PubMed Health⌕ Search

Biomedical subjects

A Harell

Publications and source records attributed to A Harell.

At least 37 records · Page 2Linked to original sources
PubMed1980

Effects of vitamin D metabolites on cellular Ca2+ and on Ca transport in primary cultures of bone cells.

Both 1,25-dihydroxycholecalciferol (1,25(OH)2D3) and 24,25-dihydroxycholecalciferol (24,25(OH)2D3) exerted direct effects on Ca2+ transport and accumulation in primary cultures of bone cells. The following changes were recorded. (1) A significant decrease in the amount of intracellular exchangeable Ca2+. (2) A marked increase in the rate constants of efflux from the 'slow'-turnover intracellular Ca pool. (3) A marked increase in the 'initial rate' of Ca influx into the cells. Thus, vitamin D metabolites caused an increase in the turnover of Ca2+ in bone cells and altered the steady-stae level of intracellular exchangeable Ca2+. Whereas the changes in the rate of efflux were abolished in the presence of inhibitors of protein synthesis, the increase in the rate of influx was not sensitive to these inhibitors. It is suggested that the changes in the two fluxes were mediated by different mechanisms and that the changes in influx were due to a direct effect of vitamin D metabolites on the cellular membranes.

24,25-Dihydroxyvitamin D 3↗
PubMed1980

Effects of calcitonin on transport and intracellular distribution of exchangeable Ca2+ in primary culture of bone cells.

The effects of calcitonin (CT) on the cellular transport and accumulation of Ca were studied in bone cells grown in primary culture. The following sequence of events was detected: (1) After 1--2 h of incubation with CT the initial rate of Ca influx into bone cells transiently increased. A longer incubation with CT (3--24 h), caused a gradual decrease in the initial rate of Ca influx, reaching a level below the control at 24 h. (2) After 2 h incubation with CT, efflux studies revealer Ca pool and (b) an increase in the accumulation of Ca in the slow-turnover Ca pool. (3) After 30 min of incubation with CT the amount of Ca in bone cells gradually increased and remained at a higher level for up to 24 h incubation with CT. It is suggested that the transient increase in the initial rate of Ca influx into bone cells, caused by CT, may provide the signal for the accumulation of Ca in the slow-turnover Ca pool, which is probably the mitochondria.

Animals↗
PubMed1980

A method for processing paraffin sections of multilayer cultured tissue.

A simple and rapid method is described for processing histological preparations from multilayer cultures growing in plastic Petri dishes, A covering collodion film is utilized to remove the tissue from the plastic dish and transfer it onto a paper block prior to embedding in Paraplast. To avoid any disruption by the collodion of the plasticware, the cultured tissue is first immersed in a solution of collodion and absolute alcohol (1:1) and then covered with pure collodion. All steps are carried out in the cold. This procedure allows morphological, histochemical, immunofluorescent, and autoradiographic studies to be carried out on serial sections of cultured tissue.

Animals↗
PubMed1979

Decreased serum 24,25-dihydroxy vitamin D concentrations in children receiving chronic anticonvulsant therapy.

Serum 24,25-dihydroxy vitamin D (24,25(OH)2D) and 25-hydroxy vitamin D (25-OHD) concentrations and the ratio between the two were measured in 31 Israeli children and adolescents receiving long-term treatment with phenobarbitone or phenytoin and in controls. 24,25 (OH)2D concentrations were significantly depressed in the patients, although the 25-OHD concentrations were similar to those in the healthy controls. In four patients with radiological evidence of osteopenia very low serum 24,25(OH)2D concentrations and serum 24,25(OH)2D: 25-OHD ratios were recorded. The findings suggest that 24,25(OH)2D deficiency may play an important part in the pathogenesis of osteomalacia in patients treated with anticonvulsant drugs and provide further indirect evidence that 24,25(OH)2D is important for normal bone structure.

Adolescent↗
PubMed1979

The diagnostic value of pharmacodynamic tests in the hyperprolactinaemic syndrome.

Patterns of prolactin (PRL) secretion were studied in a group of 18 hyperprolactinaemic patients with galactorrhoea and menstrual disorders and in a control group of thirty-two women in the early puerperium (24 h after a normal delivery) following provocative (TRH and Chlorpromazine) and suppressive (L-Dopa and bromocriptine) stimuli. Five out of the eighteen hyperprolactinaemic patients tested had radiological evidence of a pituitary tumour, and two were treated surgically. The early puerperium patients with elevated basal PRL levels (100--700 ng/ml) demonstrated a significant PRL response to the various treatments. On the other hand, in the hyperprolactinaemic group, an impaired PRL response to TRH, Chlorpromazine and L-Dopa was noted in patients with basal PRL levels higher than 30 ng/ml, whereas bromocriptine suppressed effectively PRL levels in all the hyperprolactinaemic patients tested irrespective of their basal PRL concentrations. The ratio between the fall in PRL concentrations (as percent of the baseline) after L-Dopa administration (delta%L) versus the PRL decrement after bromocriptine treatment (delta%B) was calculated. In the early puerperium group with normal pituitary prolactin secreting cells this ratio was equal to 0.8. In the hyperprolactinaemic group, the five patients with radiological evidence of a pituitary tumour had significantly lower ratios ranging from 0.2 to 0.57. These data suggest that in terms of prolactin release, prolactin producing tumour cells are intrinsically refractory to hypo thalamic dopaminergic signals. The calculation of individual delta%L/delta%B ratios may serve, therefore, as a valuable indicator for early detection of autonomous pituitary prolactin secreting cells and for evaluation of the extent of the pituitary lesion.

Adult↗
PubMed1978

Vitamin D metabolism and expression in rats fed on low-calcium and low-phosphorus diets.

1. Cholecalciferol, radioactively labelled with both (14)C and (3)H, was administered weekly for 7 weeks to rats that had been depleted of vitamin D for 4 weeks before repletion with the radioactive vitamin. This permitted measurement of the steady-state effect on vitamin D metabolism of low-calcium and low-phosphorus regimens, as compared with a normal mineral intake. These dietary manoeuvres were carried out during the last 3 weeks of repletion. Cholecalciferol, 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol were determined in plasma, intestine, kidney and bone. Ca(2+)-binding-protein content was measured in intestine and kidneys of comparable animals. 2. In rats on the low-calcium diets, 1,25-dihydroxycholecalciferol concentration was elevated in plasma, bone, kidney and intestine, and intestinal Ca(2+)-binding protein was increased to over twice the concentration found in the control animals. 3. The low-phosphorus regimens led to a decrease in plasma phosphate and 1,25-dihydroxycholecalciferol in all tissues studied, for the latter to the point where it was undetectable in plasma and bone. Intestinal and renal concentrations of Ca(2+)-binding protein were unchanged in the low-phosphate-intake group and decreased in the very-low-phosphate-intake group. 4. It is concluded that in the rat, unlike in the chick, hypophosphataemia is not associated with a stimulation of the production of 1,25-dihydroxycholecalciferol or its expression in the synthesis of Ca(2+)-binding protein. Therefore the plasma phosphate concentration does not appear to be directly involved in the regulation of the functional metabolism of vitamin D.

Animals↗
PubMed1978

Improvement in the fertility of streptozotocin-diabetic male rats following treatment with insulin and human chrionic gonadotropin.

Diabetes was produced in male rats with streptozotocin. Some of them were subsequently treated with exogenous insulin, human chorionic gonadotropin (hCG) or both. The rats were tested six weeks later for fertility, testosterone secretion and spermatogenesis. Diabetes was found to inhibit all three parameters of fertility. Accessory gland atrophy was restodred following the treatment with insulin and much improved with insulin plus hCG. In a diabetic control group on restricted food intake, insulin alone did not significantly improve fertility, whereas hCG enhanced steroidegenesis and spermatogenesis but not fertility. Treatment with both hCG and sinulsin gave the best results.

Animals↗
PubMed1977

Gonadotrophin release in ovariectomized patients. I. Suppression by clomiphene or low doses of ethinyl oestradiol.

Administration of clomiphene citrate (150 mg/day) for 5 days to twenty-four ovariectomized patients and seven normal female patients evoked a significant release of FSH and LH in the normal control group and suppressed the gonadotrophin secretion in the castrated patients. A similar suppressive effect on gonadotrophin secretion was noted in eight ovariectomized patients treated for 10 days with low doses (50 microgram/day) of ethinyl oestradiol. It is suggested that in the ovariectomized hypoestrogenic patients, clomiphene acted as an oestrogen, suppressing by a negative feedback action gonadotrophin release in a way similar to ethinyl oestradiol. In the normal control group with an adequate steroid environment, clomiphene acted (probably at the hypothalamic level) as an oestrogen antagonist and stimulated gonadotrophin secretion. In view of our findings, it seems as if the ability of anovulatory patients to respond to clomiphene treatment by increased gonadotrophin secretion depends upon the absolute concentration of the compound in the different organs and by the quantitative relation of clomiphene to the endogenous oestrogens.

Adult↗
PubMed1977

Acute effect of delta1-tetrahydrocannabinol on the hypothalamo-pituitary-ovarian axis in the rat.

Administration of delta1-tetrahydrocannabinol (delta1-THC), the principal psychoactive ingredient of cannabis, to proestrous rats (2 mg/rat, i.p., between 12.00 and 16.00 h) suppressed the proestrous rise in the plasma levels of LH, FSH and prolactin (Prl) and caused a 24 h delay in ovulation. Furthermore, the increased accumulation of prostaglandins of the E-type (PGE) in the ovaries, normally seen on the evening of proestrus, was prevented. Earlier (08.00-10.30 h) or later (18.00 h) administration of the drug on the day of proestrus was only partially effective in inhibiting ovulation. The suppressive effects of delta1-THC on ovulation and gonadotropin secretion were prevented by administration of gonadetropin releasing hormone (GnRH, 0.2 microgram/rat) 1 h after the drug, indicating that the central action of delta1-THC was exerted on the hypothalamus and not on the pituitary gland. Administration of ovine luteinizing hormore (oLH, 2.5 microgram/rat at 16.30 h on the day of proestrus restored ovulation and ovarian PGE accumulation in Nembutal-treated rats, but not in delta1-THC-treated rats; higher doses of oLH (5-10 microgram/rat) reversed the action of delta1-THC on these two parameters.

Animals↗
PubMed1977

Low cortisol and growth hormone secretion in response to methoxamine administration in obese subjects.

To investigate the hypothalamic responsiveness in obesity, changes in the levels of plasma cortisol and growth hormone (GH) were studied in 11 obese and six normal-weight subjects after hypothalamic alpha-adrenergic stimulation with methoxamine, 20 mg i.v. To allow for dose/body weight differences, five additional obese subjects received 30 mg methoxamine. Plasma GH, cortisol, insulin, free fatty acid and glucose levels were determined during the 3-h infusion of methoxamine. The responses of cortisol and GH were reduced in the obese subjects as compared with the normal-weight subjects. No significant changes in plasma glucose, free fatty acids or insulin were observed in any of the groups. The reduced responses of plasma cortisol ang GH in the obese subjects are considered to be an expression of hypothalamic underresponsiveness, since the stimuli for the secretion of these hormones are at least partially controlled by an alpha-adrenergic mechanism.

Adult↗
PubMed1976

Maternal-perinatal interrelationships of vitamin D metabolism in rats.

In pregnant rats it has been possible to show that the distribution of cholecalciferol metabolites in their fetuses reflects the distribution of these metabolites in the blood. In these experiments, pregnant rats were maintained on a vitamin D deficient diet but were supplemented with radiolabelled cholecalciferol. The metabolites found were 25-hydroxycholecalciferol and 24,25-dihydroxycholecalciferol and, to a lesser extent, cholecalciferol. 1,25-Dihydroxycholecalciferol was not detected in fetal tissues, despite the ability of fetal kidney homogenates to hydroxylate 25-hydroxycholecalciferol in C-1. Kidney homogenates of newborn pups were found to possess marked activity of 25-hydroxycholecalciferol-24-hydroxylase, which was retained even in hypocalcemic pups born to pregnant rats that were fed a low-calcium diet. Injection of radiolabeled cholecalciferol to newborn pups resulted in the formation of 25-hydroxycholecalciferol and 24,25-dihydroxycholecalciferol. 1,25-Dihydroxycholecalciferol was not detected. Tissues thought of as target organs for vitamin D (in pregnant rats), namely, intestine, kidney and bone, were found to contain none or very little 1,25-dihydroxycholecalciferol. Mammary glands obtained from lactating rats were found to contain mainly the unchanged vitamin.

Animals↗