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Biomedical subjects

R Ross

Publications and source records attributed to R Ross.

At least 361 records · Page 20Linked to original sources
PubMed1980

Gigantic monostotic fibrous dysplasia of the right humerus. A plea for advice on management.

A case of enormous enlargement and destruction of the right humerus is reported in a middle aged, right-handed, skilled manual worker. The tumour is cosmetically very ugly but right upper limb function is good. Advice from readers on the management of this case is honestly and thankfully requested, particularly information on what might be done should functional deterioration force us to undertake surgery.

Fibrous Dysplasia of Bone↗
PubMed1980

Relation of Gothic arch apex to dentist-assisted centric relation.

These data suggest that the widely held belief that thumb pressure can position the mandible consistently more posterior than the position indicated by the Gothic arch apex is unfounded. Furthermore, this study provides no evidence to support the contention that the dentist-assisted jaw relation is more reproducible than the relation indicated by the Gothic arch apex.

Adult↗
PubMed1980

Platelet-derived growth factor stimulates activity of low density lipoprotein receptors.

Partially purified platelet-derived growth factor stimulates low density lipoprotein binding and degradation in cultured aortic smooth muscle cells of monkeys by increasing the number of available low density lipoprotein receptors. When platelet-derived growth factor was added to quiescent cells, low density lipoprotein binding increased within 4-8 hr. Stimulation of low density lipoprotein receptor activity preceded stimulation of DNA synthesis by platelet-derived growth factor by 8-12 hr. Enhancement of endogenous cholesterol synthesis by platelet-derived growth factor preceded stimulation of low density lipoprotein receptor activity. These findings suggest that the platelet-derived growth factor can increase both the exogenous and endogenous supplies of cholesterol to the cell for its use during cell proliferation.

Animals↗
PubMed1980

Role of serum components in density-dependent inhibition of growth of cells in culture. Platelet-derived growth factor is the major serum determinant of saturation density.

The effects of platelet-derived growth factor and plasma components on saturation density in cultures of 3T3 cells were investigated. Both of these components of whole blood serum affect saturation density; however, when 3T3 cells become quiescent at high density in medium containing whole blood serum, only platelet-derived growth factor and fresh whole blood serum are capable of stimulating proliferation. Addition of fresh plasma- derived serum has little effect on cell growth. These results suggest that the platelet factor is the major determinant of saturation density in cultures of 3T3 cells maintained in medium supplemented with whole blood serum. Experiments were performed to investigate the mechanism by which platelet-derived growth factor regulates saturation density. We investigated the possibilities of inactivation of growth factors by proliferating cells, and the effects of cell density on the response of 3T3 cells to platelet-derived growth factor. The amount of platelet- derived growth factor required to initiated DNA synthesis increases with increasing cell density. Some inactivation of growth factors by growing cells was detected, but this depletion was only evident at high cell density. We propose that density-dependent inhibition in cultured 3T3 cells is the result both of an increased requirement for the platelet- derived growth factor as the cultures become more crowded and of inactivation of growth factor activity by growing cells.

Animals↗
PubMed1980

An endothelial cell-derived growth factor.

Cell-free plasma-derived serum (PDS) is deficient in the platelet-derived growth factor and will not support the growth of 3T3 cells, fibroblasts, or smooth muscle cells. However, when PDS-containing medium is preincubated with endothelial cells, the medium becomes modified so that it will support growth. The activity produced by the endothelial cells results from a polypeptide of 10,000 to 30,000 daltons which has several features that differ from those of the platelet-derived growth factor, including heat instability and lack of adsorption to CM Sephadex.

Animals↗
PubMed1980

Biochemical studies of two patients with the gray platelet syndrome. Selective deficiency of platelet alpha granules.

The biochemistry of platelets from two unrelated patients with the gray platelet syndrome, a deficiency of platelet alpha-granules, has been evaluated. Ultrastructural studies of their platelets revealed the number of alpha-granules to be less than 15% of normal, whereas the number of dense bodies was within normal limits. Platelets from both patients had severe deficiencies of platelet factor 4 and beta-thromboglobulin (less than 10% of normal). Sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed a marked deficiency of thrombin-sensitive protein in both patients. Analysis of the platelet-derived growth factor in one patient showed it was also markedly reduced. Levels of lysosomal enzymes, adenine nucleotides, serotonin, and catalase, and conversion of arachidonic acid by the lipoxygenase and cyclo-oxygenase enzymes, were within normal limits. The results provide important evidence to define the contents of alpha-granules and to differentiate these contents from the contents of lysosomal granules, dense bodies, and peroxisomes. Functional studies of these platelets showed deficiencies in ADP, thrombin, and collagen aggregation. The results suggest that alpha-granules or their contents make a contribution to normal platelet aggregation.

Acid Phosphatase↗
PubMed1980

Catterall grouping of Perthes' disease. An assessment of observer error and prognosis using the Catterall classification.

A study was undertaken to assess the degree of inter-observer error when a panel of observers classified the radiographs of patients with early Perthes' disease, using Catterall grouping and "at risk" signs. The anteroposterior and lateral radiographs, taken within three months of diagnosis of Perthes' disease, were available for 69 hips and were shown in turn to 10 observers. The radiological end-results were assessed at least four years from diagnosis. The results showed a poor ability of the observers to delineate Groups 1, 2 and 3, with a more satisfactory performance in Group 4 and when Groups 2 and 3 were combined. Interpretation of "at risk" signs was unsatisfactory except when there was an increase in medial joint space greater than two millimetres. The end-results correlated well with early Catterall grouping and "at risk" signs when these were correctly interpreted.

Child↗
PubMed1980

Fibroblast proliferation induced by blood cells.

Growth factors have been isolated from three cell types associated with the vascular system; the platelet, the monocyte/macrophage, and the endothelial cell. Each of these mitogens appears to have different characteristics. The platelet-derived growth factor is a cationic protein (pI 9.8) that is heat stable, of molecular weight approx. 30,000 and is located in the alpha granules of the platelet. The growth factors derived from the monocyte/macrophage and the endothelial cell each appear to be distinct and different proteins. Each of these factors was discovered as a result of the ability to induce quiescence in the G1/G0 state of cells in culture, that can be readily induced in the presence of cell free plasma-derived serum in the culture medium. Cells such as fibroblasts, smooth muscle, 3T3 cells and glial cells will remain quiescent in culture medium containing plasma-derived serum for periods up to 6 weeks. Stimulation by the platelet-derived growth factor or macrophage-derived growth factor, will commit these cells to enter S and begin cell cycle traverse. Inhibition of platelet function in vivo can be shown to inhibit intimal smooth muscle proliferation in response to endothelial injury. Thus, each of these factors may play important roles in the process of initiation of fibroplasia in wound repair, smooth muscle proliferation in atherogenesis and endothelial proliferation in response to injury.

Animals↗
PubMed1979

Platelets: cell proliferation and atherosclerosis.

Intimal smooth muscle proliferation is the hallmark of the lesions of atherosclerosis. Endothelial injury is postulated to precede this intimal smooth muscle proliferative response, which is mediated by a potent mitogenic factor derived from adherence, aggregation, and release by platelets at sites of endothelial injury. Smooth muscle proliferation is accompanied by varying amounts of connective tissue formation and intracellular and extracellular lipid deposition, dependent upon the risk factors encountered in each patient. The platelet-derived mitogen (PF) is a stable, cationic, relatively low molecular weight (10,000-30,000) protein that has been partially purified by ion exchange chromotography and gel filtration. Less than 100 ng of PF/ml culture medium can stimulate sparse 3T3 cells or smooth muscle cells, but not endothelial cells, to undergo multiple cell divisions in the presence of 5% cell-free, plasma-derived serum. The latter contains no mitogenic activity. The interaction of the platelet mitogen and plasma-derived components, including lipoproteins, plays a critical role in smooth muscle proliferation in vitro and in vivo in the induction of the lesions of atherosclerosis.

Animals↗
PubMed1979

The pathogenesis of atherosclerosis.

The pathogenesis of atherosclerosis is hypothesized to occur as a response to various forms of injury to the lining arterial endothelial cells. The resulting endothelial alterations could potentially lead to interactions between platelets in the circulation and the underlying subendothelial connective tissue or with the altered endothelial cells themselves. Such interactions provide an opportunity for platelet degranulation and release of a platelet-derived growth factor. This factor has been shown in cell culture to be an extremely potent mitogen and will induce DNA synthesis and cell multiplication of a number of cells including smooth muscle cells, fibroblasts, and other mesenchymally derived cells. Chronic endothelial injury and repeated interactions between platelet-derived mitogens, plasma components, and the underlying arterial smooth muslce cells would promote the progression of the intimal proliferative lesions of atherosclerosis that lead to the clinical sequelae associated with this disease process.

Animals↗