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摄碘过量引起地方性甲状腺肿的病理生理机理至今尚未清楚。作者比较了(?)碘地区(饮水中碘462.5μg/L)的29名甲状腺肿大儿童和含碘不高地区(饮水中碘54μg/L)的26名健康儿童的甲状腺自身抗体情况。测定抗微粒体抗体(Mab),抗甲状腺球蛋白抗体(TgAb),第二胶体抗原抗体(CA_2-Ab)和 TSH 结合抑制性免疫球蛋白(TBⅡ)。并用两种不同方法分析了经过亲和层析法纯化了的 IgG,以测定甲状腺生长刺激免疫球蛋白(TGI)的生物活性。方法一是用人工培养的豚鼠甲状腺细胞作十分敏感的细胞化学生物测定(CBA);方法二是用连续的大鼠甲状腺细胞系(FRTL-5)作有丝分裂相停止测定(MAA)。
The pathophysiological mechanism of local goiter caused by excessive iodine uptake remains unclear. The authors compared thyroid autoantibodies in 29 goiter children with iodine (iodine 462.5 μg / L in drinking water) and 26 healthy children with low iodine (iodine 54 μg / L in drinking water). Mab anti-thyroglobulin antibody (TgAb), second colloidal antigen antibody (CA_2-Ab) and TSH binding inhibitory immunoglobulin (TBII) were determined. IgG purified by affinity chromatography was analyzed by two different methods to determine the biological activity of thyroid growth stimulating immunoglobulin (TGI). The first method is to use the cultured guinea pig thyrocytes as a very sensitive cytochemical assay (CBA). The second method uses a continuous rat thyroid cell line (FRTL-5) for mitotic arrest (MAA).