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Biomedical subjects

D Woodrow

Publications and source records attributed to D Woodrow.

49 records · Page 3Linked to original sources
PubMed1987

Toxic effects of recombinant tumor necrosis factor in suckling mice. Comparisons with interferon alpha/beta.

Newborn Swiss and A2G mice were given daily subcutaneous injections for 1 week of highly purified recombinant mouse tumor necrosis factor (TNF) or mouse interferon alpha/beta. Both treatments resulted in inhibition of growth of suckling mice and severe fatty changes and necrosis in the liver. The simultaneous injection of polyclonal antibody to interferon alpha/beta abrogated the effects of interferon but did not block the effects induced by TNF. The kidneys of TNF-treated suckling mice could be distinguished from interferon-treated mice by the absence of glomerular basement membrane abnormalities and the presence of numerous rounded eosinophilic hyaline granules within the cytoplasm of the proximal tubules. Treatment of suckling mice with TNF and interferon alpha/beta induced similar changes in the spleen and thymus. Interferon treatment of suckling A2G mice resulted in the appearance of pulmonary cysts, which were not observed in TNF-treated mice. It is concluded that the pattern of lesions induced in suckling mice by mouse TNF is both similar and different from that induced by mouse interferon alpha/beta.

Animals↗
PubMed1986

Human interferons active on murine cells induce pulmonary cysts in A2G mice.

Suckling A2G mice were injected daily from birth for 8 days with highly purified human lymphoblastoid interferon (IFN) or recombinant interferons-alpha 1 or -alpha 2 rIFN-alpha 1, rIFN-alpha 2), or mouse interferon-alpha/beta (IFN-alpha/beta), or control preparations. Only mouse IFN inhibited the growth of suckling A2G mice and induced liver cell necrosis. At 56 days the mice were killed and the lungs examined for the presence of pulmonary cysts. Human lymphoblastoid IFN and rIFN-alpha 1 (and mouse IFN-alpha/beta), which exhibited significant biological activity on mouse cells in culture, induced pulmonary cysts in A2G mice. rIFN-alpha 2, which showed little or no activity on mouse cells, did not induce pulmonary cysts.

Animals↗
PubMed1986

Antibody to mouse alpha/beta interferon abrogates Pichinde virus-induced liver lesions in suckling mice.

Infection of newborn C3HeB/FeJ mice with the arenavirus Pichinde resulted in stunted growth, severe liver cell degeneration, and death. Administration of sheep anti-mouse alpha/beta interferon globulin completely abrogated liver lesions in virus-infected mice, although it did not decrease the incidence of mortality. These results indicate that endogenous interferon may be responsible for some manifestations of viral disease.

Animals↗
PubMed1984

Interferon induces pulmonary cysts in A2G mice.

Suckling A2G mice were treated for the first week of life with either partially purified or electrophoretically pure mouse alpha/beta interferon. All mice subsequently developed multiple large pulmonary cysts. The lesions were never found in interferon-treated Swiss mice and only very infrequently in interferon-treated BALB/c or F1 Swiss/A2G mice. These observations show that a brief exposure of suckling A2G mice to alpha/beta interferon can result in a severe disease that is determined by the mouse genotype.

Animals↗
PubMed1982

Severity of glomerulonephritis induced in different strains of suckling mice by infection with lymphocytic choriomeningitis virus: correlation with amounts of endogenous interferon and circulating immune complexes.

Renal lesions due to neonatal infection with lymphocytic choriomeningitis virus were studied in three different strains of mice known to produce different amounts of viral interferon. Very severe ultrastructural lesions similar to those induced by exogenous interferon were found as early as day 8 in C3H mice which produced the highest amount of interferon. Further studies could not be performed in these mice since all died by day 14. Balb/c mice produced the lowest amount of interferon and had very mild ultrastructural lesions. An intermediate pattern was found in Swiss mice. After 30 days of infection, severe immune complex type glomerulonephritis detectable by light microscopy and immunofluorescence was observed in Swiss mice whereas mild lesions only were found in Balb/c mice. Circulating immune complexes were present in both strains but in greater amounts of Swiss than Balb/c mice. These results suggest that two factors at least are important in the development of glomerulonephritis: interferon produced early in life and the load of circulating immune complexes.

Animals↗
PubMed1981

Electrophoretically pure mouse interferon inhibits growth, induces liver and kidney lesions, and kills suckling mice.

Suckling Swiss mice were injected daily for 8 days with either electrophoretically pure (EP) mouse interferon (s.a. 4.7 x 10(8) units/mg protein), major impurities obtained in the course of purification, or partially purified mouse interferon (s.a. 1.3 x 10(7) units/mg protein). Only EP or partially purified interferon inhibited growth, induced liver and kidney lesions, and killed mice. The authors conclude that interferon itself is responsible for these effects.

Animal Population Groups↗
PubMed1980

Interferon-induced disease in mice and rats.

Treatment of newborn mice with potent mouse interferon preparations resulted in an acute "early" syndrome characterized by inhibition of growth, delay in maturation of several organs, diffuse liver cell necrosis and death. When interferon treatment was discontinued at 1 week of life, mice appeared to recover, but subsequently developed a progressive glomerulonephritis ("late syndrome"). Treatment of newborn rats with potent rat interferon preparations also resulted in inhibition of growth, delay in maturation, and the subsequent development of glomerulonephritis. After infection at birth with lymphocyte choriomeningitis (LCM) virus, most strains of mice developed a similar acute early syndrome and surviving mice subsequently developed glomerulonephritis. We postulated that the endogenous interferon induced by LCM virus early in life was partially responsible for these syndromes. Administration of a potent anti-mouse interferon serum to LCM virus-infected mice neutralized the circulating endogenous interferon and inhibited the development of both the early and late syndromes. Our results suggest that large amounts of exogenous or endogenous interferon at a crucial stage of rapid growth or development of mice and rats can induce lesions in several different organs. Some lesions (i.e. the kidney) only become apparent weeks or even months after exposure to interferon.

Animals↗
PubMed1979

Cutaneous arteritis with superior vena cava obstruction.

Superior vena cava (SVC) obstruction may occur in several disorders (Urschel & Paulson, 1966) and may be associated with arteritis in Behçet's disease (Chajek & Farinaru, 1975). We report a man who had arteritis and SVC obstruction without any of the known causes.

Adult↗