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Biomedical subjects

J Seager

Publications and source records attributed to J Seager.

At least 19 recordsLinked to original sources
PubMed1995

Comparison of bupivacaine plus buprenorphine with bupivacaine alone by caudal blockade for post-operative pain relief after hip and knee arthroplasty.

In a double-blind, parallel group trial, 15 patients who were given a caudal injection of 1.8 mg kg-1 of bupivacaine after induction of anaesthesia, were compared with 15 patients in whom 7.2 mg kg-1 of buprenorphine was added to the same dose of bupivacaine, prior to knee or hip replacement surgery. The duration of analgesia was much longer (mean 606 min vs. 126 min P < 0.001) in those receiving added buprenorphine; mean morphine consumption in the first 24 h was halved (14 mg vs. 28 mg) and patient satisfaction greatly increased. There were no significant differences in the incidence of complications although the group which had added buprenorphine had a lower incidence of vomiting.

Aged↗
PubMed1987

Women and reproductive technologies: a partially annotated bibliography.

This bibliography is a resource for further information about Women and Reproductive Technologies. The references are categorized as General Information, Law and Policy Considerations, and Information about Specific Technologies. It also lists periodicals, organizations, and other bibliographies relating to this subject and is current through March 1986.

Bibliographies as Topic↗
PubMed1985

Bacterial endotoxin selectively prevents the expression of scavenger-receptor activity on human monocyte-macrophages.

Concentrations of bacterial lipopolysaccharide (LPS) as low as 1 ng/ml suppressed the activity of the scavenger receptor on cultured human monocyte-macrophages. In contrast, concentrations of LPS as high as 100 ng/ml had no effect on the activity of the low density lipoprotein (LDL) receptor. LPS and purified forms of the lipid A moiety of LPS were effective in suppressing scavenger receptor activity. However, acid hydrolysis of the labile phosphate group of the native diphosphorylated lipid A to form monophosphoryl lipid A rendered the molecule ineffective in suppressing scavenger receptor activity. LPS at a concentration of 100 ng/ml had no effect on the secretion of apolipoprotein E, phagocytic activity, tumoricidal activity, or the protein content of monocyte-macrophages. We conclude that the active component of LPS that mediates suppression of scavenger receptor activity is diphosphoryl lipid A.

Apolipoproteins E↗
PubMed1984

IgA deficiency during treatment of infantile hypothyroidism with thyroxine.

Serum IgA concentrations in five children with infantile hypothyroidism fell soon after the start of treatment with thyroxine. In one child the IgA concentration fell appreciably (to less than 0.01 g/1) and remained reduced; in the four others it returned to normal. IgM and IgG concentrations were roughly normal throughout. The deficiency in IgA concentrations may have been due to stimulation by thyroxine treatment of a T cell suppressor system that, in the original hypothyroid state, was less than normally active.

Child, Preschool↗
PubMed1983

Lymphokines secreted by an established lymphocyte line modulate receptor-mediated endocytosis in macrophages derived from human monocytes.

As little as 1 microliter of serum-free supernatant from Mo(t), an established lymphocyte line, when added to a 500-microliters incubation of macrophages derived from human monocytes, significantly decreased the receptor-mediated uptake and degradation of three cholesterol-rich molecules: low density lipoprotein (LDL); LDL complexed to dextran sulfate; and LDL modified by malondialdehyde (MDA-LDL). In contrast, the receptor-mediated uptake and degradation of mannosyl bovine serum albumin was increased three-fold. The Mo(t) supernatant did not contain competitive inhibitors of the cholesterol-rich ligands, and it did not alter macrophage receptor-independent endocytosis, protein synthesis, or phagocytosis of heat-killed yeast. The effect of the Mo(t) supernatant was specific for macrophages and was abolished by preincubation of the supernatant with trypsin, which indicates that the active substances are protein in nature. The decrease in the uptake and degradation of MDA-LDL induced by preincubating the macrophages with Mo(t) supernatant appeared to result from a decrease in the number of receptors for this ligand at the cell surface. The isolation of these lymphokines should offer new insights into macrophage receptor-mediated endocytosis, and may yield substances useful in preventing foam cell formation in atherosclerosis.

Cell Differentiation↗
PubMed1982

Lymphocyte-conditioned medium protects human monocyte-macrophages from cholesteryl ester accumulation.

Exposure of human monocyte-macrophages to as little as 50 microliters of cultured medium from lymphocytes stimulated by concanavalin A (Con A) resulted in a dramatic decrease in the activities of the low density lipoprotein (LDL) receptor pathway, the LDL-dextran sulfate pathway, and the scavenger receptor pathway. This effect was not seen when the monocyte-macrophages were exposed to culture medium from lymphocytes cultured without Con A or with Con A together with alpha-methyl mannoside or control medium without lymphocytes. The activity of 3-hydroxy-3-methyglutaryl-coenzyme A reductase also decreased in monocyte-macrophages exposed to culture medium from stimulated lymphocytes. Acyl-CoA:cholesterol O-acyltransferase activity, protein synthesis, protein content, phagocytosis of heat-killed yeast, and non-receptor-mediated endocytosis were not inhibited. Monocyte-macrophages exposed to malondialdehyde altered-LDL in the presence of stimulated lymphocyte culture medium accumulated substantially less cholesteryl esters than did cells in control medium. We propose that substances produced by stimulated lymphocytes may be useful in protecting macrophages from cholesteryl ester accumulation.

Cells, Cultured↗
PubMed1981

The metabolism of native and malondialdehyde-altered low density lipoproteins by human monocyte-macrophages.

We have recently shown that cultured human monocyte-macrophages degraded 125I-labeled low density lipoprotein (125I-nativeee-LDL) by a saturable high-affinity process with maximal velocity at 25-30 microgram protein/ml (Fogelman et al., 1980, Proc. Nat. Acad. Sci. USA. 77:2214-2218). We now describe studies of the binding of 125I-native-LDL at 4 degrees C and the effects of chloroquine, Ca2+ concentration, and reductive methylation on high-affinity 125I-native-LDL degradation that indicate that native-LDL is processed by the monocyte-macrophages via the classic LDL receptor pathway. The high-affinity degradation of 125I-native-LDL increased substantially when monocyte-macrophages were exposed to the lipoprotein deficient-fraction of serum (LPDS) for periods as brief as 4 hours, and was 25-fold greater than that of lymphocytes. Freshly isolated monocytes that had never been exposed to LPDS also demonstrated high-affinity degradation of 125I-nativ-LDL. When these monocytes were cultured for 7 days in a medium containing native-LDL at a concentration (186 microgram protein/ml) greatly in excess of that apparently needed to saturate the high-affinity process, there was more than a 10-fold increase in 125I-native-LDL high-affinity degradation. LDL modified by treatment with malondialdehyde was processed by a second high-affinity cell surface receptor that appears identical to the "scavenger" receptor that processes acetylated LDL (Goldstein, et al., 1979, Proc. Nat. Acad. Sci. USA. 76: 333-337).

Cells, Cultured↗
PubMed1981

Factors regulating the activities of the low density lipoprotein receptor and the scavenger receptor on human monocyte-macrophages.

Improved techniques of cell isolation resulted in 90 to 100 million monocytes from a single donor. Addition of low density lipoprotein (LDL) to to cultures of these cells resulted in the down regulation of LDL receptor activity. Addition of malondialdehyde-altered LDL. which enters the cell through a receptor for negatively charged proteins (the scavenger receptor), produced an even greater down regulation of the LDL receptor, indicating that both receptors are present on the same cell. Within hours of adherence of the cells, there was a dramatic decrease in the activity of both receptors. LDL receptor activity was highest during the first week in culture and then declined, despite the maintenance of a constant LDL concentration in the medium. Scavenger receptor activity surpassed LDL receptor activity by the 6th day and was maximally expressed during the second week. Increasing cell density resulted in a slight increase in the activity of the LDL receptor and a dramatic increase in scavenger receptor activity. Insulin had no significant effect on either receptor. Removing serum from the culture medium for 48 hr resulted in a 3.5-fold increase in LDL receptor activity and a 2-fold decrease in scavenger receptor activity. Twenty-four hr after the cells were re-exposed to serum, the activities of both receptors essentially returned to base line. Heat-inactivation of serum was associated with an increased cholesteryl ester content of the cells and depressed receptor activities. Scavenger receptor activity appears related to the maturation of monocytes into macrophages and is promoted by increasing cell density and serum factors that are heat labile.

Cell Membrane↗
PubMed1980

Malondialdehyde alteration of low density lipoproteins leads to cholesteryl ester accumulation in human monocyte-macrophages.

Glutaraldehyde treatment of (125)I-labeled low density lipoprotein ((125)I-native-LDL) produced a modified LDL ((125)I-glut-LDL) with a molecular weight of 10 x 10(6) or more. Malondialdehyde treatment of (125)I-native-LDL produced a product ((125)I-MDA-LDL) with a molecular weight not appreciably different from that of the original lipoprotein. However, the electrophoretic mobility of MDA-LDL indicated a more negative charge than native-LDL. (125)I-MDA-LDL was degraded by two processes: a high-affinity saturable process with maximal velocity at 10-15 mug of protein per ml and a slower, nonsaturable process. The degradation of (125)I-MDA-LDL was readily inhibited by increasing concentrations of nonradioactive MDA-LDL but was not inhibited by acetylated LDL or native-LDL even at concentrations as high as 1600 mug of protein per ml. After exposure of native-LDL to blood platelet aggregation and release in vitro, 1.73 +/- 0.19 nmol of malondialdehyde per mg of LDL protein was bound to the platelet-modified-LDL. No detectable malondialdehyde was recovered from native-LDL that had been treated identically except that the platelets were omitted from the reaction mixture. After incubation with glut-LDL, MDA-LDL, or platelet-modified-LDL for 3 days, human monocyte-macrophages showed a dramatic increase in cholesteryl ester content whereas the cholesteryl ester content of cells incubated with the same concentration of native-LDL did not. Based on these experiments we propose that modification of native-LDL may be a prerequisite to the accumulation of cholesteryl esters within the cells of the atherosclerotic reaction. We further hypothesize that one modification of LDL in vivo may result from malondialdehyde which is released from blood platelets or is produced by lipid peroxidation at the site of arterial injury.

Arteriosclerosis↗
PubMed1979

Separation of and cholesterol synthesis by human lymphocytes and monocytes.

We have devised techniques for the isolation of human monocytes which do not require the adherence of the cells to a surface. In 15 consecutive experiments using density-gradient and counterflow centrifugations, a population of mononuclear cells that was 75 +/- 11% monocytes was obtained within 2 hours of venipuncture. These cells had never been pelleted and represented approximately three-fourths of the monocytes that had been present in the whole blood. In another 22 consecutive experiments using sedimentation in gelatin followed by counterflow and density-gradient centrifugations, a population of lymphocytes that was 99.5 +/- 0.5% pure and a population of monocytes that was 94 +/- 3% pure were obtained within 3 hours of venipuncture. When these freshly isolated cells were incubated in the lipoprotein-deficient fraction of serum (d > 1.21 g/ml) or in solvent-extracted serum, the monocytes incorporated 10-20 times more [2-(14)C]acetate into sterols than did the lymphocytes. Monocytes were seen to constitute between 6 and 46% of the mononuclear cells isolated from normal individuals by the usual density-gradient centrifugation of whole blood on Ficoll-Hypaque. We conclude that future studies of cholesterol metabolism utilizing human mononuclear cells must take into account this large variation in the percentage of monocytes and their disproportionately greater activity during short-term incubations in media that induce sterol synthesis.-Fogelman, A. M., J. Seager, M. Hokom, and P. A. Edwards. Separation of and cholesterol synthesis by human lymphocytes and monocytes.

Adult↗
PubMed1977

Haemopexin, caeruloplasmin and C3: effect of diphenylhydantion.

Serum haemopexin and C3 concentrations fell and serum caeruloplasmin rose in 14 epileptic children studied prospectively during treatment with diphenylhydantoin. There was a positive correlation between the changes in haemopexin concentration and those of C3.

Adolescent↗