Biomedical subjects
Publications and source records attributed to J N Morrison.
A device to rotate valve prostheses is described. By using a polythene tubing universal joint the valve may be turned by twisting the handle of the valve rotator without altering its spatial orientation. This modification was designed to facilitate what can be a frustrating manoeuvre and should be applicable to any rotatable valve.
Reindeer inhabit a severe arctic or subarctic environment, with the young born in early spring under adverse weather conditions. The extreme northern climate imposes a major thermal challenge to the newborn, and in the present study we have examined fetal, neonatal, and young (from 2 wk before birth to 16 mo postpartum) semidomesticated reindeer from northern Finland for the presence of thermogenic brown adipose tissue. Adipose tissues were removed, mitochondria were prepared, and the proteins were separated by molecular weight and blotted onto nitrocellulose membranes. The membranes were then probed for the presence of the 32,000-relative molecular weight mitochondrial uncoupling protein (UCP) unique to brown fat by use of a rabbit anti-(ground squirrel UCP) serum. Immunoreactivity at the molecular weight characteristic of UCP was present in perirenal, abdominal, inter(pre)scapular, sternal, intralumbar, vertebral, tracheal, inguinal, and omental-mesenteral adipose tissues of newborn reindeer (0-2 days of age). No immunoreactivity was detected in coronary adipose tissue. UCP was found at high levels in interscapular and perirenal adipose tissues of fetal reindeer at 2 wk before birth. Although the protein was present during the first few days postpartum, little immunoreactivity was found at 1 mo of age, and none was evident by 2 mo. UCP and its mRNA were also apparent in perirenal adipose tissue of the newborn of another species of Cervidae, the red deer. It is concluded, on the basis of the immunologic identification of UCP, that most adipose tissues of newborn reindeer represent functional brown fat but that there is a subsequent conversion to white adipose tissue by the 2nd mo of life.(ABSTRACT TRUNCATED AT 250 WORDS)
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The effects of iron deficiency and of restriction of food intake on blood and tissue metallothionein-I (MT-I) concentrations in rats were investigated. Compared to ad libitum fed controls, MT-I concentrations in the blood cells of the iron-deficient rats were higher, whereas concentrations in pair-fed control rats were lower. Iron deficiency also increased MT-I concentrations in the bone marrow but concentrations in the liver were unchanged and those in the kidneys were reduced. The MT-I in the blood cells was associated mainly with the lighter cell fractions which were rich in reticulocytes. It is suggested that concentrations of MT-I in blood cells reflect erythropoietic activity.
Changes in metallothionein I (MT-I) levels were measured in blood and tissues of rat pups from dams given diets containing 6, 9 or 40 mg zinc/kg from wk 1 or gestation and throughout lactation. After 1, 2 and 3 wk of lactation, litters from each group were killed and tissues analyzed for MT-I. The relatively mild degree of zinc deficiency, which had no effect on fetal viability or litter size and caused only slightly lower pup weight, caused significantly lower MT-I concentrations in pup liver, thymus, plasma and red cells, particularly in pups from dams receiving 6 mg zinc/kg. Maternal zinc supply is therefore a major determinant of MT-I concentrations in neonatal tissues, and assay of this protein in blood plasma and red cells may give a useful indication of zinc status.
These studies were designed to investigate the effects of low dietary zinc, copper or selenium intake of certain types of stress and of injection of zinc, copper or cadmium on metallothionein I (MT-I) concentrations in the blood and urine of rats. The aim was to establish whether such measurements could be of value in the diagnosis of zinc deficiency. Marginal zinc deficiency rapidly caused a major decrease in MT-I levels in the blood cells and to a lesser extent in urine. Injection of zinc and also of cadmium and copper had the opposite effect and increased MT-I concentrations in both samples, although the effects of zinc on blood cells and urine were relatively transient. The MT-I in the blood cells was associated mainly with the erythrocytes. No changes in blood or urine MT-I levels were found in copper- and selenium-deficient rats. Neither cold stress nor restriction of food intake for 24 h had any significant effect on MT-I levels in the blood cells or urine. Endotoxin injection increased urinary MT-I excretion in both zinc-adequate and zinc-deficient rats but did not affect blood cell MT-I levels in either group of animals. It appears therefore that assay of erythrocyte MT levels could be of particular value in the diagnosis of zinc deficiency, especially when it is accompanied by stress or infection.
The appearance and excretion of metallothionein-I (MT-I) was studied in rats given a diet containing 1000 mg of Cu/kg for several weeks. No significant increase in MT-I concentrations in liver, plasma or bile was detected in rats with liver copper concentrations less than 600 micrograms of Cu/g fresh wt. Above this concentration, liver MT-I concentrations increased in proportion to the increase in hepatic copper content. Plasma and bile MT-I concentrations were directly related to those in the liver and were about 10 times those in normal rats. Urinary MT-I concentration also increased 10-fold within 1 week. Fractionation of bile and urine on Sephadex G-50 revealed the presence of monomeric MT-I and a range of possible degradation products of the isoprotein.
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The effects of calcium and phosphate supplements on the retention of dietary lead and the loss of lead from the body were studied in young rats. There were three experiments in which rats were given a diet containing 200 or 400 micrograms of lead/g for 3 or 6 weeks. The diet contained adequate calcium and phosphate. Calcium and phosphate supplements were given alone or together. Lead uptake after a period of lead feeding was measured by analysis of the whole gut-free carcass. Lead loss was measured by a similar analysis after the rats had received diets containing lead and then diets free of lead. The uptake of lead from the diet was reduced by about half when either dietary calcium or phosphate or both was doubled. The rate of release of body lead was decreased by calcium supplementation.
The effects of dietary protein content on lead retention were studied in young rats. In experiments lasting between 3 and 6 weeks, rats given diets containing lead and 20% casein were fed ad libitum or were pair fed with rats given diets containing 6.5 or 7.5% casein. Among rats given 20% casein, lead retention was inversely related to growth rate. A reduction of dietary protein either had no effect or reduced lead retention. In other experiments lasting 4 days and using 203Pb, given orally or intraperitoneally, the recovery of isotope in the gutfree carcass was unaffected or reduced by a reduction in dietary protein. Blood and liver lead often increased when kidney and carcass lead decreased in response to a reduction of dietary protein. Conflicting observations on the effect of low-protein diets on lead retention may thus be due to opposing effects of low dietary protein and decreases of growth rate and to different responses of different tissues.
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