Disease Mechanisms in psoriasis and psoriatic arthritis

Any hypothesis that tries to explain disease mechanisms in psoriasis and psoriatic arthritis (PsA) must take into account the containment of the inflammatory process to three specific sites: the skin, synovium, and enthesis. This article reviews the recent literature that advances our understanding of disease mechanisms at these specific sites. Additional progress will be achieved by research that focuses on common pathogenic pathways at these sites, in particular when searching for foreign candidates or autoantigens triggering the T-cell-mediated immune response.     

Prolactin directly stimulates citrate production and mitochondrial aspartate aminotransferase of prostate epithelial cells

Prolactin, in vitro, significantly increased citrate production, mAAT (mitochondrial aspartate aminotransferase) and pmAAT (precursor form of mAAT) activity of prostate epithelial cells derived from rat lateral prostate (LP) and pig prostate cultures. In contrast, prolactin had no effect on the cytosolic isozyme, cAAT. This prolactin effect appeared to be independent of testosterone. The phorbol ester TPA (12-O-tetradecanoyl-phorbol-13-acetate) induced the same effects as prolactin thereby indicating the involvement of protein kinase C. This report demonstrates that prolactin directly regulates citrate production of prostate epithelial cells and the availability of an in vitro model to elucidate the mechanism of action of prolactin.     

Psychiatric disorders in pediatric primary care. Prevalence and risk factors

Children aged 7 to 11 years visiting their primary care pediatrician for a wide range of reasons were studied to determine the one-year prevalence of DSM-III disorders and the risk factors associated with them. Parents completing the Child Behavior Checklist about their children identified problems that placed 24.7% of 789 children in the clinical range. Detailed psychiatric interviews with 300 parents and children, using the Diagnostic Interview Schedule for Children, yielded a one-year weighted prevalence of one or more DSM-III disorders of 22.0% +/- 3.4%, combining diagnoses based on either the child or the parent interview.     

Effect of growth hormone on human alveolar macrophage oxidative metabolism

BACKGROUND: Growth hormone (GH) has diverse immunological actions and has been shown to augment oxidative metabolism in rat peritoneal and porcine alveolar macrophages and both human and animal neutrophils. A study was performed to determine the effects of GH on human alveolar macrophages in vitro. METHODS: Macrophages were harvested from 10 patients undergoing bronchoalveolar lavage and incubated with 0, 10 and 100 nmol/ml GH for four hours. Oxidative metabolism was assessed by means of a fluorescent assay using FMLP and E coli as stimulants. Fluorescence was measured using flow cytometry. RESULTS: No difference in basal or stimulated oxidative metabolism was found between the GH and control groups. CONCLUSIONS: GH does not have a direct stimulatory action on human alveolar macrophages in vitro. However, this does not exclude an indirect effect in vivo. The results contrast with previous studies on animal alveolar macrophages.