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Biomedical subjects

Y Weisman

Publications and source records attributed to Y Weisman.

At least 145 records · Page 8Linked to original sources
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

Serum concentrations of 24,25(OH)2D in uremic children: a reflection of renal function.

The mean serum concentration of 24,25(OH)2D determined by competitive protein-binding radioassay was significantly lower in ten uremic children maintained on hemodialysis (0.82 +/- 0.43[SD] ng/ml) than in ten patients with impaired renal function not requiring hemodialysis (1.30 +/- 0.54 ng/ml, P less than 0.05), or in 12 normal children (2.98 +/- 1.57 ng/ml, P less than 0.01). The serum levels of 250HD were similar in all groups. There were significant (P less than 0.01) positive correlations between the serum concentration of 24,25(OH)2D or the ratio 24,25(OH)2D/25OHD and the creatinine clearance. The serum concentration of 24,25(OH)2D was significantly decreased also in six anephric adults relative to normal adult values. The data indicate that production of 24,25(OH)2D is impaired in subjects with compromised renal function. Inasmuch as the major active metabolite of Vitamin D, i.e., 1,25(OH)2D, is requried for renal synthesis of 24,25(OH)2D measurement of the latter metabolite may provide a convenient method for assessment of renal vitamin D metabolism. The role of this metabolite in the pathogenesis of renal osteodystrophy remains speculative.

Child↗
PubMed1979

Serum concentrations of 25-hydroxyvitamin D in Florida children: effect of anticonvulsant drugs.

The mean serum concentration of 25-hydroxyvitamin D (25OHD), determined by nonchromatographic radioassay, was significantly lower (P less than .02) in Florida children with epilepsy treated with anticonvulsant drugs (34.4 +/- 11.3 [SD] ng/ml) than in normal subjects (40.9 +/- 14.3), despite exposure of both groups to sunlight throughout the year. In 12% of children treated with anticonvulsant drugs, the 25OHD level was below the lowest value recorded in the control group. The mean serum concentration of 25OHD in normal Philadelphia children (27.5 +/- 9.1 ng/ml) was significantly less than in either group of Florida subjects. Annual monitoring of calcium homeostasis and vitamin D status is indicated in Southern children receiving anticonvulsant drugs, but routine vitamin D supplementation of such patients is unnecessary.

Anticonvulsants↗
PubMed1979

Response of neonatal hypocalcaemia to 1 alpha-hydroxyvitamin D3.

Administration of 1 alpha-OH-D3 to hypocalcaemic neonates (mean +/- SD, serum calcium 1.50 +/- 0.13 mmol/l) significantly increased serum calcium in all 24 infants within 48 hours after starting therapy (mean +/- SD 1.83 +/- 0.23 mmol/1). The time required to correct hypocalcaemia was significantly shorter (2.04 +/- 0.56 days) in infants treated with 1 alpha-OH-D3, than in 24 infants treated with calcium gluconate infusions (4.12 +/- 1.0 days). Treatment with 1 alpha-OH-D3 was effective, easy to maintain, and produced no side effects.

Calcium Gluconate↗
PubMed1978

Concentrations of 24,25-dihydroxyvitamin D and 25-hydroxyvitamin D in paired maternal-cord sera.

Mean serum concentrations of 24,25-dihydroxyvitamin D (24,25(OH)2D) and 25-hydroxyvitamin D (25OHD), measured by competitive radioassays, were significantly higher in maternal serum than in cord serum of term infants in both black and white subjects. There were positive correlations between maternal and cord levels of both metabolites of vitamin D. Serum concentrations of 24,25(OH)2D and 25OHD were significantly lower in white pregnant subjects than in nonpregnant women. In utero levels of 24,25(OH)2D and 25OHD probably reflect maternal stores of these metabolites.

Dihydroxycholecalciferols↗
PubMed1978

Synthesis of 1,25-dihydroxyvitamin D in the nephrectomized pregnant rat.

Pregnant rats were maintained on diets either adequate or deficient in vitamin D. On the 20th day of gestation, animals were either nephrectomized bilaterally or sham operated. Immediately therafter, four groups of nephrectomized or sham-operated pregnant rats received iv [26,27-3H]25-hydroxyvitamin D3 ([26,27-3H]25OHD3), while two groups received [1,2-3H,4-14C]D3. The animals were sacrificed 10-24 h later. The distribution of the radiolabeled metabolites of vitamin D3 was determined in extracts of maternal plasma, maternal intestinal tract, placentae, and fetuses after Sephadex LH-20 column chromatography. Both vitamin D3 and 25OHD3 crossed the placenta and entered the fetus. In anephric animals receiving [26,27-3H]-25OHD3, 24,25-dihydroxyvitamin D and a polar peak eluting in the position of 1,25-dihydroxyvitamin D [1,25(OH)2D] and 25,26-dihydroxyvitamin D were identified in extracts of maternal plasma and intestinal tracts and of placentae and fetuses. The identities of 24,25-dihydroxyvitamin D and 1,25 (OH)2D were confirmed by high pressure liquid chromatography. In rats receiving [1,2-3H,4-14C]D3, approximately 50% of the polar metabolite consisted of 1,25(OH)2D. We conclude that the anephric pregnant rat is able to synthesize 1,25(OH)2D, that the fetal portion of the feto-placental unit is the most likely site of production of this hormone, and that this metabolite of vitamin D is able to cross the placenta from the fetus to the mother.

Animals↗
PubMed1977

Measurement of 24,25 dihydroxyvitamin D in sera of neonates and children.

Serum concentration of 25OHD and 24,25(OH)2D were measured in lipid extracts of serum by competitive radioassay following separation of the metabolits by Sephadex LH-20 column chromatography. The concentration of 24,25(OH)2D in children and adolescents (3.3 +/- 1.3 SD ng/ml) was significantly greater (P less than 0.01) than the levels recorded in neonates (1.8 +/- 0.6 ng/ml), and was approximately one-tenth the concentration of 25OHD in the two populations (children 35.2 +/- 9.2 ng/ml; neonates 14.4 +/- 3.4 ng/ml, P less than 0.01). Although 24,25(OH)2D is present in significant quantities in the sera of children and adolescents, its metabolic function remains unknown at present.

Adolescent↗
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↗
PubMedDate not supplied

Differentiation of cultured mice bone marrow into osteoblast-like cells results in acquisition of sex-specific responsiveness to gonadal steroids.

We have previously demonstrated that mouse skeletal tissue, rat bone as well as rat or human derived bone cells in culture, show a sex-specific response to gonadal steroids in stimulation of the specific activity of the BB isozyme of creatine kinase (CK). This response could be modified by manipulation of the endocrine environment during early postnatal development. Moreover, pretreatment with vitamin D up-regulated the sex-specific responsiveness and sensitivity to gonadal steroids. In the present study we examine the differentiation pattern into osteoblast-like cells using dexamethasone (DEX) and 1,25 dihydroxy vitamin D3 (1,25D) and their effect on the acquisition of responsiveness to gonadal steroids by the differentiated cells. Cultured femoral bone marrow in the presence of DEX or 1,25D or both, were examined for their response to gonadal steroids by measuring the specific activities of alkaline phosphatase (AP) and CK BB. The constitutive level of CK in both male- and female-derived bone cells was decreased by DEX, by 1,25D or by both, whereas the constitutive level of AP was increased by DEX while decreased by 1,25D or by both. Following incubation of the bone marrow cultures with DEX, treatment with estradiol 17beta (E2, 30 nM, 24 h) stimulated CK activity in female derived bone cells, with no effect of treatment with dihydrotestosterone (DHT, 300 nM). In contrast, in male derived bone cells, DHT but not E2 increased CK activity. This sex-specific response was also achieved upon culturing with 1,25D and was significantly augmented by culturing with both. No response to gonadal steroids was seen with undifferentiated bone marrow cells. All cultures responded to IGF-I when cultured with or without DEX and/or 1,25D but with no augmentation by 1,25D. Gonadal steroids increased AP to a much lesser extent; but enzyme activity decreased in the presence of 1,25D. IGF-I stimulated AP slightly with no effect of 1,25D. These findings suggest that manipulation of the hormonal milieu in early stages of differentiation sequence of osteoblast-like cells, determines the subsequent selective responsiveness of the developing bone tissue to gonadal steroids.

Animals↗
PubMedDate not supplied

"Non-hypercalcemic" analogs of 1alpha,25 dihydroxy vitamin D augment the induction of creatine kinase B by estrogen and selective estrogen receptor modulators (SERMS) in osteoblast-like cells and rat skeletal organs.

We have demonstrated previously that daily treatments for 3 days with the so-called "non-hypercalcemic" analogs of 1alpha,25 dihydroxy vitamin D in ROS 17/2.8 osteoblast-like cells, stimulate the specific activity of creatine kinase BB (CK), and that such treatment with these analogs followed by a single treatment with gonadal steroids, upregulates responsiveness and sensitivity to estradiol 17beta (E(2)) for the induction of CK. This study was designed to determine if these same "non-hypercalcemic" vitamin D analogs could upregulate in vivo the response to E(2) and whether substitution of selective estrogen receptor modulators (SERMS) for E(2) would result in the same upregulation. We found that one week or 2 weeks pretreatment of prepubertal rats with vitamin D analogs led to increased induction of CK by E(2) and by the SERMS tamoxifen, tamoxifen methiodide and raloxifene, in epiphysis and diaphysis of the femur but not in the uterus. However, in contrast to their antiestrogenic activity in the uterus, there was no inhibition of E(2) action by the SERMS in skeletal tissues. The induction of mRNA for ckb in ROS 17/2.8 cells by E(2) or SERMS was demonstrated only after vitamin D pretreatment; there was no inhibition of E(2) induction by SERMS. Antagonists of vitamin D dependent calcium transport (transcaltachia) did not inhibit stimulation by vitamin D analogs. These results support the involvement of a nuclear mechanism in the upregulation of induction of CK by E(2), which may be due, in part, to the ability of vitamin D to increase estrogen receptor(s).

Animals↗
PubMedDate not supplied

Marek's disease in turkeys. I. A seven-year survey of commercial flocks and experimental infection using two field isolates.

Marek's disease virus (MDV) causes immunosuppression and tumors in chickens, but the turkey is an unusual host for the virus, and tumors caused by MDV in turkeys are unique. We describe the prevalence of turkey tumors in Israel between 1993 and 2000, their molecular diagnosis by polymerase chain reaction (PCR), and the natural distribution of herpesvirus of turkeys (HVT). Most clinical cases with tumors in commercial turkeys were diagnosed as MDV. The reproduction of Marek's disease (MD) in turkeys by two turkey MDV strains, Ar and La, was analyzed, and it was shown that these strains can induce tumors in experimental trials. The severity of experimental disease differed from those features of the original outbreak, since a less severe disease was recorded.

Animals↗