Bridgett K. Davis
University of Pittsburgh
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Featured researches published by Bridgett K. Davis.
The Journal of Urology | 1979
H. Richard Hellstrom; Bridgett K. Davis; John W. Shonnard; Trevor A. Macpherson
A case is reported of ureteral obstruction that was owing to eosinophilic pyeloureteritis, a previously unrecorded entity. The microscopic findings of extensive fibrosis and a relatively mild eosinophilic infiltrate were similar to those found in a series of eosinophilic cystitis, which was reported recently from this laboratory. Also, local injury appears to initiate some examples of eosinophilic cystitis and in the present case there was a striking history of injury 1 month before the symptoms of ureteral obstruction.
Immunogenetics | 1977
Heinz W. Kunz; Thomas J. GillIII; Barbara D. Dixon; John W. Shonnard; Bridgett K. Davis; Carl T. Hansen
The B-stock population of rats was bred for homozygosity at the loci controlling coat color. In this process, theAg-B1 andAg-B3 haplotypes became fixed in Hardy-Weinberg equilibrium. Extensive immunization and absorption studies showed that the specificities in the B-stock rats homozygous for theAg-B1 haplotype were the same as those found in the inbred F344 strain (Ag-B1), and that the specificities in the rats homozygous for theAg-B3 haplotype were the same as those found in the inbred BN (Ag-B3) strain. A homozygous line derived from the rats carrying theAg-B3 haplotype (B3) has the mixed lymphocyte reactivity and antibody responsiveness to poly (Glu52Lys33Tyr15) characteristic of the inbred strains in theAg-B4 group. Thus, it represents a naturally occurring recombination between the loci controlling MLR and immune responsiveness, on the one hand, and those controlling the Ag-B antigens on the other. Antibody responsiveness segregated with theAg-B3 haplotype in crosses between the B3 homozygotes and the low responder BUF and M520 strains; hence, this recombination is a stable one. There was no linkage of antibody formation or haplotype to coat color. The finding of a strain with a naturally occurring recombination in the major histocompatibility complex between the loci controlling mixed lymphocyte reactivity and the Ag-B histocompatibility antigens provides evidence for the separateness of these loci. Since the portion of the genetically determined mechanism controlling antibody responsiveness which is linked to the MHC was that characteristic of the MLR type, it too must lie outside the region defined by the serological specificities of theAg-B haplotype.
International Journal of Immunogenetics | 1976
John W. Shonnard; Donald V. Cramer; Paul E. Poloskey; Bridgett K. Davis; Thomas J. Gill
The Ag‐B allotype, mixed lymphocyte reactivity (MLR) and the immune response to poly(Glu52Lys33Tyr15) were assayed in male rats from the F2 hybrid and two back‐cross generations of the F344 and DA strains in order to investigate the structure of the rat major histocompatibility complex. No disparity between Ag‐B type and mixed lymphocyte reactivity was found in 263 animals. The immune response to poly(Glu52Lys33Tyr15) was closely linked to the Ag‐B locus, and both antibody production and the delayed hypersensitivity response were under polygenic control. These results suggest that the genetic loci which determine these responses in the rat are closely linked and that recombinational events between the Ag‐B and MLR loci are infrequent.
International Archives of Allergy and Immunology | 1977
Thomas J. Gill; Heinz W. Kunz; Bridgett K. Davis
The offspring of low responder F344 female rats that were immunized with poly(Glu52Lys33Tyr15) aggregated with MeBSA prior to mating showed a higher antibody response to the polypeptide antigen than did the offspring of unimmunized females. Immunization of the mothers with unaggregated polypeptide, or with DNP-BGG, did not affect the antibody response of the offspring even when high doses of antigen were used. When the polypeptide used to immunize the mothers was given as an aggregate, some crossed the placenta to the fetus. The antigen was first detected in the placenta, blood and liver of the fetus at 15 days of gestational age. After birth, it was in the liver and spleen up to 6 weeks af age, and thereafter it was present only in the bone marrow.
Cellular Immunology | 1977
Donald V. Cramer; John W. Shonnard; Bridgett K. Davis; Thomas J. Gill
A significant in vitro antigen-induced lymphocyte proliferation to poly(Glu 52 Lys 33 Tyr 15 ) was observed in sensitized splenic lymphocytes from the DA strain of rats. In segregating F2 and backcross populations the response was linked to the major histocompatibility (Ag-B or H-1) complex. Nylon wool column purification of splenic lymphocyte preparations demonstrated that the proliferative response was thymus-dependent. Alloantisera produced against lymphocytes were capable of inhibiting the proliferative response and absorption studies suggested that the antibody specificities responsible for inhibition were directed at least in part against the serologically defined histocompatibility antigens present on erythrocytes.
International Journal of Immunogenetics | 1977
Bridgett K. Davis; John W. Shonnard; Thomas J. Gill
This study examined IgM antibody produced by highly responding ACI and poorly responding F344 rats following immunization with poly(Glu52Lys33Tyr15) or poly(Glu32Lys33Tyr15) aggregated with methylated bovine serum albumin (MeBSA). The ACI rats produced both IgM and IgG plaque‐forming cells (PFC) following immunization with either form of antigen. The F344 rats did not respond to unaggregated poly(Glu52Lys33Tyr15), but they produced significant amounts of IgG PFC and extremely small amounts of IgM PFC after immunization with poly(Glu52Lys33Tyr15)/MeBSA. Both high and low responder rats had similar kinetic profiles of IgM antibody production, and this antibody had nearly identical avidity in both strains with no evidence for any maturation in avidity. thus, one of the genetic defects in the antibody response to poly(Glu52Lys33Tyr15) is an inability of the F344 strain to produce large amounts of IgM in response to this antigen.
American Journal of Clinical Pathology | 1979
H. Richard Hellstrom; Bridgett K. Davis; John W. Shonnard
JAMA | 1983
Jeffery J. Zuravleff; Victor L. Yu; John W. Shonnard; Bridgett K. Davis; John D. Rihs
Journal of Immunology | 1978
Donald V. Cramer; Bridgett K. Davis; John W. Shonnard; Otakar Štark; Thomas J. Gill
Journal of Immunology | 1975
Bridgett K. Davis; Thomas J. Gill