[Coming changes: function differentiation in the care for mentally retarded].
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The onset of hormone synthesis in the rat fetal pituitary gland was studied with the use of the peroxidase labelled antibody method. On the 16th day of fetal life, cells containing immunoreactive ACTH appeared in the primordial cell outgrowth of the Rathke's pouch. In some fetuses, also prolactin cells could be detected at the same developmental stage and these cells were present consistently on subsequent days. Differentiation of ACTH and prolactin cells was followed by onset of TSH, LH and GH synthesis on the 17th, 18th and 19th day of gestation, respectively.
Modulation of CA1 evoked electrophysiological properties (amplitude, latency, paired-pulse facilitation) by different concentrations of aldosterone (ALDO), spironolactone (SPI), and corticosterone (CT) was studied in hippocampal slice preparation from BALB/c mice. ALDO (5 nM) induced a prolonged increase of the population spike (PS) amplitude with a decrease of its latency and of the paired pulse facilitation. The same effect was observed with a solution of CT (0.5 nM) alone or combined with ALDO (0.5 nM), but no effect was observed with a solution of combined CT (0.5 nM) and SPI (500 nM). Implication of corticosteroid receptors in this response was discussed.
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In the present report, we compared activities of polymorphonuclear leukocytes (PMN) such as phagocytosis and bactericidal activity in vivo with those in vitro in sarcoma 180 (S 180)-bearing mice. Mice showed a remarkable leukocytosis and in increase in PMN fraction of peripheral blood leukocytes (PBL) after intraperitoneal injection of S 180 cells. Tumor-bearing mice infected with Escherichia coli (E. coli) intravenously and intraperitoneally showed an apparent delay in the clearance of bacteria compared to the non-tumor-bearing control mice. However, PBL of tumor-bearing mice showed a high phagocytic activity against beads and a high chemiluminescence (CL) activity. Dichlorofluorescein (DCFH) oxidation capacity of peripheral blood PMN in S 180-bearing mice after stimulation with phorbol myristate acetate (PMA) was about the same or a little stronger than that in control mice. On the contrary, serum and ascites of tumor-bearing mice strongly suppressed the phagocytic and bactericidal activities of casein-induced PMN against E. coli. During the early phase of E. coli infection, serum level of complement (C3) was not depressed in tumor-bearing hosts. From these results, it is concluded that leukocytosis and activation of functions of PMN in tumor-bearing mice were observed in vitro but they were not effective for the protection in the early phase of actual E. coli infection in vivo. The delay of in vivo clearance may be accounted for by a suppressive effect of serum components in tumor-bearing mice.
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The addition of fresh peripheral blood mononuclear cells (PBL) from four of seven patients with agammaglobulinemia to generated hemolytic plaque-forming cells (PFC) resulted in a dose-dependent suppression of PFC. This spontaneous suppressor cell activity (SSA) was restricted to the four patients who could generate a PFC response in vitro. SSA was mediated by a small subset of E-rosetting T lymphocytes characterized by theophylline-sensitive E-receptors and surface receptors for Fc-IgG. The effects of SSA were temperature dependent and reversible, and pokeweed mitogen could prevent the rapid decline of SSA observed during culture. Augmentation of SSA was achieved by agents known to increase intracellular levels of cyclic AMP, whereas lithium chloride abrogated SSA, including the drug-induced effects. Cells mediating SSA may play a role in preventing the normal transition of pre-B cells to B cells in patients with agammaglobulinemia without B lymphocytes.
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Retarded growth and disordered glucose metabolism secondary to growth hormone (GH) deficiency are associated with persistent lymphocytic choriomeningitis virus (LCMV) infection of GH-producing cells in the anterior lobe of the pituitary gland. Infected C3H/ST mice, which are H-2k haplotype, become GH deficient, and LCMV replicates in most (more than 90%) of their GH-producing cells. In contrast, BALB/WEHI and SWR/J mice, which are H-2d and H-2q, respectively, do not develop this GH deficiency, and less than 20% of their GH-producing cells are infected by virus. Yet all three strains infected at birth with LCMV strain Armstrong (ARM) carry equivalent amounts of virus in their blood, brain, heart, kidney, liver, spleen, and thymus throughout life. Of five additional H-2k murine strains tested, C3H/HEJ and CBA/N mice develop this GH-like disorder, whereas neither AKR/J, B10/BR, nor BALB/KAE mice do, indicating that the H-2K haplotype does not control the GH susceptibility. Furthermore C3H/SW mice, which have the H-2b haplotype on the C3H background, develop the disease, again negating any correlation with H-2k but inferring that the C3H background is responsible. One half of the hybrid offspring produced by crossing the C3H/ST GH-deficient strain with BALB/WEHI-resistant mice develop the disease, but the trait is not sex linked. F1 hybrid backcrosses with the susceptible C3H/ST parental strain or resistant BALB/WEHI strain indicate the involvement of more than two genes. Hence the development of a GH deficiency by LCMV-infected C3H/ST mice is not linked to the MHC haplotype, is not sex linked, and is not due to a dominant gene. Multiple genes are involved and these are related to C3H background.
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Treatment of prostaglandin (PG)H synthase purified from ram seminal vesicle microsomes with trypsin cleaves the 70-kDa subunits into 33- and 38-kDa fragments (Chen, Y.-N. P., Bienkowski, M. J., and Marnett, L. J. (1987) J. Biol. Chem. 262, 16892-16899). In contrast to a minimal decrease in cyclooxygenase activity, peroxidase activity declines rapidly following trypsin treatment. The time course for loss of guaiacol peroxidase activity corresponds closely to the time course for protein cleavage. The ability of trypsin-treated enzyme to support catalytic reduction of 5-phenyl-4-pentenyl-1-hydroperoxide in the presence of reducing substrates is significantly reduced. The products of metabolism of 10-hydroperoxy-8,12-octadecadienoic acid indicate that trypsin-treated enzyme catalyzes homolytic scission of the hydroperoxide bond in contrast to the heterolytic scission catalyzed by intact enzyme. Spectrophotometric titrations of hematin addition to trypsin-treated PGH synthase indicate approximately a 50% reduction in heme binding. These observations suggest that trypsin treatment of PGH synthase decreases the ability of the protein to bind prosthetic heme at a site that controls peroxidase activity. Comparison of the N-terminal sequence of the 38-kDa fragment of trypsin-treated PGH synthase to the amino acid sequence of the intact protein indicates that cleavage occurs between Arg253 and Gly254. Based on literature precedents and the results of the present investigations, we propose that the heme prosthetic group that controls the peroxidase activity of PGH synthase binds to the His residue of the sequence His250-Tyr251-Pro252-Arg253 located immediately adjacent to the trypsin cleavage site.
It was the purpose of our studies to achieve reevaluation of the histo- and cytomorphology of cutaneous lymphomas by means of additional enzymecyto-chemical and funtional tests. Skin biopsy specimens from 99 patients with cutaneous lymphomas and pseudolymphomas were stained for HE, Giemsa, PAS, Gormori, several hydrolytic enzymes and peroxidase. In cell suspensions extracted from skin lesions B and T cell differentiation was performed using surface markers. In addition tissue cells were tested for PHA response in suspensions and for intracytoplasmatic Ig on smears. Based on these studies cutaneous lymphomas were filed, within the "Kiel" classification of low grade and high grade malignant lymphomas according to their histological, enzymecytochemical and immunological features. It got evident that B cell and T cell lymphomas of low grade malignancy in the skin both present distinct histological patterns, indicating areas B and T cell microenvironmental specificity.
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