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Biomedical subjects

D S Yohn

Publications and source records attributed to D S Yohn.

At least 19 recordsLinked to original sources
PubMed1980

Simian virus nomenclature, 1980.

Approximately 75 simian viruses, counterparts of other animal viruses, are recognized. Nomenclature of these isolates, in general, consists of an SV (simian virus) or SA (simian agent) numerical series with no attempt to group them according to virus families. The biologic characteristics of these viruses indicate they may be classified into recognized families and groups. A simple sequential numerical designation is recommended as a nomenclature within virus families and groups. Finalization of nomenclature would follow approval by the Study Groups of the International Committee on Taxonomy of Viruses.

Adenoviruses, Simian↗
PubMed1978

Chemical carcinogen alteration of SV40 virus induced transformation of normal human cell populations in vitro.

The frequency of simian papovirus 40 (SV40) induced transformation of human cells was enhanced after pretreatment with either napthylamine-2,N-methyl-N'-nitrosoguanidine (MNNG), N-acetyl-2-fluorenylacetamide (N-Ac-AAF), benzo[a]pyrene (BP), aflatoxin B1, propane sultone (PS), beta-propiolactone, 4-nitroquinoline oxide (4-NQO), methylmethane sulfonate (MMS) or diethyl nitrosamine (DEN). Posttreatment with 4-NQO, MMS, MNNG or DEN inhibited transformation; while posttreatment with either aflatoxin B1, beta-propiolactone or napthylamine-2 did not alter transformation similar to the action of N-Ac-AAF and BP. All carcinogens that altered transformation after pretreatment damaged cellular DNA. Pretreatment or posttreatment with carcinogens 3-methylcholanthrene (3-MCA) or 7,12-dimethylbenzanthrene (7,12-DMBA), that did not damage cellular DNA also did not enhance transformation. Moreover, pre- or posttreatment with other weak or non-carcinogens that did not damage cellular DNA did not alter virus induced transformation. All foci formed in the co-carcinogen treated cultures whether the carcinogen inhibited or enhanced transformation were virus directed. While a similar pattern of response existed for carcinogens that either enhance or inhibit transformation, each of the carcinogens that enhanced or inhibited foci formation damaged cellular DNA. Moreover, those carcinogens that enhanced focus formation, compared to the carcinogens that inhibited focus formation, exhibited similar DNA damage profiles.

Carcinogens↗
PubMed1978

Biochemical activation of aryl hydrocarbon hydroxylase activity, cellular distribution of polynuclear hydrocarbon metabolites, and DNA damage by polynuclear hydrocarbon products in human cells in vitro.

Carcinogenic polynuclear hydrocarbons [7,12-dimethylbenzanthracene, 3-methylcholanthrene, and benzo(a)pyrene] were added to human skin fibroblast cell cultures. Only benzo(a)pyrene at 10 microgram/ml or above induced mixed-function hydroxylase activity, altered cell proliferation kinetics, and caused DNA damage as measured by altered grain count and bromodeoxyuridine incorporation. 3-Methylcholanthrene at concentrations as high as 15 microgram/ml was ineffective. 7,12-Dimethylbenzanthracene at 6 microgram/ml or above induced mixed-function oxygenase and stimulated DNA synthesis and cell proliferation, but at those concentrations little or no cytotoxicity or DNA damage was detected. The noncarcinogenic analogs 6,8,12-trimethylbenzanthracene, 5-fluorodimethylbenzanthracene, anthracene, and phenanthrene had no detectable effect on the human cells. It was concluded that benzo(a)pyrene can initiate all the biochemical events in human cells probably necessary to initiate transformation of human cells in vitro.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1977

Preparation of cell-free feline oncornavirus-associated cell membrane antigen.

Cell-free feline oncornavirus-associated cell membrane antigen (FOCMA) was prepared from a feline lymphoblastoid cell line of tumor origin (FL-74). Membrane fractions, separated on sucrose density gradients, and papain-solubilized products were found to contain FOCMA as determined by their capacity to inhibit reference cytotoxic cat antisera.

Animals↗
PubMed1976

Effects of steroid hormones in fetal bovine serum on plating ang cloning of human cells in vitro.

Fetal bovine sera from each of three different commercial sources were tested for their ability to support cloning of human fibroblastoid cells in vitro. Cloning efficiencies varied according to serum source. Serum (10 samples) from company A did not support growth, while sera (10 samples) from companies B and C provided adequate to excellent conditions for cloning and growth. Cells from neonatal foreskin or embryonic lung responded to each serum similarly. Bovine serum albumin type H7 from company C supported cell growth in media without serum. Sera containing 1.0 ng per ml or more of progesterone inhibited growth, whereas sera containing less than 1.0 ng per ml supported cloning and growth. In the low progesterone sera, the concentration of 17-beta-estradiol exceeded 100 pg per ml. Growth supporting sera could be made non-supportive by adding 0.1 mug per ml of progesterone. The addition to non-supporative sera of 0.1 mug per ml of 17-beta-estradiol or hydrocortisone made these sera supportive of cell growth. Addition of estrogen or hydrocortisone to a culture medium that inhibits growth, with subsequent reversal of the inhibitory effect, implies that these hormones competitively regulate growth of responsive cells in vitro.

Blood↗
PubMed1976

Influence of culture conditions of growth of FL-74 cells and feline oncornavirus cell membrane associated antigen production.

The FL-74 cell, a feline lymphoblastoid cell line derived from a tumor induced by leukemia virus, grows equally well in static suspension culture (plastic T-flask or silicone treated glass bottles) or in spinner culture. No growth was observed in unsiliconized glass bottles. Although feline leukemia virus production was nearly the same in FL-74 grown in each of the above types of vessel, the expression of the feline oncornavirus membrane associated antigen (FOCMA), as determined by membrane immunofluorescence, was more intense and more complete on cells grown in static suspension. Moreover, higher fluorescent antibody titer endpoints were observed with cells from static suspension cultures than with cells from spinner cultures, FL-74 cells grown in spinner culture, when subjected to partial synchrony by cold block or by deprivation of essential amino acids (arginine and/or isoleucine) for 12 hr, achieved a membrane fluorescent pattern for FOCMA similar to cells grown in static suspension. It is proposed that the expression of FOCMA on the cell membrane surface is cell-cycle dependent, and that the rate at which a cell passes through the cell cycle determines the pattern and intensity of the fluorescence of the cell membrane.

Antigens, Viral↗
PubMed1976

Feline oncornavirus-associated cell membrane antigen. VI. Cytotoxic antibody in cats exposed to feline leukemia virus.

Feline leukemia virus (FeLV)-infected specific pathogen-free (SPF) cats, normal uninfected SPF cats, and healthy cats from leukemic households were tested for antibody reactive to the feline oncornavirus-associated cell membrane antigen (FOCMA)-containing target cell line FL-74 by microcytotoxicity and indirect membrane immunofluorescence. Of the infected SPF animals, 81% showed concordant reactivity for the two tests. In contrast, only 55% of the healthy cats known to be naturally exposed to FeLV for long periods showed such concordance. FOCMA antibody could not be detected in normal SPF cats by either indirect membrane immunofluorescence or microcytotoxicity. Most cats in the FeLV-infected SPF group developed antibody detectable by both procedures by the fifth week post inoculation. Antibody detectable by membrane immunofluorescence persisted in a high percentage (75-90%) of the animals throughout the observation period of 19 weeks; after 9 weeks, fewer cats had antibody that was also detectable by microcytotoxicity.

Animals↗
PubMed1976

Characterization of feline T-and B-lymphocytes and identification of an experimentally induced T-cell neoplasm in the cat.

Membrane markers of feline T- and B-lymphocytes were identified for further investigation of leukemogenesis in the cat. Feline T-cells formed spontaneous erythrocyte rosettes with guinea pig (GPE) and rat erythrocytes (RE). The receptors for GPE and RE were separate entities and expressed independently on lymphoid cell membranes. The RE receptor appeared to be present only on more mature or differentiated T-cells, whereas the GPE receptor reacted with a broader population that included less differentiated T-cells. Feline B-cells bore a complement receptor that was detected by adherence of SE coated with antibody and complement. Malignant lymphoblasts obtained from thoracic fluid of cats with feline leukemia virus (FeLV)-induced thymic lymphosarcomas, as well as FL-74 cells (a FeLV-transformed feline lymphoblastoid cell line) expressed T-cell markers. These results provided definitive evidence for markers of feline T- and B-cells and identified an experimentally induced T-cell lymphosarcoma.

Animals↗
PubMed1976

Lymphocyte mitogen reactivity and enumeration of circulating B- and T-cells during feline leukemia virus infection in the cat.

Mitogen-induced blast transformation of peripheral blood lymphocytes and quantitative changes in circulating T- and B-cells were studied serially in cats inoculated with feline leukemia virus (FeLV). Concanavalin A-induced blast transformation sharply declined beginning at 5 weeks post inoculation (Pl) in FeLV-infected cats when compared to age-matched uninfected control cats. Similar but less consistent changes were seen in responses to pokeweed mitogen-induced stimulation. In most infected kittens this defect persisted until they died from thymic lymphosarcoma, 15-24 weeks Pl. An early lymphopenia, due primarily to a decrease in circulating B-cells, occurred in infected cats 5-8 weeks Pl. Following a return of total and B-lymphocytes to control values, infected cats developed increased numbers of T-cells at 16 or more weeks Pl, which correlated with circulating lymphoblastic lymphocytes bearing T-cell markers. These results correlated neoplasia arising in a thymus-derived lymphocyte population with mitogenic hyporeactivity in the preneoplastic period and suggested that FeLV-induced immune alterations may be a necessary antecedent of leukemogenesis in the cat.

Animals↗
PubMed1976

Influence of glucocorticoid, estrogen, and androgen hormones on transformation of human cells in vitro by feline sarcoma virus.

Infection of human foreskin cells (D-550) by the Snyder-Theilen strain of feline sarcoma virus produced small but countable foci and demonstrated "single-hit" dose-response kinetics. Significant quantitative and qualitative enhancement of focus formation was observed when the glucocorticoid hormones, dexamethasone, hydrocortisone, cortisol acetate, and prednisolone were added to cell cultures (1.0 mug/ml) 24 hr postinfection. However, aldosterone, while inducing qualitatively larger foci, did not bring about a quantitative enhancement in total foci number. By contrast, 17beta-estradiol, progesterone, cortisone acetate, methyltestosterone, and estrone elicited little or no effect on focus induction by Snyder-Theilen feline sarcoma virus. Evidence is suggestive of a posttranscriptional effect possibly modulating viral genome expression resulting in an increased efficiency of viral transformation, and an increased proliferation of transformed cells.

Aldosterone↗
PubMed1976

Experimental oncornavirus vaccines in the cat.

An experimental approach to the immunoprophylatic control of feline oncornavirus-mediated diseases has included induction of antivirus immunity and antibodies to the feline oncornavirus-associated membrane (tumor) antigens. A suitable model for exploring the effectiveness of killed oncornavirus vaccines in the cat has been provided by the use of feline sarcoma virus. Immunization of seven pregnant queens over a 6-week period with ultraviolet light-inactivated Gardner-Arnstein feline sarcoma virus resulted in significant protection among 12 kittens challenged with a tumor-forming Dose 90 at 7 days of age. This immunity was not present in kittens challenged at 35 days of age. Among 12 kittens born of queens immunized during pregnancy with ultraviolet light-inactivated Kawakami-Theilen feline leukemia virus and challenged with the same live virus at 4 days of age, significant protection was noted, ranging from prolongation of survival time to complete protection in 3 kittens. In general, the higher the antibody titer in the mother, the more effective the protection afforded the kittens. Immunization of 43 kittens during their first 5 weeks of life with the same vaccines used in adult cats did not immunize sufficiently to protect against feline sarcoma virus challenge at 5 weeks of age. Neutralizing antibody responses in these kittens were significantly lower than in pregnant queens. That kittens of this age are immunologically responsive was established, since complete protection of 9 kittens to feline sarcoma virus was obtained by immunization with a crude tumor extract inactivated with 5 to 7 megarads of gamma-irradiation. All these kittens developed feline oncornavirus-associated membrane antibodies while 3 developed demonstrable levels of virus-neutralizing antibodies. The results of these studies are believed indicative that killed virus vaccines and tumor vaccines can be effective immunoprophylatic measures in the control of RNA tumor virus oncogenesis in the cat. Developments in this model system should be relevant to any consideration given similar vaccines in humans.

Age Factors↗
PubMed1975

Feline oncornavirus-associated cell membrane antigen. V. Humoral immune response to virus and cell membrane antigens in cats inoculated with Gardner-Arnstein feline sarcoma virus.

Tumor growth responses in 5- to 6-week-old kittens inoculated with the Gardner-Arnstein strain of feline sarcoma virus exhibited three distinct pattern: 1) complete tumor regression or no detectable tumor growth in approximately one-third of 43 inoculated kittens, 2) rapid tumor progression which led to debilitation and death within 16.2 +/- 4.2 weeks following infection in an additional one-third, and 3) slow tumor growth or temporary regressions in the remaining third. The feline oncornavirus-associated cell membrane antigen (FOCMA) antibody response was closely correlated with tumor progression; rapid progressors had the lowest antibody titers, whereas those in the "no tumor or permanent regression" categories had the highest titers. These results agreed with those previously observed with another virus strain, the Snyder-Theilen feline sarcoma virus. Cats in the intermediate categories of tumor growth also had intermediate levels of FOCMA antibody. The presence of virus-neutralizing (VN) activity was not always correlated with anti-FOCMA activity. Animals in the rapid-progressor category, compared to the regressors or slow progressors, were more likely to have detectable VN antibody during early periods. Conversely, animals in the regressor group or group with no tumors were more likely to show an early rise in detectable anti-FOCMA activity than animals in either of the progressor groups.

Animals↗
PubMed1975

Complement-fixation-inhibition as a test for antibodies in cats and humans to C-type RNA tumor virus antigen.

The complement-fixation-inhibition (CFI) test was evaluated as a means of detecting humoral antibodies in cat sera and in human sera to mammalian C-type RNA virus interspecies antigen(s). CFI antibody titers of greater than or equal 1:2 were detected in sera from all tumor bearing (23) and normal cats (23), however, sera from most germ free cats were negative. When the same cat sera were tested for blocking antibody by the paired radioiodine labeled antibody technique the correlation between the radioimmune assay and CFI tests was 85%. Sera from 378 cancer patients and 193 normal people were tested for antibodies to the mammalian oncornavirus interspecies-specific antigen in the CFI test. This test used a rabbit antiserum prepared toward a purified feline leukemia virus (FeLV) interspecies antigen. Disrupted Rauscher murine leukemia virus (RLV) was used as source of interspecies antigen in the CFI test. A significantly (P=0.01) higher number of reactions occurred with sera from patients with lymphosarcoma (70.4%), osteosarcoma (41.0%), reticulum cell sarcoma (56.7%), and rhabdomyosarcoma (31.8%) as opposed to sera from normal individuals (6.2%). Of 51 sera from patients with acute lymphocytic leukemia 23.5% (P=0.05) were reactive. Of the sera from 88 breast cancer patients 22.7% reacted, as opposed to 7.8% of 116 normal females and 13.9% of 43 patients with benign breast disease. CFI antibody titers were shown to be dependent on RLV antigen concentration. Absorption with human A and B red blood cell (RBC) and Forssman antigen did not reduce the CFI titers in human sera whereas absorption with RLV reduced them significantly. By indirect radioimmunoelectrophoresis the antibody in selected human sera was shown to be an IgG.

Animals↗
PubMed1975

Alterations of enzymes associated with plasma membranes and cellular organelles during infection of CV-1 cells with Yaba tumor poxvirus.

The formation of cellular aggregates (foci) in CV-1 cells following infection with Yaba tumor poxvirus is dependent upon cell passage level, temperatue of incubation, and calcium concentration in the medium. Resistance of older cells can be reversed by maintaining calcium at 0.1 mM or by adding cortisone acetate (1 mug/ml), hydrocortisone, or estradiol-17beta to the cultures. In susceptible cells, foci formation was inhibited slightly by methyltestosterone and inhibited completely by dexamethasone, aldosterone and progesterone. Activities and patterns of enzymes associated with cytoplasmic membranes (alkaline phosphatase, mononucleotidase, and Na+-K+-adenosine triphosphatase) and lysosomes (beta-glucuronidase and acid phosphatase) of the younger susceptible and the older resistant CV-1 cells differed. These differences apparently occurred in concert with phenotypic changes in the membranes that reduced the mobility of older resistant cells. In susceptible culture, unifected cells migrated to the infected cell and participated in foci formation. Reduction of the calcium content to 0.1 mM apparently removed some of the constraints on mobility of the resistant cells. Although the hormones may have had a similar effect, the changes in enzyme patterns indicated basic alterations in protein synthesis. The development of resistance to foci formation occurred between the 45th and 50th passage level. Hormonal reversal of this resistance resulted in enzyme profiles that reflected the pattern of young susceptible cells.

Acid Phosphatase↗
PubMed1975

Feline oncornavirus-associated cell membrane antigen. II. Antibody titers in healthy cats from household and laboratory colony environments.

Antibody titers to the feline oncornavirusassociated cell membrane antigen (FOCMA) were determined for 447 healthy cats from laboratory colony and household environments. Only 2.7 percent of 221 cats from colony environments were antibody positive as compared to 50.4 percent of 256 cats from household environments. Incidence of FOCMA antibody and geometric mean antibody titer for pet cats from New York City representing single cat apartment habitats were substantially lower than values for unscreened cats from the Boston, Glasgow, and Detroit suburban environments. Geometric mean antibody titer for young adults in the Boston population was significantly higher than titers for kittens or aged cats. This may be due to greater mobility resulting in increased exposure to other cats. In contrast to the high frequency of FOCMA antibody positivity in pet-cat populations, less than 2 percent of the same groups were positive for virus group-specific antigen in peripheral blood leukocytes and platelets. This was interpreted as an indication that many more cats became infected with feline leukemia virus under natural conditions that the number developing persistent virus infection and/or clinical leukemia.

Animals↗