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Biomedical subjects

E R Hughes

Publications and source records attributed to E R Hughes.

At least 19 recordsLinked to original sources
PubMed1999

Ultrasonic propagation in cancellous bone: a new stratified model.

The theoretical modeling of ultrasonic propagation in cancellous bone is pertinent to improving the ultrasonic diagnosis of osteoporosis. First, this paper reviews applications of Biot's theory to this problem. Next, a new approach is presented, based on an idealization of cancellous bone as a periodic array of bone-marrow layers. Schoenberg's theory is applied to this model to predict wave properties. Bovine bone samples were tested in vitro using pulses centered at 1 MHz over various angles relative to the orientated cancellous structure. Two longitudinal modes (fast and slow waves) were observed for propagation parallel to the structure, but only one was observed for propagation normal to the structure. Angular-dependence of velocities was examined, and the fast wave was found to be strongly anisotropic. These results gave qualitative agreement with predictions of Schoenberg's theory. Although this new model is a simplification of the cancellous architecture, it has potential for future research.

Animals↗
PubMed1985

Hepatobiliary disorders in inflammatory bowel disease.

Every physician managing patients with inflammatory bowel disease should be alert to the possibility of the development of hepatobiliary disorders, especially in patients with extensive colonic involvement. There is the question concerning type of follow-up study to be instituted in patients with IBD. Elevation of the level of serum alkaline phosphatase appears to be the most useful and consistent biochemical indicator of hepatic dysfunction (101). This should be estimated at six monthly intervals. A persistent elevation of the level of serum alkaline phosphatase or more overt clinical manifestations, such as pain in the right upper quadrant, hepatomegaly, obstructive jaundice or weight loss, would all indicate the need for further investigations. This would normally take the form of roentgenologic investigation of the biliary tree and biopsy of the liver. Once a patient with IBD has been diagnosed as having one or more hepatobiliary disorders, what is the appropriate management? Each instance should be treated individually according to the nature of the disorder. In general, most of these conditions are histologic abnormalities and are of little clinical importance. There is the question of whether or not there is a role for prophylactic colectomy. There has been conflicting evidence to both support and refute the rationale that colectomy will prevent the development of, or arrest, existing disease of the liver. In the view of the authors, based upon a large experience with the management of these patients, the indication for colectomy should be based upon the severity and extent of colonic disease and almost never upon the existence of associated hepatobiliary disorders.

Adenocarcinoma↗
PubMed1983

The lung lamellar body as a functioning membrane in protein-catalyzed phosphatidylcholine transfer.

Lung lamellar bodies and liver mitochondria were used to demonstrate that soluble phospholipid transfer proteins from lung transfer phosphatidylcholine to both of these acceptors. The initial rate of transfer to lung lamellar bodies is about half that of the rate of transfer to the liver mitochondria when both acceptor membranes are present at saturating concentrations. Phosphatidylcholine unilamellar vesicles were used to demonstrate that the fatty acyl composition of the membrane phosphatidylcholine is a significant determinant of the rate of phosphatidylcholine transfer catalyzed by these proteins. The lamellar bodies have a unique phosphatidylcholine composition, and these studies suggest that this is an important factor in determining the lower initial rate of transfer to lamellar bodies. The studies have also characterized two phospholipid transfer proteins in rat lung in terms of isoelectric point. Isoelectric points for the two proteins which transfer phosphatidylcholine were found to be 5.6 +/- 0.08 and 6.2 +/- 0.03.

Animals↗
PubMed1980

Fetal lung disaturated phosphatidylcholine. Ostensible increase following exposure to dexamethasone.

Fetal rat lung removed at 15 days gestation and placed in organ culture incorporates choline into phosphatidylcholine. Addition of 10(-9) M dexamethasone resulted in increased rates of choline incorporation per micrograms protein after both 6 and 12 days culture. This concentration of dexamethasone did not increase tissue phosphatidylcholine or disaturated phosphatidylcholine. Thus, at a culture time when dexamethasone had a significant effect on choline incorporation, there was no change in either the total phospholipid or disaturated phosphatidylcholine content of the lung tissue. The transplacental administration of dexamethasone decreased fetal lung DNA and phospholipid content. At the mid-range dosage tested (400 micrograms), dexamethasone depressed DNA (51%) appreciably more than total phosphatidylcholine (28%) and disaturated phosphatidylcholine (33%). These results show that the hormone does not increase the total amount of surfactant per lung. The increased disaturated phosphatidylcholine per mg DNA results in an ostensible beneficial effect of dexamethasone on surfactant and may reflect an increased proportion of Type II cells in fetal lung both in vitro and in vivo following hormone exposure. Disaturated phosphatidylcholine per Type II alveolar cell is no doubt increased but the trade-off is fewer total cells in the lung.

Animals↗
PubMed1979

Alteration of cartilage glycosaminoglycan protein acceptor by somatomedin and cortisol.

The effect of somatomedin and cortisol on embryonic chick cartilage in vitro indicates that somatomedin stimulates 35SO4 uptake while cortisol decreases it with no effect on glycosaminoglycan turnover. Xylosyltransferase activity is increased in crude fractions of somatomedin-treated cartilage but decreased in cortisol-treated cartilage. By using a Smith-degraded proteoglycan as an exogenous acceptor, xylosyltransferase activities from both treatments were equivalent, suggesting that the enzyme was not rate limiting. The results of xylosyltransferase assays conducted by mixing enzyme and endogenous acceptor from control, cortisol-treated and somatomedin-treated cartilage, suggest both effects to be at the level of the acceptor protein.

Animals↗
PubMed1978

Differentiation of the pulmonary surfactant system. Disaturated phosphatidylcholine accumulation in fetal rat lung in vivo and in vitro.

Fetal rat lung was placed in organ culture at 15 days gestation (22 days total gestation period), before biochemical and morphological development of the pulmonary surfactant system. At the fifth day of culture numerous Type II cells containing lamellar bodies were present as determined by electron micrography. Phospholipid accumulation in the cultures increased abruptly beginning at 6 days in culture. The phospholipid which accumulated between the sixth and twelfth culture days was composed of 21--27% disaturated phosphatidylcholines. Both the percent of disaturated phosphatidylcholines in the phospholipid fraction and the qualitative pattern of accumulation as a function of time were similar to observations for fetal rat lung developing in vivo. The data presented provide evidence for development of the pulmonary surfactant system in organ culture in vitro.

Animals↗
PubMed1976

Uridine diphosphate xylosyltransferase activity in cartilage from manganese-deficient chicks.

The glycosaminoglycan content of cartilage is decreased in manganese deficiency in the chick (perosis). The activity of xylosyltransferase, the first enzyme in the biosynthetic pathway of sulphated glycosaminoglycans, was studied in the epiphysial cartilage of 4-week-old chicks which had been maintained since hatching on a manganese-deficient diet. Enzymic activity was measured by the incorporation of [14C]xylose from UDP-[14C]xylose into trichloroacetic acid precipitates. Optimal conditions for the xylosyltransferase assay were established and shown to be the same for both control and manganese-deficient cartilage. Assay of the enzyme by using an exogenous xylose acceptor showed no difference in xylosyltransferase activity between control and manganese-deficient tissue. Further, the extent of xylose incorporation was greater in manganese-deficient than in control cartilage preparations, suggesting an increase in xylose-acceptor sites on the endogenous acceptor protein in the deficient cartilage. 35S turnover in the manganese-deficient cartilage was also increased. The data suggest that the decreased glycosaminoglycan content in manganese-deficient cartilage is due to decreased xylosylation of the acceptor protein plus increased degradation of glycosaminoglycan.

Animals↗
PubMed1975

Glucocorticoid therapy in children. Effect on somatomedin secretion.

Glucocorticoids cause growth retardation in children. We have studied the effect of these hormones on serum somatomedin (Sm) levels in seven children with nephrosis. Intravenous administration of methylprednisolone sodium succinate, 2.2 mg/kg, causes a rapid fall in serum Sm activity. The activity remains suppressed during continuous therapy, but returns toward normal when medication is omitted during the course of alternate-day therapy. We conclude that one reason for growth retardation secondary to continuous glucocorticoid therapy is suppression of Sm generation. A direct effect of these hormones on the cartilage cell or induction of an Sm inhibitor cannot be excluded by the reported experiments.

Adolescent↗