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1. Pericytes contribute to pulmonary vascular remodeling via HIF2α signaling

Author

Kim, Hyunbum, Liu, Yu, Kim, Jiwon, Kim, Yunhye, Klouda, Timothy, Fisch, Sudeshna, Baek, Seung Han, Liu, Tiffany, Dahlberg, Suzanne, Hu, Cheng-Jun, Tian, Wen, Jiang, Xinguo, Kosmas, Kosmas, Christou, Helen A, Korman, Benjamin D, Vargas, Sara O, Wu, Joseph C, Stenmark, Kurt R, Perez, Vinicio de Jesus, Nicolls, Mark R, Raby, Benjamin A, and Yuan, Ke

Published
2024
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4. HLA and autoantibodies define scleroderma subtypes and risk in African and European Americans and suggest a role for molecular mimicry

Author

Gourh, Pravitt, Safran, Sarah A, Alexander, Theresa, Boyden, Steven E, Morgan, Nadia D, Shah, Ami A, Mayes, Maureen D, Doumatey, Ayo, Bentley, Amy R, Shriner, Daniel, Domsic, Robyn T, Medsger, Thomas A, Ramos, Paula S, Silver, Richard M, Steen, Virginia D, Varga, John, Hsu, Vivien, Saketkoo, Lesley Ann, Schiopu, Elena, Khanna, Dinesh, Gordon, Jessica K, Kron, Brynn, Criswell, Lindsey A, Gladue, Heather, Derk, Chris T, Bernstein, Elana J, Bridges, S Louis, Shanmugam, Victoria K, Kolstad, Kathleen D, Chung, Lorinda, Kafaja, Suzanne, Jan, Reem, Trojanowski, Marcin, Goldberg, Avram, Korman, Benjamin D, Steinbach, Peter J, Chandrasekharappa, Settara C, Mullikin, James C, Adeyemo, Adebowale, Rotimi, Charles, Wigley, Fredrick M, Kastner, Daniel L, Boin, Francesco, and Remmers, Elaine F

Subjects
Biomedical and Clinical Sciences, Immunology, Autoimmune Disease, Clinical Research, Scleroderma, Genetics, 2.1 Biological and endogenous factors, Aetiology, Inflammatory and immune system, Black or African American, Alleles, Amino Acid Sequence, Antigens, Viral, Autoantibodies, Autoantigens, Computational Biology, Datasets as Topic, Female, Genetic Predisposition to Disease, HLA Antigens, Humans, Male, Mimiviridae, Molecular Mimicry, Phycodnaviridae, Protein Structure, Secondary, Risk Assessment, Scleroderma, Systemic, Sequence Homology, Amino Acid, White People, scleroderma, HLA, autoantibodies, molecular mimicry, mimivirus
Abstract

Systemic sclerosis (SSc) is a clinically heterogeneous autoimmune disease characterized by mutually exclusive autoantibodies directed against distinct nuclear antigens. We examined HLA associations in SSc and its autoantibody subsets in a large, newly recruited African American (AA) cohort and among European Americans (EA). In the AA population, the African ancestry-predominant HLA-DRB1*08:04 and HLA-DRB1*11:02 alleles were associated with overall SSc risk, and the HLA-DRB1*08:04 allele was strongly associated with the severe antifibrillarin (AFA) antibody subset of SSc (odds ratio = 7.4). These African ancestry-predominant alleles may help explain the increased frequency and severity of SSc among the AA population. In the EA population, the HLA-DPB1*13:01 and HLA-DRB1*07:01 alleles were more strongly associated with antitopoisomerase (ATA) and anticentromere antibody-positive subsets of SSc, respectively, than with overall SSc risk, emphasizing the importance of HLA in defining autoantibody subtypes. The association of the HLA-DPB1*13:01 allele with the ATA+ subset of SSc in both AA and EA patients demonstrated a transancestry effect. A direct correlation between SSc prevalence and HLA-DPB1*13:01 allele frequency in multiple populations was observed (r = 0.98, P = 3 × 10-6). Conditional analysis in the autoantibody subsets of SSc revealed several associated amino acid residues, mostly in the peptide-binding groove of the class II HLA molecules. Using HLA α/β allelic heterodimers, we bioinformatically predicted immunodominant peptides of topoisomerase 1, fibrillarin, and centromere protein A and discovered that they are homologous to viral protein sequences from the Mimiviridae and Phycodnaviridae families. Taken together, these data suggest a possible link between HLA alleles, autoantibodies, and environmental triggers in the pathogenesis of SSc.

Published
2020

7. Multi-omics analysis identifies IgG2b class-switching with ALCAM-CD6 co-stimulation in joint-draining lymph nodes during advanced inflammatory-erosive arthritis

Author

Kenney, H. Mark, primary, Rangel-Moreno, Javier, additional, Peng, Yue, additional, Chen, Kiana L., additional, Bruno, Jennifer, additional, Embong, Abdul, additional, Pritchett, Elizabeth, additional, Fox, Jeffrey I., additional, Becerril-Villanueva, Enrique, additional, Gamboa-Domínguez, Armando, additional, Quataert, Sally, additional, Muthukrishnan, Gowrishankar, additional, Wood, Ronald W., additional, Korman, Benjamin D., additional, Anolik, Jennifer H., additional, Xing, Lianping, additional, Ritchlin, Christopher T., additional, Schwarz, Edward M., additional, and Wu, Chia-Lung, additional

Published
2023
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9. Additional file 1 of Implementation of automated behavior metrics to evaluate voluntary wheel running effects on inflammatory-erosive arthritis and interstitial lung disease in TNF-Tg mice

Author

Kenney, H. Mark, Wood, Ronald W., Ramirez, Gabriel, Bell, Richard D., Chen, Kiana L., Schnur, Lindsay, Rahimi, Homaira, Korman, Benjamin D., Xing, Lianping, Ritchlin, Christopher T., Schwarz, Edward M., and Cole, Calvin L.

Abstract

Additional file 1: Supplementary Figure 1. Depiction of lung micro-CT, segmentation, and histology in male mice. Representative cross-sectional image of lung micro-CT datasets (A.a-D.a) and associated segmentations of aerated (yellow) and tissue (blue) lung regions (A.b-D.b) are provided for each group of male mice. Representative H&E-stained lung images from TNF-Tg male sedentary versus running mice are shown, where little change in morphology was appreciated in the tissue as a whole or adjacent to the arterioles (black arrows) (E.a-F.b). Black scale bar = 500μm (E,F.a), yellow scale bar = 50μm (E,F.b). Supplementary Table 1. Sample sizes for running data. A table is provided with the sample sizes (number of animals) for each group and timepoint. For each group (WT male/female, TNF-Tg male/female), the sample sizes are shown at the following time points (days, outcomes in 10-day median blocks): 65 / 75 / 85 / 95 / 105 / 115 / 125 / 135. Reductions in sample size indicate mortality during the study period. Supplementary Table 2. Sample sizes for micro-CT outcome measures. A table is provided with the sample sizes for each group and timepoint. The groups include sedentary and running cohorts of WT male/female and TNF-Tg male/female mice. The joint micro-CT outcomes were measured as a change from a 2-month baseline. For the lung and ankle micro-CT, the males show 5 or 5.5-month measurements, while the females exhibit 3 / 4 / 5 or 5.5-month outcomes. The knee micro-CT represents outcomes at 5-month measures for both males and females. Changes in sample size across timepoints either represent exclusion of datasets due to motion artifact or animal mortality during the study period. aFinal timepoint represents 5.5-months of age and experiment unit is number of mice, bfinal timepoint represents 5-months of age and experimental unit is number of limbs, *sedentary measurements are derived from historical data in our previous publication [23].

Published
2023
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11. Multi-omics Analysis Identifies IgG2b Class-Switching with ALCAM-CD6 Co-Stimulation in Lymph Nodes During Advanced Inflammatory-Erosive Arthritis

Author

Kenney, H. Mark, primary, Rangel-Moreno, Javier, additional, Peng, Yue, additional, Chen, Kiana L., additional, Bruno, Jennifer, additional, Embong, Abdul, additional, Pritchett, Elizabeth, additional, Fox, Jeffrey I., additional, Quataert, Sally, additional, Muthukrishnan, Gowrishankar, additional, Wood, Ronald W., additional, Korman, Benjamin D., additional, Anolik, Jennifer H., additional, Xing, Lianping, additional, Ritchlin, Christopher T., additional, Schwarz, Edward M., additional, and Wu, Chia-Lung, additional

Published
2022
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16. Alterations of the Primary Cilia Gene SPAG17 and SOX9 Locus Noncoding RNAs Identified by RNA‐Sequencing Analysis in Patients With Systemic Sclerosis.

Author

Roberson, Elisha D. O., Carns, Mary, Cao, Li, Aren, Kathleen, Goldberg, Isaac A., Morales‐Heil, David J., Korman, Benjamin D., Atkinson, John P., and Varga, John

Subjects
RNA analysis, SEQUENCE analysis, BIOPSY, MONONUCLEAR leukocytes, COMPLEMENT (Immunology), B cells, SKIN, SYSTEMIC scleroderma, GENE expression, SEVERITY of illness index, VITAL capacity (Respiration), INTERFERONS, CELLULAR signal transduction, SKIN physiology, GENES, GENE expression profiling, EXTRACELLULAR space, PULMONARY gas exchange, SYMPTOMS
Abstract

Objective: Systemic sclerosis (SSc) is characterized by immune activation, vasculopathy, and unresolving fibrosis in the skin, lungs, and other organs. We performed RNA‐sequencing analysis on skin biopsy samples and peripheral blood mononuclear cells (PBMCs) from SSc patients and unaffected controls to better understand the pathogenesis of SSc. Methods: We analyzed these data 1) to test for case/control differences and 2) to identify genes whose expression levels correlate with SSc severity as measured by local skin score, modified Rodnan skin thickness score (MRSS), forced vital capacity (FVC), or diffusing capacity for carbon monoxide (DLco). Results: We found that PBMCs from SSc patients showed a strong type I interferon signature. This signal was found to be replicated in the skin, with additional signals for increased extracellular matrix (ECM) genes, classical complement pathway activation, and the presence of B cells. Notably, we observed a marked decrease in the expression of SPAG17, a cilia component, in SSc skin. We identified genes that correlated with the MRSS, DLco, and FVC in SSc PBMCs and skin using weighted gene coexpression network analysis. These genes were largely distinct from the case/control differentially expressed genes. In PBMCs, type I interferon signatures negatively correlated with the DLco. In SSc skin, ECM gene expression positively correlated with the MRSS. Network analysis of SSc skin genes that correlated with clinical features identified the noncoding RNAs SOX9‐AS1 and ROCR, both near the SOX9 locus, as highly connected, "hub‐like" genes in the network. Conclusion: These results identify noncoding RNAs and SPAG17 as novel factors potentially implicated in the pathogenesis of SSc. [ABSTRACT FROM AUTHOR]

Published
2023
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19. Engineering Advanced In Vitro Models of Systemic Sclerosis for Drug Discovery and Development

Author

De Pieri, Andrea; https://orcid.org/0000-0002-5469-7101, Korman, Benjamin D, Jüngel, Astrid, Wuertz-Kozak, Karin, De Pieri, Andrea; https://orcid.org/0000-0002-5469-7101, Korman, Benjamin D, Jüngel, Astrid, and Wuertz-Kozak, Karin

Abstract

Systemic sclerosis (SSc) is a complex multisystem disease with the highest case-specific mortality among all autoimmune rheumatic diseases, yet without any available curative therapy. Therefore, the development of novel therapeutic antifibrotic strategies that effectively decrease skin and organ fibrosis is needed. Existing animal models are cost-intensive, laborious and do not recapitulate the full spectrum of the disease and thus commonly fail to predict human efficacy. Advanced in vitro models, which closely mimic critical aspects of the pathology, have emerged as valuable platforms to investigate novel pharmaceutical therapies for the treatment of SSc. This review focuses on recent advancements in the development of SSc in vitro models, sheds light onto biological (e.g., growth factors, cytokines, coculture systems), biochemical (e.g., hypoxia, reactive oxygen species) and biophysical (e.g., stiffness, topography, dimensionality) cues that have been utilized for the in vitro recapitulation of the SSc microenvironment, and highlights future perspectives for effective drug discovery and validation.

Published
2021

21. An autoinflammatory disease with deficiency of the interleukin-1-receptor antagonist

Author

Aksentijevich, Ivona, Masters, Seth L., Ferguson, Polly J., Dancey, Paul, Frenkel, Joost, van Royen-Kerkhoff, Annet, Laxer, Ron, Tedgard, Ulf, Cowen, Edward W., Tuyet-Hang Pham, Booty, Matthew, Estes, Jacob D., Sandler, Netanya G., Plass, Nicole, Stone, Deborah L., Turner, Maria L., Hill, Suvimol, Butman, John A., Schneider, Rayfel, Babyn, Paul, El-Shanti, Hatem I., Pope, Elena, Barron, Karyl, Xinyu Bing, Laurence, Arian, Chyi-Chia R. Lee, Chapelle, Dawn, Clarke, Gillian I., Ohson, Kamal, Nicholson, Mark, Gadina, Massimo, Yang, Barbara, Korman, Benjamin D., Gregersen, Peter K., van Hegen, P. Martin, Hak, A. Elisabeth, Huizing, Marjan, Rahman, Proton, Douek, Daniel C., Remmers, Elaine F., Kastner, Daniel L., and Goldbach-Mansky, Raphaela

Subjects
Autoimmune diseases -- Causes of, Autoimmune diseases -- Drug therapy, Gene mutations -- Research, Interleukin-1 -- Health aspects, Interleukin-1 -- Usage
Abstract

An autoinflammatory disease involving skin and bone, which is caused by mutations in IL1RN, the gene encoding the interleukin-1-receptor antagonist, is reported. The term deficiency of the interleukin-1-receptor antagonist or DIRA is used to denote the life-threatening systemic disease.

Published
2009

23. Pathological pulmonary vascular remodeling is induced by type V collagen in a model of scleroderma

Author

Marangoni, Roberta Goncalves, primary, Korman, Benjamin D., additional, Parra, Edwin R., additional, Velosa, Ana Paula P., additional, Barbeiro, Hermes V., additional, Martins, Vanessa, additional, dos Santos, Angela B.G., additional, Soriano, Francisco, additional, Teodoro, Walcy R., additional, Silva, Pedro Leme, additional, Tourtellotte, Warren, additional, Capelozzi, Vera L., additional, Varga, John, additional, and Yoshinari, Natalino H., additional

Published
2021
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25. Tumor Necrosis Factor Induces Obliterative Pulmonary Vascular Disease in a Novel Model of Connective Tissue Disease–Associated Pulmonary Arterial Hypertension

Author

Bell, Richard D., primary, White, R. James, additional, Garcia‐Hernandez, Maria L., additional, Wu, Emily, additional, Rahimi, Homaira, additional, Marangoni, Roberta G., additional, Slattery, Pamelia, additional, Duemmel, Stacey, additional, Nuzzo, Marc, additional, Huertas, Nelson, additional, Yee, Min, additional, O'Reilly, Michael A., additional, Morrell, Craig, additional, Ritchlin, Christopher T., additional, Schwarz, Edward M., additional, and Korman, Benjamin D., additional

Published
2020
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26. HLAand autoantibodies define scleroderma subtypes and risk in African and European Americans and suggest a role for molecular mimicry

Author

Gourh, Pravitt, primary, Safran, Sarah A., additional, Alexander, Theresa, additional, Boyden, Steven E., additional, Morgan, Nadia D., additional, Shah, Ami A., additional, Mayes, Maureen D., additional, Doumatey, Ayo, additional, Bentley, Amy R., additional, Shriner, Daniel, additional, Domsic, Robyn T., additional, Medsger, Thomas A., additional, Ramos, Paula S., additional, Silver, Richard M., additional, Steen, Virginia D., additional, Varga, John, additional, Hsu, Vivien, additional, Saketkoo, Lesley Ann, additional, Schiopu, Elena, additional, Khanna, Dinesh, additional, Gordon, Jessica K., additional, Kron, Brynn, additional, Criswell, Lindsey A., additional, Gladue, Heather, additional, Derk, Chris T., additional, Bernstein, Elana J., additional, Bridges, S. Louis, additional, Shanmugam, Victoria K., additional, Kolstad, Kathleen D., additional, Chung, Lorinda, additional, Kafaja, Suzanne, additional, Jan, Reem, additional, Trojanowski, Marcin, additional, Goldberg, Avram, additional, Korman, Benjamin D., additional, Steinbach, Peter J., additional, Chandrasekharappa, Settara C., additional, Mullikin, James C., additional, Adeyemo, Adebowale, additional, Rotimi, Charles, additional, Wigley, Fredrick M., additional, Kastner, Daniel L., additional, Boin, Francesco, additional, and Remmers, Elaine F., additional

Published
2019
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31. A candidate gene study reveals association between a variant of the Peroxisome Proliferator-Activated Receptor Gamma (PPAR-γ) gene and systemic sclerosis

Author

Marangoni, Roberta Goncalves, primary, Korman, Benjamin D, additional, Allanore, Yannick, additional, Dieude, Philippe, additional, Armstrong, Loren L, additional, Rzhetskaya, Margarita, additional, Hinchcliff, Monique, additional, Carns, Mary, additional, Podlusky, Sofia, additional, Shah, Sanjiv J, additional, Ruiz, Barbara, additional, Hachulla, Eric, additional, Tiev, Kiet, additional, Cracowski, Jean-Luc, additional, Varga, John, additional, and Hayes, M Geoffrey, additional

Published
2015
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32. Chromosome 7q Region Associated with Female Rheumatoid Arthritis in a British Population Fails to Replicate in a North American Case-Control Series

Author

Korman, Benjamin D, Seldin, Michael F, Taylor, Kimberly E, Le, Julie M, Lee, Annette T, Plenge, Robert M, Amos, Christopher I, Criswell, Lindsey A, Gregersen, Peter K, Kastner, Daniel L, and Remmers, Elaine F

Subjects
Adult, Male, Sex Characteristics, Genotype, Middle Aged, Polymorphism, Single Nucleotide, Article, Linkage Disequilibrium, United Kingdom, Arthritis, Rheumatoid, Case-Control Studies, North America, Humans, Female, Sex Distribution, Chromosomes, Human, Pair 7
Abstract

The single-nucleotide polymorphism (SNP) rs11761231 on chromosome 7q has been reported to be sexually dimorphic marker for rheumatoid arthritis (RA) susceptibility in a British population. We sought to replicate this finding and to better characterize susceptibility alleles in the region in a North American population.DNA from 2 North American collections of RA patients and controls (1,605 cases and 2,640 controls) was genotyped for rs11761231 and 16 additional chromosome 7q tag SNPs using Sequenom iPlex assays. Association tests were performed for each collection and also separately, contrasting male cases with male controls and female cases with female controls. Principal components analysis (EigenStrat) was used to determine association with RA before and after adjusting for population stratification in the subset of the samples for which there were whole-genome SNP data (772 cases and 1,213 controls).We failed to replicate an association of the 7q region with RA. Initially, rs11761231 showed evidence for association with RA in the North American Rheumatoid Arthritis Consortium (NARAC) collection (P=0.0073), and rs11765576 showed association with RA in both the NARAC (P=0.038) and RA replication (P = 0.0013) collections. These markers also exhibited sex differentiation. However, in the whole-genome subset, neither SNP showed significant association with RA after correction for population stratification.While 2 SNPs on chromosome 7q appeared to be associated with RA in a North American cohort, the significance of this finding did not withstand correction for population substructure. Our results emphasize the need to carefully account for population structure to avoid false-positive disease associations.

Published
2009

33. STAT4: Genetics, Mechanisms, and Implications for Autoimmunity Review for Current Allergy and Asthma Reports

Author

Korman, Benjamin D., Kastner, Daniel L., Gregersen, Peter K., and Remmers, Elaine F.

Subjects
Arthritis, Rheumatoid, Immunity, Active, Animals, Humans, Lupus Erythematosus, Systemic, Autoimmunity, Genetic Predisposition to Disease, Protein Tyrosine Phosphatase, Non-Receptor Type 22, STAT4 Transcription Factor, skin and connective tissue diseases, Polymorphism, Single Nucleotide, Article, Autoimmune Diseases
Abstract

Recent advances in genetics and technology have led to breakthroughs in understanding the genes that predispose individuals to autoimmune diseases. A common haplotype of the signal transducer and activator of transcription 4 (STAT4) gene has been shown to be associated with susceptibility to rheumatoid arthritis, systemic lupus erythematosus, and primary Sjögren's syndrome. STAT4 is a transcription factor that transduces interleukin-12, interleukin-23, and type 1 interferon cytokine signals in T cells and monocytes, leading to T-helper type 1 and T-helper type 17 differentiation, monocyte activation, and interferon-gamma production. Although the evidence for this association is very strong and well replicated, the exact mechanism by which polymorphisms in this gene lead to disease remains unknown. In concert with the identification of other disease-associated loci, elucidating how the variant form of STAT4 modulates immune function should lead to an improved understanding of the pathophysiology of autoimmunity.

Published
2008

34. Inflammatory expression profiles in monocyte-to-macrophage differentiation in patients with systemic lupus erythematosus and relationship with atherosclerosis

Author

Korman, Benjamin D, primary, Huang, Chiang-Ching, additional, Skamra, Carly, additional, Wu, Peggy, additional, Koessler, Renee, additional, Yao, David, additional, Huang, Qi, additional, Pearce, William, additional, Sutton-Tyrrell, Kim, additional, Kondos, George, additional, Edmundowicz, Daniel, additional, Pope, Richard, additional, and Ramsey-Goldman, Rosalind, additional

Published
2014
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35. Genome-wide association study identifies variants in the MHC class I, IL10, and IL23R-IL12RB2 regions associated with Behçet's disease

Author

Remmers, Elaine F, primary, Cosan, Fulya, additional, Kirino, Yohei, additional, Ombrello, Michael J, additional, Abaci, Neslihan, additional, Satorius, Colleen, additional, Le, Julie M, additional, Yang, Barbara, additional, Korman, Benjamin D, additional, Cakiris, Aris, additional, Aglar, Oznur, additional, Emrence, Zeliha, additional, Azakli, Hulya, additional, Ustek, Duran, additional, Tugal-Tutkun, Ilknur, additional, Akman-Demir, Gulsen, additional, Chen, Wei, additional, Amos, Christopher I, additional, Dizon, Michael B, additional, Kose, Afet Akdag, additional, Azizlerli, Gulsevim, additional, Erer, Burak, additional, Brand, Oliver J, additional, Kaklamani, Virginia G, additional, Kaklamanis, Phaedon, additional, Ben-Chetrit, Eldad, additional, Stanford, Miles, additional, Fortune, Farida, additional, Ghabra, Marwen, additional, Ollier, William E R, additional, Cho, Young-Hun, additional, Bang, Dongsik, additional, O'Shea, John, additional, Wallace, Graham R, additional, Gadina, Massimo, additional, Kastner, Daniel L, additional, and Gül, Ahmet, additional

Published
2010
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36. The chromosome 7q region association with rheumatoid arthritis in females in a british population is not replicated in a North American case–control series

Author

Korman, Benjamin D., primary, Seldin, Michael F., additional, Taylor, Kimberly E., additional, Le, Julie M., additional, Lee, Annette T., additional, Plenge, Robert M., additional, Amos, Christopher I., additional, Criswell, Lindsey A., additional, Gregersen, Peter K., additional, Kastner, Daniel L., additional, and Remmers, Elaine F., additional

Published
2008
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37. Common variants at CD40 and other loci confer risk of rheumatoid arthritis

Author

Raychaudhuri, Soumya, primary, Remmers, Elaine F, additional, Lee, Annette T, additional, Hackett, Rachel, additional, Guiducci, Candace, additional, Burtt, Noël P, additional, Gianniny, Lauren, additional, Korman, Benjamin D, additional, Padyukov, Leonid, additional, Kurreeman, Fina A S, additional, Chang, Monica, additional, Catanese, Joseph J, additional, Ding, Bo, additional, Wong, Sandra, additional, van der Helm-van Mil, Annette H M, additional, Neale, Benjamin M, additional, Coblyn, Jonathan, additional, Cui, Jing, additional, Tak, Paul P, additional, Wolbink, Gert Jan, additional, Crusius, J Bart A, additional, Horst-Bruinsma, Irene E van der, additional, Criswell, Lindsey A, additional, Amos, Christopher I, additional, Seldin, Michael F, additional, Kastner, Daniel L, additional, Ardlie, Kristin G, additional, Alfredsson, Lars, additional, Costenbader, Karen H, additional, Altshuler, David, additional, Huizinga, Tom W J, additional, Shadick, Nancy A, additional, Weinblatt, Michael E, additional, de Vries, Niek, additional, Worthington, Jane, additional, Seielstad, Mark, additional, Toes, Rene E M, additional, Karlson, Elizabeth W, additional, Begovich, Ann B, additional, Klareskog, Lars, additional, Gregersen, Peter K, additional, Daly, Mark J, additional, and Plenge, Robert M, additional

Published
2008
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39. Genetic Risk Factors for Rheumatoid Arthritis Differ in Caucasian and Korean Populations.

Author

Hye-Soon Lee, Korman, Benjamin D., Le, Julie M., Kastner, Daniel L., Remmers, Elaine F., Gregersen, Peter K., and Sang-Cheol Bae

Subjects
*RHEUMATOID arthritis, *AUTOIMMUNE diseases, *NUCLEOTIDES, *GENETIC polymorphisms
Abstract

The article discusses the study which determines whether rheumatoid arthritis (RA) is a susceptible loci in Caucasian and Korean populations with the formulation of autoimmune disease-associated gene. Researchers evaluated the disease-associated nucleotide single-nucleotide polymorphism (SNP) to seek novel coding variants to disease in the area. The study found that genetic risk factors for RA are different in Caucasian and Korean patients in different ethnic groups of genetic risk.

Published
2009
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40. Pulmonary Hypertension: How to Best Treat the Different Scleroderma Phenotypes?

Author

Korman BD, Lachant DJ, and Castelino FV

Subjects
Humans, Phenotype, Hypertension, Pulmonary etiology, Hypertension, Pulmonary therapy, Scleroderma, Systemic complications, Scleroderma, Systemic therapy
Abstract

Pulmonary hypertension (PH) is a leading cause of morbidity and mortality in systemic sclerosis (SSc). PH is a heterogenous condition and several different forms of PH are associated with SSc, including pulmonary arterial hypertension (PAH) resulting from a pulmonary arterial vasculopathy, PH due to interstitial lung disease, PH due to left heart disease, and PH due to thromboembolic disease. Extensive research has led to an improved understanding of the mediators involved in the pathogenesis of SSc-PH. Initial combination therapy is the preferred treatment approach for SSc-PAH and requires coordinated care with a multidisciplinary team including rheumatology, pulmonology, and cardiology., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Published
2023
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41. Pathological pulmonary vascular remodeling is induced by type V collagen in a model of scleroderma.

Author

Marangoni RG, Korman BD, Parra ER, Velosa APP, Barbeiro HV, Martins V, Dos Santos ABG, Soriano F, Teodoro WR, Silva PL, Tourtellotte W, Capelozzi VL, Varga J, and Yoshinari NH

Subjects
Adult, Animals, Case-Control Studies, Collagen Type V metabolism, Disease Models, Animal, Female, Hemodynamics, Humans, Middle Aged, Pulmonary Artery immunology, Pulmonary Artery metabolism, Pulmonary Artery physiopathology, Rabbits, Scleroderma, Systemic immunology, Scleroderma, Systemic metabolism, Scleroderma, Systemic physiopathology, Collagen Type V immunology, Lung blood supply, Pulmonary Artery pathology, Scleroderma, Systemic pathology, Vascular Remodeling
Abstract

Objective: The pulmonary vascular remodeling in systemic sclerosis (SSc) is poorly understood and animal models are lacking. Type V collagen (COLV) is elevated in SSc and is implicated in the pathogenesis, and immunization with human COLV induces SSc-like skin and lung changes in rabbits and mice. Here we tested the hypothesis that COLV immunization will induce pathological and functional changes that phenocopy SSc-associated pulmonary vascular disease., Methods: Pulmonary vascular changes in rabbits immunized with human COLV were extensively characterized by a combination of histology, electron microscopy and immunohistochemistry. Physiologic changes induced by COLV in explanted pulmonary artery rings were evaluated. The pattern of histopathologic alterations and gene expression induced in immunized rabbits were compared to those in SSc patients., Results: COLV immunization was accompanied by striking pulmonary vascular abnormalities, characterized by reduced capillary density, perivascular inflammation, endothelial cell injury and collagen accumulation, that closely phenocopy changes seen in SSc patients. Moreover, pulmonary arteries from immunized rabbits showed impaired ex vivo vascular relaxation. Expression of COL5A2 was significantly increased in the lungs from immunized rabbits (p = 0.02), as well as in patients with SSc (P = 0.02)., Conclusion: COLV immunity in rabbits is associated with marked vascular remodeling in the lung that phenocopies early-stage human SSc-associated pulmonary vascular disease. COLV immunization therefore represents a novel approach to model SSc pulmonary vascular pathology. Moreover, our findings suggest that COLV might represent a novel pathogenic autoantigen in SSc and future studies with the present model should be developed for possible association with PAH., (Copyright © 2021 Elsevier GmbH. All rights reserved.)

Published
2021
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