RESUMO
The effect of the 44-amino-acid peptide human pancreatic GH releasing factor (hpGRF-44) upon the secretion of GH was studied in control and hypothyroid adult male rats. In animals rendered hypothyroid by ingestion of propylthiouracil (PTU), basal and hpGRF-44-stimulated secretion of GH was depressed in vivo. Administration of T4 together with PTU prevented the decline in basal and hpGRF-provoked GH secretion in vivo. HpGRF-44-stimulated release of rat GH was also impaired in vitro, an effect partially reversed by administration of low doses of T4 in vivo. The depressed in vitro secretion of GH could not be restored in hypothyroidism pituitaries by incubation of the glands with T3. Thus, hypothyroidism blunts hpGRF-44-stimulated secretion of GH in vivo and in vitro in the hypothyroid adult male rat.
Assuntos
Hormônio Liberador de Hormônio do Crescimento/farmacologia , Hormônio do Crescimento/metabolismo , Hipotireoidismo/metabolismo , Animais , Técnicas In Vitro , Masculino , Ratos , Tiroxina/sangue , Tiroxina/farmacologiaRESUMO
Granulocytopenic patients with an intravascular catheter are at increased risk for infection with Staphylococcus epidermidis. During the intervals when the catheters are not being used for infusions, it is customary to maintain patency of the catheter lumen with a solution containing heparin. We show that heparin does not inhibit the growth of S. epidermidis isolated from the catheter of an infected patient. A 20-mg/ml solution of disodium EDTA, a chelating agent which effectively anticoagulates blood at this concentration, was shown to be bactericidal for an initial inoculum of 10(3) CFU of staphylococci per ml in 24 h. Vancomycin, an antibiotic which is often employed to treat Staphylococcus infections, was also bactericidal for initial inocula of 10(3) CFU/ml at doses of 6.7 micrograms/ml, a drug concentration in the therapeutic range. When 10(3) staphylococci per ml were cultured in the presence of catheter segments and disodium EDTA or vancomycin, subcultures of the catheters showed minimal or no growth, respectively. In contrast, when cultured with heparin alone, subcultures showed abundant growth. In view of its low cost, effectiveness as an anticoagulant, and bactericidal activity, EDTA should be studied as a replacement for heparin solutions for the maintenance of intravenous catheters in granulocytopenic patients.
Assuntos
Cateteres de Demora/efeitos adversos , Ácido Edético/farmacologia , Infecções Estafilocócicas/prevenção & controle , Staphylococcus epidermidis/efeitos dos fármacos , Heparina/farmacologia , Humanos , Testes de Sensibilidade Microbiana , Staphylococcus epidermidis/crescimento & desenvolvimento , Vancomicina/farmacologiaRESUMO
Menstrual cycle characteristics may reflect underlying endocrine patterns that influence the risk of breast cancer. Most previous studies of menstrual function and breast cancer risk have used retrospective reports of menstrual bleeding, which may be unreliable. To examine this association, the authors conducted a mail survey among 997 women who had recorded menstrual events prospectively over as many as 50 years, beginning in 1934. Compared with women with a median menstrual cycle length of 26-29 days, women who had cycles of extreme length at ages 25-29 years had a nearly twofold increased incidence of breast cancer (for a median cycle length of less than 26 days, adjusted relative risk (RR) = 1.9, 95% CI 0.9-4.1; for > or = 34 days, RR = 1.9, 95% CI 0.9-3.9). Statistical adjustment was made for age, family history of breast cancer, parity, age at menopause, age at first pregnancy, and Quetelet index (weight (kg)/height (m)2). Adjusting for age and other potential confounders and restricting the analysis to women who did not use hormones, women who experienced either a lesser (< 150) or a greater (> 350) cumulative number of cycles had an increased incidence of breast cancer (adjusted RR = 1.9, 95% CI 0.3-10.6, and RR = 1.8, 95% CI 0.5-6.0, respectively) compared with women who experienced 150-350 cycles. The findings are discussed in the context of current hormonal theories of breast cancer etiology.