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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Long-term bone marrow cultures are dependent on the formation in vitro of an adherent cell layer that supports hematopoiesis. We have grown bone-marrow-adherent cells, termed stromal colony-forming units, or CFU-ST, as isolated adherent colonies, and examined some of their growth requirements. Bone marrow mononuclear cells separated from aspirates by density centrifugation and cultured in medium supplemented with fetal calf serum or human plasma gave rise to adherent colonies (CFU-ST). An average of 23.4 +/- 2.1 (mean +/- SEM, n = 19) CFU-ST were produced by 10(5) bone marrow mononuclear cells. CFU-ST could not be cultured from similarly prepared peripheral blood mononuclear cells. The colonies were composed of spindle cells, flat cells, and fat-containing cells, with all three types often present in the same colony, suggesting derivation from a common progenitor. Cells were negative for nonspecific esterase and factor VIII antigen. Hydrocortisone added to the cultures at concentrations of 10(-7) M induced the formation of adipose cells in the center of one-third to one-half of the colonies but did not affect CFU-ST number. Human platelet-poor plasma and platelet-rich plasma were substituted for fetal calf serum in the medium. When all determinations for four experiments were averaged, platelet-rich plasma gave 17.8 +/- 1.2 (mean +/- SEM, n = 16) colonies, whereas platelet-poor plasma gave only 0.2 +/- 0.1 colonies (n = 15). When purified platelet-derived growth factor (PDGF) was added to platelet-poor plasma, growth of CFU-ST was enhanced, and a dose-response relationship was found between size of colonies and concentration of added PDGF. Granulocyte-macrophage colony stimulating factor added to cultures had no effect on the growth of CFU-ST.
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PMID:Human bone marrow stromal cell colonies: response to hydrocortisone and dependence on platelet-derived growth factor. 301 48

Corticotropin-releasing hormone (CRH) plays a key role in coordinating neuroendocrine, metabolic and behavioral responses in stress and affective disorders. To further investigate the effects of enhanced pituitary-adrenocortical activity upon sleep-related phenomena we administered four intravenous injections of 50 micrograms human (h)-CRH or saline to 11 normal males at 10 p.m., 11 p.m., 12 p.m. and 1 a.m. and measured plasma levels of cortisol and growth hormone (GH) as well as sleep EEG recordings throughout the night. Treatment with h-CRH resulted in a significant increase of mean (+/- SEM) cortisol secretion between 11 p.m. and 3 a.m. (h-CRH: 100.6 +/- 9.5 ng/ml; saline: 39.0 +/- 1.5 ng/ml; p less than 0.01). This initial cortisol increase after repeated h-CRH stimulations was followed by a period of attenuated plasma cortisol between 3 and 7 a.m. (h-CRH: 70.3 +/- 7.0 ng/ml; saline: 115.5 +/- 8.0 ng/ml; p less than 0.01). Cortisol surges after h-CRH were associated with a significant blunting of sleep-related GH release expressed as areas under concentration curves (h-CRH: 1.245 +/- 0.32 ng/ml/min.10(3); saline: 2.462 +/- 0.92 ng/ml/min.10(3), p less than 0.01). In addition to these hormonal effects, h-CRH induced a decrease of REM and slow wave sleep (stages III and IV) while the amount of more shallow sleep (stages I and II) increased. These effects upon sleep structure were more pronounced during the second part of the night.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of intravenous corticotropin-releasing hormone upon sleep-related growth hormone surge and sleep EEG in man. 326 35

After a bolus of 2 mg/kg, propofol was given by continuous infusion (150 micrograms/kg/minute for 30 minutes and then 100 micrograms/kg/minute) supplemented with nitrous oxide for anaesthesia during ear surgery in 12 patients. Cardiovascular changes were not significant except for a decrease in heart rate after 60 minutes. Acid-base balance was unaffected by the amount of fatty emulsion. Cortisol levels showed a nonsignificant decrease during the prolonged administration of propofol but had recovered completely by one hour following anaesthesia. Mean blood concentrations of propofol were 10.5 micrograms/ml (SEM 1.2) at the onset of unconsciousness, between 3.4 and 4.5 micrograms/ml during continuous infusion and 2.9 micrograms/ml (SEM 0.3) on awakening. Patients opened their eyes 6 minutes (SEM 1) after discontinuation of the infusion, and were responsive at 7.5 minutes (SEM 0.5), which suggests that propofol infusion can be used safely for surgery of 2 hours' duration.
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PMID:Propofol combined with nitrous oxide-oxygen for induction and maintenance of anaesthesia. 349 22

The effects of fasting between Days 8 and 16 of the estrous cycle on plasma concentrations of luteinizing hormone (LH), progesterone, cortisol, glucose and insulin were determined in 4 fasted and 4 control heifers during an estrous cycle of fasting and in the subsequent cycle after fasting. Cortisol levels were unaffected by fasting. Concentrations of insulin and glucose, however, were decreased (p less than 0.05) by 12 and 36 h, respectively, after fasting was begun and did not return to control values until 12 h (insulin) and 4 to 7 days (glucose) after fasting ended. Concentrations of progesterone were greater (p less than 0.05) in fasted than in control heifers from Day 10 to 15 of the estrous cycle during fasting, while LH levels were lower (p less than 0.01) in fasted than in control heifers during the last 24 h of fasting. Concentrations of LH increased (p less than 0.01) abruptly in fasted heifers in the first 4 h after they were refed on Day 16 of the fasted cycle. Concentrations (means +/- SEM) of LH also were greater (p less than 0.05) in fasted (11.2 +/- 2.6 ng/ml) than in control (4.7 +/- 1.2 ng/ml) heifers during estrus of the cycle after fasting; this elevated LH was preceded by a rebound response in insulin levels in the fasted-refed heifers, with insulin increasing from 176 +/- 35 pg/ml to 1302 +/- 280 pg/ml between refeeding and estrus of the cycle after fasting. Concentrations of LH, glucose and insulin were similar in both groups after Day 2 of the postfasting cycle. Concentrations of progesterone in two fasted heifers and controls were similar during the cycle after fasting, whereas concentrations in the other fasted heifers were less than 1 ng/ml until Day 10, indicating delayed ovulation and (or) reduced luteal function. Thus, aberrant pituitary and luteal functions in fasted heifers were associated with concurrent fasting-induced changes in insulin and glucose metabolism.
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PMID:Relationships between insulin and glucose metabolism and pituitary-ovarian functions in fasted heifers. 351 23

Cortisol was infused, intravenously, for 4 h continuously into 5 chronically cannulated ovine fetuses at 111-120 days of gestation (term is 142-152 days). The dose used was 100 micrograms/h, and raised fetal blood cortisol concentrations from 8.2 +/- 4.0 to 56.5 +/- 19.0 nmol/l (values are mean +/- SEM). The effects observed were a 4-5 fold increase in sodium and chloride excretion, a doubling of potassium excretion and free water clearance, no significant changes in urine pH, urea and creatinine excretions, and an increase in urine osmolality from 129 +/- 7.5 to 154.4 +/- 11.3 mosmol/kg water. There were no significant changes in any of the measured parameters in 5 fetuses infused with 0.9% NaCl for 4h. It is suggested that the hyponatremia and inability to retain sodium observed in many premature or very low birth weight babies may be due to the fact that their kidneys are behaving as fetal rather than neonatal organs and responding to the high plasma cortisol concentrations found in such babies with a natriuresis.
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PMID:Cortisol is natriuretic in the immature ovine fetus. 402 Mar 17

Cortisol, added to 1 ml incubation medium containing 3-4 X 10(5) isolated guinea-pig adrenal cells, provoked a decrease in basal and ACTH (250 pg)-stimulated cortisol production, in correlation with the amounts used (50 ng-2,000 ng). A decrease in aldosterone production could be seen when cortisol concentrations reached or exceeded 1,000 ng/ml. There were no variations in either androgens (delta 4-androstenedione, dehydropiandrosterone) or 17-hydroxyprogesterone. Only 11-deoxycortisol was slightly increased. Using increasing concentrations of ACTH (50-250 pg), both in the absence and in the presence of 1,000 ng cortisol, it was noted that the inhibition induced by cortisol was of a competitive type and could be overcome by ACTH. This decrease in cortisol was concomitant with an increase in 11-deoxycortisol. Neither corticosterone nor dexamethasone reduced cortisol production. In addition, it was shown that the conversion of tritiated 11-deoxycortisol to radioactive cortisol increased significantly under the influence of 250 pg ACTH (mean relative variation of 21.7% +/- 7.7 (SEM), n = 6, P less than 0.05); but decreased significantly under the combined effect of 1,000 ng exogenous cortisol and the same dose of ACTH: (mean relative variation of 4.3% +/- 1 (SEM), n = 8, P less than 0.005). There is therefore reason to believe that the concentrations of cortisol at the adrenal level modulate the stimulation induced by ACTH and that this self-adjustment forms part of the control mechanisms involved in corticosteroidogenesis.
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PMID:Inhibition of cortisol production in isolated guinea-pig adrenal cells. 608 31

Ouabain-sensitive Na+-K+-stimulated ATPase was measured in red cell membranes using a spectrophotometric assay. The mean enzyme level in patients in the depressed state (1.2 nM/mg protein per min +/- 0.18 SEM) was lower lower than that in well-state patients (2.0 +/- 0.26) and hypomanic patients (2.4 +/- 0.31). Lithium treatment itself did not alter ATPase levels. Levels in patients in the well state were not significantly different from controls and thus ATPase does not constitute a "trait" marker for affective illness. Plasma cortisol level was higher in well-state patients (15.9 micrograms/dl +/- 1.46) than in controls (11.5 +/- 0.75). There were no significant differences in cortisol in these single morning samples during different mood states. Cortisol level correlated negatively with ATPase level in the total group of patients (r = 0.42, p less than 0.005), especially in those who were euthymic. These data indicate a relationship between cortisol and ATPase levels in affectively ill patients. Ouabain-sensitive NaK ATPase may be useful as an indicator of state in affective illness; plasma cortisol may be continuously elevated in some individuals with affective disorder.
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PMID:Red cell ouabain-sensitive Na+-K+-adenosine triphosphatase: a state marker in affective disorder inversely related to plasma cortisol. 629 47

We examined the effects of synthetic human beta-endorphin (beta END) and a stable methionine (Met)-enkephalin analogue on aldosterone and cortisol secretion rates in anesthetized, hypophysectomized, and nephrectomized dogs and compared them to those of (1-39) ACTH. The circulation of the adrenal glands was completely isolated on the arterial and venous sides (Hilton Pouch). The peptides were infused to deliver 3 pmol/min into the aortic "pouch." Blood was collected from the vena caval pouch, which received blood only from the adrenal gland. Secretion rates of aldosterone and cortisol were calculated as the product of adrenal blood flow and venous steroid concentration. Duplicate steroid measurements were obtained during a control period, at 10, 30, and 50 min of peptide infusion and during a postcontrol period. BetaEND increased aldosterone secretion rate from 2.4 +/- 0.5 ng/min (mean +/- SEM) to 3.2 +/- 0.9 ng/ min at 10 min (N.S.), 8.2 +/- 2.5 ng/min (P less than 0.05) at 30 min and 11.0 +/- 3.7 ng/ min (P less than 0.05) at 50 min of infusion. Cortisol secretion rate was not affected by infusion of betaEND. Infusion of the stable Met-enkephalin analogue D-alanine2; Metphenylalanine4, Met(O)-enkephalin-ol or saline alone had no effect on aldosterone or cortisol secretion rates. ACTH infusion increased mean aldosterone secretion rate by approximately 215% and significantly stimulated cortisol secretion rate. These results indicate that beta END selectively stimulates aldosterone secretion with a potency similar to that of an equimolar dose of ACTH.
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PMID:Beta endorphin selectively stimulates aldosterone secretion in hypophysectomized, nephrectomized dogs. 629 40

In the intact, unstressed ovine fetus, both plasma immunoreactive adrenocorticotrophin (ACTH) and blood cortisol concentrations increased after 121 days gestation. The mean ACTH and cortisol concentrations in intact fetuses of 90-121, 122-135 and 136-144 days gestation were for ACTH 20.4 +/- 3.9 (50) (mean +/- SEM, n), 30.2 +/- 5.6 (26) and 56.0 +/- 6.3 pg/ml (37) respectively, and for cortisol 0.07 +/- 0.01 (24), 0.17 +/- 0.03 (21) and 0.64 +/- 0.13 microgram/100 ml (15), respectively. After 121 days ACTH and cortisol concentrations were correlated positively. Cortisol infused into intact or adrenalectomized fetuses and corticosterone infused into adrenalectomized fetuses suppressed fetal plasma ACTH concentrations. In summary, ACTH and cortisol increase concomitantly after 122 days, so that it is highly probable that ACTH is the trophic stimulus for fetal adrenal maturation. The suppression of ACTH by cortisol and corticosterone suggests that these are the natural feedback regulators. It is proposed that while the mechanism for cortisol feedback may exist early in gestation, it is not until after 121 days that feedback control of ACTH becomes evident and physiologically important.
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PMID:Development of the pituitary-adrenal axis in chronically cannulated ovine fetuses. 630 92

Pergolide mesylate is a synthetic ergoline with dopamine agonist properties. The endocrine profile was studied in a double blind crossover design in six normal males. Circulating PRL, TSH, GH, LH, FSH, and cortisol were measured in the basal state and after TRH (500 micrograms iv) administration at 4.5, 11.5, and 23.5 h after placebo or pergolide (100 micrograms orally). Pergolide caused suppression of basal PRL from 2-8 ng/ml to less than 2 ng/ml commencing 60 min after administration and persisting throughout the 23.5-h study period. For the three TRH tests, a suppression of peak PRL (mean +/- SEM) response to TRH of 54.6 +/- 5.1 vs. 1.9 +/- 0.5, 45.2 +/- 4.1 vs. 4.5 +2- 0.6, and 34.4 +/- 2.9 vs. 6.9 +/- 1.4 ng/ml, respectively, for placebo and pergolide was noted. Basal TSH levels were unaffected by pergolide, but after pergolide the peak TSH response to the first two TRH challenges was blunted (placebo vs. pergolide: 12.3 +/- 1.2 vs. 6.8 +/- 1.0 and 14.8 +/- 2.0 vs. 9.6 +/- 1.0, respectively); however, the third TSH response (9.8 +/- 1.1 vs. 9.3 +/- 1.2) was not blunted after pergolide. GH secretion was stimulated by pergolide with a consistent pulse observed within 60 min of pergolide administration and an enhancement in the number and amplitude of subsequent GH pulses throughout the 24-h period. Cortisol levels rose after pergolide and returned to levels seen on the control day at 16.5 h. FSH levels were unaffected but LH levels were lowered pergolide. Side effects including nausea, vomiting, and hypotension were observed in all subjects. Pergolide is a potent dopamine agonist with the anticipated endocrine profile and clinical effects; its long duration of actions offers promise of single daily dose therapy for hyperprolactinemia.
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PMID:Pergolide mesylate: its effects on circulating anterior pituitary hormones in man. 679 9


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