[Xanthogranulomatous pyelonephritis].
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Biomedical subjects
Publications and source records attributed to C Koch.
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Guinea-pigs immunized with reactive 2,4-dinitrophenyl (DNP) sensitizer in Freund's complete adjuvant develop delayed-onset reactivities to the reactive DNP sensitizer and to DNP protein conjugates as well as to PPD. We have studied the role of various lymph node lymphocyte populations from these animals in producing the lymphokine macrophage agglutination factor (MAggF) and effecting antigen induced blast transformation. The production of MAggF, when elicited by reactive sensitizer or PPD, was readily inhibited by low doses of a particular cytotoxic rabbit and anti-T (thymus-dependent)-lymphocyte serum and complement, while the production of MAggF when elicited by DNP protein conjugate was inhibited only by higher doses of anti-T-cell serum. These results in vitro paralleled earlier observations in vivo. In contrast, PPD induced blast transformation was only inhibited by high doses of anti-T-cell serum and not by low doses. Chromatography of sensitized lymph node cells over anti-Ig-containing columns (to remove B cells) affected neither MAggF production nor blast transformation. Our data suggest that these in vitro responses are mediated by two different subpopulations of T cells.
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Severe combined immunodeficiency (SCID) was diagnosed in a girl immediately after birth; her older brother had SCID and was successfully reconstituted by bone marrow transplantation from his uncle. She was isolated in a laminar air flow bench and decontaminated. The father differed by one HLA-A antigen but was HLA-Dw2 homozygous like the patient; his lymphocytes showed a slight response to the patient's cells in mixed lymphocyte culture (MLC). At the age of 2 1/2 months and again at 5 months, she was given a bone marrow transplant from the father. During the entire course the patient had no infections, and apart from a transient eosinophilia she had no signs of graft-versus-host reaction. Immunological reconstitution was nearly complete at 9 months of age, when she was recontaminated. One year later plasma immunoglobulin concentrations are in the low normal range (IgG and IgM) or decreased (IgA); tests of cell-mediated immunity are normal. Apart from slight upper respiratory infections, the patient has been healthy. Physical and psychological development have been normal.
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The shape of the survival curve for cells inactivated by tritium decay in DNA is modified by the presence of halogenated pyrimidines in the DNA in a manner analogous to their effect on X-ray induced reproductive death. The large shoulder found for tritium suicide is removed completely by coincorporation of 10(-6) M IUdR. The oxygen enhancement ratio for 125I and tritium disintegrations in unsynchronized Chinese hamster cells was determined for cells permitted to accumulate damage from these events at 4 degrees C. The oxygen enhancement ratio for 125I induced damage is 1.4. This is much smaller than the OER found for tritium decay which is similar or more than that found for X-ray exposure under the same conditions. These results suggest that the nature of the lesions produced by 125I decay in DNA are analogous to those produced by high LET radiation while those lesions produced by tritium are similar to lesions produced by roentgen rays. In synchronous V79 cells the effects of 125I induced damage in different regions of the mammalian cell DNA was examined taking advantage of the fact that DNA replication in hamster nuclei follows a time-dependent three dimensional pattern. The experiments indicate that 125I decays accumulated in the G2-period of the cell cycle have different efficiences for the induction of reproductive death depending on the region of the DNA which is labeled. The efficiency for the induction of reproductive death appears to be a maximum in DNA that replicates in V79 cells near the end of the DNA replication cycle. Electron capture events are dramatically efficient in the production of lethal chromosome aberrations. In CHO cells synchronized in the G1-stage of the cell cycle stored in the frozen state the efficiency for the induction of dicentric and ring chromosomes is 0.03. The dose response curve for the induction of these aberrations is linear in contrast to the curvilinear response found for roentgen ray exposure under the same conditions. Data on this kind suggest that there may exist "critical" regions within mammalian cell nuclei where chromatin fibers from two different chromosomes are in close proximity to each other and both are damaged non-repairably by a single electron capture event.
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Immune response in chickens to the multichain copolymer (T,G)-A--L 2030 is analysed. Previous work has shown that responsiveness is not linked to the B-complex. Three different antibody specificities could be distinguished. From the data it is proposed that the response to the backbone of (T,G)-A--L (poly-DL-alanine) influences the responses to the side chain determinants (primarily the (T,G)-determinant). Thus the anti-(T,G) response in chickens is determined by at least two different loci, the B-complex, and another, as yet unidentified locus which determines the response to the poly-DL-alanine determinant. A third antibody specificity is directed against G-A--L and is only detectable in chickens which are high responders to poly-DL-alanine.
We have examined the effect in mixed leucocyte culture (MLC) with rat cells of the IgG fraction of alloantibodies against the major histocompatibility complex (anti-BN major) and against some of the minor histocompatibility antigens. Anti-BN major specifically inhibited the MLC response, both when BN cells were responding and stimulating cells. Absorption with BN erythrocytes completely removed the haemagglutinating antibodies but had no effect of MLC inhibition, while absorption with BN lymphocytes removed MLC inhibition as well as haemagglutinating antibodies. The F(ab')2 fragments of anti-BN major did not inhibit MLC, although they still had the capacity to combine specifically with BN lymphocytes. We therefore suggest that the inhibition of MLC responses by alloantibodies is either because of a cytotoxic effect (even if cytotoxicity could not be demonstrated in unmixed cultures) or a blocking of antibody-coated lymphocytes by Fc receptor-bearing cells. Antibodies against minor histocompatibility antigens did not inhibit MLC.
The multichain co-polymer poly(Tyr,Glu)-polyAla--polyLys, designated (T,G)-A--L, is normally thought to present only the poly(Tyr,Glu) sequences, designated (T,G), as antigenic determinants. Evidence is presented indicating that at least two different determinants in the (T,G)-A--L antigen are recognized by chickens. Studies in a partly inbred high-responder chicken strain reveal two major determinant systems: the (T,G) and the A--L in the (T,G)-A--L antigen. For one serum the antigenic determinant of the A--L backbone is shown to be a poly-D-alanine.
Autoradiographic studies have shown that radioiodinated TIGAL binds in vitro to a small but varying fraction of lymphoid cells from bursectomized, agammaglobulinemic chickens, whereas no binding of radioiodinated TGAL or a variety of other radioiodinated antigens can be observed. The binding of [125I]TIGAL is inhibited by antigen-antibody complexes. Radioiodinated antigen-antibody complexes are bound to a similar proportion of the lymphoid cells from bursectomized chickens, and this binding is inhibited by preincubation of the cells with unlabeled TIGAL but not with TGAL. These results indicate a cross-reaction at the level of Fc receptors between determinants on TIGAL and on IgG.
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