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Biomedical subjects
Publications and source records attributed to G Jones.
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A case is described of a mixed manually dominant man with a right parietal infarction who demonstrated reversals in object manipulation. Although mirror reversals in parietal lobe dysfunction and right-left spatial reversal in conjunction with mirror writing have been reported previously, object and spatial reversal to this extent has not been reported. The theoretical implications of the absence of mirror writing here, in relation to side of brain lesion and handedness, are discussed.
In vitro metabolism of 25-hydroxy-24-oxovitamin D3 was studied in kidney homogenates from vitamin D-supplemented chickens and rats. In chicken homogenates, 25-hydroxy-24-oxovitamin D3 was converted predominantly to 23,25-dihydroxy-24-oxovitamin D3, 24,25-dihydroxyvitamin D3, and 23,24,25-trihydroxyvitamin D3. In rat homogenates, 25-hydroxy-24-oxovitamin D3 was not converted to either 24,25-dihydroxyvitamin D3 or 23,24,25-trihydroxyvitamin D3, but it was converted to 23,25-dihydroxy-24-oxovitamin D3 and 23-hydroxy-24,25,26,27-tetranorvitamin D3. The latter metabolite was not produced by the chicken preparations. The stereochemical configuration at C-24 of the 24,25-dihydroxyvitamin D3 produced by chicken homogenates was determined to be S. This contrasts with the R configuration of 24,25-dihydroxyvitamin D3 produced by 24-hydroxylation of 25-hydroxyvitamin D3. These results suggest that chickens have an enzyme that can reduce the 24-oxo group to 24S-hydroxyl group, whereas rats do not.
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We report a resurgence of yaws in the Solomon Islands and describe the combined clinico-serological survey and mass penicillin treatment campaign to define and curb it.
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By cochromatography, mass spectrometry, and chemical derivatization, we have shown that a metabolite isolated from the perfused rat kidney incubated with 24-(R),25-dihydroxyvitamin D3 is indistinguishable from chemically synthesized 24,25,26,27-tetranor-23-hydroxyvitamin D3. The new metabolite is also produced from 24-oxo-25-hydroxyvitamin D3 but not from 23(S),25-dihydroxyvitamin D3. Enzymes required for the synthesis of the new metabolite are absent in the vitamin D deplete animal but are induced along with the 25-hydroxyvitamin-D3 24-hydroxylase by vitamin D repletion. The pathway of 24,25-dihydroxyvitamin D3 metabolism in the perfused kidney is stimulated by pre-treatment of the rat with large doses of vitamin D3, suggesting that the pathway is a degradative one.
Since several aspects of the effects of vitamin A and 1 alpha,25-dihydroxyvitamin D3 (1,25-(OH)2D3) on bone metabolism are quite similar, we examined the possibility that vitamin A effects on bone were mediated through the regulation of cytosolic 1,25-(OH)2D3 receptors. A clonal osteoblast-like cell line derived from rat osteosarcoma (ROS 17/2) was used as a model system. Vitamin A acid (retinoic acid) in concentrations ranging from 10(-8) to 10(-5) M was found to elicit a dose-dependent increase in 1,25-(OH)2D3 binding in these cells. This effect was maximal after 24 h, was independent of cell density, and was inhibited by actinomycin D (0.05-0.5 microgram/ml). The 1,25-(OH)2D3 binding macromolecule in cytosol preparations from both vehicle- and retinoic acid-treated cells had a sedimentation coefficient of 3.2 S and binding specificities for vitamin D3 metabolites in the order: 1,25-(OH)2D3 greater than 25-(OH)-D3 greater than 24,25-(OH)2D3. Sucrose density gradient analysis, vitamin D3 metabolite displacement studies, and saturation and Scatchard analyses all indicated that the specific increase in 1,25-(OH)2[3H]D3 binding in these cells was the result of a selective increase in the number of specific 1,25-(OH)2D3 receptors.
We describe identical twins concordant for exstrophy of the cloaca and myelocystocele. Their management and subsequent course was strongly influenced by prenatal ultrasound recognition of neural tube defects in both twins and severe renal dysplasia in one of the fetuses. The genetic aspects of this case are consistent with existing causal theories of exstrophy of the cloaca.
The effect of local application of various solutions on leucocyte adherence to the wall of small blood vessels in the microcirculation of the rat mesentery was examined. Leucocyte adhesion was produced by local application of zymosan-activated complement. Solutions of EDTA, lignocaine and prostacyclin when applied locally cause the release of a high proportion of leucocytes previously firmly adherent to the endothelium of venules and small veins without producing any significant change in the rate of blood flow through the affected vessels. Acetylcholine injected intravenously increases the rate of blood flow through the mesenteric microcirculation several fold but has no apparent effect on pre-existing leucocyte sticking. The findings suggest that in normal small blood vessels production of prostacyclin by vascular endothelium may inhibit adhesion of leucocytes to the vascular wall. When endothelium is injured local production of prostacyclin may be inhibited sufficiently to permit adhesion of leucocytes to the injured endothelium and so induce the earliest stage in the emigration of leucocytes into the area of injury. Lignocaine may possibly inhibit leucocyte sticking by increasing local production of prostacyclin, but the mode of action of EDTA and many other aspects of the mechanism responsible for leucocyte sticking remain obscure.
Utilization of orthodontic services may be influenced as much by the social and cultural setting as by objective criteria. The public's assessment of dental irregularity and its perceptions of the psychosocial implications of malocclusion may be critical factors in the utilization of available services. To test these assumptions, two communities with historic differences in the availability and utilization of orthodontic services were selected as survey sites (Lexington, Kentucky, and Cardiff, Wales). Three-hundred eighty-five sixth grade children (11 to 12 years of age) and 123 of their parents were interviewed concerning dental esthetics, treatment need, and knowledge about, attitudes toward, and value placed on orthodontic treatment. Although the Lexington respondents had greater personal and indirect knowledge about such services, they did not have more positive perceptions about treatment; nor did they value straight teeth more highly. There were no significant differences between the groups' judgement of dental esthetics or assessment of treatment need. The differences in utilization of services in the two communities could not be explained in terms of differences in attitude toward malocclusion and orthodontic treatment.
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Cultured skin fibroblasts from normal individuals and from patients with Duchenne muscular dystrophy spread equally rapidly when seeded on a glass substratum. Exposure to the ionophore monensin substantially suppresses normal and dystrophic fibroblast spreading in serum-free media for up to at least 100 min. Preincubation of normal fibroblasts with monensin causes a further reduction in cell spreading. Dystrophic fibroblasts fail to spread as well as normal cells after monensin preincubation. Such findings indicate that there is a delay in the secretion of functional adhesive surface proteins in monensin-preincubated normal fibroblasts and that this lag period is significantly longer in dystrophic fibroblasts. These data are consistent with findings of altered adhesive and secretory properties of fibroblasts from patients with Duchenne muscular dystrophy.
We have shown that thyroid hormones have a direct effect on the renal metabolism of 25-hydroxyvitamin D3 (25OHD3). Using a new high performance chromatographic technique based upon a cyano-bonded packing, we studied the metabolism of [26,27-3H]25OHD3 in the isolated perfused rat kidney in vitro. We measured the rate of synthesis of 24,25-dihydroxyvitamin D3 [24,25-(OH)2D3], 24-oxo-25-hydroxyvitamin D3 [24-oxo-25OHD3], and 24-oxo-23,25-dihydroxyvitamin D3 [24-oxo-23,25-(OH)2D3] by the kidneys of vitamin D-replete [D(+)] rats and the rate of synthesis of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] by the kidneys of vitamin D-deplete [D(-)] rats. Synthesis of 24,25-(OH)2D3 increased significantly at 2 and 6 h of perfusion in perfused kidneys treated with T3, T4, and TSH as compared to untreated controls. Synthesis of 24-oxo-25OHD3 increased at 2 and 6 h and that of 24-oxo-23,25-(OH)2D3 increased at 6 h in T3- and TSH-treated groups. Perfused kidneys from vitamin D(-) rats treated with T3, T4, and TSH synthesized significantly decreased amounts of 1,25-(OH)2D3 at 2, 4, and 6 h. TRH treatment of kidneys from either vitamin D(+) or D(-) rats caused no significant changes in synthesis of any vitamin D metabolites when compared with appropriate controls. These results suggest T3, T4, and perhaps TSH, but not TRH, have a direct effect on renal 25OHD3 metabolism.
A group of grain-fed heifers became stiff, and some sternally recumbent, upon exercising after winter confinement. All but 2 affected heifers gradually recovered after IM injections of Se-vitamin E and IV infusion of Ca-Mg solution. Though serum assays failed to detect low Se levels, the presumptive diagnosis was based upon clinical signs and a good response to Se-vitamin E treatment.
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