17ß-estradiol replacement therapy induces eNOS, nNOS and estrogen receptor ß in hypophysectomized rats with inflamed footpads.

Nitric oxide (NO) plays a key role in inflammation. It is partly produced by three forms of NOS: eNOS of inflammatory cells, nNOS of neural cells and iNOS (inducible isoform). Estrogens can cause an anti-inflammatory effect, although it is not yet clear through which NOS isoforms. The aim of this study was to evaluate the role of the different NOS isoforms, as well as estrogen receptors (ERs) α and ß, on the anti-inflammatory effects of estrogens. To avoid the influence of endogenous glucocorticoids or sexual hormones, male rats were hypophysectomized. Animals were segregated into two control groups (no-treatment control group and SHAM-operated animals) and three hypophysectomized groups (no-hormonal treatment, with estradiol-17ß, or with testosterone replacement treatment). Freund's complete adjuvant (1 mg) was administered to the footpad of all animals. Measurements were made based on footpad inflammation (with a plethysmometer) such as eNOS, nNOS, iNOS and ER α and ß protein expression (by immunohistochemistry principle/method) on days 1, 7 and 14. Only estradiol decreased inflammation, accompanied by increased levels of eNOS and nNOS and differential expression of ERs α and ß in the inflammatory infiltrate. The higher levels of estradiol-induced eNOS and nNOS ocurred perhaps through the activation of ER ß.

[Evaluation of the tuberculin reaction in health occupation students] . / Evaluación de la respuesta a la tuberculina en estudiantes del área de la salud.

A cross-sectional study was done at the University of Antioquia, MedellIn, Colombia, to evaluate the response to a tuberculin skin test among students in undergraduate health programs (medicine, odontology, nursing, and bacteriology) as compared to undergraduate students in nonhealth programs. The study included students from the beginning, middle, and end of the university's academic programs. The sample of 490 students included 273 from health programs and 217 from nonhealth programs. Participants were randomly selected using lists provided by the university registrar, for the second semester of 1998. The presence of a BCG vaccination scar was determined, and all the participants were also questioned about TB-related risk factors. Tuberculin skin test reactivity was evaluated by the size of induration 72 hours after intradermal injection of two tuberculin units of purified protein derivative RT 23. There were no differences in tuberculin reactivity between students from the health programs and from the nonhealth programs, irrespective of the academic level. However, there was a significantly higher proportion of positive skin tests among students with a BCG scar. These results suggest that undergraduate health students do not have extensive contact with TB patients or with clinical samples from such patients. Nevertheless, the results do not rule out TB as an occupational risk for health personnel.