No abstract

Inoculation of newborn mice with lymphocytic choriomeningitis (LCM) virus resulted in decreased weight gain, liver cell necrosis, and death. Injection of potent sheep immunoglobulin against mouse interferon markedly inhibited these manifestations of LCM virus disease despite the fact that these treated mice had 100-fold more LCM virus in their serum. We conclude that interferon induced by LCM virus is responsible in large part for the syndrome of growth inhibition, liver cell necrosis, and death observed in LCM virus-infected suckling mice.

A marked difference was observed in the severity of disease in lymphocytic choriomeningitis (LCM) virus-infected suckling BALB/c, Swiss, and C3H mice. BALB/c mice had minimal liver lesions and none died, whereas C3H mice had extensive liver lesions and all mice died. An intermediate pattern was oberved for Swiss mice (36% mortality). Although there was no difference in the titers of LCM virus in the plasma or liver between these three strains of mice, there was a marked difference in the amount of interferon produced and the duration of interferonemia. C3H mice produced more interferon than Swiss mice which produced more interferon than BALB/c mice, indicating a direct correlation between the amount of interferon induced by LCM virus and the extent of disease. Inoculation of a potent anti-mouse interferon globulin markedly reduced the incidence of mortality in virus-infected C3H mice. BALB/c mice were as sensitive to the effects of interferon as C3H mice because daily administration of potent interferon preparations did induce disease in this strain. This ensemble of results supports our contention that endogenous interferon is in large part responsible for the manifestaions of acute LCM virus disease in suckling mice.

The local wavenumber and a multimodel wavenumber are complex attributes derived from a complex analytic signal. These quantities have been used to interpret anomalies arising from contacts, thin sheets, and horizontal cylinders. A new multimodel wavenumber can be used for computing depths of 2-D thick dikes and 2-D sloping steps. These two multimodel wavenumbers have been incorporated into a depth-estimation algorithm based on automatic curve matching. This algorithm works on profile data and has three appealing features: (1) the most appropriate of these five models is selected automatically; (2) the automatic curve matching uses a least-squares technique to reject responses that do not conform to the model assumptions; and (3) interference from distant sources can be accounted for as a base-level shift of the multimodel wavenumber curves. Applying the automatic technique to survey data from the Western Canada sedimentary basin yields four thick dikes between 3400 and 4300 m below sensor. These depths are equivalent to 2.2 and 3.1 km below sea level, which is consistent with the basement depths derived from drillhole information. Using these solutions as a starting point in an iterative forward modeling exercise, the measured data were explained with a geologically reasonable model.

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.