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Biomedical subjects

Y Weisman

Publications and source records attributed to Y Weisman.

At least 109 records · Page 6Linked to original sources
PubMed1986

Stimulation of creatine kinase activity by calcium-regulating hormones in explants of human amnion, decidua, and placenta.

We have used stimulation of the activity of the brain type creatine kinase (CK) isoenzyme as a response marker to examine the effects of vitamin D metabolites, PTH, and calcitonin in cultured explants of placenta, decidua, and amnion from normal human deliveries. We found a biological response to PTH in placenta and amnion and to vitamin D metabolites in all three tissues. In the amnion, CK activity increased 2.3-fold after 24 h of incubation in 2.5 nM 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3], 3.8-fold when incubated with 12.5 nM 24,25-dihydroxyvitamin D3 [24,25-(OH)2D3] and 2.7-fold when incubated with 10 U/ml bovine PTH. In the decidua, 24,25-(OH)2D3, but not 1,25-(OH)2D3 or bPTH caused a 1.7-fold increase in CK activity. In contrast, the placenta responded to 1,25-(OH)2D3 with a 1.6-fold increase in CK activity and to bPTH, with a 1.7-fold increase but did not respond to 24,25-(OH)2D3. Bovine calcitonin (100 ng/ml) had no effect on CK activity in any of the three tissues. Nearly all CK in both the unstimulated and stimulated explants was the brain type isoenzyme. CK activity increased significantly between 1 and 4 h after hormonal treatment in all experiments. The enzyme activity rose steeply with dose and reached a significant increase, and usually a plateau, at hormone concentrations considered to be physiological in vivo. [3H]Thymidine incorporation into DNA increased in parallel to stimulation of CK activity in all experiments, except that PTH did not increase DNA synthesis in the placenta. PTH did cause an increase in cAMP production in explants of amnion (1.5-fold) and placenta (2.6-fold).

Amnion↗
PubMed1985

Autoradiographic localization of 24R,25-dihydroxyvitamin D3 in epiphyseal cartilage.

There is emerging evidence for specific binding sites and biologic action for 24,25(OH)2D3 in the epiphyseal cartilage. The present study was undertaken to identify the target cells of 24,25(OH)2D3 in the epiphyses of rat bone using an autoradiographic technique. Pieces of epiphyseal cartilage obtained from 4-day-old vitamin D-deficient rats were incubated for 15 or 60 min with [3H]-24,25(OH)2D3 in the presence or absence of 100-fold excess of 25(OH)D3, 1,25(OH)2D3, or 24R,25(OH)2D3. The pieces were prepared for autoradiographic study by a new modified fixation method. Cytoplasmic and nuclear concentration of radioactivity was observed in all cell layers of the epiphyseal cartilage except for the hypertrophic cartilage zone. The highest concentration of radioactivity was seen in the proliferating chondroblasts of the columnar zone. After 15 min of incubation the radioactivity was seen mainly in the cell membrane and cytoplasm, whereas at 60 min radioactivity was also prominent in the nuclei. The competition with excess of cold metabolites revealed that only 24R,25(OH)2D3 caused a significant decrease in cytoplasmic and nuclear radioactivity. These data support the biochemical studies showing that the epiphyseal cartilage is a target tissue for 24,25(OH)2D3.

24,25-Dihydroxyvitamin D 3↗
PubMed1985

Retinol transport proteins and concentrations in human amniotic fluid, placenta, and fetal and maternal sera.

1. The proteins binding retinol, and retinol concentrations, were determined in amniotic fluid, placental cytosol and in the fetal and maternal circulation. 2. In non-pregnant women, plasma retinol was almost exclusively found in a transthyretin-retinol-binding-protein complex whereas, in pregnant women, retinol-binding-protein-bound retinol was observed not complexed to transthyretin. This latter fraction increased in concentration with fetal age. These two fractions were the major retinol-protein complexes in amniotic fluid and their relative amounts changed with progress of gestation. 3. In fetal blood both of these fractions were again found, with higher proportions of retinol-binding-protein-bound retinol in the umbilical artery than in the umbilical vein.

Amniotic Fluid↗
PubMed1985

Defective binding and function of 1,25-dihydroxyvitamin D3 receptors in peripheral mononuclear cells of patients with end-organ resistance to 1,25-dihydroxyvitamin D.

Lectin-induced DNA synthesis by peripheral mononuclear cells from 17 normal donors was inhibited (40-60%) by 1,25-dihydroxyvitamin D3 (1,25[OH]2D3) at physiological concentrations (10(-10)-10(-9) M). The lymphocytes acquire specific receptors for 1,25(OH)2D3 upon activation by the lectins. This process precedes the inhibitory effect of 1,25(OH)2D3. We studied lymphocytes from six patients from four different kindreds with the syndrome of hereditary end-organ resistance to 1,25(OH)2D (the so-called vitamin D-dependent rickets type II). In five patients (three kindreds) peripheral blood mononuclear cells did not acquire receptors for 1,25(OH)2D3 upon phytohemagglutinin-induced activation. Moreover, in contrast to normal lymphocytes, the mitogenic stimulation of these patients' lymphocytes by phytohemagglutinin and concanavalin A was not inhibited by 1,25(OH)2D3. Activated lymphocytes of the sixth patient from a fourth kindred exhibited normal binding of [3H]1,25(OH)2D3 but the hormone failed to inhibit the mitogenic stimulation. A similar pattern of the vitamin D effector system was previously observed in fibroblasts cultured from skin biopsies of the same group of patients. The conclusions from these findings are: (a) the inhibition of mitogenic stimulation by 1,25(OH)2D3 is mediated by specific functional receptors to the hormone; and (b) the receptors for 1,25(OH)2D3 in mononuclear cells are probably controlled genetically by the same mechanisms as the effector system in well-characterized target organs of the hormone, such as intestine and kidney.

Adolescent↗
PubMed1985

Does 1,25-dihydroxyvitamin D participate in the regulation of hormone release from endocrine glands?

The presence of receptors for 1,25-dihydroxyvitamin D3 in the pituitary, pancreas, testis, and ovary has raised the question of a possible direct role for 1,25-dihydroxyvitamin D (1,25(OH)2D) in the regulation of hormone synthesis and secretion. To evaluate this problem, six children with the syndrome of resistance to 1,25(OH)2D with rickets and alopecia underwent dynamic tests of insulin, TSH, PRL, GH, and testosterone secretion. Oral glucose loading resulted in normal glucose curves, subnormal peak insulin responses of 12-20 microU/ml in three hypocalcemic patients, and normal peak serum insulin values of 30-40 microU/ml in two normocalcemic patients. Basal serum, TSH, PRL, T4, and T3 concentrations were normal in all patients. Peak serum TSH values after TRH were 11-17 and 16-32 microU/ml in the hypo- and normocalcemic patients, respectively. The PRL response to TRH stimulation in either hypocalcemic or normocalcemic patients was normal [mean 26.2 +/- 5.1 (SD) ng/ml]. Peak serum GH levels were greater than 8 ng/ml in all five patients studied after one or more of the various stimuli. Serum testosterone concentrations after hCG stimulation were normal in the three patients studied (4.1-8.0 ng/ml). Thus, in children with resistance to 1,25(OH)2D, we could find no significant abnormalities in hormone secretion from the pituitary, pancreas, and testis apart from those presumably due to the hypocalcemia itself.

Calcitriol↗
PubMed1984

Stimulation of creatine kinase BB activity by 1 alpha,25-dihydroxycholecalciferol and 24R,25-dihydroxycholecalciferol in rat tissues.

Vitamin D metabolites stimulate creatine kinase BB activity in organs of vitamin D-deficient rats. In epiphyses of long bones, creatine kinase BB activity increases 2.6-fold 24 h after injection of 24R,25-dihydroxycholecalciferol but not of 1 alpha,25-dihydroxycholecalciferol. Contrariwise, 1 alpha,25-dihydroxycholecalciferol, but not 24R,25-dihydroxycholecalciferol, increases creatine kinase BB activity in diaphyses and in kidney. Neither metabolite affects creatine kinase activity in duodenal mucosa.

24,25-Dihydroxyvitamin D 3↗
PubMed1984

Rapid diagnosis of congenital adrenal hyperplasia by high performance liquid chromatography.

This manuscript describes methods for the quantitation of serum concentrations of 17-hydroxyprogesterone and 11-deoxycortisol (Compound S) employing reverse-phase high-performance liquid chromatography (HPLC) and ultraviolet (UV) absorbance which are applicable to the diagnosis of congenital adrenal hyperplasia due to deficiencies of 21- and 11-hydroxylase activities, respectively. These methods are simple, specific, precise and rapid. Data obtained by the HPLC-UV methods are highly correlated (p less than 0.001) with radioimmunoassay measurements.

17-Hydroxycorticosteroids↗
PubMed1984

1,25-Dihydroxyvitamin D resistance, rickets, and alopecia.

Two unrelated kindreds with four affected children having 1,25-dihydroxyvitamin D resistance, rickets, and alopecia are described. The children exhibited early onset of severe rickets with hypocalcemia, hypophosphatemia, elevated serum alkaline phosphatase levels, and secondary hyperparathyroidism. Radiography showed diffuse demineralization and classic changes of rickets. All affected children had total-body alopecia. Serum levels of 1,25-dihydroxyvitamin D3 were elevated and rose to extremely high values during treatment, with no apparent change in the mineral disorder. However, secondary hyperparathyroidism and hypophosphatemia did remit during treatment despite persistently low calcium levels. Skin biopsy was performed in the parents and affected children in one kindred. Analysis of 1,25-dihydroxyvitamin D3 receptors in cultured fibroblasts indicated apparent normal receptors in the parents and undetectable receptors in both affected children. After long periods of treatment with vitamin D metabolites and mineral replacement, healing took place in the older child in each kindred. These data suggest that the healing occurred spontaneously as the children reached seven to nine years of age rather than as a result of the treatment. The biochemical lesion in these children appeared to be a genetically transmitted defect in the 1,25-dihydroxyvitamin D3 receptor. The mechanisms by which healing was initiated and maintained remain to be elucidated.

Alopecia↗
PubMed1984

The role of 17 beta-estradiol in the recovery from oviductal prolapse in layers.

Plasma 17 beta-estradiol concentrations, thecal estrogen content, and uterine prostaglandin synthetase activity were measured in healthy and prolapsed hens as well as in layers that recovered after exposure to low intensity lighting (250 or 50 lx). The effect of estradiol benzoate injections (100 ng, 3 X per week) in hens exposed to high intensity light (greater than 500 lx) was also studied. Prolapsed hens had significantly lower plasma 17 beta-estradiol concentrations (60 +/- 12 pg/ml; mean +/- SEM) than recovered (374 +/- 40 pg/ml) or healthy hens (475 +/- 45 pg/ml). Theca cells from recovered hens had a significantly higher content of 17 beta-estradiol (.7 ng/5 X 10(5) cells) than theca cells from normal or prolapsed birds (.3 ng/5 X 10(5) cells). Microsomes prepared from the uteri of prolapsed hens converted significantly less arachidonic acid to prostaglandin metabolites (4.4%) than did microsomes from healthy or recovered birds (9.0%). Treatment of prolapsed hens with estradiol benzoate resulted in 89% of the birds recovering within 3 weeks compared to a 4% recovery rate in the controls. We conclude that restoration of peripheral 17 beta-estradiol concentrations to normal levels was concomitant with recovery in prolapsed birds, and suggest that the estrogen exerts its effect by raising the level of prostaglandin synthetase activity in the uterus.

Animals↗
PubMed1983

The effects of 24R,25-dihydroxycholecalciferol and of 1 alpha,25-dihydroxycholecalciferol on ornithine decarboxylase activity and on DNA synthesis in the epiphysis and diaphysis of rat bone and in the duodenum.

The effect of cholecalciferol metabolites on ornithine decarboxylase activity and on DNA synthesis in developing long bones was investigated in vitamin D-depleted rats. In the epiphysis there was a 6.4-fold increase in ornithine decarboxylase activity 5 h after a single injection of 24R,25-dihydroxycholecalciferol but not of 24S,25-dihydroxycholecalciferol or other vitamin D metabolites. In comparison, in the diaphysis and duodenum, 1 alpha,25-dihydroxycholecalciferol, but not other vitamin D metabolites, caused a 3-3.5-fold increase in the enzyme activity. The enzyme activity in the tissues examined attained a maximal value at 5 h after the injection of the metabolites. The activity of ornithine decarboxylase in the epiphysial region increased dose-dependently as the result of a single injection of 24R,25-dihydroxycholecalciferol and attained a maximal value at a dose between 30 and 3000 ng. In addition, administration of 24R,25-dihydroxycholecalciferol, but not 24S,25-dihydroxycholecalciferol or other metabolites, caused within 24 h a 1.7-2.0-fold increase in [3H]thymidine incorporation into DNA of the epiphyses of tibial bones. In comparison, 1 alpha,25-dihydroxycholecalciferol caused a 1.5-fold increase in [3H]thymidine incorporation into DNA of the diaphyses and of the duodenum. The present data indicate that 24R,25-dihydroxycholecalciferol is involved in the regulation of epiphyseal growth, whereas 1 alpha,25,dihydroxycholecalciferol stimulates the proliferation of cells in the diaphysis of long bones and in the intestinal mucosa.

24,25-Dihydroxyvitamin D 3↗
PubMed1983

The effect of tiamulin administered by different routes and at different ages to turkeys receiving monensin in their feed.

Healthy turkeys receiving 80 ppm monensin in their feed were injected at 26, 40 and 61 days of age with tiamulin at dosages of 12.5 and 25 mg/kg body weight. The aim of the study was to develop a regime for medicating with tiamulin turkeys receiving monensin in their feed, and which would circumvent the known toxicity created by the simultaneous administration of the two drugs. One injection of 12.5 mg/kg tiamulin up to the age of 61 days or 2 injections of 12.5 mg/kg tiamulin up to 40 days of age caused no mortality or adverse reaction.

Age Factors↗
PubMed1983

Vitamin D metabolites in amniotic fluid.

To provide further data on vitamin D metabolism in pregnancy, the concentrations of 25-hydroxyvitamin D (25OHD; n = 72), 24,25-dihydroxyvitamin D [24,25-(OH)2D; n = 70], and 1,25-(OH)2D (n = 59) were measured in amniotic fluid by competitive protein-binding radioassays. At term, the mean (+/- SE) concentrations of 25OHD and 24,25-(OH)2D in amniotic fluid (810 +/- 76 and 37.5 +/- 5.4 pg/ml, respectively) were significantly lower (P less than 0.01) than those at 16-18 weeks gestation (1707 +/- 2.67 and 149 +/- 3 pg/ml, respectively). Similarly, the concentrations of 25OHD in pooled amniotic fluid samples, as determined by high pressure liquid chromatography and UV absorbance detection at 254 nm, were 664 +/- 188 pg/ml at term and 1240 +/- 294 pg/ml at midgestation. In comparison, no difference could be found between the mean concentrations of 1,25-(OH)2D at term (4.3 +/- 0.8 pg/ml) and those at midgestation (3.3 +/- 0.4 pg/ml). However, in 14 of 39 amniotic fluid samples obtained at term (35.9%), the concentration of 24,25-(OH)2D was undetectable, while the level of 1,25-(OH)2D was increased. The reciprocal relationship between 24,25-(OH)2D and 1,25-(OH)2D found in more than a third of the amniotic fluid samples at term may be due to a regulatory mechanism responding to the increased fetal demand for calcium in the final stages of pregnancy.

25-Hydroxyvitamin D 2↗