Effect of Hypercapnia and Hypocapnia on Tryptophan and Tyrosine Hydroxylation in Rat Brain

The effects of induced hypo- and hypercapnia upon the rate of hydroxylation of tryptophan and tyrosine in the rat brain were studied by measuring the accumulation of 5-HTP and DOPA following administration of the aromatic L-aminoacid decarboxylase inhibitor 3-hydroxybenzylhydrazine HC1 (NSD 1015). The results suggest that the hydroxylation of tryptophan varies directly with the tissue Po₂- On the other hand, the hydroxylation of tyrosine did not show a simple relationship to Po₂ but appeared to be influenced by pH changes.     

Effect of metabolic cage housing on immunoglobulin A and corticosterone excretion in faeces and urine of young male rats

Six 8-week-old Sprague-Dawley rats were studied for 9 days divided into three periods of 3 days each: before transferral to metabolism cages, during metabolic cage housing and after return to their home cages. Faeces were collected daily when the animals were housed in their home cages and every 6 h when the animals were housed in metabolic cages during which time urine was also collected every 6 h. The rate of weight gain was slightly reduced during the 3 days in metabolic cages and the animals produced significantly larger amounts of faeces when housed in metabolic cages than when housed in their home cages. The total faecal excretion of corticosterone (nanograms excreted per hour per kilogram body weight) and immunoglobulin A (IgA) (milligrams excreted per hour per kg body weight) quantified by enzyme-linked immunosorbent assays (ELISAs) exhibited a clear diurnal rhythm in the metabolic cage. Urinary excretions of corticosterone and IgA also followed a clear diurnal cycle. The mean daily amounts of corticosterone excreted were not significantly affected by cage change and by housing in metabolic cages. However, the excretion of faecal IgA was significantly reduced during the 3 days after the period in metabolic cages. Taken together the results indicate that metabolic cage housing is mildly stressful for young adult male rats.     

Analysis of HLA-DRB and -DQB gene RFLPs in DR7 homozygous cell lines: associations with Dw11, Dw17 and DB1

The DR7-associated Dw specificities, Dw11, Dw17 and DB1 were investigated with regard to DRB- and DQB-gene polymorphism, as revealed by RFLP analysis using the restriction enzyme TaqI. In the 22 DR7 homozygous cell lines investigated, each of these Dw specificities was found to correlate to one specific RFLP defined DR-DQ haplotype. In addition, a clear linkage disequilibrium to a specific HLA-B locus allele for each Dw specificity was noted, indicating that the Dw subtypes of DR7 often are associated with a conserved HLA-B-DR-DQ haplotype. Only one genetically homozygous cell line, PLH, deviated from these correlations. This cell line, notably derived from an individual with a deletion of the 21-hydroxylase B-gene (21-OHB), caries the HLA haplotype Bw47, DR7, DQw2, DB1, but displayed a DRB RFLP otherwise found in association with Dw17.     

Activation of Lyt-2+ T cells by antibodies towards brain-associated antigens. I. Accessory cell requirement and role of Fc receptors in the induction of reactivity to interleukin 2

The present report describes a system where essentially all Lyt-2+ T cells are selectively activated by rabbit anti-mouse brain antibodies (RaMB) to interleukin 2 (IL 2) reactivity. High efficiency of RaMB-mediated induction was obtained by a 5 h incubation with antibodies at high cell density of Sephadex G-10-nonadherent spleen cells. No in situ production of IL 2 by RaMB-treated cells was detected, and proliferative responses were entirely dependent on exogeneous IL 2. RaMB-induced IL 2 reactivity was found to require accessory cells which are Fc receptor positive, and clearly distinct from those required to induce T cell proliferation in mixed lymphocyte cultures. We conclude that Lyt-2+ T cells are triggered to IL 2 reactivity by Fc receptor-mediated presentation of RaMB antibodies. The mechanism of induction by RaMB antibodies is discussed.     

Enzyme-linked immunosorbent assay for immunological diagnosis of human tularemia.

The enzyme-linked immunosorbent assay (ELISA) was applied for immunological diagnosis of human tularemia, using lipopolysaccharide from Francisella tularensis as antigen. Sera collected from patients, healthy individuals, and vaccinated volunteers were investigated for antibodies against F. tularensis by ELISA and tube agglutination. In ELISA all sera were titrated with a polyspecific anti-immunoglobulin enzyme conjugate. A limited number of consecutive sera from individual patients were also investigated for immunoglobulin G (IgG) and IgM antibodies by means of immunoglobulin class-specific conjugates. On an average ELISA was more than 10-fold as sensitive as tube agglutination. Two weeks after onset of disease, sera from patients had significantly higher titers in ELISA than sera from healthy controls. High titers persisted after more than 2 years. Significant amounts of both IgG and IgM antibodies were present within 1 to 2 weeks after infection. The antibody activity increased during the first month, without any significant change of the relation between IgG and IgM titers. After 2.5 years the IgG/IgM titer ratio of sera from patients was significantly increased. Within 6 weeks after vaccination sera from about half of the vaccinees had significantly elevated titers in ELISA. Titers observed after vaccination were generally lower than those found after infection. An elevated ELISA titer can be of diagnostic importance by the end of the first week of illness. A significant increase of titer in consecutive serum samples indicates a diagnosis of tularemia. Determination of IgG and IgM antibodies may be of value in determing whether a positive titer of a single serum sample is of longstanding or recent origin.     

Bactericidal and cytotoxic effects of hypothiocyanite-hydrogen peroxide mixtures

Lactoperoxidase catalyzes the oxidation of thiocyanate by hydrogen peroxide into hypothiocyanite, a reaction which can protect bacterial and mammalian cells from killing by hydrogen peroxide. The present study demonstrates, however, that lactoperoxidase in the presence of thiocyanate can actually potentiate the bactericidal and cytotoxic effects of hydrogen peroxide under specific conditions, such as when hydrogen peroxide is present in the reaction mixtures in excess of thiocyanate. The toxic agent was also formed in the absence of lactoperoxidase in a reaction between hypothiocyanite and hydrogen peroxide. Sulfate, sulfite, cyanate, carbonate, and ammonia, which have been postulated to be formed in the chemical oxidation of hypothiocyanite by hydrogen peroxide, were not bactericidal and did not potentiate the bactericidal effect of hydrogen peroxide. Cyanosulfurous acid, the only other postulated product of the chemical oxidation of hypothiocyanite by hydrogen peroxide, may be the killing agent.