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Biomedical subjects

R M Leach

Publications and source records attributed to R M Leach.

At least 91 records · Page 5Linked to original sources
PubMed1985

Avian tibial dyschondroplasia. I. Ultrastructure.

Tibial dyschondroplasia is an abnormality of the growth cartilage that occurs in chickens and other rapidly growing animals. The disease is characterized by a mass of avascular opaque cartilage, which is continuous with the growth plate of the proximal tibia and extends into the metaphysis. In this study electron micrographs revealed that chondrocytes in the hypertrophic zone of the growth plate were normal in appearance with the exception that the cells did not undergo complete hypertrophy. In the proximal region of the lesion, cells began to undergo necrotic changes suggestive of an energy depletion. These changes included dilatation and vesiculation of the endoplasmic reticulum, enlargement of the paranuclear space, mitochondrial swelling with dilatation of the intracristal spaces and the appearance of electron-dense, flocculent material in the mitochondrial matrix, chromatin margination, and dilatation of the Golgi saccules. Chondrocytes also occurred with rarefied cytoplasm and atrophic Golgi saccules. A few cartilage cells in the proximal region of smaller lesions contained crescentic caps of condensed chromatin in the nuclei, which is indicative of apoptosis. These cells also exhibited dilated endoplasmic reticulum and lamellar bodies; and sometimes, in the proximal region of the lesion, they appeared to be condensed and convoluted. This process continued in the mid and distal regions. The condensed necrotic cells appeared as amorphous osmiophilic masses with karyorrhexic and pyknotic nuclei. Matrix vesicles were observed at all levels of the lesion, but calcified only at the distal edge of the lesion, where mineralization of both matrix and cells occurred. The resulting shell of mineral may act as a diffusion barrier.

Animals↗
PubMed1985

Avian tibial dyschondroplasia. II. Biochemical changes.

Biochemical parameters (dry matter, DNA, protein, cAMP, and calmodulin) were measured in tibial dyschondroplastic (TD) cartilage. This abnormal cartilage, which is a mass of unmineralized, unvascularized cartilage found in the proximal metaphysis of the tibiotarsus and tarsometatarsus, was compared with normal epiphyseal growth plate and hypertrophic cartilage obtained from day-old embryonic cone. The latter tissue is an example of cartilage which rapidly undergoes vascularization and mineralization. When compared with normal growth plate, tibial dyschondroplastic cartilage was found to contain lower amounts of dry matter, DNA, protein, cAMP, and calmodulin. This cartilage did not respond to factors in serum which stimulate 35S uptake. Although the above two types of cartilage contained similar amounts of ash, TD cartilage had less phosphorus and potassium and more sodium than the growth plate. The two types of cartilage had similar lysozyme activity and proteoglycan (hexosamine) content. In many of the parameters measured, day-old hypertrophic cartilage was similar to the normal growth plate. However, these tissues did differ in DNA, protein, ash, and lysozyme content. Substantially greater amounts of ash and lysozyme were found in the hypertrophic cartilage, which appeared to be related to events of mineralization and vascularization of this cartilage. These events did not occur in the abnormal cartilage cells found in the tibial dyschondroplastic lesion.

Animals↗
PubMed1985

Avian tibial dyschondroplasia. III. Electron probe analysis.

Tibial dyschondroplastic (TD) lesions and their associated growth plates, obtained from chickens, were prepared by freeze-drying and embedding in an anhydrous epoxy resin. Quantitative electron probe analysis was performed on dry, unstained sections. Levels of Na, Mg, P, S, Cl, K, and Ca were determined in cytoplasm (endoplasmic reticulum), mitochondria, and extracellular matrix of the proliferative, prehypertrophic, and early hypertrophic zones of the growth plate and in the proximal, mid, and distal regions of the lesion. A zone of calcification in the growth plate was absent. The concentration of elements in all regions of the TD growth plate was the same as found in an earlier study for normal growth plate. The cytoplasm of proximal lesion chondrocytes was similar to that of early hypertrophic chondrocytes. However, in the remainder of the lesion there was a progressive increase in cellular Na, S, Cl, and Ca and a progressive loss of P. In matrix, there was less S and K than expected in all regions of growth plate and lesion, except in the proliferating zone. Also, in matrix of the distal lesion there was less Na and Cl. The levels of Na, S, Cl, and K in matrix may have been lowered by their adsorption into the condensed masses of dead cells. Mitochondria acquire only half as much Ca and P as normal and release it earlier than usual (ie, early prehypertrophic cells, rather than chondrocytes of the lower hypertrophic zone). There were no granules in mitochondria of the cells at all levels of the lesion, even though anhydrous methods were used. The first sign of the disease appears in the matrix of the growth plate, where it seems that S and K are in abnormally low amounts. Although there are sufficient levels of Ca and P present, the matrix does not calcify. The cartilage remains avascular, and the cells appear to be dying. The event that triggers the chondrocytes of the growth plate to form an abnormal uncalcified matrix is not known.

Animals↗
PubMed1985

Effects of deficient and adequate dietary magnesium concentrations on body magnesium concentrations in wethers.

Effects of 2 dietary Mg concentrations (deficient and adequate: 0.04 and 0.12 g of Mg/100 g of dry matter, respectively) on body fluid and tissue Mg concentrations and performance of wether lambs were evaluated in a 28-day trial. Nine blood and 6 urine samples were collected from each wether. After 28 days, CSF and wool samples were collected, and diet, body fluids, and tissues were analyzed for mineral concentration. Diet effects on serum and urine Mg concentrations were noticed after day 3 (P less than 0.01; P less than 0.05, respectively). Mean serum and urine Mg concentrations for 6 sampling periods were correlated (r = 0.83, P less than 0.001; No. of samples = 12). The effect of dietary Mg on CSF Mg concentrations approached significance (P less than 0.10). Effects of diet on cardiac muscle, liver, and 3rd metatarsal bone Mg contents or hematologic criteria were not observed. Diet affected wool and kidney cortex Mg contents (P less than 0.02). Individual mean 28-day serum Mg concentration was correlated with wool Mg content (r = 0.73, P less than 0.05; n = 8) and with kidney cortex Mg content (r = 0.75, P less than 0.05; n = 8). Wethers fed low Mg diet excreted less urine Ca (P less than 0.001) and had slightly lower serum Ca and K values (P less than 0.10) than did wethers fed high Mg. Significant differences in cardiac muscle, liver, spleen, or kidney cortex Ca contents were not observed. Wethers fed low Mg diet consumed less dry matter and gained less weight (P less than 0.001) than did wethers fed high Mg diet. Body fluid and tissue macromineral concentrations of 1 wether with hypomagnesemic tetany are presented for prognostic and diagnostic purposes.

Animals↗
PubMed1985

Switch hair as an indicator of magnesium and copper status of beef cows.

Samples of switch hair, blood, and urine were obtained periodically over 5.5 months from 11 Angus and 13 Angus-Charolais cows grazing either all-grass or grass-legume swards. Liver samples were obtained at the end of the study. Hair growth rate and mineral concentrations in switch hair (magnesium [Mg], copper [Cu]), blood serum (Mg, Cu), urine (Mg), and liver (Cu) were determined. Significant (P less than 0.05) hair-growth rate differences were observed among sampling periods (daily mean = 0.58 +/- 0.01 mm). Angus black-pigmented switch hair contained more (P less than 0.001) Mg than did the light-pigmented Angus-Charolais hair. The effect of season was observed on hair Mg and Cu and on serum Mg (P less than 0.01). Serum and hair Mg concentration correlated in both breed groups after removal of individual cow treatment effects (Angus: r = 0.58, P less than 0.001, n = 64; Angus-Charolais: r = 0.46, P less than 0.001, n = 76). Likewise, urine Mg and hair Mg concentrations correlated (Angus: r = 0.35, P less than 0.05, n = 53; Angus-Charolais: r = 0.26, P less than 0.05, n = 63). Sward type had a pronounced effect on serum and urine Mg concentrations and a slight effect on hair Mg concentrations (P less than 0.10) only during midsummer. Cattle with switch hair Mg values less than 25 to 30 mg (light pigmentation) and 100 to 125 mg (black pigmentation)/kg of dry matter (DM) may be hypomagnesemic.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

The effect of dietary manganese deficiency on cholesterol and lipid metabolism in the estrogen-treated chicken and the laying hen.

Three experiments were conducted to determine the affect of dietary manganese on cholesterol and lipid metabolism in avian species. In the first experiment, day-old chicks were fed a manganese-deficient (4.8 micrograms/g) and a manganese-supplemented (104.8 micrograms/g) diet for 4 weeks after which time they were injected with estrogen (5 mg diethylstilbestrol per kilogram body weight). Manganese deficiency did not significantly alter plasma or liver cholesterol in either group. Estrogen administration significantly increased plasma cholesterol concentration in both dietary groups and liver cholesterol in the manganese-deficient group. In the second experiment, 15-week-old White Leghorn pullets were fed a manganese-deficient (4.5 micrograms/g) diet for 10 weeks. Although dietary manganese deficiency significantly decreased hepatic manganese and cholesterol concentrations, it did not affect hepatic cholesterol and fatty acid synthesis, liver lipid, plasma or egg yolk cholesterol. Similar results were obtained in the third experiment with older (36-week-old) laying hens given similar manganese-deficient and adequate diets. These results indicate that dietary manganese deficiency in the avian species does not result in a significant alteration of cholesterol and lipid metabolism.

Animals↗
PubMed1983

The effect of dietary manganese deficiency on cholesterol and lipid metabolism in the Wistar rat and in the genetically hypercholesterolemic RICO rat.

Two experiments were conducted to determine the effect of dietary manganese on cholesterol and lipid metabolism in the Wistar rat and the genetically hypercholesterolemic RICO rat. Weanling animals were placed on a manganese-deficient (0.12 microgram/g) and a supplemented diet (100.12 micrograms/g). Mean body weights, hepatic fatty acid synthesis and liver manganese concentration significantly decreased in the deficient group of Wistar rats. Plasma cholesterol, VLDL (very low density lipoprotein) and HDL (high-density lipoprotein) cholesterol, hepatic cholesterol synthesis, liver cholesterol and lipid concentrations were not significantly affected by manganese deficiency. Mean body weights and hepatic manganese content were lower in the manganese-deficient group in both normal and hypercholesterolemic RICO rats. Manganese deficiency significantly decreased LDL cholesterol concentration in the hypercholesterolemic RICO rats. Manganese deficiency had no significant effect on hepatic cholesterol and fatty acid synthesis, plasma cholesterol, VLDL and HDL cholesterol concentrations, liver lipid and liver cholesterol concentration in either group of RICO rats. These results indicate that dietary manganese deficiency does not result in significant alterations in cholesterol and lipid metabolism in the rat.

Animals↗
PubMed1983

The effect of manganese deficiency upon the ultrastructure of the eggshell.

Manganese deficiency in the laying hen results in decreased egg production and eggshell thickness. Eggshells from deficient hens show specific changes in appearance characterized by translucent areas. Examination of these translucent areas with the scanning electron microscope revealed changes in the ultrastructure of the shell. The most prominent feature was large irregular mammillary knobs probably due to the fusion of several mammillary cores during the early phases of eggshell formation. Chemical analysis of the organic matrix of the eggshell showed a decrease in hexosamine and hexuronic acid content consistent with the known role of manganese in polysaccharide synthesis. Studies on the characteristics of the polysaccharide chains isolated from normal eggshells suggested that these polysaccharides were considerably different from those isolated from cartilage proteoglycans.

Animals↗
PubMed1982

A comparison of the in vitro lipogenic rates and other physiologic parameters in two strains of lean and obese chickens.

Selection for abdominal fat pad size in mature hens has yielded two divergent strains of lean and obese chickens. The females in the obese line have been shown to have a greater amount of total body lipid by six weeks of age. Liver slices from 6- and 17-week old obese chickens incorporated significantly more 3H2O into extracted fractions of total lipid and saponified fatty acids. Palmitate esterification by abdominal fat pad slices from 12-week old pullets was the same for both strains when activity was expressed per unit weight of tissue. The twofold difference in size between the lean and obese fat pads at this age, however, indicates a significantly greater degree of total esterification in the obese birds. At 6-, 12-, and 17-weeks of age, the two lines exhibited similar concentrations of plasma glucose, total protein, and triglycerides.

Adipose Tissue↗
PubMed1982

The developmental characteristics of two strains of chickens selected for differences in mature abdominal fat pad size.

Genetic selection for mature abdominal fat pad size has resulted in establishing lean and obese lines of chickens. Although the selection was made with mature hens, studies with the progeny showed that obesity could develop as early as 6 weeks of age. Body weights in the two lines diverged by 7 weeks of age although significant differences in feed intake were not seen until the fourteenth week. A pair-feeding study was conducted from 7 through 17 weeks of age. The results showed that pair-feeding greatly reduced the lipid deposited in the obese line. The two strains differed substantially in carcass lipid content, but the proportion of total body lipid contributed by the carcass, viscera, and abdominal fat pad was similar in both lines.

Adipose Tissue↗
PubMed1980

Localization of lysyl oxidase in hen oviduct: implications in egg shell membrane formation and composition.

Lysyl oxidase activity was found in the isthmus (the membrane-forming region) of the hen's oviduct in a copper-rich region proximal to the shell gland. Desmosine and isodesmosine, cross-linking compounds associated with mature elastin, were found in hydrolysates of the shell membrane, confirming the necessity for lysyl oxidase in its biosynthesis. Shell membranes from hens fed a copper-deficient diet or a diet supplemented with beta-aminopropionitrile had a reduced content of desmosine and isodesmosine.

Amino Acid Oxidoreductases↗
PubMed1980

Intracellular distribution of copper and zinc in sheep: effect of age and dietary levels of the metals.

This study was conducted to assess the effects of age and dietary levels of copper and zinc on the intracellular distribution of these metals in sheep, the domestic species most susceptible to copper toxicity. Hepatic copper concentration was lower in newborn lambs than in 30- and 60-day old lambs and its distribution in neonates differed significantly from that in the older animals and from that observed in newborn and adult rats. Sheep previously maintained on a low-copper diet for 50 days were then fed diets containing 2.2, 11.3 or 47.0 microgram Cu/g diet with and without zinc supplementation (543 or 46 microgram Zn/g diet, respectively) for 60 days. Ceruloplasmin activity, total plasma copper and hematocrit were lower in zinc-supplemented sheep. Hepatic copper concentration was not reduced by zinc supplementation but was increased with each increase in dietary copper; the distribution pattern was significantly altered as hepatic copper increased. Hepatic zinc concentration and distribution were not affected by diet. Sheep fed the highest level of copper had higher copper concentrations in the mucosa of the small intestine and in kidney cortex. The concentrations of zinc in the kidney and of copper and zinc in diaphragm muscle and bile were not affected by diet.

Aging↗
PubMed1980

Copper- and zinc-binding proteins in sheep liver and intestine: effects of dietary levels of the metals.

Liver cytosol from sheep fed diets containing 2.2, 11.3 or 47 microgram Cu/g diet with or without supplemental zinc (543 or 46 microgram Zn/g diet), fractionated on Sephadex G-100, yielded three main copper- and zinc-containing proteins with approximate molecular weights of greater than 150,000, 27,000 and 10,000. Amino acid analysis of the 10,000-molecular-weight proteins were of the metallothionein type. Copper-chelatin was not present in sheep liver cytosol. Copper concentration of the metallothionein fraction increased (P less than 0.01) as dietary copper increased from 2.2 to 11.3 microgram Cu/g, but did not increase further when dietary copper increased to 47 microgram Cu/g in unsupplemented sheep. A low-molecular-weight (approximately 3,500) copper-, but not zinc-containing fraction appeared at this highest level of copper. Zinc supplementation of the diet increased not only the zinc content of the metallothionein fraction but also its copper content, most dramatically in sheep fed the highest copper level. In intestinal mucosal cytosol, no copper and little zinc was associated with the metallothionetin fraction which was not affected by dietary treatment. Evidence from this study suggests that sheep have limited capacity to synthesize metallothionein in response to increased dietary copper.

Animals↗
PubMed1980

Metabolism of abnormal cartilage cells associated with tibial dyschondroplasia.

Similarities in morphology between copper-deficient cartilage and abnormal cartilage associated with tibial dyschondroplasis (TD) led to studies dealing with copper metabolism and its possible relation to TD. Abnormal cartilage and copper deficient cartilage cells both oxidize significantly less glucose to CO2 and water when compared to normal epiphyseal and day-old hypertrophic cartilage cells. Plasma ceruloplasmin levels and cartilage copper content were not different between normal birds and those affected wth TD, which seemed to rule out a genetic defect in copper metabolism as being partly responsible for the abnormal cartilage occurrence. Mitochondrial marker enzyme activities were investigated, and abnormal cartilage showed a significant decrease in activity of both cytochrome oxidase and citrate synthase. The yield of mitochondria on a percent of total activity basis was quite low from both normal and abnormal cartilages, and, thus, an absolute conclusion with regard to mitochondrial impairment cannot be made at this time.

Animals↗