Search PubMed⌕ Search

Biomedical subjects

L V Avioli

Publications and source records attributed to L V Avioli.

At least 307 records · Page 17Linked to original sources
PubMed1973

Abnormal bone mineral maturation in the chronic uremic state.

X-ray diffraction analysis of bone from chronically uremic but nonacidotic rats with normocalcemia and hyperphosphatemia revealed smaller apatite crystals and an increase in the X-ray amorphous mineral fraction when compared to age-matched, pair-fed control animals, indicating less advanced mineral maturation in the uremic animals. Studies in animals with varied degrees of chronic renal insufficiency revealed a progression of the bone crystal maturational defect with advancing uremia.

Animals↗
PubMed1972

On death and dying.

Explore the source record for details and available documents.

Attitude of Health Personnel↗
PubMed1972

Intestinal calcium transport: the role of sodium.

The role of sodium in intestinal calcium transport was investigated in everted rat intestine. Ethacrynic acid, but not ouabain, inhibited calcium transport. However, ouabain did inhibit net water transport and, therefore, sodium transport, establishing the dissociation of the two transport processes. In addition to a magnesium-dependent adenosine triphosphatase (activated by sodium and potassium), a phosphatase dependent on sodium and calcium was localized to the lateral and basal membrane fractions of the mucosal cell. Activity of the latter phosphatase, similar to calcium transport in intact tissue, was inhibited by ethacrynic acid and not by ouabain. Sodium, therefore, may participate in the calcium transport process by activating an enzyme complex, dependent on adenosine triphosphate, that mediates calcium transport.

Adenosine Triphosphatases↗
PubMed1972

Phenobarbital-induced alterations in vitamin D metabolism.

The metabolic fate of intravenously injected vitamin D(3)-1,2-(3)H (D(3)-(3)H) was studied in two normal individuals on chronic phenobarbital therapy. Silicic acid column chromatography of lipid-soluble plasma extracts obtained serially for 96 hr after D(3)-(3)H injection demonstrated a decreased plasma D(3)-(3)H half-life and increased conversion to more polar metabolites. The polar metabolites formed included several with chromatographic mobility similar to known biologically inactive vitamin D metabolites and one with chromatographic mobility identical to 25-hydroxycholecalciferol. Disappearance of this latter material was also accelerated. A child with rickets and a normal volunteer studied before and after a 2 wk course of phenobarbital therapy demonstrated similar alterations in D(3)-(3)H metabolism. When liver microsomes from 3-wk-old Sprague-Dawley rats treated with phenobarbital were incubated with D(3)-(3)H, polar metabolites were produced with chromatographic mobility similar to the plasma D(3)-(3)H metabolites from phenobarbital-treated humans. Similar incubations employing 25-hydroxy-cholecalciferol-26-27-(3)H as the substrate also demonstrated an increased conversion to polar metabolites. The data suggest that the reported increased incidence of osteomalacia observed in patients on chronic anticonvulsant therapy may be the result of an accelerated conversion of vitamin D and its active metabolite, 25-hydroxycholecalciferol, to polar metabolites by druginduced liver microsomal enzymes.

Adult↗
PubMed1972

Effect of magnesium depletion on responsiveness to parathyroid hormone in parathyroidectomized rats.

Hypocalcemia and resistance to exogenous parathyroid hormone have been reported in several clinical states associated with magnesium deficiency. On the basis of such observations, it has been suggested that magnesium depletion per se may result in impaired responsiveness of the adenyl cyclase-adenosine 3',5'-monophosphate (3',5'-AMP) system. To test this hypothesis, 4 wk old male parathyroidectomized rats were maintained on normal or magnesium-deficient diets for 4 wk and their responses to parathyroid hormone compared. Serum magnesium and calcium fell progressively in the magnesium-deficient group. Despite clinical and biochemical evidence of severe magnesium deficiency in these animals, renal production and excretion of 3',5'-AMP in response to parathyroid hormone was normal both in vitro and in vivo. Additionally, administration of either dibutyryl 3',5'-AMP or parathyroid extract to fasting magnesium-depleted rats produced a normal increase in serum calcium. Parathyroid hormone infusion studies demonstrated normal renal and skeletal responsiveness as measured by urinary excretion of calcium, magnesium, phosphate, and hydroxyproline. These data show that the effect of parathyroid hormone on 3',5'-AMP formation and excretion, the responsiveness of skeletal tissue to 3',5'-AMP, and the renal and skeletal system responses to parathyroid hormone are not altered by pure magnesium deficiency in the parathyroidectomized rat.

Adenosine Monophosphate↗
PubMed1972

Effect of experimental chronic renal insufficiency on bone mineral and collagen maturation.

The effect of chronic renal disease on bone matrix and mineral maturation was evaluated in rats with experimental renal insufficiency of 2-11 wk duration utilizing bromoform-toluene gradient fractionation of bone powder, pulse labeling experiments with (45)Ca and proline-(3)H differential extraction, and X-ray diffraction techniques.Maturation defects in both collagen and mineral ((45)Ca) metabolism were documented as early as 2 wk after the induction of uremia, when total bone calcium, inorganic phosphate, and hydroxyproline content were unchanged. The maturational defect progressed with advancing uremia despite insignificant changes in plasma pH and calcium, and normal bone carbonate levels. Although circulating levels of 25-hydroxycholecalciferol were significantly lower than normal in the uremic animals, pretreatment with either this vitamin D metabolite or vitamin D(3) itself failed to alter the observed changes in skeletal maturation.

Animals↗