Measurement of sex-steroid-binding plasma protein in serum of healthy individuals in prepuberty and puberty (74 males and 94 females) was performed using a radioimmunoassay procedure. An age-related decrease of serum SBP was demonstrated during these ages in both sexes. In parallel studies, the serum level of testosterone, oestradiol and dehydroepiandrosterone was evaluated in subjects under 20 years of age. A rise of serum dehydroepiandrosterone levels in both sexes was observed to occur at approximately 8 years of age, being a little bit earlier than the ages for testosterone to rise in males and for oestradiol to rise in females, both of them being at about 10 years of age, respectively. When the testosterone/sex-steroid-binding plasma protein ratio was evaluated as an index of free testosterone concentration in serum, a sharp increase of the ratio was found to occur at 10 years of age and to continue during puberty in both sexes with more marked increment in males than in females. It was suggested that the decrease of SBP in puberty might be largely influenced by alteration in the hormonal balance of testosterone, oestradiol and dehydroepiandrosterone.
NOD mouse-derived beta-cell-specific cytotoxic T-cell (beta-CTL) clones are diabetogenic in adult NOD mice, but only if co-injected with splenic CD4+ T-cells from diabetic animals. This investigation was initiated to determine whether infiltration of pancreatic islets by beta-CTL is a major histocompatibility complex (MHC) class I-restricted response, and whether beta-CTL has a direct cytopathic effect on beta-cells in vivo. Pancreatic islets from BALB/c (H-2d) or B6 (H-2b) mice were transplanted under the renal capsule of streptozotocin (STZ)-induced diabetic (NOD x BALB/c) F1 (H-2Kd, H-2Dd,b) or NOD x B6) F1 (H-2Kd,b, H-2Db) mice, respectively. H-2Kd-restricted beta-CTL clones from NOD mice were transfused into euglycemic mice within 3 days after transplantation. In all of the H-2d islet-grafted (NOD x BALB/c) F1 mice that received the beta-CTL clones, the beta-CTLs homed into the grafts, recruited host Mac-1+ cells and CD4+ and CD8+ T-cells, and caused diabetes within 7 days. In contrast, none of the H-2b islet-grafted (NOD x B6) F1 mice who received the beta-CTL clones and none of the H-2d islet-grafted (NOD x BALB/c) F1 mice who received a non-beta-cell cytotoxic CTL clone (N beta-CTL) developed graft inflammation or diabetes. Depletion of CD4+ T-cells in H-2d islet-grafted (NOD x BALB/c) F1 mice did not prevent beta-CTL clone-induced diabetes but reduced its severity. In contrast, when the beta-CTL clones were injected > 8 days after transplantation, none of the H-2d islet-grafted (NOD x BALB/c) F1 mice became diabetic or developed graft inflammation. We conclude that (1) islet-derived beta-CTLs can destroy beta-cells in vivo; (2) infiltration of grafted islets by beta-CTLs is an MHC class I-restricted response; (3) beta-CTLs can recruit naive CD4+ T-cells to the site, leading to further beta-cell damage; and (4) revascularized islet grafts are, like pancreatic islets of irradiated adult NOD mice, "sequestered" from circulating beta-CTLs.
The effects of antithyroid drugs and related agents on human neutrophil function were studied. Neutrophil function was mainly assessed through oxygen radical formation as determined by chemiluminescence (CL) response, superoxide anion (O\m=-\2)generation and hydrogen peroxide production. Propylthiouracil (PTU) at a therapeutic concentration (10 \g=m\g/ml) inhibited CL response evoked by phorbol myristate acetate (PMA) and other stimulators. The inhibitory effect was not enhanced by pre-incubation of neutrophils with PTU and not exerted through a direct cytotoxic effect of the drug. It was not related to the kind of stimulators to evoke CL response in neutrophils either. However, the inhibitory effect disappeared when PTU was removed from the reaction mixture for CL response.PTU did not inhibit O\ m=-\ 2 generation but markedly inhibited hydrogen peroxide production in neutrophils or activity of hydrogen peroxide in vitro. Morphologically, the unique change of cellular configuration of chemotactic neutrophils caused by N-formyl-methionylleucyl-phenylalanine (FMLP) was not influenced with PTU. Since hydrogen peroxide is mainly derived from O\ m=-\ 2, these observations suggest that PTU may have a scavenger effect on hydrogen peroxide activity. Inhibition of CL response in neutrophils was also demonstrated with methimazole (MMI), thiouracil and thiourea, but not with imidazole and uracil, which suggests that their inhibitory effect on CL response in neutrophils may be closely related to the antithyroid activity.
The serum concentration of sex-steroidbinding plasma protein (SBP) was measured with radioimmunoassay for 92 patients with Graves' disease, 36 males and 56 females, as well as 92 age-and sexmatched controls. In 24 male patients with hyperthyroidism, the mean SBP concentration was 6.4 \m=+-\0.2 (mean \ m=+-\ sd) \g=m\g/ml, whereas it was 2.3 \ m=+-\ 0.2 \g=m\g/ml for the controls. The mean SBP concentration in 28 female patients with hyperthyroidism was 7.4 \m=+-\0.6 \g=m\g/ml , whereas it was 3.2 \m=+-\0.6 \g=m\g/ml for the controls. In Graves patients who were euthyroid following treatment, SBP levels were decreased near normal in both sexes. There was a significant correlation between T4 and SBP concentrations as well as between T3 and SBP concentrations in patients with Graves' disease in both sexes, with a better correlation in females. Increased SBP in untreated Graves' disease initiated to decline within a month following administration of antithyroid drugs, taking over 3 months to decline to the normal range.
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