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Steroids antibody specificity

A stepwise approach to therapy was proposed for cases of ocular toxocariasis. For eye disease alone, local and periocular or systemic steroids should be used, with surgery (vitrectomy, membrane peel) when appropriate. For eye disease unresponsive to steroids, a specific anthelmintic agent is added and systemic steroids are continued (e.g., thiabendazole 50 mgAg per day for 7 days plus prednisolone 0.5 to 1.0 mg/kg per day). For eye disease with systemic symptoms (VLM) or high antibody levels, local steroids and mydriatics are used, in addition to oral thiabendazole and oral steroids from the outset. [Pg.630]

Haptens.—Haptens have been prepared from steroid hormones by reactions at C-3 or C-17, or in the pregnane side-chain. Antibody specificity is often improved, however, by anchoring the steroid through a middle-ring site to the protein, so that both ends of the steroid component of the complex are exposed for recognition in the antibody-forming process. [Pg.310]

Although a proper choice of solvent improves the selectivity of extraction, a large number of closely related steroids, chromogenic substances, and other nonspecific materials are also extracted with the steroids. Removal of such contaminants, especially those that will interfere in the final estimation, is important when the antibody specificity used to measure the steroid is relatively low. With high specificity and high affinity antibodies, this becomes less of an issue and is now more the rule than the exception. [Pg.2035]

Arevalo JH, Hassig CA, Stura EA, Sims MJ, Taussig MJ, Wilson IA. Structural analysis of antibody specificity. Detailed comparison of five Fab -steroid complexes. J Mol Biol 1994 241 663-690. [Pg.616]

Fig. 3 Demonstration of antibodies specific for drug metabolite in a patient who developed acute thrombocytopenia after taking the non-steroidal antiinflammatory drug naproxen. Serum from the patient contained an IgG antibody that recognized normal platelets in the presence of naproxen glucuronide in a flow cytometric assay. Antibody binding was not promoted by naproxen. However, positive reactions were obtained with drug metabolites isolated from the same urine ( urinary metabolites ) and with purified naproxen glucuronide. No reaction was obtained with 6-0-desmethyl naproxen, another metabolite of naproxen. Mean fluorescence intensity values are shown in parentheses (from Bougie and Aster 2001)... Fig. 3 Demonstration of antibodies specific for drug metabolite in a patient who developed acute thrombocytopenia after taking the non-steroidal antiinflammatory drug naproxen. Serum from the patient contained an IgG antibody that recognized normal platelets in the presence of naproxen glucuronide in a flow cytometric assay. Antibody binding was not promoted by naproxen. However, positive reactions were obtained with drug metabolites isolated from the same urine ( urinary metabolites ) and with purified naproxen glucuronide. No reaction was obtained with 6-0-desmethyl naproxen, another metabolite of naproxen. Mean fluorescence intensity values are shown in parentheses (from Bougie and Aster 2001)...
Nonspecific immunosuppressive therapy in an adult patient is usually through cyclosporin (35), started intravenously at the time of transplantation, and given orally once feeding is tolerated. Typically, methylprednisone is started also at the time of transplantation, then reduced to a maintenance dose. A athioprine (31) may also be used in conjunction with the prednisone to achieve adequate immunosuppression. Whereas the objective of immunosuppression is to protect the transplant, general or excessive immunosuppression may lead to undesirable compHcations, eg, opportunistic infections and potential malignancies. These adverse effects could be avoided if selective immunosuppression could be achieved. Suspected rejection episodes are treated with intravenous corticosteroids. Steroid-resistant rejection may be treated with monoclonal antibodies (78,79) such as Muromonab-CD3, specific for the T3-receptor on human T-ceUs. Alternatively, antithymocyte globulin (ATG) may be used against both B- and T-ceUs. [Pg.42]

K2. Kobayashi, N., Oiwa, H., and Goto, J., Production and characterization of group-specific monoclonal antibodies recognizing nonamidated, glycine- and taurine-amidated ursodeoxycholic acid 7-W-acetylglucosaminides. J. Steroid Biochem. Mol. Biol. 64, 171-177 (1998). [Pg.169]

More than 90% of patients with myasthenia gravis have circulating antibodies directed against a subunit of the acetylcholine receptor/ Immunosuppressive drugs and steroids help to cut down on these autoantibodies, and many patients are benefit-ted by removal of the thymus. Newer approaches involve specific immunotherapy aimed at increasing tolerance to either T cells or to B cells.C/d For example, oral ingestion of purified acetylcholine receptors to desensitize the body s response or inhibition of production of 11-2. [Pg.1864]

Laitinen T, Kankare JA, Perakyla M (2004) Free energy simulations and MM-PBSA analyses on the affinity and specificity of steroid binding to antiestradiol antibody, Proteins, 55(1) 34—43... [Pg.331]


See other pages where Steroids antibody specificity is mentioned: [Pg.160]    [Pg.392]    [Pg.43]    [Pg.279]    [Pg.166]    [Pg.90]    [Pg.159]    [Pg.547]    [Pg.2035]    [Pg.88]    [Pg.103]    [Pg.392]    [Pg.171]    [Pg.219]    [Pg.853]    [Pg.220]    [Pg.227]    [Pg.118]    [Pg.392]    [Pg.402]    [Pg.65]    [Pg.68]    [Pg.75]    [Pg.228]    [Pg.3]    [Pg.87]    [Pg.249]    [Pg.158]    [Pg.323]    [Pg.344]    [Pg.150]    [Pg.246]    [Pg.247]    [Pg.250]    [Pg.262]    [Pg.382]    [Pg.24]    [Pg.26]    [Pg.457]    [Pg.341]    [Pg.98]   
See also in sourсe #XX -- [ Pg.157 , Pg.158 , Pg.202 ]




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