Zobrazeno 1 - 10
of 24
pro vyhledávání: '"C. A. Laskin"'
Publikováno v:
Clinical and Experimental Obstetrics & Gynecology. 45:699-701
Autor:
C A Clark, C A Laskin
Publikováno v:
Lupus. 24:773-773
Publikováno v:
The Journal of rheumatology. 27(12)
To determine the prevalence of anti-beta2-glycoprotein I antibodies (anti-beta2-GPI) in patients with systemic lupus erythematosus (SLE), and to assess their association with and predictive value for the clinical classification criteria of the antiph
Autor:
J D, Douketis, M A, Crowther, J A, Julian, K, Stewart, D, Donovan, E A, Kaminska, C A, Laskin, J S, Ginsberg
Publikováno v:
Thrombosis and haemostasis. 82(3)
The optimal intensity of oral anticoagulant therapy for the prevention of thromboembolism in patients with antiphospholipid antibodies (APLA) and systemic lupus erythematosus is controversial. Retrospective studies have suggested that patients with A
Autor:
I N, Bruce, C A, Laskin
Publikováno v:
The Journal of rheumatology. 24(8)
Publikováno v:
The Journal of rheumatology. 18(12)
Established solid phase assays for anticardiolipin antibodies (aCL) are often characterized by high levels of nonspecific binding. As a result, only very high levels of aCL have been reported to be associated with a variety of clinical conditions inc
Publikováno v:
The Journal of Immunology. 133:1325-1331
Because recombinant inbred lines, which are homozygous at most loci, can have any combination of parental genes, the numbers and the association of genes responsible for traits can be suggested by examining phenotypic distribution in these lines. Suc
Publikováno v:
The Journal of Immunology. 137:1867-1873
Murine lupus is characterized by the production of numerous autoantibodies and immune complex glomerulonephritis. Anti-DNA antibodies are the hallmark of this disorder and may be associated pathogenetically with the glomerulonephritis. The cellular m
Publikováno v:
The Journal of Immunology. 127:1743-1747
Publikováno v:
The Journal of Immunology. 131:1121-1125
We report experiments designed to determine if the tolerance defect in NZB mice results from i) failure of NZB cells to become tolerant, or ii) the ability of NZB cells to interfere actively with the development of tolerance. The results indicate tha