Search PubMed⌕ Search

Biomedical subjects

R B Rucker

Publications and source records attributed to R B Rucker.

At least 91 records · Page 5Linked to original sources
PubMed1979

Additional evidence for a proform to tropoelastin from chick aorta.

Evidence is presented for the presence of precursor to tropoelastin in chick arterial extracts. The precursor is approx. 100 000 daltons in size. It is suggested to be a precursor to tropoelastin (72 000 daltons). This protein may be observed in culture in vitro if appropriate precautions are taken to inhibit proteolysis. Once synthesized, it appears to be converted into tropoelastin within 10--20 min. The protein may also be detected in vivo. When 1-day-old cockerels were fed on a copper-deficient diet (less than 1 p.p.m. to inhibit cross-linking) containing epsilon-aminohexanoic acid (0.2%) to retard proteolysis and then injected wiht [3H]valine, extraction of arterial proteins 12h after injection resulted in detection of two major peaks of [3H]valine-labelled protein with pI values of pH 7.0 and 5.0 respectively. The protein that focused at pH 7.0 was estimated to be about 100 000 daltons in size and could be shown to be converted into a more basic protein with the properties of tropoelastin. It is speculated that the protein with pI 5.0 may be yet another extension peptide. The data appear to be in keeping with similar observations by ourselves and others that a proform of tropoelastin exists, and, in at least one step before conversion into tropoelastin, exists as a 100 000-dalton protein subunit.

Animals↗
PubMed1979

Clinical signs of anemia in vitamin A-deficient rats.

Young rats weighing 150 g (initial weight) were fed diets sufficient or deficient in vitamin A. Postweaning rats were used in order to retard the rapid onset of vitamin A deficiency. The effects of the deficiency were studied with respect to impairment of hematopoietic function and anemia. Values for hemoglobin and hematocrit provided evidence of anemia before the signs of severe vitamin A deficiency became apparent. These included alopecia, ocular lesions, and low levels of retinol in plasma and liver. At the point where liver stores of vitamin A were virtually depleted, however, estimates for serum iron, hematocrit, and hemoglobin were elevated to control levels. The latter phenomenon appeared to result from hemoconcentration. These data suggest that anemia may be a component of vitamin A deficiency, but might be masked by the dehydration that accompanies severe depletion of vitamin A.

Alopecia↗
PubMed1978

Inhibition of elastolysis by proteinase inhibitors from chick plasma and aorta.

Chick plasma contains inhibitor(s) against trypsin and elastase which also appear to retard the degradation of tropoelastin by arterial tissue extracts. Chick aorta extracts also contain similar inhibitors against elastase and trypsin. Both levels of the plasma inhibitor(s) and inhibitor(s) extracted from thoracic aorta increase during early stages of growth and maturation. There is a three- to four-fold increase in the levels of the inhibitor(s) in chick plasma and aorta between one to four weeks after hatching. Of particular interest are the observations that the presence of the inhibitor(s) retards the conversion of soluble elastin (tropoelastin) to smaller elastin peptides. Subsequently, it is speculated that in addition to other vital roles, such proteinase inhibitors may also act in regulating elastogenesis and elastin fiber formation.

Animals↗
PubMed1978

Hematopoietic studies in vitamin A deficiency.

Recent studies of experimental vitamin A deficiency in man led the authors to conclude that anemia may result from lack of vitamin A. A review of numerous nutrition surveys in underdeveloped countries enhanced the suspicion that deficiency of vitamin A does contribute to the prevalence of anemia. Preliminary studies of vitamin A-deficient rats confirmed previous observations that anemia may result from lack of this vitamin. The livers of these animals had very low concentrations of vitamin A but normal or increased concentrations of iron. The finding of anemia is in contrast with other reports that vitamin A deficiency may cause elevated values for hemoglobin and hematocrit. The authors suggest that loss of taste and smell as a result of deficiency may account for refusal of experimental animals to eat and drink enough to prevent inanitation and dehydration. The resulting hemoconcentration may mask the true hematological picture, which is one of anemia.

Adolescent↗
PubMed1977

Nutritional copper deficiency and penicillamine administration: some effects on bone collagen and arterial elastin crosslinking.

Nutritional copper deficiency effects marked changes in the crosslinking of collagen and elastin, presumably in relationship to copper's role as a cofactor for lysyl oxidase. Lysyl oxidase controls one of the initial steps in the crosslinking of elastin and collagen, i.e., the conversion of peptidyl lysine or hydroxylysine residues to peptidyl alpha-aminoadipic-delta-semialdehyde derivatives. Once lysine-derived aldehydic functions in collagen and elastin are formed, crosslinks occur via aldol and Schiff-base type condensations. A decrease in the degree of crosslinking results in changes in the biomechanical properties of both collagen- and elastin-rich tissues. Some of these changes are described with respect to chick bone and aorta. Likewise, penicillamine blocks crosslinking reactions. In this case, however, it is probably because of the formation of thiazolidine complexes between penicillamine aldehydic functions. The administration of penicillamine at different levels to young growing chicks allows the isolation of fibrous insoluble elastin varying in aldehyde content.

Amino Acids↗
PubMed1977

Effect of ethane-1-hydroxy-1,1-diphosphonate (EHDP) and dietary fluoride on biomechanical and morphological changes in chick bones.

There are only a few papers in the literature in which parameters related to bone strength are examined over wide range of fluoride concentrations. In this report, chicks were used and fed diets containing fluoride added at 0, 50, 200, or 800 ppm in preparation for measurements on bone strength. The diets were fed for 20 days. After 10 days, the birds were also injected daily with solutions containing either isotonic saline or 5 mg of ethane-1-hydroxy-1,1-diphosphonate (EHDP) as phosphorus/kg body weight or 10 mg of EHDP as phosphorus/kg body weight. The effects of added fluoride and EHDP on bone morphology and the biomechanical properties of bone were then examined. The rate of bone formation was assessed using histological and tetracycline labeling techniques. Administration of high fluoride and/or EHDP resulted in significant changes in bone morphology. The changes effected by the administration of EHDP appeared independent of fluoride induced changes. Biomechanical studies also indicated that both high levels of fluoride and EHDP caused a significant reduction in bone torsional breaking strength. The reductions in breaking strength were independent of changes in body size.

Animals↗
PubMed1977

Scoliosis in chickens.

Scoliosis developed in 55 per cent of sexually mature birds (68 per cent of male and 46 per cent of female birds) in a highly inbred line of chickens originally produced from white Leghorns. The curve could first be detected at five to six weeks of age and progressed until spontaneous fusion of the thoracic vertebrae occurred. Studies of these chickens indicated that abnormalities of growth and development of the spine are not the primary cause of the scoliosis. Preliminary studies of the paravertebral musculature also indicated that simple muscle imbalance is not responsible for the curve. Initial studies of collagen extracted from the scoliotic line of chickens showed it to be more soluble than similar collagen extracted from white Leghorn controls.

Animals↗
PubMed1976

Arterial elastin synthesis in the young chick.

In the growing chick a marked stimulation in soluble and mature arterial elastin synthesis occurs 2 and 5 weeks after hatching. Measurement of [3H]valine and [3H]proline incorporation into arterial soluble protein during this period indicated that most of the label is found in a 70 000 dalton protein subunit. The labeled soluble subunit had the characteristics of native soluble elastin or tropoelastin. During the period in which the greatest percentage increase in mature elastin occurs, the highest specific activities of soluble [3H]valine-labeled protein were observed. These changes were striking and suggest a developmental period for the growing chick in which factors related to elastin metabolism may be more easily studied.

Aging↗
PubMed1976

Formation in vitro of ascorbic acid 2-sulfate.

The sulfation of ascorbic acid by an ascorbic acid sulphotransferase was investigated using rat liver and colon homogenates. When Na2 35 SO4 or 3'-phosphoadenylyl [35S]sulfate (P-Ado-P-35S) and ascorbic acid were used as substrates, chromatographic behavior of the reaction products on thin-layer cellulose suggested that ascorbic acid 2-[35S]sulfate was formed. With Na2 35SO4 as the source of radioactive sulfate in the assay system, ATP was found to be an obligatory cofactor. Incorporation of [35S]sulfate frofrom Na2 35SO4 into ascorbic acid 2-[35S]sulfate was also decreased when ATP sulfurylase inhibitors were added to the system. P-Ado-O35S alone in the assay without ATP was an extemely effective sulfating agent. In addition, liver and colon homogenates from vitamin A deficient and sufficient rats were used in one of the studies. Vitamin A deficiency appeared to have little effect on ascorbic acid 2-sulfate formation.

Animals↗
PubMed1976

Arterial elastin.

Explore the source record for details and available documents.

Amino Acid Sequence↗
PubMed1976

Vitamin A deficiency and the metabolism of glycosaminoglycans and ascorbic acid in the rat.

Weanling rats were fed diets with and without the addition of retinyl palmitate at 6,500 units/kg. The supplemented groups were fed either ad libitum or food was restricted daily to that amount consumed by the group of rats receiving the unsupplemented diet. After a 10 week experimental period, signs of vitamin A deficiency were observed (growth plateau, xerophthalmia) and liver values as retinol were only 1% of control values. Relative to the two control groups, vitamin A deficiency resulted in approximately 30% lower liver, 50% lower blood and 40% lower urinary ascorbic acid. Vitamin A deficiency did not appear to result in significant and direct impairment of GAG sulfate metabolism. Although the total amount of GAG in rat skin was increased, the composition of GAG fractions did not appear to be altered by vitamin A deficiency. Studies regarding the incorporation and disappearance of 35S-sulfate in vivo into GAG fractions obtained from skin indicated no serious impairment in GAG turnover with vitamin A deficiency. Twenty-four hour urine samples were also collected for estimation of 35SO4 excreted in GAG and non-GAG fractions. Likewise, little change was observed with respect to radioactivity associated with sulfate fractions excreted in urine. Although many previous studies have directly linked vitamin A with sulfation of GAG, the results reported here suggest that if there is an alteration in GAG sulfate metabolism, it is probably an indirect consequence of vitamin A status.

Animals↗