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Biomedical subjects

Y Weisman

Publications and source records attributed to Y Weisman.

At least 55 records · Page 3Linked to original sources
PubMed1995

Antigenic heterogeneity of avian paramyxoviruses of serotype 2 ("Yucaipa-like") isolated from domestic and wild birds in Israel.

Thirty-three viruses of PMV-2 serotype isolated in Israel from domestic and wild birds during epizooty of a respiratory disease in 1979-1981 were studied comprehensively in comparison with a set of reference PMV-2 viruses using cross reaction hemagglutination inhibition tests, elution-hemagglutination pattern and pattern of migration of viral proteins in polyacrylamide gel electrophoresis. The results demonstrated considerable heterogeneity amongst the local isolates by the above three criteria which were not correlated with each other. There was no significant correlation between the differences found and chronology of isolation of the viruses. The results indicated that there may have been simultaneous co-circulation of different PMV-2 strains in the local avian reservoir at the beginning of the epizootic rather than temporal accumulation of variants as a result of antigenic drift of an "ancestor" virus which caused the initial infection.

Animals↗
PubMed1995

Pretreatment with 1,25(OH)2 vitamin D or 24,25(OH)2 vitamin D increases synergistically responsiveness to sex steroids in skeletal-derived cells.

We demonstrated previously that vitamin D metabolites modulate the response of bone and cartilage cells to 17 beta-estradiol (E2) and dihydrotestosterone (DHT) both in cell cultures and in vivo. In the present study, we investigated to what extent pretreatment with 1,25(OH)2D3 or 24,25(OH)2D3 would reduce the minimal effective dose of E2, DHT or progesterone (P) required for stimulation of DNA synthesis and creatine kinase specific activity in cultured osteoblast-like ROS 17/2.8 cells and in rat embryo epiphyseal cartilage cells, and to what extent such pretreatment would increase the maximal response. We measured responses to sex steroids after pretreatment of the cells for 5 days with 0.02% ethanol vehicle or with the vitamin D metabolites 1,25(OH)2D3 (0.12 nM), or 24,25(OH)2D3 (1.2 nM) singly or in combination. Pretreatment of ROS 17/2.8 cells with 1,25(OH)2D3, but not 24,25(OH)2D3, increased synergistically their response to E2 but not to P, and did not affect their lack of response to DHT. Pretreatment of epiphyseal cartilage cells with either 1,25(OH)2D3 or 24,25(OH)2D3 increased synergistically their DNA synthetic response to all three steroids, but their CK response only to E2 or DHT. The minimal dose for causing a significant response to E2 in ROS 17/2.8 cells or to either E2 or DHT in epiphyseal cartilage cells was reduced 10-fold after pretreatment with vitamin D metabolites. After pretreatment, the maximal response was more than doubled in ROS 17/2.8 cells; epiphyseal cartilage cells showed a similar 10-fold decrease in the dose required for maximal response to E2 or DHT; the improvement in the response to P was significant only for DNA synthesis. We conclude that pretreatment with the appropriate vitamin D metabolite(s) both reduces by an order of magnitude, or more, the amount of sex steroids needed to stimulate skeletal derived cells and increases synergistically the maximal response of the cells.

24,25-Dihydroxyvitamin D 3↗
PubMed1995

Low-dose adrenocorticotropin test reveals impaired adrenal function in patients taking inhaled corticosteroids.

The aim of the present study was to examine the use of low-dose ACTH-(1-24) stimulation for assessment of adrenal function and the detection of mild adrenal insufficiency. The criteria for normal response to ACTH-(1-24) are a peak cortisol level of more than 500 nmol/L (18.1 micrograms/dL) and an increment of the cortisol level above the basal one of more than 200 nmol/L (7.2 micrograms/dL). These criteria were satisfied by 32 of 33 healthy children and adults subjected to an ACTH-(1-24) dose 500 times lower (0.5 micrograms/1.73 m2) than the dose of 250 micrograms in the standard test. At 20 min, the peak cortisol level was the same in the low-dose test [(621 +/- 28 nmol/L) (22.5 +/- 1.0 microgram/dL)] as in the standard ACTH test [(654 +/- 31 nmol/L) (23.7 +/- 1.1 microgram/dL)]. Of 46 asthmatic patients who had been treated with inhaled beclomethasone dipropionate (482 +/- 42 micrograms/m2 daily; n = 32) or budesonide (507 +/- 62 micrograms/m2 daily; n = 14) for over 6 months, 16 (35%) failed to reach a cortisol peak of more than 500 nmol/L (18.1 micrograms/dL) following stimulation with 0.5 micrograms ACTH-(1-24)/1.73 m2. Of these, 11 (24%) showed a cortisol increment of less than 200 nmol/L (7.2 micrograms/dL). These 16 patients, showing insufficient response to low-dose ACTH-(1-24), also had a significantly lower (P < 0.01) mean 24-h urinary free cortisol excretion [(71 +/- 10 nmol/m2.24 h) (25.7 +/- 3.6 micrograms/m2.24 h)] than patients who responded normally [(118 +/- 11 nmol/m2.24 h) (42.8 +/- 4.0 micrograms/m2.24 h). Nonetheless, all but one of the poor responders to a 0.5 microgram ACTH showed normal stimulation with the standard 250 micrograms ACTH test. Therefore, it appears that a low-dose ACTH test is capable of revealing mild adrenal insufficiency, which is not detected by the standard high-dose ACTH test.

Administration, Inhalation↗
PubMed1995

Amniotic fluid and plasma levels of parathyroid hormone-related protein and hormonal modulation of its secretion by amniotic fluid cells.

Parathyroid hormone-related (PTHrP), the major mediator of humoral hypercalcemia of malignancy, may also regulate placental calcium flux, uterine contraction and fetal tissue development. In the present study, we demonstrated that the mean immunoreactive PTHrP concentrations in amniotic fluid at mid-gestation (21.2 +/- 3.7 pmol/l) and at term (19.0 +/- 2.7 pmol/l) were 13-16-fold higher than levels measured in either fetal (1.6 +/- 0.1 pmol/l) or maternal plasma (1.4 +/- 0.3 pmol/l) at term and equal to levels found in plasma of patients with humoral hypercalcemia of malignancy. In vitro studies pointed to three possible sources of PTHrP in amniotic fluid: cultured amniotic fluid cells, cells derived from the amniotic membrane overlying the placenta and placental villous core mesenchymal cells. Treatment of cultured amniotic fluid cells with human prolactin, human placental lactogen (hPL) or human growth hormone (100 micrograms/l) increased PTHrP secretion after 24 h by 43%, 109% and 90%, respectively. Insulin-like growth factors I and II (100 micrograms/l), insulin (100 micrograms/l) and epidermal growth factor (EGF) (10 micrograms/l) increased PTHrP secretion by 53%, 46%, 68% and 118%, respectively. The stimulation of PTHrP secretion by EGF or by hPL was both time- and dose-dependent. In contrast, calcitriol and dexamethasone (10 nmol/l) decreased PTHrP secretion by 32% and 75%, respectively. Estradiol, progesterone, dihydrotestosterone and human chorionic gonadotropin had no effect on PTHrP secretion. These findings support the notion that PTHrP may play a physiological role in the uteroplacental unit and demonstrate that human amniotic fluid cells could be a useful model for studying the regulation of PTHrP production and secretion by hormones and growth factors.

Amniotic Fluid↗
PubMed1995

Anti-idiotypic antibody as an oestrogen mimetic: removal of Fc fragment converts agonist to antagonist.

Previous studies indicated that the anti-idiotypic antibody (clone 1D5) caused an increase in uterine creatine kinase (CK) activity when administered in vivo to immature female rats, indicating that the antibody has oestrogenic-like activity. It was, therefore, of interest to investigate the structural requirements of clone 1D5 to act as an oestrogen mimetic in an in vitro model system. In the present study, the effect of clone 1D5 and its proteolytic fragments, F(ab')2, Fab' and Fc on CK activity was examined in cultured skeletal cells having functional oestrogen receptor (ER). Incubation of female-derived calvaria cells or epiphyseal cartilage cells with clone 1D5 (8.33 nM) or oestradiol (E2) (30 nM) for 24 h caused a significant increase in CK activity, indicating that clone 1D5 acted as an agonist. On the other hand, incubation of male-derived calvaria cells devoid of a functional ER with clone 1D5 or E2 did not have any effect on CK activity. Incubation of female-derived calvaria cells with clone 1D5 and E2 did not result in any further increase in CK activity, whereas dihydrotestosterone (DHT) did not alter the response to clone 1D5. The CK response to clone 1D5, in female-derived calvaria cells was time- and dose-dependent and could be inhibited in a dose-dependent manner by the oestrogen antagonist tamoxifen. In contrast, the proteolytic fragments of clone 1D5, the F(ab')2 dimer (12 nM) and the Fab' monomer (24 nM), and the Fc fragment (28 nM) did not have E2-like activity in these cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Hereditary 1 alpha,25-dihydroxyvitamin D-resistant rickets resulting from a mutation in the vitamin D receptor deoxyribonucleic acid-binding domain.

Hereditary 1 alpha,25-dihydroxyvitamin D-resistant rickets (HVDRR) is a genetic disease that results from mutations in the gene encoding the vitamin D receptor (VDR). In this study of two siblings showing classical features of HVDRR, cultured dermal fibroblasts were used to characterize their VDR and assess responsiveness to 1,25-dihydroxyvitamin D3 treatment. The VDR displayed normal affinity and binding capacity for [3H]1,25-dihydroxyvitamin D3; however, the cells failed to exhibit induction of 25-hydroxyvitamin D 24-hydroxylase activity when treated with hormone. A decreased affinity of liganded VDR for DNA cellulose suggested that the defect was localized to the DNA-binding domain. Exons 2 and 3 of the VDR gene, which encode the two zinc fingers in the DNA-binding domain, were amplified and sequenced by polymerase chain reaction. Both siblings exhibited a G to A missense mutation (CGG to CAG) in exon 3, which results in the replacement of Arg77 by Gln at the base of the second zinc finger. This mutation has been described previously in two unrelated cases of HVDRR by Sone et al. It is unclear at this time whether these kindreds might be distantly related and, therefore, harbor the same mutation, or whether this represents a mutational hot spot in the VDR gene.

Amino Acid Sequence↗
PubMed1993

A paralytic-like disease of the ostrich (Struthio camelus masaicus) associated with Clostridium chauvoei infection.

Two adult Masai ostriches in a zoological collection became recumbent. The birds could not raise the neck or the head, had difficulties in breathing, and died eight and 13 days, respectively, after the first clinical signs appeared. On post mortem examination the heart had a globous appearance accompanied by gelatinous atrophy. The lungs were hyperaemic and oedematic, while the intestines had prominent haemorrhages in their mucosa. The liver and kidney were enlarged, and the former had also necrotic foci. Smears taken from the hyperaemic regions of the intestines and the necrotic foci of the liver were positive to Clostridium chauvoei after staining with specific fluorescein-labelled antiserum. No other pathogenic agents were identified or isolated from these birds. This report appears to be the first of a pathogenic condition associated with C chauvoei in an avian species.

Acute Disease↗