Search PubMed⌕ Search

Biomedical subjects

R Ross

Publications and source records attributed to R Ross.

At least 343 records · Page 19Linked to original sources
PubMed1982

Factors affecting the secretion of phosphate in parotid saliva in the sheep and goat.

The relationship between the concentration of phosphate in plasma and parotid saliva was studied in six conscious sheep and a goat, either intact or thyroparathyroidectomized (t.x.p.t.x.), under conditions designed to minimize marked fluctuations in flow rate of saliva. A linear relationship between acutely induced changes in plasma phosphate concentration and the phosphate level in saliva has been demonstrated in both intact and t.x.p.t.x. animals. Dietary phosphorus depletion caused adaptation of salivary phosphate concentration so that less was secreted at a given concentration of plasma phosphate. Attention is drawn to the similarity between this phenomenon and that already described for the proximal renal tubule. Parathyroid hormone (PTH) was shown to reduce the salivary phosphate concentration with little or no effect on phosphataemia. The administration of 1,25-dihydroxycholecalciferol (1,25(OH)2CC) also caused a reduction in salivary phosphate concentration despite hyperphosphataemia and hypercalcaemia. It is suggested that salivary phosphate concentration can be influenced directly by the concurrent level of plasma phosphate but that this relationship can be modified by the circulating concentration of 1,25(OH)2CC and indirectly by PTH via increased production of 1,25(OH)2CC.

Animals↗
PubMed1982

Dopamine regulates canine plasma beta-endorphin-immunoreactivity levels.

Intravenous administration of the dopamine antagonists domperidone and metoclopramide elevates canine plasma beta-endorphin immunoreactivity. Pretreatment with dopamine, but not dexamethasone, inhibits this effect. Sephadex G-50 chromatography shows that this response is due to beta-endorphin-like peptides, not beta-lipotropin. These findings indicate that pituitary beta-endorphin secretion is tonically inhibited by dopamine and suggest that the intermediate lobe is the source of this secretion.

Animals↗
PubMed1982

Calcium homeostasis in the fetal pig.

Acute studies have been carried out with pregnant sows and their fetuses during the last 2 weeks of gestation. In blood samples obtained simultaneously it was shown that the concentrations of ionized calcium, calcitonin and parathyroid hormone (PTH) in fetal plasma were all greater than the corresponding values in maternal plasma. In contrast, the fetal concentrations of 24,25-dihydroxy vitamin D3 were lower than maternal and those of 1,25-dihydroxy vitamin D3 were not significantly different. In one experiment the circulatory level of fetal PTH was shown to be higher than in the sow by both an immunoradiometric assay and a very sensitive cytochemical assay. The latter showed the fetal: maternal ratio to be approximately three. This inappropriately high level of fetal PTH was unaffected by short term hypocalcaemic and hypercalcaemic changes in the fetal circulation. Although part of this fetal PTH may have been secreted in response to the action of beta-catecholamines released as a result of the experimental conditions, the transplacental gradient of PTH was also demonstrated in the chronically catheterized fetus. A short term period of either hypercalcaemia or hypocalcaemia induced in the mother was without consistent effect upon plasma calcium concentration in the fetus. However, an increase in ionized calcium concentration in the fetal plasma was found to follow the cessation of a period of maternal hypocalcaemia. It can be seen that the porcine fetus possesses the important elements of a calcium homeostatic mechanism, namely parathyroid hormone, calcitonin and the biologically active metabolites of vitamin D. Although the degree of independence from the mother is somewhat less than in the sheep, it is concluded that the porcine fetus is largely autonomous with respect to calcium homeostasis.

Animals↗
PubMed1981

Early changes in phosphatidylinositol and arachidonic acid metabolism in quiescent swiss 3T3 cells stimulated to divide by platelet-derived growth factor.

We added platelet-derived growth factor to cultures of quiescent Swiss 3T3 cells to investigate early changes in lipid metabolism related to initiation of cell cycle traverse. In a series of experiments that focused on lipid degradation we added the growth factor to cells that had been prelabeled with myoinositol, glycerol, or arachidonic acid. We observed the following mitogen-dependent effects: a decline of radioactivity in cell phosphatidylinositol within 2 to 5 min that progressed to 25 to 50% during the 1st h, a transient rise of radioactivity in cell diacylglycerol that peaked at 10 min, a gradual increase of radioactivity in monoacylglycerol in the medium, and a concomitant increase of radioactivity in medium-free fatty acid. In experiments that focused on lipid biosynthesis, we added the growth factor to cells and pulse-labeled them with radioactive precursors. We observed increased incorporation within 60 min of myoinositol into phosphatidylinositol, arachidonic acid into phosphatidylinositol, diacylglycerol, and phosphatidylethanolamine, and choline into phosphatidylcholine. These results support the possibility that action of platelet-derived growth factor on Swiss 3T3 cells leads to release of diacylglycerol from phosphatidylinositol, that some of the released diacylglycerol is hydrolyzed to monoacylglycerol and arachidonic acid, and that these lipid products are in part reconverted to phosphatidylinositol and other lipids.

Animals↗
PubMed1981

Human monocyte-derived growth factor(s) for mesenchymal cells: activation of secretion by endotoxin and concanavalin A.

Cultured peritoneal macrophages have previously been shown to release a potent mitogen for mesenchymal cells. Peritoneal macrophages are derived from peripheral blood monocytes, one of the principal inflammatory cells associated with numerous tissue responses to injury. Cultured human monocytes can be activated by endotoxin or concanavalin A to secrete a potent growth factor(s) that is active on human smooth muscle cells, human fibroblasts and 3T3 cells. The optimal conditions for activation of monocyte release of this monocyte derived growth factor(s) MDGF) were to expose 5-day-old monocyte cultures (initially plated at 6.8 X 10(5) cells/ml medium) to 10 microgram/ml endotoxin or 6 microgram/ml concanavalin A for approximately 20 hr. Monocytes can secrete MDGF into serum-free medium supplemented with 0.15% bovine serum albumin, MDGF stimulates both DNA synthesis and increase in cell number and is trypsin-sensitive, heat labile and nondialyzable. The relationship of MDGF to other monocyte products and its potential importance in wound repair and atherogenesis are discussed.

Amino Acid Sequence↗
PubMed1981

Phenotype-dependent response of cultured aortic smooth muscle to serum mitogens.

Smooth muscle cells from the aortic media of adult pigs and monkeys have been grown in primary culture by plating cells enzymatically dissociated from the intact aorta. During the first 6 d these cells are in the "contractile" phenotype. That is, they contract slowly in response to angiotensin II and their cytoplasm is filled with both thick and thin myofilaments. In this state they do not incorporate [3H]thymidine into DNA or proliferate in response to normolipemic or hyperlipemic whole blood serum (WBS). After 7 d in culture the cells undergo a spontaneous modulation of phenotype to a "synthetic" state where they cannot be stimulated to contract and their cytoplasm is filled with organelles usually associated with synthesis of secretory protein. Thick myosin-containing filaments can no longer be demonstrated. When challenged with normolipemic or hyperlipemic WBS the cells incorporate [3H]thymidine into DNA and undergo logarithmic growth. It is suggested that when smooth muscle is the contractile phenotype (as normally exists for most cells in the aortic media of adult animals) it does not divide when challenged with serum mitogens but can undergo a change of phenotype to a synthetic state in which division can be stimulated.

Animals↗
PubMed1981

Screening for toxoplasmosis in pregnancy.

The prevalence of antibody against Toxoplasma gondi in a population of 715 pregnant women has been evaluated by two methods: indirect haemagglutination antibody (IHA) and indirect fluorescent antibody (IFA) test and all positive sera were checked by the dye test. Five hundred of the study population were questioned on diet and on animal contact to elucidate a possible relation to the prevalence of antibody. Results are expressed in international units (IU) of antibody against T gondi. Of the 715 sera, 171 were positive by IHA and 173 by IFA. One hundred and sixty-seven sera were positive by both tests, ninety-eight (58%) correlating exactly, as to the concentration of antibody. The ten sera which were not positive by both tests all had detectable antibody at the minimum concentration only (12 IU). The dye test confirmed all sera positive by both tests with the exception of three. It also confirmed one of four sera positive by IHA antibody alone and two of six positive by IFA alone. All sera that proved dye test-negative had low antibody concentrations (12 IU) by IHA or IFA. The IHA test, which is commercially available in kit form, would be suitable for use as a screening test during pregnancy. The estimated annual rate of antibody acquisition over the age range 16-40 years is 1.2% per annum with the highest rate in the 36-40 age group (2.5% per annum) and the lowest in the 26-30 age group (0.4% per annum). The clinical history was not significantly different between those with and those without antibody against T gondi but significantly more women in the 36-40 age group had a history of animal contact than those in the 26-30 age group. No conclusive evidence of recent or current infection was found.

Adolescent↗
PubMed1981

Endothelium and arteriosclerosis.

Endothelium, platelets and macrophages can each provide growth factors that may participate in atherosclerotic lesion initiation or progression, or both. These mitogens, coupled with alternations in endothelial integrity or function resulting from a variety of different risk-associated factors, such as hyperlipidaemia, hypertension, tobacco smoke, antibodies, infections, or homocystinaemia, may provide the basis for the intimal proliferative smooth muscle cell response of atherosclerosis. Platelets, endothelium or macrophages may be important in lesion initiation and progression in some circumstances but not in others, depending upon the extent and type of endothelial "injury'.

Animals↗
PubMed1980

Modulation of epidermal growth factor receptors on 3T3 cells by platelet-derived growth factor.

Platelet-derived growth factor does not compete with epidermal growth factor (EGF) for binding to EGF receptors on the murine 3T3 cell surface, but it modulates EGF receptors in two ways: (i) it induces a transient down regulation of EGF receptors and (ii) it inhibits EGF-induced down regulation of EGF receptors. These data suggest a common cellular internalization mechanism for the receptors for both hormones.

Animals↗
PubMed1980

Increased fluid pinocytosis, induced by action of platelet-derived growth factor on quiescent arterial smooth muscle cells, does not require increased cholesterol biosynthesis.

In the current report we provide evidence that the increased rate of cholesterol biosynthesis mediated by platelet-derived growth factor in the cell cycle of monkey (Macaca nemestrina) arterial smooth muscle cells can be separated from the increased rate of fluid pinocytosis using inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase.

Animals↗
PubMed1980

Studies of morphologically atypical ("sprouting") cultures of bovine aortic endothelial cells. Growth characteristics and connective tissue protein synthesis.

Morphologic and biochemical studies were performed on cultures of bovine aortic endothelial cells which had developed a second growth pattern that has been referred to as "sprouting" (Gospodarowicz and Mecher, '78; Schwartz '78). These morphologically atypical cells undergrew the intact endothelial cell monolayer and appeared only after the cells had reached confluence. They were ultrastructurally very similar to endothelial cells, but synthesized reduced amounts of fibronectin and a predominance of type I procollagen, rather than the types III and IV procollagens synthesized by monolayer endothelial cells. It is suggested that these cells represent phenotypically altered endothelial cells that differ in biosynthesis of secreted proteins and display a reduced contact-inhibition.

Animals↗