The suppression of antibody formation by passively administered antibody is influenced by the dose and nature of the antigen, type of immunization procedure, ratio of antibody to antigen, species origin and characteristics of the antiserum used, as well as the species selected for immunization. In guinea pigs, diphtheria antitoxin formation can be effectively suppressed by an intravenous injection of excess homologous or heterologous antitoxin as long as 5 days after toxoid immunization and after delayed-type hypersensitivity to toxoid has developed. Following the period of antibody suppression which lasts 2 to 7 weeks, serum antibody can usually be demonstrated. It is proposed that this delayed immunization results from dissociation of antigen, since diphtheritic paralysis and death can be produced in guinea pigs and rabbits by the intravenous injection of toxin-antitoxin precipitates formed in antitoxin excess. This syndrome is prevented by injection of excess horse antitoxin 1 hour after injection of the toxin-antitoxin complexes.
Distal elongation of the hamstrings was performed for contracture due to neurogenic disorders in 66 patients. A follow-up study on 34 of the patients with cerebral palsy is reported here. The success of the operation was judged by functional evaluation including joint measurement and gait analysis. The advantages of this operation and the need for prolonged aftercare are discussed.
Quantitative studies of antibody formation in experimental animals have been facilitated by the use of labeled proteins (1, 2). After equilibration following intravenous injection, labeled antigen is eliminated from the circulation in two exponential phases: the first and slower rate is due to non-immune catabolism; the second and rapid decline is caused by the production and release into the circulation of specific antibody (3, 4).In this study, guinea pigs have been injected with relatively minute amounts of a small bacteriophage, 4~X 174, which has been traced in the circulation utilizing the plaque-forming capacity of the virus. With this method it has been possible to detect an immune elimination as early as 24 hours after injection. The early detection of antibody was facilitated by the small amounts of antigen employed. It has also been shown that there is a close resemblance between the kinetics of the primary and secondary antibody response to this bacteriophage. Materials and MethodsPhage.--Str~J.us of ~bX 174 and T2 were kindly supplied to us by Dr. E. Lennox. ~bX was grown in Escherickia coli strain C in glycerol-easamino acid medium (5). The lysed culture was centrifuged at low speed to remove cell debris. Purification was then accomplished by precipitation with ammonium sulfate, passage through a DEAE cellulose anion exchange column, and elution with 0.1 M ammonium acetate (6). This purified stock containing 10 n plaque-forming particles per ml was kept at 4°C in ammonium acetate buffer pH 7.4 conraining 0.01 per cent gelatin. Dilutions of this stock were used for almost all the immunization experiments.
Nerve growth factor (NGF) is a protein essential for the development and maintenance of the peripheral sympathetic nervous system, causing responsive neurones to increase in size and to extend neurites. Biochemically, the selective induction of tyrosine hydroxylase (TH) and dopamine beta-hydroxylase key enzymes in catecholamine biosynthesis is one of its most characteristic effects. Both the morphological and biochemical effects are modulated by glucocorticoids, suggesting a close relationship between specific effects of NGF and hormone action. NGF has been shown to induce an increase in adrenal cyclic AMP in intact but not in hypophysectomised rats, and so we have looked directly at the effect of systemic administration of NGF on the hypothalamo-pituitary-adrenal axis. We report here that NGF induced an enhanced secretion of adrenocorticotropin (ACTH) and a prolonged increase in plasma glucocorticoid concentration after intravenous (i.v.) injection. Such effects could have important implications for the biological activity of NGF.
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