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Biomedical subjects

J A Hamilton

Publications and source records attributed to J A Hamilton.

At least 325 records · Page 18Linked to original sources
PubMed1980

Lipoprotein-X: carbon-13 nuclear magnetic resonance studies on native, reconstituted, and model systems.

Lipoprotein-X (LP-X), a lipoprotein isolated from human cholestatic plasma by ethanol--acetate precipitation and zonal ultracentrifugation, has been studied by 13C NMR at 67.9 MHz. Spectra of LP-X and its three subfractions are markedly different from those of normal human high-density lipoprotein3 (HDL3) or low-density lipoprotein (LDL). Spectra of LP-X are characterized by the presence of unusually broad resonance lines, especially those attributable to C6 of unesterified cholesterol (160--260 Hz) and to C beta of phospholipid glyceride (240--290 Hz). In contrast, the CH2O, CH2N, and N(CH3)3 choline resonances have line widths comparable to those of normal LDL and HDL3. For the subfraction LP-X1, spin--lattice relaxation times (T1) of the fatty acyl olefin resonances at 129.8 and 128.0 ppm and of the unesterified cholesterol C6 at 120.1 ppm were measured to be 675, 766, and 162 ms, respectively. These times are comparable to those measured for the corresponding resonances in single bilayer vesicles whose lipid composition approximates that of LP-X. The three LP-X subfractions isolated by zonal ultracentrifugation gave spectra which are identical, within experimental error, as judged qualitatively from their appearance and quantitatively from the line widths of selected resonances. In addition, 13C NMR spectra of sonicated total LP-X lipids are similar to spectra of the intact native lipoprotein. This study suggests (a) that motions of lipids in LP-X as probed by 13C NMR are similar to the motions of lipids found in model vesicular systems, (b) that the motions of the cholesterol rings and phospholipid fatty acyl chains are significantly more restricted in LP-X than in HDL3 and LDL, and (c) that the motions of the phosphoryl moieties in all three systems are similar.

Centrifugation, Zonal↗
PubMed1980

Tumor-promoting phorbol esters stimulate hematopoietic colony formation in vitro.

Tumor-promoting phorbol esters stimulated mouse bone marrow cells to form myeloid colonies in agar cultures without added colony-stimulating factors. The colony-stimulating ability of various phorbol esters correlated well with their ability to promote skin tumors in vivo. These results suggest that phorbol esters mimic the action of specific colony-stimulating factors that regulate growth.

Animals↗
PubMed1980

Stimulation of macrophage plasminogen activator activity by colony-stimulating factors.

Colony-stimulating factors (CSFs) stimulate granulocyte-macrophage praoduction from single hemopoietic progenitor cells. Various preparations of purified CSFs of two different subclasses have been shown here to stimulate a plasminogen-dependent fibrinolytic (plasminogen activator) activity from resident and starch-induced mouse peritoneal macrophages. Lymphocyte supernatants also stimulate macrophage plasminogen activator (PA) activity. Since they contain colony stimulating activity, it is possible that one or more subclasses of CSF in these supernatants is responsible for this effect. Since both colony-stimulating and macrophage growth activities have been detected at inflammatory sites, these findings could reflect a role for CSF in inflammatory processes.

Animals↗
PubMed1980

Regulation of the plasminogen activator activity of macrophage tumor cell lines.

Four murine monocyte-macrophage cell lines, WEHI-3, J774, RAW 264.10 and PU5-1.8, synthesize and secrete the proteolytic enzyme, plasminogen activator. Lymphocyte conditioned medium, 12-0-tetradecanoyl-phorbol-13-acetate and Concanavalin A enhance the enzyme activity of these lines, while low concentrations of anti-inflammatory glucocorticoids and also cholera toxin reduce the enzyme activity. These observations are similar to those found for mouse peritoneal exudate macrophages. It is suggested, therefore, that these cell lines might be useful models to delineate the cellular mechanisms involved in the control of the synthesis and secretion of macrophage plasminogen activator and of other macrophage secretory products, particularly those resulting from lymphocyte-macrophage interaction.

Animals↗
PubMed1980

Macrophage stimulation and the inflammatory response to asbestos.

Chrysotile fibers injected into the peritoneal cavity of mice elicit a cellular exudate. Macrophages appearing in this exudate produce high levels of the neutral protease, plasminogen activator, when compared with the resident peritoneal macrophage population. In contrast, the levels of lysozyme and two lysosomal enzymes are the same for the two macrophage types. The asbestos-induced macrophages producing the plasminogen activator appear to have descended from recently divided precursors. Low concentrations of anti-inflammatory glucocorticoids inhibit macrophage plasminogen activator synthesis. Preliminary experiments indicate that different asbestos types induce hyperemia in skin, and also shorten the partial thromboplastin time of plasma and generate the release of kinins. These observations could be interrelated and are suggested as representing some aspects of the inflammatory response of the host to asbestos exposure.

Acetylglucosaminidase↗
PubMed1980

Stimulation of macrophage prostaglandin and neutral protease production by phorbol esters as a model for the induction of vascular changes associated with tumor promotion.

A series of phorbol esters stimulates prostaglandin E production from both resident and starch-induced mouse peritoneal macrophages. The relative potencies of these compounds parallel their abilities both to elevate macrophage plasminogen activator levels and to function as tumor promoters in a mouse skin carcinogenesis model. Low concentrations of antiinflammatory glucocorticoids, such as dexamethasone, inhibit the enhanced prostaglandin E synthesis as a result of 12-O-tetradecanoylphorbol-13-acetate action. The same glucocorticoids also inhibit the enhanced plasminogen activator production. On the basis of these observations, it is suggested that there might be a relationship between macrophage phospholipase activation and plasminogen activator synthesis. It is also suggested that these data might be providing insight into how 12-O-tetradecanoylphorbol-13-acetate and certain structural analogs elicit an inflammatory response and behave as tumor promoters in mouse skin.

Animals↗
PubMed1976

High-field 13C NMR Studies of certain normal and abnormal human plasma lipoproteins.

High-field (63.4 kilogauss) Fourier transform nuclear magnetic resonance spectroscopy 13C in natural abundance has been used to study the structural organization and molecular dynamics of constituent lipids of normal human very low-density lipoproteins (VLDL) and low-density lipoproteins (LDL). The same method was used to study the abnormal beta-VLDL of two type III hyperlipoproteinemia patients having markedly differing ratios of VLDL cholesterol to triglyceride (0.3 and 0.6, respectively). Resolution obtained at 63.4 kilogauss has made possible the assignment of several additional resonances of cholesterol ring carbon atoms, not resolved in earlier studies at lower fields, in the VLDL spectra. The rotational reorientation of the ring portion of cholesteryl esters in VLDL (normal) and beta-VLDL (abnormal) is not highly anisotropic and is similar to that for cholesteryl esters disolved in excess triolein. The rotations of cholesteryl esters in LDL are more highly anisotropic and significantly more restricted. The results suggest that the structural organization of the lipid components in beta-VLDL resembles that found in normal VLDL but differs significantly from that for normal LDL.

Cholesterol↗