[Importance of vitamin D doses in bone mineralization in preterm infants].
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Biomedical subjects
Publications and source records attributed to M Moya.
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A newborn male patient with a partial trisomy 13q22----qter, derived from a maternal translocation (13;15)(q22;p11) is reported. This non-frequent chromosomal anomaly leads to a characteristic phenotype easily recognizable from other craniosynostosis syndromes, in which the cranial malformation is often associated with auricular and limb defects. This phenotype includes: cranial malformation, characteristic facies, mental and developmental retardation, urologic and genital anomalies, polydactily, abnormal muscular tonicity and convulsive status. Our patient, a "pure" partial trisomy, without other associated chromosomal anomaly, is compared with the published cases.
From olden time the resistance and capacitance of the living body were measured by alternating current bridge and the impedance diagram was made by rend 1/omega c using orthogoual axises, and it showes an arch. But by this research the impedance diagram of the Nitella was a line those are measured by finite alternating current. Formerly the frequencies were from 0.2Kc to 20Kc, but by this research the capacitance are nothing at over 4Kc.
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In this new method for quantifying vitamin D in infants' formulas and breast milk, after repeated lipid extraction, samples are further purified by passage through Sep-Pak cartridges, followed by liquid chromatography, then quantified by competitive protein-binding assay. Analytical recovery is estimated by use of added 3H-labeled vitamin D. For repeated assays of a reconstituted proprietary powdered milk formula in two runs, the intra-assay vitamin D values were 9.0 (SD 1.4) (n = 6) and 8.9 (SD 1.6) micrograms/L (n = 7) (t = 0.07). Assay of a proprietary liquid formula yielded values of 14.9 (SD 0.9) micrograms/L (n = 6). For each, the results agreed with the vitamin D content shown on the label. Vitamin D concentrations in breast milk from two groups of lactating mothers of different social class and nutritional status were 2.3 (SD 1.4) (n = 7) and 2.0 (SD 1.7) micrograms/L (n = 7). Overall recoveries ranged from 65 to 75%. Only 2 mL of milk is required, which facilitates sample collection, and the assay is less time-consuming than other current methods.
The tox228 gene encoding the non-toxic, immunologically cross-reactive CRM228 mutant diphtheria toxin (DT) has been cloned downstream of the PR promoter and the cro translational initiation region of bacteriophage lambda carried by plasmid pCQV2 (Queen, 1983). Efficient transcription but no appreciable amount of a translational product corresponding to complete DT could be detected in Escherichia coli hosts. Deletion of 320 bp from the C-terminal region of the B-fragment of DT, and fusion of the truncated tox228 gene to lacZ yielded several hybrid beta-galactosidases (beta Gal) in an E. coli lon- strain in addition to beta Gal. The various DT fragments fused to beta Gal were immunologically reactive and were identified with antibodies specifically directed against the A- or the B-fragment of DT. Antibodies raised against the DT-beta Gal fusion proteins in guinea pigs cross-reacted with wild-type DT and its B-fragment and protected Vero cells in tissue culture against the lethal action of DT. Immunized guinea pigs survived upon injection of a five-fold lethal dose of wild-type DT.
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Four siblings are presented with a malformative syndrome. All were born to an epileptic woman treated with phenytoin and valproic acid. A considerable high fetal pathology is found. Perhaps increased teratogenic effects are related with this pharmacological association not previously described.
We report a newborn female with neonatal hyperthyroidism, born to a mother with Graves disease treated with potassium iodide and carbimazole. At four months she had some breast development, a bone age advance of one year, and elevated levels of FSH and estradiol. Later on the prolactin level was also raised, while LH and TSH values continued low. Posteriorly, irregular cutaneous pigmentation, brown in colour, was evident on the neck and trunk, and a McCune-Albright syndrome was suspected. The relationship between these conditions and treatment of them is discussed.
It has been recently shown (Larkin, J. M., M. S. Brown, J. L. Goldstein, and R. G. W. Anderson, 1983, Cell, 33:273-285) that after a hypotonic shock followed by incubation in a K+-free medium, human fibroblasts arrest their coated pit formation and therefore arrest receptor-mediated endocytosis of low density lipoprotein. We have used this technique to study the endocytosis of transferrin, diphtheria toxin, and ricin toxin by three cell lines (Vero, Wi38/SV40, and Hep2 cells). Only Hep2 cells totally arrested internalization of [125I]transferrin, a ligand transported by coated pits and coated vesicles, after intracellular K+ depletion. Immunofluorescence studies using anti-clathrin antibodies showed that clathrin associated with the plasma membrane disappeared in Hep2 cells when the level of intracellular K+ was low. In the absence of functional coated pits, diphtheria toxin was unable to intoxicate Hep2 cells but the activity of ricin toxin was unaffected by this treatment. By measuring the rate of internalization of [125I]ricin toxin by Hep2 cells, with and without functional coated pits, we have shown that this labeled ligand was transported in both cases inside the cells. Hep2 cells with active coated pits internalized twice as much [125I]ricin toxin as Hep2 cells without coated pits. Entry of ricin toxin inside the cells was a slow process (8% of the bound toxin per 10 min at 37 degrees C) when compared to transferrin internalization (50% of the bound transferrin per 10 min at 37 degrees C). Using the indirect immunofluorescence technique on permeabilized cells, we have shown that Hep2 cells depleted in intracellular K+ accumulated ricin toxin in compartments that were predominantly localized around the cell nucleus. Our study indicates that in addition to the pathway of coated pits and coated vesicles used by diphtheria toxin and transferrin, another system of endocytosis for receptor-bound molecules takes place at the level of the cell membrane and is used by ricin toxin to enter the cytosol.
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We have designed az method for the assessment of trabecular bone mass (TBM) in a central portion of L4 by means of CT scanning. A total of 29 normal individuals of different ages from both sexes, and 19 hemodialysis patients were studied. 3 selected patients were also studied 1 year later. A good in vivo reproducibility was demonstrated in a dog after repositioning. A positive inverse correlation was observed in the control group between age and TBM supporting the reliability of this method. As reported by others in the postmortem bone mineral analysis of L4, a majority of patients (78.9%) showed a normal or high TBM. From a total of 5 patients with increased TBM only 2 showed radiological osteosclerosis, and 4 of them presented advanced subperiostal resorption suggesting a pathogenetic role of excessive circulating PTH in the genesis of osteosclerosis. A total of 4 had decreased TBM and only 2 of them showed radiological demineralization, 2 patients with decreased TBM, 1 of them under anticonvulsant therapy, experienced a considerable increase in the TBM after 1 year of 25OHD3 therapy. We conclude that this method can be an important help in the early detection of management of renal osteodystrophy.
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