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194 results on '"Chang, D. M."'

18. Invasive aspergillosis in patients with systemic lupus erythematosus: a retrospective study on clinical characteristics and risk factors for mortality.

Author

Hung, M. L., Liao, H. T., Chen, W. S., Chen, M. H., Lai, C. C., Tsai, C. Y., and Chang, D. M.

Subjects
ASPERGILLOSIS, PLASMAPHERESIS, CYTOMEGALOVIRUS diseases, RESPIRATORY diseases, STEROIDS
Abstract

Objective The objective of this paper is to analyze the clinical features, outcomes, mortality risk factors, and all-cause mortalities of invasive aspergillosis (IA) in patients with systemic lupus erythematosus (SLE). Methods Medical records were reviewed to identify SLE patients with IA from January 2006 to June 2017, at Taipei Veterans General Hospital, Taiwan. A total of 6714 SLE patients were included. Clinical/laboratory parameters and treatment outcomes were analyzed. Results Four patients (19.0%) had definite and 17 had probable (81.0%) IA. Seven patients (33.3%) survived and 14 died (66.7%). Concurrently, there were 19 pneumonias (90.5%), 17 cases of other infections (81.0%), eight bacteremia (38.1%), nine cytomegalovirus (CMV, 42.7%) and six Candida (28.6%) infections. In all 55 blood cultures, 38 (69.1%) yielded gram-negative bacilli, of which carbapenem-resistant A. baumannii accounted for eight (21.1%); 17 (30.9%) yielded gram-positive cocci, of which methicillin-resistant S. aureus accounted for six (35.3%); and vancomycin-resistant Enterococcus accounted for four (23.5%). Daily steroid dose ≥ 20 mg (hazard ratio (HR) 2.00), recent pulse steroid therapy (HR 2.80), azathioprine (HR 2.00), rituximab (HR 2.00), plasmapheresis (HR 2.00), acute respiratory distress syndrome (HR 2.00), concurrent infections (HR 5.667) and CMV viremia (HR 1.75) were higher in the fatality group. All p values were less than 0.05. Septic shock (n = 7, 50% in the fatality group) is the most common cause of mortality. Conclusions High daily steroid dosing, recent pulse steroid therapy, azathioprine, rituximab, concurrent infections, and CMV viremia were mortality risk factors for IA in SLE. [ABSTRACT FROM AUTHOR]

Published
2018
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19. Vascular and upper gastrointestinal effects of non-steroidal anti-inflammatory drugs: meta-analyses of individual participant data from randomised trials

Author

Baigent, Colin, Bhala, N., Emberson, J., Merhi, A., Abramson, S., Arber, N., Baron, J. A., Bombardier, C., Cannon, C., Farkouh, M. E., Fitzgerald, G. A., Goss, P., Halls, H., Hawk, E., Hawkey, C., Hennekens, C., Hochberg, M., Holland, L. E., Kearney, P. M., Laine, L., Lanas, A., Lance, P., Laupacis, A., Oates, J., Patrono, C., Schnitzer, T. J., Solomon, S., Tugwell, P., Wilson, K., Wittes, J., Adelowo, O., Aisen, P., Al Quorain, A., Altman, R., Bakris, G., Baumgartner, H., Bresee, C., Carducci, M., Chang, D. M., Chou, C. T., Clegg, D., Cudkowicz, M., Doody, L., Miedany, Y. E. l., Falandry, C., Farley, J., Ford, L., Garcia Losa, M., Gonzalez Ortiz, M., Haghighi, M., Hala, M., Iwama, T., Jajic, Z., Kerr, D., Kim, H. S., Kohne, C., Koo, B. K., Martin, B., Meinert, C., Muller, N., Myklebust, G., Neustadt, D., Omdal, R., Ozgocmen, S., Papas, A., Patrignani, P., Pelliccia, Francesco, Roy, V., Schlegelmilch, I., Umar, A., Wahlstrom, O., Wollheim, F., Yocum, S., Zhang, X. Y., Hall, E., Mcgettigan, P., Midgley, R., Moore, R. A., Philipson, R., Curtis, S., Reicin, A., Bond, J., Moore, A., Essex, M., Fabule, J., Morrison, B., Tive, L., Davies, K., and Yau, F.

Subjects
medicine.medical_specialty, Gastrointestinal Diseases, Perforation (oil well), coronary disease, Placebo, anti-inflammatory agents, non-steroidal, blood vessels, Diclofenac, vascular, Internal medicine, medicine, naproxen, Humans, Myocardial infarction, Vascular Diseases, medicine (all), Stroke, ibuprofen, anti-inflammatory, business.industry, Vascular disease, Anti-Inflammatory Agents, Non-Steroidal, General Medicine, Articles, Ibuprofen, medicine.disease, stroke, gastrointestinal, diclofenac, myocardial infarction, cyclooxygenase 2 inhibitors, Heart failure, Anesthesia, Settore MED/11 - MALATTIE DELL'APPARATO CARDIOVASCOLARE, gastrointestinal tract, business, anti-inflammatory agents, non-steroidal, gastrointestinal diseases, humans, vascular diseases, medicine.drug
Abstract

BACKGROUND: The vascular and gastrointestinal effects of non-steroidal anti-inflammatory drugs (NSAIDs), including selective COX-2 inhibitors (coxibs) and traditional non-steroidal anti-inflammatory drugs (tNSAIDs), are not well characterised, particularly in patients at increased risk of vascular disease. We aimed to provide such information through meta-analyses of randomised trials. METHODS: We undertook meta-analyses of 280 trials of NSAIDs versus placebo (124,513 participants, 68,342 person-years) and 474 trials of one NSAID versus another NSAID (229,296 participants, 165,456 person-years). The main outcomes were major vascular events (non-fatal myocardial infarction, non-fatal stroke, or vascular death); major coronary events (non-fatal myocardial infarction or coronary death); stroke; mortality; heart failure; and upper gastrointestinal complications (perforation, obstruction, or bleed). FINDINGS: Major vascular events were increased by about a third by a coxib (rate ratio [RR] 1·37, 95% CI 1·14-1·66; p=0·0009) or diclofenac (1·41, 1·12-1·78; p=0·0036), chiefly due to an increase in major coronary events (coxibs 1·76, 1·31-2·37; p=0·0001; diclofenac 1·70, 1·19-2·41; p=0·0032). Ibuprofen also significantly increased major coronary events (2·22, 1·10-4·48; p=0·0253), but not major vascular events (1·44, 0·89-2·33). Compared with placebo, of 1000 patients allocated to a coxib or diclofenac for a year, three more had major vascular events, one of which was fatal. Naproxen did not significantly increase major vascular events (0·93, 0·69-1·27). Vascular death was increased significantly by coxibs (1·58, 99% CI 1·00-2·49; p=0·0103) and diclofenac (1·65, 0·95-2·85, p=0·0187), non-significantly by ibuprofen (1·90, 0·56-6·41; p=0·17), but not by naproxen (1·08, 0·48-2·47, p=0·80). The proportional effects on major vascular events were independent of baseline characteristics, including vascular risk. Heart failure risk was roughly doubled by all NSAIDs. All NSAID regimens increased upper gastrointestinal complications (coxibs 1·81, 1·17-2·81, p=0·0070; diclofenac 1·89, 1·16-3·09, p=0·0106; ibuprofen 3·97, 2·22-7·10, p

Published
2013
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20. Le Grand Pari(s) Le projet d'une ville poreuse

Author

Équipe, Studio, Secchi, Bernardo, Vigano', Paola, Fabian, Lorenzo, Giannotti, Emanuel, Pellegrini, Paola, Calò, A, Chang, D. M., Cos, T, Fonty, N, and Pagnacco, A.

Subjects
grand paris
Published
2010

22. Preferential Binding to Elk-1 by SLE-Associated IL10 Risk Allele Upregulates IL10 Expression

Author

Sakurai, D., Zhao, J., Deng, Y., Kelly, J. A., Brown, E. E., Harley, J. B., Bae, S. C., Alarcón-Riquelme, M. E., Edberg, J. C., Kimberly, R. P., Ramsey-Goldman, R., Caeiro, F., Soriano, E. R., Bertoli, A., Prigione, C., Ramos, F. A., Romero, E. J., Tsao, B. P., Chen, W., Truedsson, L., Yu, C. Y., Migliarese, S., García, M. A., Marcos, J. C., Eimon, A., Sánchez-Román, J., Battagliotti, C. G., Kaufman, K. M., Vyse, T. J., Jacob, C. O., Gaffney, P. M., Sebastiani, G. D., Ramón, Enrique de, Hahn, B. H., Song, Y. W., Grossman, J. M., Sivils, K. M., James, J. A., Kamen, D. L., Gilkeson, G. S., Niewold, T. B., D'Alfonso, Sandra, Merrill, J. T., Martín, J., Scofield, R. H., Chang, D. M., Criswell, L. A., Langefeld, C. D., Stevens, A. M., Cantor, R. M., Frostegård, Johan, Boackle, S. A., Kim, J. H., Choi, J., Pons-Estel, B. A., Freedman, Barry I., Sabio, José Mario, Anaya, J. M., Ortego-Centeno, N., Callejas-Rubio, J. L., González-Escribano, María Francisca, Buchanan, G., Graf, C. E., Paira, S., Galeazzi, M., Witte, Torsten, Lauwerys, B. R., Endreffy, E., Kovács, L., Vasconcelos, C., Silva, B. M. da, Scherbarth, H. R., Catoggio, L. J., Manni, J., Caprarulo, C., Guillerón, C., Marino, P. C., Motta, E. L., Gamron, S., Drenkard, C., Menso, E., Allievi, A., Roverano, S., Tate, G. A., Bertero, E., Presas, J. L., Navarro, S. M., Parque, S., Grimaudo, S., Palatnik, S. A., Abdala, M., Acevedo, E., Bearzotti, M., Santos, C. D., Alvarellos, A., Berbotto, G. A., Jorfen, M., Marcos, A. I., Perandones, C. E., Cucho, M., Torre, I. G. de la, Ríos, M. C., Moctezuma, J. F., Ceceña, M. M., Petri, M. A., Vilá, Luis M., Reveille, J. D., Alarcón, G. S., Sakurai, D., Zhao, J., Deng, Y., Kelly, J. A., Brown, E. E., Harley, J. B., Bae, S. C., Alarcón-Riquelme, M. E., Edberg, J. C., Kimberly, R. P., Ramsey-Goldman, R., Caeiro, F., Soriano, E. R., Bertoli, A., Prigione, C., Ramos, F. A., Romero, E. J., Tsao, B. P., Chen, W., Truedsson, L., Yu, C. Y., Migliarese, S., García, M. A., Marcos, J. C., Eimon, A., Sánchez-Román, J., Battagliotti, C. G., Kaufman, K. M., Vyse, T. J., Jacob, C. O., Gaffney, P. M., Sebastiani, G. D., Ramón, Enrique de, Hahn, B. H., Song, Y. W., Grossman, J. M., Sivils, K. M., James, J. A., Kamen, D. L., Gilkeson, G. S., Niewold, T. B., D'Alfonso, Sandra, Merrill, J. T., Martín, J., Scofield, R. H., Chang, D. M., Criswell, L. A., Langefeld, C. D., Stevens, A. M., Cantor, R. M., Frostegård, Johan, Boackle, S. A., Kim, J. H., Choi, J., Pons-Estel, B. A., Freedman, Barry I., Sabio, José Mario, Anaya, J. M., Ortego-Centeno, N., Callejas-Rubio, J. L., González-Escribano, María Francisca, Buchanan, G., Graf, C. E., Paira, S., Galeazzi, M., Witte, Torsten, Lauwerys, B. R., Endreffy, E., Kovács, L., Vasconcelos, C., Silva, B. M. da, Scherbarth, H. R., Catoggio, L. J., Manni, J., Caprarulo, C., Guillerón, C., Marino, P. C., Motta, E. L., Gamron, S., Drenkard, C., Menso, E., Allievi, A., Roverano, S., Tate, G. A., Bertero, E., Presas, J. L., Navarro, S. M., Parque, S., Grimaudo, S., Palatnik, S. A., Abdala, M., Acevedo, E., Bearzotti, M., Santos, C. D., Alvarellos, A., Berbotto, G. A., Jorfen, M., Marcos, A. I., Perandones, C. E., Cucho, M., Torre, I. G. de la, Ríos, M. C., Moctezuma, J. F., Ceceña, M. M., Petri, M. A., Vilá, Luis M., Reveille, J. D., and Alarcón, G. S.

Abstract

Immunoregulatory cytokine interleukin-10 (IL-10) is elevated in sera from patients with systemic lupus erythematosus (SLE) correlating with disease activity. The established association of IL10 with SLE and other autoimmune diseases led us to fine map causal variant(s) and to explore underlying mechanisms. We assessed 19 tag SNPs, covering the IL10 gene cluster including IL19, IL20 and IL24, for association with SLE in 15,533 case and control subjects from four ancestries. The previously reported IL10 variant, rs3024505 located at 1 kb downstream of IL10, exhibited the strongest association signal and was confirmed for association with SLE in European American (EA) (P = 2.7×10-8, OR = 1.30), but not in non-EA ancestries. SNP imputation conducted in EA dataset identified three additional SLE-associated SNPs tagged by rs3024505 (rs3122605, rs3024493 and rs3024495 located at 9.2 kb upstream, intron 3 and 4 of IL10, respectively), and SLE-risk alleles of these SNPs were dose-dependently associated with elevated levels of IL10 mRNA in PBMCs and circulating IL-10 protein in SLE patients and controls. Using nuclear extracts of peripheral blood cells from SLE patients for electrophoretic mobility shift assays, we identified specific binding of transcription factor Elk-1 to oligodeoxynucleotides containing the risk (G) allele of rs3122605, suggesting rs3122605 as the most likely causal variant regulating IL10 expression. Elk-1 is known to be activated by phosphorylation and nuclear localization to induce transcription. Of interest, phosphorylated Elk-1 (p-Elk-1) detected only in nuclear extracts of SLE PBMCs appeared to increase with disease activity. Co-expression levels of p-Elk-1 and IL-10 were elevated in SLE T, B cells and monocytes, associated with increased disease activity in SLE B cells, and were best downregulated by ERK inhibitor. Taken together, our data suggest that preferential binding of activated Elk-1 to the IL10 rs3122605-G allele upregulates IL10 expressio

Published
2013

23. Identification of a systemic lupus erythematosus susceptibility locus at 11p13 between PDHX and CD44 in a multiethnic study

Author

Lessard, C. J., Adrianto, I., Kelly, J. A., Kaufman, K. M., Grundahl, K. M., Adler, A. J., Williams, A. H., Gallant, C., Anaya, J. M., Bae, S. C., Boackle, S. A., Brown, E. E., Chang, D. M., Criswell, L. A., Edberg, J. C., Freedman, Barry I., Gregersen, Peter K., Gilkeson, G. S., Jacob, C. O., James, J. A., Kamen, D. L., Kimberly, R. P., Martín, J., Merrill, J. T., Niewold, T. B., Park, Su-Yeon, Petri, M., Pons-Estel, B. A., Ramsey-Goldman, R., Reveille, J. D., Song, Y. W., Stevens, A. M., Tsao, B. P., Vilá, Luis M., Vyse, T. J., Yu, C. Y., Guthridge, J. M., Bruner, G. R., Langefeld, C. D., Montgomery, C. G., Harley, J. B., Scofield, R. H., Gaffney, P. M., Moser, K. L., Lessard, C. J., Adrianto, I., Kelly, J. A., Kaufman, K. M., Grundahl, K. M., Adler, A. J., Williams, A. H., Gallant, C., Anaya, J. M., Bae, S. C., Boackle, S. A., Brown, E. E., Chang, D. M., Criswell, L. A., Edberg, J. C., Freedman, Barry I., Gregersen, Peter K., Gilkeson, G. S., Jacob, C. O., James, J. A., Kamen, D. L., Kimberly, R. P., Martín, J., Merrill, J. T., Niewold, T. B., Park, Su-Yeon, Petri, M., Pons-Estel, B. A., Ramsey-Goldman, R., Reveille, J. D., Song, Y. W., Stevens, A. M., Tsao, B. P., Vilá, Luis M., Vyse, T. J., Yu, C. Y., Guthridge, J. M., Bruner, G. R., Langefeld, C. D., Montgomery, C. G., Harley, J. B., Scofield, R. H., Gaffney, P. M., and Moser, K. L.

Abstract

Systemic lupus erythematosus (SLE) is considered to be the prototypic autoimmune disease, with a complex genetic architecture influenced by environmental factors. We sought to replicate a putative association at 11p13 not yet exceeding genome-wide significance (p < 5 × 10-8) identified in a genome-wide association study (GWAS). Our GWA scan identified two intergenic SNPs located between PDHX and CD44 showing suggestive evidence of association with SLE in cases of European descent (rs2732552, p = 0.004, odds ratio [OR] = 0.78; rs387619, p = 0.003, OR = 0.78). The replication cohort consisted of >15,000 subjects, including 3562 SLE cases and 3491 controls of European ancestry, 1527 cases and 1811 controls of African American (AA) descent, and 1265 cases and 1260 controls of Asian origin. We observed robust association at both rs2732552 (p = 9.03 × 10-8, OR = 0.83) and rs387619 (p = 7.7 × 10-7, OR = 0.83) in the European samples with pmeta = 1.82 × 10-9 for rs2732552. The AA and Asian SLE cases also demonstrated association at rs2732552 (p = 5 × 10-3, OR = 0.81 and p = 4.3 × 10-4, OR = 0.80, respectively). A meta-analysis of rs2732552 for all racial and ethnic groups studied produced pmeta = 2.36 × 10-13. This locus contains multiple regulatory sites that could potentially affect expression and functions of CD44, a cell-surface glycoprotein influencing immunologic, inflammatory, and oncologic phenotypes, or PDHX, a subunit of the pyruvate dehydrogenase complex. © 2011 The American Society of Human Genetics.

Published
2011

45. Aspirin differentially regulates endotoxin-induced IL-12 and TNF-alpha production in human dendritic cells.

Author

Ho, Ling-Jun, Chang, Deh-Ming, Shiau, Hen-Yih, Chen, Chen-Hung, Hsieh, Tsai-Yuan, Hsu, Yu-Lin, Wong, Chih-Shung, Lai, Jenn-Haung, Ho, L J, Chang, D M, Shiau, H Y, Chen, C H, Hsieh, T Y, Hsu, Y L, Wong, C S, and Lai, J H

Subjects
ASPIRIN, DENDRITIC cells, PHYSIOLOGY, BIOCHEMISTRY, CELL culture, COMPARATIVE studies, DOCUMENTATION, DOSE-effect relationship in pharmacology, INTERLEUKINS, PHENOMENOLOGY, RESEARCH methodology, MEDICAL cooperation, NUCLEOTIDES, POLYMERASE chain reaction, REFERENCE values, RESEARCH, TUMOR necrosis factors, EVALUATION research, REVERSE transcriptase polymerase chain reaction, LIPOPOLYSACCHARIDES, PHARMACODYNAMICS
Abstract

Objective: In the development of autoimmune diseases, dendritic cells (DC) play critical roles. Here, we examined the effect of aspirin on lipopolysaccharide (LPS)-induced DC activation.Methods: The monocyte-derived DC were established. The cytokine production was measured by ELISA, reverse transcriptase/polymerase chain reaction, or intracellular staining analyzed by flow cytometry. The expression of cell surface molecules was determined by flow cytometry.Results: Aspirin inhibited LPS-induced DC maturation and costimulatory molecules expression. Aspirin, at therapeutic concentrations, also decreased LPS-induced IL-12 and IL-10 production. In contrast, the LPS-induced TNF-alpha production was enhanced by aspirin. The differential effects of aspirin on IL-12 and TNF-alpha production may not be due to down-regulation of cyclooxygenase activities.Conclusion: The various effects of aspirin on LPS-stimulated DC may influence the understanding of the diverse immunomodulatory mechanisms of this anti-inflammatory drug. [ABSTRACT FROM AUTHOR]

Published
2001
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