Attitudes about treatment of coronary heart disease among women and men presenting for exercise testing

In recent years, several potent gonadotropin-releasing hormone (GnRH) analogues have become available for female contraception and one of them (buserelin) has been tested in lactating women. However, the possible effects on infants due to the transference of the analogue through breast milk have not been studied. The present work evaluated the effect of oral buserelin on urinary LH secretion in male infants. A total of 19 healthy full-term boys (aged 2-4 months) were included in the study. Infants received orally a single dose of a GnRH agonist mixed with breast milk. Urine samples were collected prior to, and 4-6 and 24 h after treatment for LH measurement. The results disclosed a significant increase in LH urine level in the sample taken 4-6 h after buserelin administration. Twenty-four hours after GnRH agonist ingestion, the LH level returned to baseline level. The present study demonstrated that GnRH analogue administered orally to infants escapes from gastrointestinal inactivation and induces a significant rise in LH levels 4-6 h after treatment.     

Histamine-and isoprenaline-evoked stimulation of cAMP formation in chick cerebral cortex

Histamine (HA) and isoprenaline (ISO) strongly stimulated cAMP formation in chick cerebral cortical slices. The effects of HA and ISO were selectively antagonized by HA H2-receptor blockers (aminopotentidine, ranitidine) and beta-adrenoceptor blocker propranolol, respectively. The combination of HA (0.1-100 microM) and ISO (0.1-10 microM) produced some additive effects when the drugs were used at low concentrations, i.e. 0.1-1 microM but not when HA was applied at 10 or 100 microM doses (which evoked nearly maximal effect). It is suggested that HA H2-like receptors and beta-adrenoceptors (whose activation leads to stimulation of cAMP formation) are localized in the same subpopulation of cortical cells, in which they probably utilize a common and limited pool of cAMP-generating system.     

Hypoxia effects on hypothalamic corticotropin-releasing hormone and anterior pituitary cAMP

AIM: To study the effects of acute and chronic hypoxia on hypothalamus-anterior pituitary-adrenocortex axis. METHODS: Rats and pikas were exposed to different altitude and periods. Animals were injected with CRH, Arg and NE in the third ventricle of the brain of rats. RESULTS: Anterior pituitary cAMP and plasma corticosterone levels of rats obviously increased during 1 h of hypoxia. cAMP was increased from 2.23 +/- 0.13 of control group to 7.7 +/- 0.7 of 5 km and 13.4 +/- 1.9 nmol/g wet tissue of 8 km, respectively. i.c.v. CRH, Arg and NE all activated HPA axis. The effects of CRH were most potent. CRH 2 microL 0.75 nmol i.c.v increased anterior pituitary of cAMP from 3.5 +/- 0.4 of control to 22.4 +/- 2.2 nmol/kg wet tissue. Stimulating altitude of 5000 m resulted in a 16.9% decrease in corticosterone level (P < 0.05), 8000 m resulted in a 47.5% decrease (P < 0.01) after hypoxia for 25 d. Hypoxia did not activate HPA axis in pikas. CONCLUTION: 1) Hypoxia stress activates the secretion of corticotrophin (ACTH) via cAMP; 2) Adrenocotical function of rats decays during chronic hypoxia; 3) Arg and NE regulate the secretion of plasma corticosterone and synthesis of pituitary cAMP at the hypothalamus level; 4) Hypoxia tolerance of the pika was high.     

Chronic growth stimulation of human adult melanocytes by inflammatory mediators in vitro: implications for nevus formation and initial steps in melanocyte oncogenesis

In the human epidermis, melanocytes are distributed at a distance from each other. In contrast, melanocytes in nevi, which are considered benign neoplasms of melanocytes, are grouped in nests. Although still not well defined, environmental factors are thought to play an important role in the development of nevi. We found that chronic growth stimulation by leukotriene C4, a compound found in increased amounts in inflamed skin, induced pleiotropic modifications in the normal melanocyte phenotype. These changes include loss of contact inhibition and formation of structures resembling tumor spheroids. In parallel with these changes, there was a constitutive expression of Fos protein. Switching these cultures to medium supplemented with phorbol ester sustained growth with reversion of the altered phenotype. In contrast, a cAMP stimulator, cholera toxin, induced features of terminal differentiation. Our findings suggest a role for inflammatory mediators in human epidermal melanocytes. This observation provides insight into melanocyte growth alterations which may have relevance in early stages of melanocyte oncogenesis.