Zobrazeno 1 - 6
of 6
pro vyhledávání: '"Sapna Chadha"'
Autor:
CA Roberton, Sapna Chadha, D S Cunninghame Graham, David D'Cruz, Dorothea Nitsch, B Griffiths, Timothy J. Vyse, Andrew Russell, Tim J. Fernandez-Hart, John C. Whittaker
Publikováno v:
Genes & Immunity. 6:422-429
Altered function of selectin glycoprotein adhesion molecules may modulate severity and organ-specific manifestations of autoimmune and inflammatory disease via changes in leukocyte trafficking. Serum concentrations of selectin molecules have been sug
Autor:
Lisa Farwell, Timothy J. Vyse, John D. Rioux, Sapna Chadha, Liz Lightstone, Mark J. Daly, Katie Miller
Publikováno v:
European Journal of Human Genetics. 13:669-676
Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease that is caused by genetic and environmental factors. The tumour necrosis factor (TNF) superfamily of genes play a central role in immune regulation and have been proposed to be inv
Autor:
Duncan R. Hewett, Fredrik Enlund, Phil Robinson, Kathryn L. Cantone, Colin W. Dykes, Lena Samuelsson, Chee Gee See, Doug S. Montgomery, John H. Riley, Gunnar Swanbeck, Purvis Ij, Chris Christodolou, Sapna Chadha, Jan Wahlström, Paul M. Matthews, Joanne Polding, Tommy Martinsson, Charlotta Enerbäck, Devi Smart, Allen D. Roses, Annica Inerot, Mary Plumpton
Publikováno v:
Genomics. 79:305-314
Psoriasis is a chronic inflammatory disease of the skin with both genetic and environmental risk factors. Here we describe the creation of a single-nucleotide polymorphism (SNP) map spanning 900-1200 kb of chromosome 3q21, which had been previously r
Autor:
Peter Charles, Saowalak Hunnangkul, Michelle M. A. Fernando, Timothy J. Vyse, Pedro Pessôa-Lopes, Peter J. Norsworthy, Benjamin Rhodes, Cheri A. Roberton, Charles Mackworth-Young, John C. Whittaker, David A. Isenberg, Dorothea Nitsch, Sapna Chadha
Publikováno v:
Arthritis and rheumatism. 58(4)
Objective To determine whether key features of systemic lupus erythematosus (SLE), namely, production of non-nuclear antibodies (anti-C1q and anticardiolipin antibodies [aCL]) and depletion of complement components C3 and C4, aggregate in families. I
Autor:
John D. Rioux, Timothy J. Vyse, Sapna Chadha, Lisa Farwell, Katie Miller, Steven H. Sacks, Mark J. Daly
Publikováno v:
European journal of human genetics : EJHG. 14(1)
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with partially understood aetiology. The 1p36 region has been previously linked with SLE and harbours tumour necrosis factor receptor (TNFR) genes. Functional and genetic data implic
Publikováno v:
Arthritis Research
The aetiology of systemic lupus erythematosus (SLE) is unknown. However, there is good evidence to support a genetic contribution in lupus, including a number of mouse strains that are genetically predisposed to develop lupus. Several groups have pub