Immature female rats received implants containing 17 beta-estradiol on postnatal day 28 at 0900 h, followed 24 h later by either blank capsules or progesterone. Between 1500-1600 h on the day of progesterone (or blank capsule) implantation, these rats, a group of unoperated or sham controls, and a group of estrogen-progesterone-treated immature male rats were killed and perfused, and their brains processed for immunocytochemistry of c-fos antigen and LHRH. LHRH neurons consistently expressed c-fos after estrogen-progesterone treatment in females but not males; in only one of four females examined was c-fos induced after estrogen treatment. No fos was associated with LHRH neurons in the control groups. The LHRH neurons that expressed c-fos were located in the preoptic area and anterior hypothalamus; more rostral LHRH cells did not appear stimulated. These data demonstrate that gonadal steroids, administered in a paradigm that predictably produces timed stimulation of LH release, induce c-fos in LHRH neurons. The induction of c-fos in LHRH neurons provides a potentially useful and powerful tool for studying LHRH activation at the cellular level.

The present study was carried out to determine how active surveillance for methicillin-resistant Staphylococcus aureus (MRSA) could be improved by the use of enrichment broth and the inclusion of extra-nasal sites with nares cultures. Molecular typing was also performed to identify colonization by single or multiple strains. Surveillance cultures for MRSA were obtained from 650 patients on admission to a medical and surgical intensive care unit (ICU) in Taiwan. MRSA was detected on directly plated vs. broth-enrichment cultures in any site at 10.0% vs. 24.2%, nares 8.2% vs. 17.5%, throat 4.8% vs. 13.4%, axilla 1.2% vs. 9.1%, and perineum 1.8% vs. 9.5%, respectively. Nares cultures alone detected only 81.5% and 72.5% of all colonized patients by direct and broth-enriched cultures, respectively. The molecular typing of 68 isolates from 17 patients revealed that multisite isolates were largely indistinguishable within each patient, but four patients had multiple subtypes and another three patients had different clonotypes. The detection of MRSA carriers was considerably enhanced by broth-enrichment cultures at multiple anatomic sites and simultaneous colonization by multiple strains at different sites can occur. Epidemiological studies are needed to determine the likelihood of subsequent nosocomial infection among colonized patients detected via direct nasal versus broth-enriched cultures from multiple sites.

Previous studies have shown that progesterone inhibits endothelial cell proliferation through a nuclear receptor-mediated mechanism. Here, we further demonstrate that progesterone at physiologic levels (5 - 500 nM) dose- and time-dependently inhibited DNA synthesis of cultured human umbilical vein endothelial cells (HUVEC). The mRNA and protein levels of p21, p27, and p53 in HUVEC were increased by progesterone. The formation of CDK2-p21 and CDK2-p27 were increased and the CDK2 activity was decreased in the progesterone-treated HUVEC. The progesterone-inhibited [3H]thymidine incorporation was completely blocked when the expressions of p21 and p27 were knocked-down together. Transfection of HUVEC with dominant negative p53 cDNA prevented the progesterone-induced increases in p21 and p27 promoter activity and protein level, decreases in thymidine incorporation, and capillary-like tube formation. Matrigel angiogenesis assay in mice demonstrated the antiangiogenic effect of progesterone in vivo. These findings demonstrate for the first time that progesterone inhibited endothelial cell proliferation through a p53-dependent pathway.