The fall in household size and the rise of the primary individual in the United States

The long-term fall in household size in the United States is discussed within the framework of the aging of the population, continuing as the effects of fertility and mortality decline accumulate. Using distributions of households by size from U.S. census data 1790-1970 and a components of change analysis on primary individuals for 1950-1974, household changes are related to demographic change for the periods 1790-1900, 1900-1950, and 1950-1974. Fertility and mortality declines have unambiguous impact on household size until the increases in primary individuals begin. But these, too, have a theoretically interesting, if indirect relationship to population structure.     

Androgen receptor dependent and independent activities of testosterone on hepatic microsomal drug metabolism

Administration of testosterone for 6 days to intact female and castrate male BALB/cJ mice stimulated hepatic microsomal ethylmorphine N-demethylase activity and cytochrome P-450 content by 50-75%. Testosterone also stimulated hepatic microsomal NADPH-oxidase activity, but to a lesser degree. To probe the mechanism of this effect of androgens, two antiandrogens (cyproterone acetate and flutamide) were employed. Since cyproterone acetate was a potent stimulator of hepatic microsomal ethylmorphine N-demethylase activity and cytochrome P-450 content, no antiandrogenic activity of this steroid could be detected. By contrast, flutamide alone had little effect on either ethylmorphine N-demethylase activity or cytochrome P-450 content. However, this drug effectively blocked the stimulatory effects of testosterone on ethylmorphine N-demethylase activity and cytochrome P-450 content but not on NADPH-oxidase activity. This effect was not species specific, since flutamide also prevented androgen stimulation of ethylmorphine metabolism in adult castrate and prepubertal male Fisher rats. The testosterone-induced increase of hepatic weight and microsomal protein content was not affected by the administration of flutamide. The observations are consistent with the hypothesis that androgens have two distinct effects on the liver. First, testosterone may act as a general, nonspecific stimulant of liver weight and microsomal protein content which is independent of the androgen receptor. Secondly, testosterone action in the liver may be expressed via an androgen-specific or androgen receptor-dependent mechanism which controls, in part, the cytochrome P-450-dependent demethylase system.