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Biomedical subjects

D L Vredevoe

Publications and source records attributed to D L Vredevoe.

36 records · Page 2Linked to original sources
PubMed1980

Cadmium and the reticuloendothelial system (RES). A specific defect in blood clearance of soluble aggregates of IgG by the liver in mice given cadmium.

The ability of the reticuloendothelial system (RES) to bind and catabolize soluble stable heat aggregates of 125I-IgG (A-IgG) was studied in mice given oral cadmium. Cadmium caused a delay in the circulation clearance of A-IgG in intact animals. The defect was due to impaired liver uptake of A-IgG and correlated with increased liver cadmium. Subsequent catabolism of bound A-IgG by liver slices was not affected. The defect was specific in that clearance of aggregated human serum albumin and colloidal carbon was normal in cadmium mice; this suggests that cadmium may affect either Fc or complement receptors of Kupffer cells in liver.

Animals↗
PubMed1977

A discrepancy in XC and oncogenicity assays for murine leukemia virus in AKR mice.

Studies of murine leukemia virus expression in AKR mice are presented. Material from in vivo and in vitro sources of normal tissues and lymphomas was assayed for in vitro infectivity, using the XC plaque assay, and for oncogenicity, by assessing lymphoma-accelerating capacity after inoculation into newborn animals. Normal tissues from healthy young AKR mice up to 7 months of age were found to have XC but not oncogenic activity. XC activity persisted, and weak oncogenic activity appeared in older mice. Cocultivation of normal young cells with NIH Swiss mouse embryo cells did not result in the appearance of oncogenic activity, although XC virus increased in titer. A cell-free filtrate of a virus-accelerated lymphoma was studied for host range. Virus as measured by polymerase and gs antigen was found to be propagated on NIH Swiss mouse embryo and wild mouse embryo cells, but not on human rhabdomyosarcoma, normal rat kidney, rabbit corneal, and BALB/c embryo cells. Virus as measured by the XC assay grew better on NIH Swiss mouse than on BALB/c embryo cells. Both of these cell lines propagated virus as measured by the oncogenicity assay. Supernatants from an in vitro cell line from a virus-accelerated lymphoma did not produce XC plaques but were oncogenic. Those from two cell lines of spontaneous lymphomas were negative with both assays. Cultivation of supernatants from these cultured lymphoma cells with NIH Swiss mouse embryo cells resulted in material which produced small plaques on the XC assay. These findings are interpreted as showing the presence of two viruses in AKR mice. One is XC positive and present throughout life. The other is oncogenic, appears later in life, and could be a separate virus or a variant of the first one.

AKR murine leukemia virus↗
PubMed1976

Therapy of transplanted lymphomas.

Allogeneic cells or cell products containing murine leukemia virus were effective in curtailing growth of a transplanted CBA lymphoma, which was originally induced by Gross virus and then maintained by syngeneic cell passage. All allogeneic cells or products effective in therapy of this lymphoma expressed virus as tested by the XC cell in vitro infectivity assay. Some of the materials also expressed virus as assayed by oncogenicity in vivo. A therapeutic effect was not demonstrated with allogeneic cells or cell products laking these virus activities. Syngeneic lymphoma cells were ineffective. Protected animals did not develop lymphoma when rechallenged several months later. Mechanisms for this therapy with virus were proposed.

AKR murine leukemia virus↗
PubMed1976

Virion interaction in mouse lymphomas.

Virion expression in filtrates of lymphomas in AKR/J or C3H/HeJ mice was assayed by two techniques: (a) in vitro infectivity (XC assay), or (b) acceleration of oncogenicity in vivo (O assay). The two assays appeared to detect different virus populations or activities. This was shown when the same filtrates were tested in parallel by the XC and O tests and opposite results were obtained on the two assays, e.g., XC+ 0- or XC- O+. It was postulated that two viruses, termed "XC+" and "O" to correspond to the assays used to detect them, were involved in oncogenesis. When lymphomas originally virus induced were passaged by cells in 2- to 3-month-old syngeneic AKR or C3H mice, oncogenic activity of filtrates of these transplanted lymphomas decreased as cell passages increased. These filtrates from C3H lymphomas also had decreased XC activity as cell passages increased. Normal lymphoid tissue from 1- to 5-month-old AKR mice was XC+ O-, while from C3H mice it was XC- O-. Thus, the two strains modified activities lacking in their normal tissues. Filtrates highly oncogenic in XC+ newborn AKR mice were oncogenic in C3H newborn mice only when sufficient XC+ virus was in the inoculum received by the XC- C3H mice. Thus the XC+ virus appeared to play a synergistic role with a postulated O virus in oncogenesis.

AKR murine leukemia virus↗
PubMed1975

Virus expression and immunoprophylaxis of a murine lymphoma.

CBA mice tested with a rapidly lethal transplanted lymphoma could survive challenge when pretreated with allogeneic lymphoma cells or other material expressing murine leukemia virus (MuLV). Protection resulted when recipients were given injections of AKR and C3H transplanted lymphomas or selected normal AKR and SJL tissues, filtrates of which give positive assays for MuLV by in vitro and/or in vivo tests. There was no protection when recipients were given injections of C3H lymphomas or C3H normal tissues that failed to have positive assays for virus.

Animals↗
PubMed1970

Decreased growth capacity of passaged gross virus-induced mouse lymphomas after incubation with antithymocytic sera.

AKR or C3H/HeJ transplanted mouse lymphomas, originally induced by Gross virus, could be neutralized by in vitro incubation with an immunosuppressive rabbit anti-mouse thymus cell serum. Neutralization was measured by significantly increased latent periods or decreased incidence (at a minimum of 90 days post-transfer) of lymphoma in syngeneic recipients of lymphoma cells incubated with antithymocytic serum when compared with syngeneic recipients of lymphoma cells incubated with normal rabbit serum.

Journal Article↗
PubMed1970

Increased Incidence of Lymphoma in C3H/HeJ Adult Mice Injected with Gross Virus and Antithymocytic Serum.

An increased incidence of lymphoma in adult C3H/HeJ mice injected with antithymocytic serum as compared with normal rabbit serum during a course of one to four weekly intraperitoneal injections of cell-free filtrates of Gross virus-induced lymphomas was noted. The latent period of lymphoma ranged from 119 to 298 days after initiation of treatment. The incidence tended to increase as the number of injections of cell-free filtrate was increased, with a maximum incidence reached at three injections.

Journal Article↗
PubMedDate not supplied

Natural killer cell anergy to cytokine stimulants in a subgroup of patients with heart failure: relationship to norepinephrine.

Heart failure is a disease characterized by chronically high levels of plasma norepinephrine and anergy in the cytotoxicity of circulating natural killer (NK) lymphocytes. This study shows that NK anergy extends to a significantly reduced cytotoxicity in response to the powerful NK stimulants, interleukin (IL)-2 and interferon (IFN)-alpha. Fifteen patients with heart failure, New York Heart Association stage III or IV, were studied for NK-cell-mediated cytotoxicity. The patients were divided into two groups based upon their NK cytotoxicity function: (1) those who had minimal baseline cytotoxicity and failed to respond following stimulation by IL-2 and IFN-alpha (n = 6), and (2) those who were about at the level of normal controls, and were responsive to IL-2 and IFN-alpha (n = 9). There was no relationship between the anergy and the etiology of the heart failure, laboratory indicators of heart failure, serum albumin or sodium, state anxiety, age or sex of the subjects. There was a statistically significant negative correlation between the response of NK cells to the stimulators IL-2 and IFN-alpha and the level of plasma norepinephrine in the heart failure patients. This was corroborated by in vitro testing of direct effects of norepinephrine on normal NK cells, which indicated that baseline cytotoxicity and the ability of these cells to respond to IL-2 were inhibited in a dose-dependent manner. The findings indicate that the NK cell anergy seen in heart failure patients extends to the response to the stimulators IL-2 and IFN-alpha in a subgroup of patients.

Adult↗