By George C. Tsokos
George Tsokos and a panel of authoritative clinicians and researchers synthesize the newest findings from throughout mobilephone and molecular biology with the fundamental rules of rheumatology to create the 1st textbook of molecular rheumatology. those demonstrated specialists describe the biochemical mechanisms during which apoptosis, telephone signaling, supplement, lipids, and viruses give a contribution to sickness expression, and element either immune and nonimmune mobilephone functionality in rheumatic illnesses. Their overview of the key rheumatic illnesses integrates the mobile, biochemical, and molecular organic mechanisms which are very important in rheumatic illness pathogenesis. Path-breaking and illuminating, rules of Molecular Rheumatology expands the envelope of scientific knowing to bare the organic roots underlying rheumatologic ailment, in addition to the character and roles of the strong new therapeutics now rising for its optimum remedy.
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Extra info for Principles of Molecular Rheumatology (Current Molecular Medicine)
And Cuellar, M. L. (1998) Retrovirus-associated rheumatic syndromes, in Arthritis and Allied Conditions. (Koopman, W. ), Williams & Wilkins, Baltimore, p. 2361. 14. , and Leroy, J. P. (1998) Lymphoma with regression after methotrexate withdrawal in a patient with rheumatoid arthritis. Role for the Epstein-Barr virus. Rev. D Rhumatisme, Eng. Ed. 65, 283–286. 15. , Farhi, D. , and Fanucchi, M. P. (1998) Reversible Epstein-Barr virus associated T cell non-Hodgkin’s lymphoma in a patient with rheumatoid arthritis undergoing chronic immunosuppressive therapy.
BMoMLV The presence of the unique amino acid sequence QTDRED in the nitrogenase protein of Klebsiella and HLA B27 is thought to be a pathogenetic factor in seronegative spondylarthropathies (52). Along the same line, the “shared epitope” QKRAA sequence from the third hypervariable region of HLA DRB1*0401, which has been found in numerous human pathogens, is associated with susceptibility to RA (53). A hallmark of the self-destructive autoimmune process in patients with SLE is the production of circulating antinuclear autoantibodies (ANAs).
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