L’administration de thyrocalcitonine à I’homme normal détermine une excrétion rénale accrue de phosphates et de calcium. Le coefficient de réabsorption tubulaire des phosphates est diminué. Au cours d’une perfusion de phosphates, la thyrocalcitonine diminué la quantité de phosphates réabsorbés en méme temps que le coefficient de réabsorption tubulaire. Ces faits sont attribués à une diminution de la réabsorption tubulaire de ces deux ions, les variations de la filtration glomérulaire étant insuffisantes pour en rendre compte. L’excrétion rénale des ions H+ n’est pas modifiée de manière reproductible. Les mêmes résultats étant observés chez deux hypoparathyroïdiens et un hyperparathyroïdien, on en conclut que l’hyperphosphaturie est indépendante d’une modification de la sécrétion de parathormone. La connaissance des effets de la thyrocalcitonine sur l’excrétion rénale des phosphates doit intervenir dans l’interprétation des temps précoces des épreuves d’hypercalcémie provoquée.
The antigonadal effects of GnRH agonists (GnRH-A) are mediated both through pituitary and testicular inhibitory mechanisms in the rat. To investigate these effects in men, we studied patients having no gonadotropin secretion and compared their testicular response to hCG in the absence or in the presence of GnRH-A. Thirteen patients with acquired pituitary hypogonadotropism had plasma testosterone levels below 1.5 ng/ml and no gonadotropin responses to acute GnRH administration (100 micrograms iv). Testicular responsiveness was evaluated using a single im injection of hCG (5000 IU im). Plasma levels of testosterone, dihydrotestosterone, androstenedione, 17-hydroxyprogesterone (17-OHP), and progesterone were determined before and 4, 12, 24, 48, and 72 h after hCG stimulation. The same protocol was also used in the same patients on day 4 of a 6-day course of treatment with the GnRH-A, D-Ser-(TBU)6, des-Gly NH2 GnRH ethylamide (Buserelin) (3 sc injections of 250 micrograms/day). During the first 4 days of GnRH-A administration, plasma LH, FSH, and testosterone levels were measured daily in order to establish the completeness of the gonadotropin deficiency. Before treatment with hCG, plasma testosterone levels were 0.56 +/- 0.15 and 0.96 +/- 0.22 ng/ml (mean +/- SE) in the absence of GnRH-A and during GnRH-A administration, respectively. The administration of hCG elicited a significant increase in plasma testosterone in both situations; integrated testosterone concentrations were 123.7 +/- 24.9 and 155.5 +/- 27.9 ng/ml . 72 h (P greater than 0.1) in the absence of GnRH-A and during GnRH-A administration, respectively. Likewise the ratios of 17-OHP to progesterone, androstenedione to 17-OHP, and dihydrotestosterone to testosterone after hCG injection were similar in the presence or absence of GnRH-A. Since short term administration of buserelin did not inhibit hCG-induced testosterone secretion in patients with gonadotropin deficiency, we suggest that Buserelin does not grossly modify the function of testicular steroidogenesis enzymes. The antigonadal effects of GnRH-A in man appear to be mediated exclusively through the pituitary.
ParisThe effect of passively administered anti-2,4-dinitrophenyl (DNP) IgG, and IgG2 antibodies o n their own production has been studied.Guinea pigs were immunized with immune complexes emulsified in complete Freund's adjuvant. These complexes were made at 4 times equivalence with IgG, and/or IgC2 anti-DNP antibodies having the same affinity. Humoral IgGl and IgG, anti-DNP antibody contents were assayed at weekly intervals, and 4 and 10 days after a booster injection of antigen in saline given on the 12th week.Active anti-DNP IgC, antibody production is strongly inhibited by passive IgG2, IgG, and F(ab'), antibody fragments.Active anti-DNP IgG, antibody production of the same animals is inhibited by passive IgG2 and F(ab')2, t o an extent similar t o active IgC, antibody inhibition, but the response after boosting is normal. On the other hand, passive IgGl antibodies lead t o a delayed enhanced active IgG, antibody response.The effect of a 1 : 1 mixture of both passive antibody classes is intermediate t o what is observed with either class alone.These differential effects according t o the class ( i e . the Fc fragment) of the passive antibodies used show the importance of immune complexes in not only the quantitative, but also the qualitative, regulation of the immune response.
The effect of passively administered IgG1 and IgG2 anticarrier antibodies on the IgG1 and IgG2 antihapten response has been studied.
Guinea pigs were immunized with dinitrophenylated bovine gamma globulin mixed with purified IgG1 or IgG2 antihuman gamma globulin antibodies, i.e., antibodies directed against a limited range of the carrier determinants. Humoral IgG1 and IgG2 anti-DNP antibody contents were assayed at weekly intervals and 4 to 10 days after a booster injection of antigen in saline given on the 12th wk.
The main finding was the sustained suppressive effect of passive IgG1 anti-carrier antibodies on the active IgG1 antihapten response.
This result is compared with the enhancing effect of passive IgG1 antihapten antibodies and is discussed in the light of T cell-B cell and hapten-carrier relationships, leading to the proposal of a regulatory function of the Fc portion of the IgG1 anticarrier antibody, combined with the antigen, on the T cell.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.