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D D Anthony

Publications and source records attributed to D D Anthony.

32 records · Page 2Linked to original sources
PubMed1981

Induction of uterine cancer with inactivated herpes simplex virus, types 1 and 2.

A series of studies were performed to evaluate the oncogenic potential of inactivated herpes simplex viruses types 1 (HSV-1) and 2 (HSV-2) in the mouse cervix. HSV-1 or HSV-2 prepared in HEp-2 cell cultures and inactivated by exposure to formalin or ultraviolet light was applied to the mouse cervix for periods ranging from 20 to 90 weeks. Control mice were exposed for the same period to control fluids. Vaginal cytologic preparations from all animals were examined weekly to detect epithelial abnormalities. Animals were sacrificed and histopathological studies were carried out when cellular changes seen on vaginal smears resembled those indicative of premalignant or malignant changes as previously established in a similar model system using coal tar hydrocarbons. Other animals were exposed for periods up to 90 weeks, or until there was cellular evidence of invasive cancer. Cytologic and histologic materials were coded and evaluated without knowledge of whether they were from virus-exposed or control animals. Premalignant and malignant cervical lesions similar to those that occur in women were encountered in 78 to 90% of the virus-exposed animals. All controls were normal. Invasive cancer was detected in 24 to 60% of the animals and dysplasia was found in 18 to 66%. The yield of invasive cancer was twice as great after exposure to ultraviolet-inactivated HSV-2 as compared with formalin-inactivated virus. Various histologic grades of carcinoma of the cervix and endometrium were found. No primary lesions were found in the vagina or ovaries.

Adenocarcinoma↗
PubMed1980

Conformational changes in deoxyribonucleic acid during transcription.

Circular dichroism (CD) was used to examine changes in secondary structure of calf thymus DNA during in vitro transcription. Formation of a binary complex between DNA and RNA polymerase (nucleoside triphosphate:nucleotidyltransferase, EC 2.7.7.6) did not alter the CD spectrum of the DNA. Alterations in ellipticity in the spectral region between 245 and 300 nm occurred during synthesis of RNA. This change was consistent with a B- to A-like form transition in polynucleotide conformation. The increment of ellipticity consisted of two separate compounds; component I was insensitive to treatment with pancreatic ribonuclease whereas component II was a ribonuclease labile fraction. Cleavage by restriction endonucleases did not produce or significantly alter the ellipticity of transcription. In contrast, between 50% and 60% of the component I ellipticity was sensitive to pancreatic DNase I. The data indicate that component I is a property of DNA and suggest that the alteration in secondary conformation which affects this component extends cooperatively beyond the DNase I insensitive DNA-RNA polymerase complexes.

Animals↗
PubMed1975

Changes in ribosomal RNA processing paths in resting and phytohemagglutinin-stimulated guinea pig lymphocytes.

Processing of rRNA was examined in resting and phytohemagglutinin-stimulated guinea pig lymphocytes. Synthesis of 1.7 (28S) and 0.7 (18S) X 10(6) dalton rRNA was more than 4-fold greater in phytohemagglutinin-stimulated than in resting cells. A 5- to 10-fold increase in flux of molecules through a 2.3 X 10(6) dalton RNA occurred without a concurrent change in the flux through a 2.6 X 10(6) dalton fraction in phytohemagglutinin-stimulated cells. In both resting and phytohemagglutinin-stimulated lymphocytes, the 2.3 X 10(6) dalton intermediate equilibrated with [3H]methyl label and pulse-chased prior to the 2.6 X 10(6) dalton RNA. The data indicate at least two processing paths in guinea pig lymphocytes; one proceeds to rRNA via a 2.3 X 10(6) dalton intermediate, and another proceeds via a 2.6 X 10(6) dalton RNA. The increase in rRNA synthesis in phytohemagglutinin-stimulated cells occurs primarily through that path containing the 2.3 X 10(6) dalton intermediate.

Animals↗
PubMed1973

Relationship of replication and transcription of Simian Virus 40 DNA.

RNA produced by the Simian Virus 40 (SV40) mutant tsA30 during lytic infection of kidney cells of African green monkeys was examined by RNA-DNA competition-hybridization. This mutant is temperature-sensitive in a function (gene A) that regulates synthesis of viral DNA. No detectable difference between mutant RNA synthesized at the permissive temperature (33 degrees ) and wild-type viral RNA was found. During continuous infection with the mutant at the restrictive temperature (41 degrees ) only early viral RNA was produced. When mutant DNA and late RNA synthesis were initiated at the permissive temperature, a shift to the restrictive temperature rapidly terminated synthesis of viral DNA but not that of late viral RNA. The data indicate that the function of gene A is required before synthesis of late viral RNA and that after initiation, the production of late RNA continues without further expression of gene A or concomittant viral DNA synthesis.

Animals↗
PubMedDate not supplied

Wegener granulomatosis simulating bacterial endocarditis.

Cardiac involvement in Wegener granulomatosis is uncommon. We report a case of Wegener granulomatosis that presented as culture-negative endocarditis with aortic valvular vegetation. The clinical manifestations included gingival hyperplasia, gangrenous digital infarcts, mononeuritis multiplex, high fever, inflammatory arthritis, pansinusitis, splenic infarct, and aortic valvular vegetation, which underscore the difficulty of distinguishing systemic vasculitis from bacterial endocarditis. Contrary to the common notion that valvular vegetation is invariably associated with bacterial endocarditis, this case proves that such findings can occur in Wegener granulomatosis as well. Clinicians are guided toward early treatment with corticosteroids and cyclophosphamide to prevent fatal complications.

Aortic Valve↗
PubMedDate not supplied

Immunization with TCR Vbeta10 peptide reduces the frequency of type-II collagen-specific Th1 type T cells in BUB/BnJ (H-2q) mice.

OBJECTIVE: Collagen induced arthritis (CIA) in mice is mediated by synergistic T cell and humoral immune responses specific for type II collagen (CII). We have previously shown that in arthritic joints of BUB mice (TCR Vbetaa, H-2q) the TCR repertoire is enrichedfor Vbeta10 expressing T cells, and that immunization with a Vbeta10 peptide (Vbeta10p) prevents the phenotypic expression of disease. The objective of the present study was to understand how immunization with a synthetic TCR Vbeta peptide affected the development of the pathogenic CII-specific immune response in BUB mice. METHODS: Arthritic and protected animals were tested for Vbeta10p- and CII-specific cytokine production by a highly specific and sensitive ELISA spot assay, andfor CII-specific antibody production by standard ELISA. In adoptive transfer experiments, Vbeta10p-specific LN cells (INF-gamma producing) were injected into naive mice prior to immunization with type-II collagen/CFA. RESULTS: Immune cells from arthritic animals produced IFN-gamma and IL-2, without IL-4 and IL-5 in response to CII and an immunodominant epitope, A2, derivedfrom CII. Serum from these mice contained anti-CII antibodies of both IgGI and IgG2a subtypes. Our results show for thefirst time that immunization with Vbeta10p resulted in Vbeta10p-specific IFN-gamma and IL-2 production that was restricted to the CD4+ T cell subset. Emergence of this Vbeta10p-specific immune response was associated with a dramatic decrease in the frequency of CII and A2-specific, cytokine producing T cells in arthritis protected mice. Protective immunity was cell mediated and could be adoptively transferred. In contrast, the protective immunization had only a marginal effect on the anti-CII antibody response indicating that the CII specific humoral immune response was not significantly affected. CONCLUSION: Immunization with TCR Vbeta10p leads to expansion of a population of Vbeta10p- specific CD4+ Tcells. This anti-TCR Vbeta10p specific type 1 cytokine producing immune response was protective in adoptive transfer studies and appears to inhibit the expansion of the pathogenic anti-CII cellular immunity. Additionally, the anti-TCR Vbeta10p-specific cellular immune response was mediated by CD4+ T cells and these T cells did not produce IL-4 or IL-5. Thus, our results suggest that protection against CIA in mice immunized with synthetic TCR Vbeta10p was achieved by a specific down-regulation of the CII-specific Thl type cellular immune response and not via immune deviation.

Animals↗