No abstract

Prenatal care has long been endorsed as a means to identify mothers at risk of delivering a preterm or growth-retarded infant and to provide an array of available medical, nutritional, and educational interventions intended to reduce the determinants and incidence of low birth weight and other adverse pregnancy conditions and outcomes. Although the general notion that prenatal care is of value to both mother and child became widely accepted in this century, the empirical evidence supporting the association between prenatal care and reduced rates of low birth weight emerged slowly and has been equivocal. Much of the controversy over the effectiveness of prenatal care in preventing low birth weight stems from difficulties in defining what constitutes prenatal care and adequate prenatal care use. While the collective evidence regarding the efficacy of prenatal care to prevent low birth weight continues to be mixed, the literature indicates that the most likely known targets for prenatal interventions to prevent low birth weight rates are (1) psychosocial (aimed at smoking); (2) nutritional (aimed at low prepregnancy weight and inadequate weight gain); and (3) medical (aimed at general morbidity). System level approaches to impact the accessibility and the appropriateness of prenatal health care services to entire groups of women and population-wide health promotion, social service, and case management approaches may also offer potential benefits. However, data on the effectiveness of these services are lacking, and whether interventions focused on building cohesive, functional communities can do as much or more to improve low birth weight rates as individualized treatments has yet to be explored. The ultimate success of prenatal care in substantially reducing current low birth weight percentages in the United States may hinge on the development of a much broader and more unified conception of prenatal care than currently prevails. Recommendations for actions to maximize the impact of prenatal care on reducing low birth weight are proposed both for the public and for the biomedical, public health, and research communities.

No abstract

The role of hCG in the regulation of testicular steroid production in human fetuses from 14 to 20 weeks gestational age was studied. Saturable binding of 125I-hCG to testicular homogenates was demonstrated, and physiologic concentrations of hCG were able to stimulate testosterone formation in testicular minces without the addition of exogenous precursors. In five fetses of 16-20 weeks gestational age, the capacity to bind hCG varied from 25.6 to 42.2 pg/mg wet tissue. The association constant of binding was 1.07+/-0.12 X 10(10) M-1. Testicular minces from six other fetuses (gestational age 14-19 weeks) were incubated in the presence of concentrations of 0, 0.5, 5 or 50 ng/ml NIH-hCG (1 mg=10,000 IU), which are within the physiologic range. Preincubation of 30 min in excess buffer was necessary to observe clear differences in testosterone production rates between controls and hCG stimulated testicular tissues. The greatest increase in testosterone production occurred when the hCG concentration was increased from 0.5 to 5 ng/ml. Little additional stimulation was observed at a concentration of 50 ng/ml. Maximal production rates of up to 12 ng/mg tissue/h were seen. It is concluded that human fetal testes bind hCG, and that physiologic levels of hCG stimulate fetal testicular testosterone formation in vitro at this stage of gestation.

Prenatal health promotion and psychosocial services have associated benefits to enrollees that should matter to Medicaid health plans and their providers.