Adequacy of testing, empiric treatment, and referral for adult male emergency department patients with possible chlamydia and/or gonorrhoea urethritis.

This study evaluated the adequacy of testing, empiric treatment and referral for further evaluation of adult male emergency department (ED) patients with possible chlamydia and/or gonorrhoea urethritis. Of 968 adult male ED patients, 84% were tested for chlamydia and gonorrhoea, 16% for HIV and 27% for syphilis; 92% received empiric treatment for chlamydia and gonorrhoea and 71% were referred for further evaluation; of those tested, 29% were infected with chlamydia, gonorrhoea or both; and 3% of those tested had a positive syphilis test. The results of logistic regression modelling indicated that testing, treatment and referral were not related to a history of sexual contact with someone known to have a sexually transmitted disease or to the patient's ultimate diagnosis of a laboratory-confirmed infection. Compliance with Centers for Disease Control and Prevention (CDC) recommendations for chlamydia and gonorrhoea testing and treatment regimens was high, but was poor for HIV testing. More explicit guidance from CDC regarding syphilis testing and referral for further evaluation is needed.

A recombinant DNA bio-assay for selenium in blood.

The trace element selenium (Se) is included in the form of selenocysteine (Sec) at the active site of several prokaryotic and eukaryotic proteins known as selenoproteins (SePro). The growing implications of SePro in cell physiology and human health point to the need for an adequate means of assessing Se status in biological fluids. Here, we describe a new approach based on a recombinant DNA construct, in which the expression of the 'lacZ gene in Escherichia coli is proportionally and specifically driven by UGA-directed Sec incorporation. Se status is determined in samples of rat blood first treated by acid hydrolysis for protein degradation. As compared to other methods, this simple, sensitive bioassay (BIO) for determining Se status seems to be unique in its ability to measure all functional Sec residues in SePro in blood serum.

Effect of selenium deficiency on type I 5'-deiodinase.

The type I iodothyronine 5'-deiodinase (5'-DI) present in rat liver and kidney has recently been demonstrated to be a selenoprotein. The goal of the present study was to examine in detail the effect of selenium (Se) deficiency on 5'-DI at the protein and mRNA levels. In weanling rats fed a selenium-deficient (Se(-)) diet for 6 weeks, 5'-DI activity was decreased 91 and 69% relative to control activities in liver and kidney, respectively. Administration of 3,5,3'-triiodothyronine resulted in a 2-fold increase in 5'-DI activity in control animals, but had little or no effect on 5'-DI activity in Se(-) animals. Western analysis using a specific antiserum directed against a bacterial fusion protein containing the carboxyl-terminal half of the 5'-DI protein demonstrated that this decrease in 5'-DI activity in Se(-) animals was explained by a marked decrease in 5'-DI protein. Administration of Se to Se(-) animals resulted in parallel increases in 5'-DI protein and activity over a 72-h time period. It was also shown that selenium deficiency was accompanied by a 40% decrease in 5'-DI mRNA levels in the kidney, but not in the liver. In both tissues, the administration of 3,5,3'-triiodothyronine resulted in increased 5'-DI mRNA levels which were not altered by selenium status. These studies indicate that selenium deficiency decreases 5'-DI activity by decreasing the amount of 5'-DI protein. The mechanism of this impairment in enzyme synthesis appears to be a defect in translation, presumably due to a block in the UGA-directed selenocysteine incorporation in selenium deficiency.

Effects of moderate dietary phosphorus restriction on intestinal absorption and external balances of phosphorus and calcium in growing female rabbits.

The effects of moderate dietary P restriction on intestinal net fluxes and external balances of P and Ca were studied in growing female albino rabbits that were fed a P-deficient diet for 10 consecutive days while they were housed in metabolism cages. Intestinal P secretion occurred during the first 24 h of P restriction and thereafter changed to absorption. During recovery, when the rabbits were consuming a normal diet, P absorption was significantly greater than either prerestriction control values or than in a separate group of time control rabbits. Phosphorus balance was negative during the 1st day of P restriction but thereafter became positive. This pattern occurred because intestinal P secretion changed to absorption and because urinary losses of P were negligible. Intestinal Ca absorption increased within 24 h of P restriction, reached maximal values by 4 days, and remained elevated for each of the remaining 6 days that dietary P was low. It also was elevated compared to P-sufficient time controls for 8 days after replenishment of dietary P. Despite increased intestinal absorption, Ca balance was significantly reduced during P restriction because of substantial hypercalciuria. Thus, selective dietary P restriction reduced the positive balances of both P and Ca that are characteristic of growth. We conclude that in growing rabbits moderate dietary P restriction induces both intestinal and renal adaptations that conserve this mineral; concomitantly, positive Ca balance is reduced. With dietary P replenishment, adaptations persist to restore the positive mineral balances that were lost because of dietary P restriction during growth.

Renal responses to phosphorus deprivation in young rabbits.

To evaluate the renal adaptations to dietary P deprivation, young growing female rabbits were fed a P-deficient diet for 10 consecutive days while they were housed in metabolism cages. Urinary Ca excretion rates increased markedly within 24 h of P deprivation, remained high for each of the 10 days that dietary P was low, and returned to control values within 24 h of consuming a normal-P feed. The hypercalciuria was attributable to both an increased filtered load and decreased tubular reabsorption of Ca. Urinary P excretion rates decreased gradually in response to a low P diet and reached a nadir only after 9 days of deprivation. Urinary P excretion rates recovered to control values within 24 h of feeding a normal-P diet. Increased tubular reabsorption of P alone accounted for the hypophosphaturia. Plasma P concentration was reduced significantly after 10 days of dietary P deprivation, and this was associated with a significant increase in plasma calcitriol concentration. We conclude that dietary P deprivation in the rabbit effects the hypophosphatemia, hypophosphaturia, and hypercalciuria that characterize this condition in rats, dogs, and humans. Furthermore, the elevation in plasma calcitriol concentration that has been observed with dietary P deprivation in healthy rats and humans also occurs in the laboratory rabbit.