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Biomedical subjects

J E Russell

Publications and source records attributed to J E Russell.

69 records · Page 4Linked to original sources
PubMed1979

The relationship of biochemical and histometric determinants of uremic bone.

Simultaneous histometric and biochemical analyses were performed on 16 bone biopsy specimens taken from eight patients with chronic renal failure. The bone calcium and phosphorus contents are inversely related to the relative volume of microscopically measured, nonmineralized bone matrix (osteoid) and to the percentage of trabecular surface covered by this tissue. The magnesium content of uremic bone is positively correlated with the quantity of osteoid. Skeletal calcium and phosphorus contents correlate inversely with the osteoblast population, and phosphorus relates directly to the volume of trabecular bone. Bone hydroxyproline content does not correlate significantly with any histometric variable. As one may now infer biochemical conclusions about the uremic skeleton from morphological observations, these data may facilitate interpretation of nondecalcified histological sections of bone.

Bone and Bones↗
PubMed1975

The nature of the collagen cross-links in bone in the chronic uraemic state.

The cross-links from NaB3H4-reduced bone collagen of chronically uraemic rats and pairfed controls were compared. The ratio of the reduced cross-links deltadelta'-dihydroxylysinonorleucine to delta-hydroxylysinonorleucine was significantly increased in the uraemic animals. The observed increment in the dihydroxylysinonorleucine:hydroxylysinonorleucine ratio was accentuated as the uraemic state advanced. The data indicate that osteodystrophy of chronic renal insufficiency is characterized by an alteration of the quantitative relations between cross-links and aldehydic precursors of bone collagen.

Animals↗
PubMed1975

Experimental renal osteodystrophy. The response to 25-hydroxycholecalciferol and dicholomethylene diphosphate therapy.

Bone mineral and matrix maturation in chronically uremic, nonacidotic rats were investigated after 25-hydroxcholecalciferol (25OHD) and/or dichloromethylene diphosphonate (C12MDP) therapy utilizing bromoform-toluene density gradient fractionation and X-ray diffraction analyses. The bromoform-toluene density gradient analyses demonstrated that the progressive accumulation of less dense, more immature bone characteristic of progressive uremia was reversed by 25OHD and/or C12MDP therapy for a 2-wk period, and that after 4 wk of therapy the maturational profile of bones from chronically uremic animals treated with 250HD and/or C12MDP was comparable to that from nonuremic littermates. X-ray diffraction analysis revealed that by the 4th wk of therapy with 25OHD and C12MDP both the degree of crystallinity and the crystal size/perfection parameters in the uremic bones were comparable to those of nonuremic, pair-fed control littermates. Treatment for 4 wk with 25OHD resulted in enlarged and/or more perfect apatite crystallites, while C12MDP alone slightly inhibited crystal growth and/or perfection after 2 wk of treatment. Soft tissue calcification was diminished in uremic animals treated for 4 wk with C12MDP or a combined C2MDP/25OHD regimen, the latter being much more effective in this regard. The accumulated data in this study support the premise that the attendant accelerated bone resorption, soft tissue calcification, and abnormal mineralization and maturation of the skeletal tissue, well documented to characterize experimental ranal insufficiency, may be alleviated with therapeutic dosages of 25OHD and/or C12MDP.

Animals↗
PubMed1975

25-hydroxycholecalciferol-enhanced bone maturation in the parathyroprivic state.

In vitro evidence presently favors a direct osteolytic effect of biologically active vitamin D metabolites. Studies were designed to evaluate the effect of 25-hydroxycholecalciferol (25OHD3) on bone collagen and mineral maturation in vivo and its dependence on parathyroid hormone (PTH). After treatment of sham-operated control and parathyroidectomized (PTX) mature rats with either 25OHD3 or an oil vehicle for 2 wk, tibial bone mineral-collagen maturation was quantitated by bromoform-toluene density gradient fractionation techniques. Intestinal calcium absorption was measured by in vivo 45Ca transport procedures. In contrast to the control group, the response to 25OHD3 of PTX rats was dramatic. Bone mineral and matrix maturation were both accelerated by 25OHD3 treatment without concomitant reduction in total bone mineral or collagen content or changes in the intestinal calcium absorption. These observations support the premise that biologically active vitamin D metabolites stimulate bone tissue maturation, and that PTH is not required in this regard.

Animals↗
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↗
PubMed1973

Development of verbal control over bizarre gestures of retardates through imitative and nonimitative reinforcement procedures.

Two retardates, manifesting hand gestures and minimal instructional control, were trained by imitative reinforcement procedures to imitate a response that was in contrast to gesturing. Next, with the contrast response continuing to be imitatively reinforced, gesturing was reduced by nonimitative reinforcement procedures; while providing facial and gesture cues, the adult said, "Do not do this". Imitative and nonimitative procedures were found to have the same effects on the contrast response as on the gesturing response, such that imitative procedures increased both responses, whereas nonimitative procedures decreased both. Nonperformance of gesturing was further maintained when (1) explicit verbal directions for nongesturing were superimposed upon the demonstrational-facial-verbal cues as these collective stimuli were faded out and (2) food reinforcers for nongesturing were gradually removed while social consequences continued to be administered.

Journal Article↗
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↗
PubMedDate not supplied

Growth and maturation of mandibular bone in otherwise totally immobilized rhesus monkeys.

The effects of 14 days of total postcranial body immobilization (in plaster casts) on the mineralization rate and on the maturation of matrix and mineral moieties in the rhesus jaw were studied by tetracycline labeling and by density gradient methods, respectively. Immobilization did not alter the rates of periosteal and endosteal mineralization in the dense cortical bone from the lingular region of the jaw, but it did impair mineralization in osteonal bone. Osteons that continued to show radial closure did so at a normal rate. In the more trabecular cortex (premolar region) in young monkeys (3-6 kg body weight), immobilization impaired bone mineralization, as shown by lower ratios of calcium and inorganic phosphorus to hydroxyproline (Ca/HO-Pr;Pi/HO-Pr), and it reduced the rate at which the newly formed bone and mineral moieties matured. In older monkeys (6-10 kg body weight) immobilization did not alter Ca/HO-Pr and Pi/HO-Pr ratios or impair tissue maturation. These changes tended to normalize within 7 to 14 days after decasting.

Age Factors↗