Twenty four young (mean age 29-2 years, range [25][26][27][28][29][30][31][32][33][34][35] and 21 elderly (mean age 66-5, range 60-80) healthy subjects collected their urine in timed aliquots over 24 hours. The elderly subjects had been selected for their fitness by clinical and laboratory examinations and all lived independently at home. Sodium and potassium excretions were reduced in the elderly subjects compared with the young subjects, potassium excretion considerably so. This was despite similar 24 hour urine volumes and total solute excretion by both groups.The ratios of rates of excretion of water, electrolytes, and solutes during the night to the rates of excretion during the day were found to be higher in the elderly than the young subjects.Reduced day to night ratios of urinary excretion may be partly responsible for complaints of nocturia and sleep disturbance in elderly people. Introduction For many years it has been known that urine flow is lower at night than during the day in healthy subjects.' There is also an accompanying nocturnal reduction in electrolyte excretion.2 It has been speculated that reduction in urine flow at night in mammals may have evolved to permit undisturbed sleep.3Several studies of excretory rhythms in old patients have been reported.4-9 The first study was of patients in psychiatric hospitals4 5; the second of elderly patients in hospitals long term6; the third of nine patients in hospital, only two of whom were

No abstract

We recently noted that immature rats failed to exhibit a normal uterine response to exogenously administered estradiol as assessed by both biochemical (induction of gene expression) and morphological (altered uterine and vaginal histology, and size) end points. An initial analysis suggested that this was due to a high degree ofestrogenization from a dietary source which was producing a near maximal uterotrophic response prior to hormone treatment. Subsequent chemical analysis indicated that the feed in question contained high amounts of two well-known phytoestrogens, genistein (210 mglkg) and daidzen (14 mg/kg), and the lot of feed in question produced a large uterotrophic ect when fed to immature ovariectomized rats. These findings illustrate that, despite increased awareness of phytoestrogens, some batches of animal feed contain very high amounts of estrogenic components which have marked efects on in vivo end points of hormone action. These observations have important implications for both basic research and screenin methods that utilize in uivo approaches.

We recently noted that immature rats failed to exhibit a normal uterine response to exogenously administered estradiol as assessed by both biochemical (induction of gene expression) and morphological (altered uterine and vaginal histology and size) end points. An initial analysis suggested that this was due to a high degree of estrogenization from a dietary source which was producing a near maximal uterotrophic response prior to hormone treatment. Subsequent chemical analysis indicated that the feed in question contained high amounts of two well-known phytoestrogens, genistein (210 mg/kg) and daidzen (14 mg/kg), and the lot of feed in question produced a large uterotrophic effect when fed to immature ovariectomized rats. These findings illustrate that, despite increased awareness of phytoestrogens, some batches of animal feed contain very high amounts of estrogenic components which have marked effects on in vivo end points of hormone action. These observations have important implications for both basic research and screening methods that utilize in vivo approaches.ImagesFigure 2Figure 3

Estradiol produces a large increase in the uterine level of c-fos mRNA, which is maximum in 3 h. The administration of progesterone antagonizes this estrogen-induced increase in protooncogene transcript levels in both the rat and mouse. The inhibitory effect of progesterone is observed within 1 h after hormone treatment and persists for 9-18 h. In the rat, this effect can be observed at a dose of 0.25 mg progesterone and is maximum at a dose of 2.5 mg. A similar inhibition of fos mRNA levels after estrogen administration is produced by the glucocorticoid dexamethasone, but not by androgens or mineralocorticoids. Progesterone does not block the induction of c-jun or c-myc mRNA by estradiol. Uterine levels of c-fos mRNA observed after treatment with the phorbol ester phorbol 12-myristate 13-acetate are not decreased by a 3-h pretreatment with progesterone. Under the conditions of our experiments, progesterone does not decrease occupied levels of nuclear estrogen receptors in the uterus after estradiol administration. These findings are consistent with a mechanism in which progesterone inhibits transcriptional activation by the estrogen receptor at the level of the c-fos gene.