,X. M. Cheng,Jian Shen,Lixin He,Xiaoshan Xu,Xifan Wu
Physics , 2013, DOI: 10.1103/PhysRevB.90.014436
Abstract: Using combined theoretical and experimental approaches, we studied the structural and electronic origin of the magnetic structure in hexagonal LuFeO$_3$. Besides showing the strong exchange coupling that is consistent with the high magnetic ordering temperature, the previously observed spin reorientation transition is explained by the theoretically calculated magnetic phase diagram. The structural origin of this spin reorientation that is responsible for the appearance of spontaneous magnetization, is identified by theory and verified by x-ray diffraction and absorption experiments.
Specific Variants in the MLH1 Gene Region May Drive DNA Methylation, Loss of Protein Expression, and MSI-H Colorectal Cancer
Miralem Mrkonjic,Nicole M. Roslin,Celia M. Greenwood,Stavroula Raptis,Aaron Pollett,Peter W. Laird,Vaijayanti V. Pethe,Theodore Chiang,Darshana Daftary,Elizabeth Dicks,Stephen N. Thibodeau,Steven Gallinger,Patrick S. Parfrey,H. Banfield Younghusband,John D. Potter,Thomas J. Hudson,John R. McLaughlin,Roger C. Green,Brent W. Zanke,Polly A. Newcomb,Andrew D. Paterson,Bharati Bapat
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0013314
Abstract: We previously identified an association between a mismatch repair gene, MLH1, promoter SNP (rs1800734) and microsatellite unstable (MSI-H) colorectal cancers (CRCs) in two samples. The current study expanded on this finding as we explored the genetic basis of DNA methylation in this region of chromosome 3. We hypothesized that specific polymorphisms in the MLH1 gene region predispose it to DNA methylation, resulting in the loss of MLH1 gene expression, mismatch-repair function, and consequently to genome-wide microsatellite instability.
Empirical Analysis of Dynamic Linkages between China and International Stock Markets  [PDF]
Thomas C. Chiang, Xiaoyu Chen
Journal of Mathematical Finance (JMF) , 2016, DOI: 10.4236/jmf.2016.61018
Abstract:

This paper investigates the dynamic conditional correlations (DCC) of stock returns between China and international markets. Statistics suggest that stock-return correlations across markets are time-varying, displaying a structural change triggered by an upward shift in China’s adoption of financial liberalization and the occurrence of the worldwide financial crisis. The dynamic correlations are closely tied to geographic location: the highest correlation is with Hong Kong, followed by Taiwan and Korea; the correlations with Europe and the US are low. The DCC series are negatively associated with the relative P/E ratios and are positively associated with the risk from the US market.

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