PubMed Health⌕ Search

Biomedical subjects

C Fortier

Publications and source records attributed to C Fortier.

At least 37 records · Page 2Linked to original sources
PubMed1981

Science and the universities.

The university system in Canada, as well as its method of funding, was built on the expectation of growth. It is now necessary to consider what effect the expected decline in enrollment may have on the ability of the university system to serve national needs. Neither the government nor the universities have had any experience that would fit them for carrying out effectively, humanly, and economically the kind of contraction that may be required, while still maintaining the quality of education. Such an adjustment is going to require the best efforts of the universities and the two senior levels of government working in concert, as well as the support of the public. Parallels are drawn with the situation in the United States.

Canada↗
PubMed1976

[Adrenocortical responses to ACTH (author's transl)].

To characterize by a mathematical model the dynamics of adrenocortical responses to ACTH, the concentration of plasma corticosterone was measured following a series of injections and perfusions of ACTH to dexamethasone-treated male rats. A similar slope was observed during the rise of plasma corticosterone following graded pulse inputs, and the steady-state corticosterone secretion rate was shown to increase proportionally to the perfusion rate of ACTH up to saturation corresponding to maximal secretion. The data will be used, concurrently with our model of the dynamics of plasma cortiscosterone, for the identification of a mathematical model of the adrenocortical response to ACTH.

Adrenal Cortex↗
PubMed1975

Feedback inhibition of adrenocorticotropin release by corticosterone infusions in the adrenalectomized rat.

Advantage was taken of a specific and sensitive bioassay for rat plasma adrenocorticotropin (ACTH) based on the dispersion of rat adrenal cells with trysin, to investigate the relationship between plasma corticosterone concentration and inhibition of ACTH release under steady-state conditions achieved by graded rates (0-5.12 mug/min per 100 g body weight) of intravenous infusion of the steroid for 45 min in 28-day adrenalectomized rats. In contrast to prior reports involving suppression of stress-induced ACTH release, the inhibitory effect of corticosterone was shown, under our experimental conditions, to be exerted also on the basal rate of ACTH secretion. Indeed, a slight though not significant decrease of plasma ACTH concentration was observed with the corticosterone infusion rate of 0.64 mg/min per 100 g body weight, and further progressive and highly significant drops in concentration were recorded for infusion rates of 2.56 and 5.12 mg/min per 100 g body weight. An increase of the metabolic clearance rate of corticosterone, observed as a function of the infusion rate, was ascribed to saturation by the steroid of the plasma transcortin binding sites.

Adrenal Cortex↗
PubMed1975

Interactions between the pituitary, thyroid and adrenal cortex during acute exposure to cold or to electric shocks in the rat.

In intact rats acclimated to 25 +/- 1 degrees C, acute exposure to cold resulted in simultaneous stimulation of TSH and ACTH secretion. The plasma TSH response to cold was identical at temperatures varying from +14 to -10 degrees C, whereas the adrenocortical response increased proportionally to the severity of cold. Acute stimulation of ACTH secretion by exposure to a stressful situation (electrical shocks) did not alter the TSH response to cold. Conversely, acute blockade of the pituitary-adrenocortical response by dexamethasone treatment did not enhance the TSH response to cold. Chronic stimulation of ACTH secretion resulting from adrenalectomy did not interfere with the TSH response during subsequent exposure to cold. However, a reduced adrenocortical response to cold was observed during chronic hypersecretion of TSH resulting from previous thyroidectomy. These findings do not support the hypothesis of an inverse relationship between TSH and ACTH secretions during acute cold exposure, but rather suggest that these secretions are independent.

Adrenal Cortex↗
PubMed1975

Relationship between ACTH release and corticosterone binding by the receptor sites of the adenohypophysis and dorsal hippocampus following infusion of corticosterone at a constant rate in the adrenalectomized rat.

The amount of corticosterone bound to proteins in the adenohypophysis and dorsal hippocampus was studied concurrently with the plasma ACTH concentration in 4-week adrenalectomized male rats under steady-state conditions achieved by infusing the steroid at a constant rate for 45 min. Corticosterone binding was measured by gel chromatography on Sephadex LH-20, using a TE buffer containing 0.4 m NaCl. No saturation was observed in whole homogenates and supernatants with increasing plasma corticosterone concentrations. However, corticosterone binding by the pituitary and by one of two types of hippocampal receptors evidenced saturation within our range of corticosterone infusion rates, indeed. Scatchard plots allowed us to distinguish two types of binding sites in the hippocampus. The first, saturated at a low corticosterone concentration has an association constant of 3.0 times 10-8 M-1 with a number of binding sites estimated at 150 times 10- minus 15 mol/mg protein, whereas the second is associated with non-specific binding. The adenohypophysis shows only one kind of binding site with an association constant of 3.6 times 10-8 m- minus 1 and a number of sites estimated at 989 times 10- minus 15 mol/mg protein. A suggestive relationship was observed between ACTH inhibition by corticosterone and saturation of the pituitary binding sites. Our data are consistent with the possible involvement of corticosterone binding by specific sites in the negative feedback regulation of ACTH release.

Adrenalectomy↗