Search PubMed⌕ Search

Biomedical subjects

J E Harrison

Publications and source records attributed to J E Harrison.

At least 109 records · Page 6Linked to original sources
PubMed1984

Proliferation of arterial smooth muscle cells incubated in serum from brain-stimulated rats.

Platelet deficient serum prepared from rats subjected to acute electrical stimulation of the lateral hypothalamus demonstrated mitogenic activity when added to incubating media supporting growth of homologous arterial smooth muscle cells in vitro. This activity did not appear to be related to the presence of platelet-derived growth factor, hyperlipidemic lipoproteins or increased amounts of insulin. Plasma arginine vasopressin concentration was elevated in these animals, but further investigation is required to determine if this elevation is causally related. Since hypothalamic stimulation is also associated with severe endothelial injury in vivo, the mitogenic activity of the blood of such animals could induce proliferation of SMC which have migrated into the arterial intima. Such features have been observed in chronically stimulated animals and may be of relevance for the role of neural factors in atherogenesis.

Animals↗
PubMed1984

The effect of diet calcium on fluoride toxicity in growing rats.

The effect of dietary Ca in response to fluoride (F) treatment was investigated in rats. Rats were maintained on either adequate (0.5%) or high (2.0%) dietary Ca and given for 5 weeks, NaF in drinking water. The minimum NaF levels that inhibited body growth and reduced survival were 300 mg/L with 0.5% diet Ca and 550 mg/L with 2.0% diet Ca. With these toxic F doses, bone histology showed increased formation surfaces and thickened osteoid seams (osteoid index 6-7%). Fluoride doses 30% below toxic levels (200 and 350 mg/L for 0.5 and 2.0% diet Ca, respectively) had no demonstrable effect on bone. Additional diet Ca reduced F absorption from 76 +/- 3 to 47 +/- 3% for 0.5 and 2.0% diet Ca, respectively. Comparable absorbed doses of F produced comparable effects on bone and body growth but, with additional dietary Ca, these effects were observed with 50% lower serum and bone F levels. Variable response to NaF therapy can be produced in rats by alterations in dietary Ca alone. Results indicate that for clinical treatment the NaF dose needs to be adjusted on an individual basis but neither serum nor bone F levels can be used reliably to establish optimal doses.

Animals↗
PubMed1984

Changes in body composition in patients with small-cell lung cancer. The effect of total parenteral nutrition as an adjunct to chemotherapy.

y composition was studied in 31 patients receiving chemotherapy for small-cell lung cancer. Patients were randomly assigned to receive either 4 weeks of total parenteral nutrition (study group) or to continue a self-regulated oral diet (control group). The relationship between height and total body nitrogen was altered initially for patients who had lost more than 5% of body weight. During the 4 weeks of parenteral nutrition, body weight, total body fat, and total body potassium, but not total body nitrogen, increased significantly in the study group (p less than 0.001). However, after parenteral nutrition was stopped, body weight and potassium levels in the study group fell significantly and to the same extent as in the control group. Nitrogen levels showed an overall fall in the 32 weeks of observation for both groups. After the period of parenteral nutrition, the decrease in body fat was significantly greater in the control group than in the study group (p less than 0.05). Thus, parenteral nutrition increased body fat and total body potassium, but not total body nitrogen.

Adipose Tissue↗
PubMed1983

Effect of a weight-reducing high-protein diet on the body composition of obese adolescents.

The effect of a three-month period on a high-protein reducing diet on body composition was studied in 17 obese adolescents, aged 12.5 to 17.4 years. Body composition was assessed by estimating fat-free body mass from four skin-fold thicknesses, total body potassium by natural potassium 40 abundance, and total body nitrogen by prompt gamma ray analysis. Weight loss was 15% of initial body weight. Total body nitrogen loss was only 4.8% (not significant), while total body potassium fell by 13.2%. Change in fat-free body mass estimated from skin-fold thicknesses constituted approximately 44% of the total weight lost. There was no correlation between changes in total body potassium and total body nitrogen, suggesting that total body potassium cannot be used to predict total body nitrogen in a changing nutritional state.

Adipose Tissue↗
PubMed1983

Radical acetoacetate oxidation by myeloperoxidase, lactoperoxidase, prostaglandin synthetase, and prostacyclin synthetase: implications for atherosclerosis.

When the myeloperoxidase-catalyzed peroxidation of acetoacetate proceeds in the presence of piperidinooxy free radical, methyl glyoxal is formed, and the nitroxide group is reduced to the secondary amine. A mechanism is advanced wherein an alpha-carbon-centered acetoacetate radical, generated by the peroxidase, forms an unstable adduct with the nitroxide group, subsequently decomposing to the observed products. Formation of methyl glyoxal, detected as its bis-2,4-dinitrophenylhydrazone by radial thin-layer chromatography, represents a method of determining free radical acetoacetate peroxidation by other peroxidases. It is shown that lactoperoxidase, prostaglandin synthetase, and prostacyclin synthetase generate methyl glyoxal with requirements identical to those of myeloperoxidase. With prostaglandin synthetase, arachidonic acid could replace the supporting peroxide. Substantiation that the catalyst for the reaction in aortic microsomes was prostacyclin synthetase was obtained by showing that 15-hydroperoxyarachidonic acid strongly inhibited the activity (5). The finding that these peroxidases catalyze radical acetoacetate oxidation could have broad implications for cellular damage via lipid peroxidation (7). Specifically, radical oxidation of acetoacetate by prostacyclin synthetase is proposed to be a link between cardiovascular risk factors and the initiation of atherosclerosis.

Acetoacetates↗
PubMed1982

Endothelial morphology and plasma total and high density lipoprotein cholesterol changes in hypothalamically stimulated squirrel monkeys fed a modified atherogenic diet.

Experimental animals fed atherogenic diets show endothelial damage, impairment of endothelial regeneration and plasma lipid changes characterized by elevation of LDL and decrease of HDL cholesterol concentrations. Previous studies in this laboratory disclosed that chronic electrical stimulation of the lateral hypothalamus was associated with electron-microscopic evidence of endothelial injury in rats and squirrel monkeys maintained on basal (low fat/cholesterol-free) diets. In the present investigation squirrel monkeys fed similar diets supplemented with "modest" amounts of caloric fat and cholesterol were subjected to chronic lateral hypothalamic stimulation for periods as long as 20 months with the expectation that endothelial injury would be greater than in the absence of the supplements. The expectations were not substantiated. Endothelium was found to be surprisingly intact by electron microscopy and similar to that of implanted nonstimulated controls. A further observation of interest was the cholesterolemic response, notably in the HDL fraction, observed in both groups, but more striking in experimental animals. The data suggest that an interaction between a modified lipid/cholesterol diet and hypothalamic stimulation may lead to elevation of plasma HDL cholesterol concentration and preservation of endothelial integrity. Further investigation is required to determine whether these two events are causally related.

Animals↗
PubMed1982

Increased bone apposition in primary hyperparathyroidism: measurements based on short interval tetracycline labeling of bone.

Bone biopsies of 23 subjects suffering from primary hyperparathyroidism, which was proven by the demonstration of parathyroid pathology during neck surgery, were studied by morphometric analysis and short interval sequential tetracycline labelling and compared with those of 13 patients without metabolic bone disease. In 19 of these patients, abnormalities were found in the trabecular volume, resorption surface, formation surface, or in various combinations. However, no constant pattern of bone changes was observed. In 4 patients, the bone morphometric parameters were normal. The bone apposition rate, on the other hand, was elevated in all 23 subjects. The rate was re-evaluated in 4 patients 6 wk to 3 mo following successful parathyroid surgery. It fell back within the control range. These findings confirm the observation in experimental animals that parathyroid hormone stimulates bone apposition in vivo and give support to the rationale of using this hormone in the treatment of osteoporosis.

Adolescent↗
PubMed1982

Plasma vitamin D metabolite levels in phosphorus deficient rats during the development of vitamin D deficient rickets.

Plasma levels of the vitamin D metabolites were related to changes in bone morphology during the development of rickets in rats deprived of phosphorus and vitamin D. Weanling rats were studied at 1, 3, and 5 wk after onset of diets deficient in phosphorus or in both phosphorus and vitamin D. Bone histology and morphometry were carried out and measurements were made of 45Ca and 32P absorption, serum Ca and P, and plasma 25(OH)D3, 24,25(OH)2D3 and 1,25(OH)2D3. After 1 wk of vitamin D restriction, the plasma levels of 25(OH)D3 and 24,25(OH)2D3 were non-detectable (less than 0.5 and less than 0.8 ng/ml). The plasma 1,25(OH)2D3 level was elevated at 1 wk (105.5 pg/ml) and fell to 19 pg/ml by 5 wk. At 1 wk mild rachitic lesions in epiphyseal cartilage were observed despite the elevated 1,25(Oh)D3 level. Serum Ca and P levels and values for 45CA and 32P absorption decreased and the severity of the rickets increased with the fall in plasma levels of 1,25(OH)2D3. In Vitamin D replete, phosphate deficient rats the epiphyseal cartilage was normal throughout the 5 wk study period. Our results provide further evidence that physiological levels of 1,25 (OH)2 D3 will not prevent rickets without adequate plasma concentrations of either 25(OH)D3 or 24,25(OH)2D3.

Animals↗
PubMed1982

Antagonism by meseclazone and other nonsteroidal anti-inflammatory drugs of bradykinin-induced bronchospasm.

Bradykinin-induced bronchoconstriction is due, in part, to release of TXA2 and prostaglandins. Intravenous administration of meseclazone and other nonsteroidal anti-inflammatory drugs caused a dose-dependent inhibition of bronchoconstriction resulting in the following order of descending potency: isoproterenol congruent to indomethacin greater than fenoprofen greater than tolmetin greater than aspirin greater than naproxen congruent to ibuprofen greater than phenylbutazone greater than diflunisal greater than meseclazone greater than 5-CSA. This order of potency does not correlate with that obtained with these compounds for in vitro relaxation of tracheal smooth muscle, an effect which may be related to inhibition of prostaglandin synthesis.

Animals↗
PubMed1981

Protective effect on vitamin D2 on bone apposition from the inhibitory action of hydrocortisone in rats.

Using the technique of short interval sequential tetracycline labeling, it was documented that the apposition of mineralized bone matrix in adult male Sprague-Dawley rats was inhibited by hydrocortisone. The inhibition occurred as early as six days after the onset of the treatment and was dose dependent over a dose range of 0.62 to 20 mg per kg body weight per day. Vitamin D2 supplements by injection protected bone from this hydrocortisone action. 64 I. U. of vitamin D2 injected daily was able to prevent the inhibition of bone apposition by 20 mg per kg body weight per day of hydrocortisone. The results imply that vitamin D or its metabolites may compete with hydrocortisone in some cellular mechanisms and support the usefulness of vitamin D supplements in the treatment and the prevention of steroid-induced osteoporosis.

Animals↗
PubMed1981

Total body bone mineral and lean body mass by dual-photon absorptiometry. III. Comparison with trunk calcium by neutron activation analysis.

Dual-photon absorptiometry using 153Gd (44 and 100 keV) was used to measure the bone mineral content (BMC) of the trunk and of the total body (TBBM) in 7 volunteers with no overt bone disease. These values were compared to those obtained with partial-body neutron activation of calcium (trunk Ca). The trunk Ca seemed to represent best a 60 x 30 cm area; the correlation coefficient with the corresponding BMC in that area was 0.97 (SEE congruent to 7%). Trunk Ca was also highly correlated with TBBM (r = 0.96; SEE = 8%) and with radius BMC (r = 0.92; SEE = 11%), but the correlations with the BMC of smaller subareas of the trunk were lower (r congruent to 0.9; SEE approximately 12%). The BMC of the lumbar spine was only moderately correlated with trunk Ca, radius BMC and TBBM (r approximately 0.82; SEE approximately 18%), and only slightly more associated with trunk BMC (r approximately 0.88; SEE approximately 14%). The BMC of the combined lumbar-thoracic spine showed higher correlations with trunk Ca, radius BMC and TBBM (r approximately 0.87; SEE approximately 13%), and trunk BMC (r = 0.93; SEE approximately 10%). An accurate and sensitive measure of spinal status requires a direct measurement of that area.

Adult↗
PubMed1981

Effect of hypothalamic stimulation on the endothelial morphology of the aorta in the conscious squirrel monkey.

The role of neurogenic factors in the development of atherosclerosis has not previously been studied in detail. In recent years evidence has accumulated to implicate endothelial injury as a primary stimulus for the proliferation of myo-intimal cells resulting in the formation of the early morphologic lesion. In the present investigation, the effect on aortic endothelial morphology of repetitive electrical stimulation of the lateral hypothalamus in the conscious, unrestrained squirrel monkey, maintained on a cholesterol-free low-fat diet, has been studied. Stimulation was performed with a self-powered, miniaturized electronic stimulator connected to indwelling electrodes. Implanted nonstimulated animals served as controls. Endothelial injury in the form of cell degeneration, denudation, with plasma insudation and partial junctional separation were observed electron-microscopically in stimulated animals compared with controls. These alterations were found to be independent of hypercholesterolemia and/or hypertension. Possible pathways for the induction of injury in this neurogenic model are: (1) direct, through neural circuits from the brain to the vessel wall, and (2) indirect, by elaboration of angiopathic substances inside or outside of the CNS, released into the circulation and transported to the vessel wall where they exert their effects. Reversibility of the endothelial injury progression to established lesions and mechanisms involved remain to be determined in further investigations.

Animals↗