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R D Cardiff

Publications and source records attributed to R D Cardiff.

141 records · Page 8Linked to original sources
PubMed1971

Immunological and biophysical separation of dengue-2 antigens.

Antigenic compositions of slowly sedimenting dengue-2 hemagglutinin (SHA) and soluble complement-fixing antigen (SCF) were compared with the virion (rapidly sedimenting hemagglutinin, RHA) by radioimmune precipitation (RIP), RIP inhibition, kinetic neutralization, and neutralization blocking tests with the use of hyperimmune mouse ascitic fluids. RHA and SHA were unable to inhibit completely the RIP of each other by anti-RHA, and neutralization by anti-RHA was not blocked by SHA. This indicated that SHA is serologically related, but not identical, to RHA. SHA differed from RHA in that SHA lacked the "core" polypeptide but contained the two envelope polypeptides. In addition, SHA contained a polypeptide with a molecular weight of 16,500 daltons and a suggestion of several other proteins. These data, when considered with other evidence, suggest that SHA is a special form of "incomplete virus." SCF was unable to inhibit the RIP of SHA or RHA or to block neutralizing antibodies. Further, anti-SCF did not neutralize RHA or precipitate significant levels of SHA or RHA. Polyacrylamide gel electrophoresis separated SCF from structural polypeptides by molecular size. This evidence suggests that SCF is a nonstructural antigen.

Acrylates↗
PubMed1970

Dengue virions and antigens in brain and serum of infected mice.

The temporal relationships of the production of infectious dengue-2 virus and its antigens were investigated in intracerebrally infected suckling mice. Infectious virus, a slowly sedimenting noninfectious hemagglutinin (SHA), and a noninfectious soluble complement-fixing antigen (SCF) were found in the brain. Serum contained high concentrations of SCF antigen relative to infectivity when compared to SCF to infectivity ratios in the brain. Degradation of virions by Tween-80 and ether produced two antigens with sedimentation characteristics similar to the noninfectious antigens occurring naturally in infected tissues. However, the virionderived SHA differed from native SHA when examined by electron microscopy and by equilibrium centrifugation in cesium chloride. Virion-derived SCF (as well as the virions and both SHA antigens) was denatured by sodium lauryl sulfate (SLS) and 2-mercaptoethanol (2-ME), whereas native SCF retained its complement-fixing activity. SLS and 2-ME treatment of dengue-1 and dengue-2 sucrose-acetone antigens increased their serotypic specificity. The hemagglutinin present in sucrose-acetone antigens was predominantly native SHA.

Animals↗
PubMedDate not supplied

Hairy cell leukemia has a B-cell genotype.

The phenotype and, by inference, the cell of origin of some lymphocytic neoplasms has been defined by surface marker studies; however, the precise cellular origin of other neoplasms of the lymphoid system is still unknown. For example, with reference to hairy cell leukemia (HCL), cell marker data has been used in support of a monocytic, a T cell, or a B cell origin. If hairy cell leukemia is a B cell-derived neoplasm, the controversy may be resolved by genotyping the cells, using the rearrangement of immunoglobulin genes as a marker of the B cell nature of the process. Rearrangement of these genes is detected using the Southern blot technique and cloned probes specific for the JH segment of the immunoglobulin genes. In this study, the arrangement of the immunoglobulin genes was analysed in normal tissue, in two accepted B cell lymphomas and in nine cases of hairy cell leukemia. DNA from peripheral blood leukocytes (two patients) and from the spleen (seven patients) revealed a discrete new JH restriction fragment length in the leukocytes of hairy cell leukemia cases. The presence of rearranged restriction fragments is interpreted as evidence of the existence of clonal B cell populations. Three of six samples had rearranged kappa light chain fragments. We conclude that most cases of hairy cell leukemia have a B cell genotype. The use of genotyping has wider application in the analysis of hematological malignancies.

B-Lymphocytes↗
PubMedDate not supplied

Proto-neoplasia revisited: the molecular biology of mouse mammary hyperplasia.

The mouse mammary tumor model is a well characterized multistep tumor system which has been used to study characteristics of protoneoplastic and neoplastic lesions of the breast. The ability to transplant mammary epithelial tissue or cells into gland cleared fat pads makes this system more powerful and versatile than most tumor models. Transplantability has provided sufficient tissue to allow sequential molecular analysis of protoneoplastic tissue, making studies of clonality and oncogene activation during tumorigenesis possible. It has also been extensively used for the study of a wide range of carcinogenic agents. The recent development of transgenic mice and transgenic mammary gland technologies provide exciting new avenues of research by providing the opportunity for prospective in-vivo studies of carcinogenesis.

Animals↗
PubMedDate not supplied

Delayed wound healing and disorganized neovascularization in transgenic mice expressing the IP-10 chemokine.

IP-10 is a member of the alpha or cysteine-X amino acid-cysteine (CXC) chemokine family of chemotactic cytokines. High levels of IP-10 expression have been detected in a number of chronic human inflammatory conditions, including psoriasis, a common inflammatory disease of the skin. IP-10 has been shown to chemoattract activated T cells, inhibit the proliferation of endothelial cells, and inhibit the growth of tumors in vivo. To determine the capacity of IP-10 to modulate the inflammatory response in vivo, we have created transgenic mice that constitutively express IP-10 from keratinocytes. These mice developed normally and, in general, did not spontaneously recruit leukocytes into the skin or other organs that expressed the transgene. In addition, the transgenic mice had a normal cutaneous contact hypersensitivity cellular immune response. However, IP-10 transgenic mice had an abnormal wound healing response characterized by a more intense inflammatory phase and a prolonged and disorganized granulation phase with impaired blood vessel formation. These results have demonstrated that IP-10 can inhibit the neovascularization associated with a physiological response in vivo and have revealed a novel biologic activity of IP-10 as an inhibitor of wound healing.

Animals↗