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Biomedical subjects

R G Olsen

Publications and source records attributed to R G Olsen.

At least 109 records · Page 6Linked to original sources
PubMed1981

Feline oncovirus-associated cell membrane antigen and feline leukemia virus group-specific antigen expression in bone marrow and serum.

Feline retrovirus-induced possible preneoplastic lesions were identified by detection of feline oncovirus-associated cell membrane antigen (FOCMA) in bone marrow (BM) and mesenteric lymph nodes of noninbred, domestic short- or long-hair kittens. Cell-bound FOCMA was detected 1-3 weeks after feline leukemia virus (FeLV) infection and at least 6 months before a tumor was evident. BM FOCMA was detected earlier and reached higher levels at early periods in cats that became persistently viremic. Serum FeLV group-specific antigen (gsa) increased more rapidly and reached a higher level in cats that became persistently viremic, but nonviremic cats still had detectable gsa as late as 7-9 months after FeLV infection, even in the presence of high levels of viral antibody. The presence in nonviremic cats of FeLV gsa in sera and FOCMA in BM and sera suggests that these cats may have a persistent, low-level FeLV infection.

Animals↗
PubMed1981

Determinants of susceptibility and resistance to feline leukemia virus infection. I. Role of macrophages.

The role of autochthonous peritoneal feline macrophages (M theta) in the age-related resistance of cats to feline leukemia virus (FeLV) was investigated by a study of the functional properties and FeLV susceptibility of M theta from kittens and adult cats and the effect of hydrocortisone (HC) and silica on M theta-FeLV interactions. Although the phagocytic functions of isolated M theta from kittens and adults were equivalent, the mean FeLV susceptibility of M theta from kittens was five times that of M theta from adult cats, thus establishing a direct correlation between the age-related susceptibility of cats and M theta from cats to FeLV. M theta of viremic cats were found to be infected with FeLV in vivo; virus titers were slightly higher than those obtained after in vitro infection of M theta, M theta from cats that had experienced regressive FeLV infection were not significantly more resistant to FeLV infection in vitro than were M theta from naive adult specific-pathogen-free cats. HC, which has been shown to enhance the in vivo FeLV susceptibility of cats, also enhanced the permissiveness of M theta from cats to FeLV in vitro (600-fold for M theta from adult cats and 200-fold for M theta) from kittens. M theta permissiveness to FeLV was highly sensitive to HC and occurred in M theta infected in vivo or in vitro. In parallel with the effect of HC on the natural resistance of cats to FeLV, administration of silica before virus inoculation also markedly enhanced the FeLV susceptibility of adult cats. Silica was toxic for isolated M theta but not for lymphocytes in vitro, and silica produced monocytopenia and neutrophilia, delayed skin allograft rejection, and augmented feline oncovirus-associated cell membrane antigen antibody responses in vivo. These experiments indicate that M theta were linked to the natural resistance of cats to FeLV and that the temporary elimination of M theta functions (e.g., by silica) and/or the conversion of the M theta-FeLV relationship from a nonpermissive to a permissive state (e.g., by corticosteroids) resulted in failure of early virus containment, in persistent virus amplification in hemolymphatic tissues, and in subsequent FeLV-related proliferative or antiproliferative disease.

Age Factors↗
PubMed1981

Determinants of susceptibility and resistance to feline leukemia virus infection. II. Susceptibility of feline lymphocytes to productive feline leukemia virus infection.

The interplay between feline leukemia virus (FeLV) and feline lymphocytes (lc) infected in vitro or in vivo was investigated. Surface marker analysis and viral infectivity (VI) assays of lc populations were used to determine susceptibility of lc subsets to FeLV. The principal FeLV-replicating cell in the mesenteric lymph node of persistently infected, preleukemic cats was a nonadherent, complement receptor (CR)-bearing lc (B-cell). The lymph nodes of preleukemic cats also had increased numbers of uninfected T-cells [cells forming rosettes with guinea pig erythrocytes (GPE)] and cells with receptors for the Fc portion of 7S IgG (Fc gamma R cells) as compared with lymph nodes of age-matched specific-pathogen-free (SPF) cats. The induction of productive infection of feline peripheral blood mononuclear leukocytes (PBL) in vitro depended on a 48-hour in vitro preincubation period before virus exposure. The equivalent susceptibility of whole and adherent cell-depleted PBL to productive infection and the failure of hydrocortisone to enhance viral infection were compatible with identification of the FeLV-replicating cell as an lc. Furthermore, lc from susceptible SPF kittens replicated 50 times as much FeLV as did lc from resistant adult SPF cats. The Ic productively infected with FeLV after in vitro exposure were more precisely identified with the use of Ficoll-Isopaque density gradient separations of rosetted and nonrosetted lc. Whole PBL, GPE rosette-positive PBL (T-cells), and CR-positive PBL (B-cells) were permissive to FeLV infection, and maximal VI was evident at 14 days after exposure. The substantial (1,325-fold) increment in VI found in the Fc gamma R-depleted PBL suggested a role for Fc gamma R cells in the containment of FeLV infection. Unstimulated mononuclear leukocytes from blood, spleen, lymph node, thymus, and marrow were susceptible to productive FeLV infection after in vitro exposure. The degree of spontaneous DNA synthesis in marrow, thymus, and spleen but not lymph node or PBL was inversely related to permissiveness to viral replication. Mitogen activation of lc was associated with decreased viral replication when either T-cell mitogens (concanavalin A, phytohemagglutinin, or pokeweed mitogen) or a B-cell mitogen (dextran sulfate) was used. Virus production by spleen cells and PBL was enhanced twofold to tenfold by prior lc stimulation by the B-cell mitogen, lipopolysaccharide, or protein A-bearing Staphylococcus aureus, a mitogen for feline T-cells with Fc gamma R. Both productively infected (preincubated) and nonproductively infected (freshly isolated) PBL transferred infectious FeLV to autochthonous peritoneal macrophages (M theta); most of the virus in PBL-peritoneal M theta cocultures was produced by adherent cells, irrespective of whether the adherent or nonadherent cell population was inoculated originally.

Age Factors↗
PubMed1981

Feline leukemia virus-induced erythroid aplasia: in vitro hemopoietic culture studies.

Colony forming unit (CFU) assays were developed for feline granulocyte-macrophage (CFUGM), early erythroid (day 2 CFUE), and late erythroid (day 7 CFUE) colonies in methylcellulose medium. Feline CFUGM and both day 2 and day 7 CFUE were enhanced by feline macrophage conditioned medium and late CFUE often were intimately associated with macrophages. Kittens were inoculated with the Kawakami-Theilen (KT) strain of feline leukemia virus (FeLV) and sequential changes in marrow CFU determined. Erythroid aplasia, characterized by progressive non-regenerative anemia, lymphopenia, and a profound decrease in early and late CFUE but not CFUGM was induced by 3 to 5 weeks after FeLV-KT inoculation. The susceptibility of kittens to FeVL-induced erythroid aplasia was strongly age-related; neonatal kittens were most sensitive and substantial natural resistance developed by 4 weeks of age. The results demonstrate that FeLV-KT infection induced a rapid and selective suppression of erythroid progenitor cells and represents a suitable model of experimentally-induced acquired erythroid aplasia.

Anemia, Aplastic↗
PubMed1981

Evidence for microwave-induced acoustical resonances in biological material.

Pulse bursts of microwave energy were used to stimulate resonant-type acoustical response in a rectangular muscle-equivalent model and in a spherical brain-equivalent model. The rectangular model was irradiated using a military radar transmitter at 5.655 GHz, 200 kW peak, and the spherical model was irradiated using a pulse-type cavity oscillator at 1.10 GHz, 4 kW peak. Hydrophone transducers were implanted in the models to record the microwave-induced mechanical vibrations. Four properly timed radar pulses produced a threefold increase in the acoustical amplitudes in the muscle model. In the spherical model, a pulse train of three properly timed microwave pulses doubled the stress wave amplitudes as recorded by the implanted hydrophone. These results show that certain pulse parameters of microwave irradiation can be adjusted to increase the intensity of induced mechanical vibrations in both rectangular and spherical tissue equivalent models.

Acoustics↗
PubMed1980

Microwave-induced pressure waves in a model of muscle tissue.

Microwave-induced mechanical stress waves were studied in simulated muscle tissue. Pulsed microwave energy at 5.655 GHz induced pressure waves that were recorded with a hydrophone transducer. Each pulse produced a peak power density greater than 1.5 kW/cm2. Microwave absorption measurements within the model showed energy deposition to be mostly confined to a region within 2 cm of the irradiated surface. The average specific absorption rate (SAR) at the surface of the sample was about 100 W/kg. The microwave-induced stress wave propogated at a velocity of 1,600 m/sec with peak pressures of approximately 300 pascals and was detectable after having traveled a total distance of 0.61 m on a path that included two reflections at model-container interfaces.

Absorption↗
PubMed1980

Far-field microwave dosimetry in a rhesus monkey model.

Dosimetric measurements were made in a muscle-equivalent model of an adult rhesus monkey subjected to far-field irradiation at 1.29 GHz. Profiles of microwave-induced heating in the model were obtained at eight locations, and a gradient-layer whole-body calorimeter was used to measure total absorbed energy. Average specific absorption rate (SAR) was calculated both from the calorimeter experiments and from the local temperature measurements. Thermographic imaging techniques were used to qualitatively show the microwave-induced surface heating patterns. For this model the calculated average SAR was 0.15 9W/dg)/(mW/cm2) which, at 1.29 GHs, makes the absorption cross section 84% of the geometric shadow cross section. The SAR is about three times that predicted for a prolate spheroidal model of similar mass. A disproportionally high absorption occurred in the legs of the model positioned parallel to the E-polarization because of what is believed to be partial-body resonance.

Absorption↗
PubMed1980

Feline sarcoma virus induced in vitro progression from premalignant to neoplastic transformation of human diploid cells.

Human diploid cells morphologically transformed by feline sarcoma virus were serially propagated under selective cell culture conditions. When injected into nude mice prior to passage in soft agar (0.35%), morphologically transformed cells did not produce tumors. However, when propagated under selective cell culture conditions, transformed cells grew in soft agar and, when injected subcutaneously into the subcapsular region of the n mu/n mu mice, produced neoplastic nodules histopathologically interpreted as fibromas. Karyological examination of cell populations grown out from the tumors confirmed that the tumors were composed of human cells. Examination of electron micrographs of the excised tumor tissue revealed the presence of budding virus particles. Tumor cells isolated from nude mice and morphologically transformed cells both contained the feline oncornavirus-associatied cell membrane antigen. It was concluded that expression of feline oncornavirus-associated cell membrane antigen is associated with an early stage of feline retrovirus-induced carcinogenesis, namely focus formation. In addition, it was shown that FeLV-FeSV can induce morphological transformation in human cells in vitro and that there is a requirement for the cells to passage through soft agar before subsequent tumor formation (neoplastic transformation) can be demonstrated.

Animals↗
PubMed1980

Suppression of mitogen-induced blastogenesis of feline lymphocytes by in vitro incubation with carcinogenic nitrosamides.

Effects of brief in vitro incubation with nitrosamides on the lymphocyte blast transformation (LBT) response of feline peripheral blood mononuclear cells (PMC) to concanavalin A (con A) was studied. Incubation for 1/2 hr with 10--100 microgram/ml methylnitrosourea (MNU) or 0.1-2.01 microgram/ml methyl-N-nitrosoquanidine (MNNG) caused marked suppression of the normal LBT response. This effect was not due to cytotoxicity, since viability experiments showed no significant decrease in viability for any concentration of either MNU or MNNG. MNU caused suppression when added to PMC cultures 24 hr, but not 48 hr, after initiation of stimulation with con A. Biologically inactivated MNU also caused suppression of the LBT response, similar in magnitude to active MNU. Finally, serum from cats immunologically suppressed by MNU did not cause suppression of the LBT response of normal feline PMC. It was concluded that the immunosuppressive properties of MNU previously noted in vivo are probably due to a direct suppressive effect on lymphocytes and/or macrophages, and that the decreased LBT response to con A of MNU-treated PMC is an accurate reflection of the immunosuppression seen in vivo.

Animals↗
PubMed1979

Enhancement of feline leukemia virus-induced leukemogenesis in cats exposed to methylnitrosourea.

The effect of methylnitrosourea (MNU), a potent resorptive carcinogen, was evaluated for its influence on the susceptibility of adult cats to infection and induction of oncornavirus disease by feline leukemia virus (FeLV). Young adult cats at an age previously demonstrated to be highly resistant to FeLV, were injected intravenously with moderately toxic doses (15-20 mg/kg) of MNU alone or with infections FeLV (Rickard strain). Following exposure to virus and chemical, cats were monitored for antibody to the feline oncornavirus-associated cell membrane antigen (FOCMA), viremia by direct infectivity and the presence of gsa in peripheral blood leukocytes, and for toxic effects of MNU by hemogram analyses on peripheral blood. Of 8 cats injected with MNU + FeLV, 6 developed persistent viremia, 5 of which became debilitated from thymic lymphoma. Only 1 of 6 non-MNU-treated and infected cats of the same age became transiently viremic. FOCMA antibody development was markedly depressed in MNU + FeLV inoculated cats compared with cats inoculated with FeLV alone. Results show that MNU was apparently responsible for the obliteration of age-related susceptibility in cats to FeLV infection and induction of FeLV-related disease, and suggest that in nature exposure to toxic chemical carcinogens may act as factors which determine susceptibility to feline oncornaviruses in the cat.

Age Factors↗
PubMed1979

The effects of methylnitrosourea on the immune system and hematopoietic system of adult specific pathogen free cats.

The effects of a single non-carcinogenic dose of 15 mg/kg methylnitrosourea (MNU) on the immune and hematopoietic systems of adult specific-pathogen-free (SPF) cats were determined. The cell-mediated-immune (CMI) system was markedly suppressed, as evidenced by: (i) Prolonged cutaneous allograft retention time (41-84 days); (ii) Decreased lymphocyte blast transformation response to mitogens (2% of pretreatment response to pokeweed mitogen or concanavalin A) and antigen (12% of untreated control cat response to keyhole limpet hemocyanin); (iii) Reduced number of absolute erythrocyte-rosetting T-cells in the peripheral blood. This immunosuppression lasted at least 3 months, the duration of the experiment. Suppression of the hematopoietic system was also noted as evidenced by: (i) Peripheral lymphopenia lasting 3 months and neutropenia lasting 3 weeks; (ii) Bone marrow hypocellularity lasting 3 weeks; (iii) Hypoplasia of neutrophilic precursors lasting 3 weeks and erythroid precursors lasting 4 days. It was concluded that a single non-carcinogenic dose of MNU induces a prolonged suppression of the CMI system and a brief suppression of hematopoiesis in adult SPF cats. The immunosuppression may in part be responsible for the previously observed increased susceptibility to feline leukemia virus infection and disease of adult SPF cats treated with MNU.

Animals↗
PubMed1979

Recovery of soluble feline oncornavirus-associated cell membrane antigen from large volumes of tissue culture fluids.

Feline oncornavirus-associated cell membrane antigen (FOCMA), which is released spontaneously in tissue culture, was harvested from large volumes of culture fluid. Continuous-flow molecular filtration was the method of choice for concentrating the component. The yield of antigen recovered, as determined by cytotoxicity inhibition, was equal to that recovered with concentration in cellulose membrane tubing against polyethylene glycol and half that obtained by lyophilization. The latter two techniques were found to be impractical for handling large volumes of material. However, lyophilization was used for the final concentration step following volume reduction to approximately 300 ml in the molecular filtration system. Antigen yields were equivalent when removing salt by constant-volume molecular washing, prior to concentration in the filtration system, or when removing salt by conventional diffusion through cellulose membrane tubing.

Animals↗
PubMed1979

Preliminary studies: far-field microwave dosimetric measurements of a full-scale model of man.

Measurements of microwave heating were made in a full-size, upright human model. The 75-Kg model, composed of electrically simulated muscle, was placed in the far-zone of a standard-gain horn inside an absorber-lined chamber. Pulsed energy at 1.29 GHz was obtained from a military radar transmitter (AN/TPS-1G) and produced radiation at 6-14 mW/cm2 average power density at the location of the model. Microwave heating at the front surface was measured at nine locations on the phantom. Measurements at several depths within the phantom were also made at a central location to gain information on the depth-of-penetration of the microwave energy. Results of the frontal surface measurements and of the penetration study permitted a calculation of the approximate whole-body average specific absorption rate (SAR) when the model's long axis was parallel to the E-field vector. For a normalized power density of 1 mW/cm2 at a frequency of 1.29 GHz, the whole-body average SAR approximated 0.03 W/Kg. This result agrees well with theoretical predictions based on absorption in prolate spheroidal models of man.

Humans↗
PubMed1979

Inhibition of human lymphocyte mitogen and antigen response by a 15,000-dalton protein from feline leukemia virus.

Peripheral blood lymphocyte response of normal human subjects to mitogens and antigens was suppressed by a 15,000-dalton protein (p15) from a C-type feline leukemia virus. Four of six subjects were suppressed 70 to 96% when responding to concanavalin A or phytohemagglutinin in the presence of 5.0 microgram of p15. The three subjects who responded to streptokinase-streptodornase and Candida were suppressed 68 to 91% when cultured with 5.0 microgram of p15. The subviral protein did not appear to be cytotoxic at doses reported. Lymphocyte membrane studies with fluorescein isothiocyanate-concanavalin A revealed a reduction in concanavalin A-induced cap formation of 51 to 91% in the presence of the same dose of p15. These results demonstrate that in vitro immunological dysfunction in human lymphocytes can be induced by a C-type virion protein.

Antigens↗
PubMed1979

Immunosuppressive properties of a virion polypeptide, a 15,000-dalton protein, from feline leukemia virus.

The 15,000-molecular-weight polypeptide (p15) of feline leukemia virus (FeLV) was shown to impair normal lymphocyte function in vitro and to abrogate immunity to feline oncornavirus disease in vivo. FeLVp15 suppressed concanavalin A-induced blast transformation of normal feline lymphocytes by 68%, while other virion proteins had no effect. p15 suppression was not due to toxicity, nor was p15 a competitive inhibitor of concanavalin A binding. Capping of receptors for concanavalin A on normal feline lymphocytes also was inhibited by either inactivated FeLV or FeLV p15. Groups of cats were immunized with either killed feline oncornavirus-associated cell membrane antigen bearing tumor cells or tumor cells plus FeLV p15. After challenge with feline sarcoma virus, three of four p15-treated cats developed progressive fatal fibrosarcoma as compared to one of five non-p15-treated cats. The cats receiving p15 also had lower cytotoxic antibody titers against feline oncornavirus-associated cell membrane antigen (mean peak titer, 1:6) than did the non-p15 group (1:74). These data support the hypothesis that the immunosuppression in cats infected with FeLV is mediated by FeLV p15.

Animals↗
PubMed1979

Mobility of lymphocyte surface membrane concanavalin A receptors of normal and feline leukemia virus-infected viremic felines.

The virus-associated depression of concanavalin A mitogenesis which accompanies feline leukemia virus-induced cat lymphoma was investigated by comparing lymphocyte surface receptor mobility of normal cats to that of viremic diseased animals. The mechanics of feline lymphocyte receptor mobility were studied using fluorescein-conjugated concanavalin A to quantitate lymphocyte capping. The results of a study of 21 disease-free animals showed that cat lymphocytes undergo appreciable concanavalin A capping, with a mean capping rate of 17% under conditions developed in this study. In contrast, morphologically normal peripheral blood lymphocytes of six feline leukemia virus-infected viremic cats, with or without lymphoma, exhibited a mean capping of only 7%, significantly less than that of the control animals (p less than 0.005). These findings suggest that a membrane-related lymphocyte deficiency accompanies the development of virus-induced lymphoma in the cat.

Animals↗