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Biomedical subjects

C J Meade

Publications and source records attributed to C J Meade.

At least 37 records · Page 2Linked to original sources
PubMed1985

B lymphocyte receptors and polyphosphoinositide degradation.

Resting B lymphocytes can be activated and induced to proliferate by antibodies against their antigen receptors (anti-lg). We demonstrate an early increase in the level of [3H]inositol trisphosphate in [3H]inositol-labeled murine B cells, which suggests breakdown of phosphatidylinositol bisphosphate by phospholipase C. In line with this, the level of [3H]1,2-diacylglycerol was also elevated after incubation of [3H]arachidonic-acid-labeled B cells with anti-Ig. Anti-lg also caused a rapid increase in the level of cytosolic Ca2+ in B cells. In contrast, two other polyclonal B cell activators, lipopolysaccharide and phorbol myristate acetate, failed to induce any of these effects. Our results suggest that anti-lg may induce B cell growth via phosphoinositide degradation and Ca2+ mobilization, and that phorbol myristate acetate, and possibly lipopolysaccharide, bypass these initial events.

Animals↗
PubMed1984

gamma-Hexachlorocyclohexane stimulation of macrophage phospholipid hydrolysis and leukotriene production.

gamma-Hexachlorocyclohexane stimulates arachidonic acid release from macrophage phospholipids. It is also a powerful stimulator of leukotriene C4 production, yet (by comparison with zymosan) produces only a small effect on prostaglandin production. This suggests that synthesis of leukotrienes and prostaglandins can be independently regulated. The most likely mechanism of action of gamma-hexachlorocyclohexane is through its effect on phosphatidylinositol metabolism.

Animals↗
PubMed1984

One-dimensional thin-layer chromatographic separation of the lipids involved in arachidonic acid metabolism.

A one-dimensional thin-layer chromatographic separation technique is described that separates the phospholipids and neutral lipids that are principally involved in arachidonic acid metabolism from each other, and from arachidonic acid and its eicosanoid derivatives. The technique is useful in studies on changes in arachidonic acid metabolism following cell stimulation. Balance sheets may be drawn up between the loss of radioactivity from phospholipids, and the gain in free fatty acid, eicosanoids, and esterified lipids of the phosphatidylinositol cycle.

Animals↗
PubMed1983

The separation of leukotrienes and hydroxyeicosatetraenoic acid metabolites of arachidonic acid by high performance liquid chromatography (HPLC).

The following high performance liquid chromatography system was found suitable for separating most lipoxygenase metabolites of arachidonic acid: Techsphere 5-C18 column, eluting solvent methanol:water:acetic acid (65:35:0.06 v/v), pH 5.3. Comparisons with other packing materials and solvent systems are described. The method could be used to identify lipoxygenase products released from mouse macrophage cells stimulated with gamma-hexachlorocyclohexane. Detection limits between 1 and 10 ng were obtained.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1981

Obesity: can some fat cells enlarge while others are shrinking?

CBA mice were made obese by injection with gold thioglucose (GTG). After receiving transplants of "lean" and "GTG-obese" fat under separate kidney capsules, the host mice were fed a restricted diet for three weeks. Over this period, the fat cells in the lean grafts enlarged whereas the fat cells in the GTG-obese grafts shrank. Concurrent fat loss and fat gain can therefore take place.

Adipose Tissue↗
PubMed1981

The relationship between hyperglycaemia and renal immune complex deposition in mice with inherited diabetes.

Kidney lesions were studied by light microscopy and immunofluorescence in diabetic (db/db) and obese (ob/ob) mutant mice. The db/db mutation was studied both on the C57Bl/KsJ genetic background (where it produces severe hyperglycaemia) and on the C57Bl/6J background (where hyperglycaemia is only mild). In all cases, more IgG, IgM and C3 were deposited in the renal glomeruli of mutant mice than in the glomeruli of normal (+/?) mice of equivalent age. First signs of immunoglobulin deposition occurred at a slightly younger age than first signs of C3 deposition or histological change (mainly mesangial thickening). Insulin deposits were occasionally seen in the glomeruli of older mutant mice and immunoglobulin eluted from diabetic mouse kidneys had anti-insulin activity. Increased anti-DNA activity was present in the serum of older mutants. In those mutants with severe hyperglycaemia, the macula densa and distal convoluted tubules also contained immunoglobulin deposits, probably derived from the glomerular mesangium. Urine from diabetic mice contained high molecular weight material reacting with antisera to Fab or kappa but not the Fc portion of immunoglobulin. We conclude that diabetic mice have immune complexes in the kidney containing antibodies against insulin and possibly other antigens. We find no evidence that hyperglycaemia itself is the direct cause of glomerular immune complex deposition, although there may be a link between hyperglycaemia and tubular dysfunction.

Animals↗
PubMed1980

Site differences in fat cells of New Zealand obese mice--a transplantation study.

Fat cells from the gonadal fat pad of New Zealand obese mice are larger than those from the subcutaneous fat pad. When fat is transplanted to a third, common site (beneath the kidney capsule), this difference in size largely disappears, suggesting it is the location of the fat cells rather than of intrinsic differences between the cells that account for their different sizes.

Adipose Tissue↗
PubMed1979

Is genetically transmitted obesity due to an adipose tissue defect?

1. The aim of this investigation was to ascertain of a variety of obese rodents whether the primary cause of fat cell enlargement lay in the fat cell itself, or in its environment. Rodents studied were the mutant mice 'diabetic' (db/db), 'adipose' (dbad/dbad), and 'yellow obese' (Ay/+), New Zealand obese mice, CBA mice made obese with gold thioglucose, and obese BIO 4.24 hamsters. 2. Gonadal fat of obese or lean genotype was transplanted under the kidney capsule of an obese or lean host. Grafts were left in place for at least one month, then examined histologically to measure fat cell diameters, from which fat cell masses were calculated. 3. Immunological rejection of grafts was avoided either by using mice syngeneic except for the obesity producing mutation (db/db, dbad/dbad or Ay/+) or by transplanting into F1 hybrids (NZO X BALB/c) made by mating the strains acting as donors of obese or lean fat. Transplantation of fat between lean BIO 4.22 hamsters and obese BIO 4.24 hamsters was possible because these had common histocompatibility antigens. 4. In all the forms of murine obesity studied, 'lean' fat cells enlarged in an obese recipient to the size typical of cells in 'obese' fat whilst 'obese' fat cells shrunk in a lean recipient to, at least, the size typical of 'lean' fat. Lean hamster fat cells also enlarged in an 'obese' environment and 'obese' hamster cells shrunk in a 'lean' environment. 5. Environment therefore contributes to the determination of fat cell size in all the rodents studied, and in several rodents (db/db, dbad/dbad, Ay/+, and gold thioglucose obese mice) our results showed that environmental factors are of paramount importance in determining cell size, and factors associated with the fat cell itself make a negligible contribution.

Adipose Tissue↗
PubMed1979

Effects of the obese (ob/ob) genotype on spleen cell immune function.

Spleen cells from mice homozygous for the obese (ob) mutation killed DBA/2 mastocytoma target cells less well than spleen cells from lean littermates or unrelated age-and sex-matched controls of the same strain. Killing was impaired only when the attacker cells were primed in vivo, not following in vitro priming. Hence the effect of the ob/ob genotype is not to produce an irreversible functional change in the lymphocyte, but rather to produce an environment in which lymphocytes are less able to react to priming antigen. Not only were the spleen cells of in vivo primed obese mice less active than those of lean controls, but also their number per spleen was significantly decreased. Such a quantitive difference was no longer found in adrenalectomised animals, but the qualitative difference in spleen cell cytotoxic activity still occurred. This suggests that adrenocortical hyperfunction may affect immune function in obese mice, without necessarily being the only factor in the in vivo environment of obese mouse spleen cells capable of depressing cellular immune reactivity.

Adrenalectomy↗
PubMed1979

How arachidonic acid depresses thymus weight.

Subcutaneous injection of arachidonic acid depresses thymus weight. This is unlikely to be a stress effect, since arachidonic acid is equally active in adrenalectomised animals. Amongst other fatty acids tested, those capable of being metabolised to arachidonic acid have greater thymolytic activity than those which are not arachidonic acid precursors. Thymolysis is significantly inhibited by indomethacin, a drug which blocks the conversion of arachidonic acid to prostaglandins.

Adrenalectomy↗
PubMed1978

Obesity: do fat cells from genetically obese mice (C57BL/6J ob/ob) have an innate capacity for increased fat storage?

Fat tissue from the genetically obese mouse (C57BL/6J ob/ob) and its lean littermate (+/?) was transplanted into lean hosts(+/+). Chemical induced obesity in the host mice caused no greater increase in the size of 'obese' fat cells than it did in the size of 'lean' fat cells. 'Obese' fat cells, therefore, have no innate capacity for increased fat storage.

Adipose Tissue↗
PubMed1978

Reduction by linoleic acid of the severity of experimental allergic encephalomyelitis in the guinea pig.

This paper reports the effects of supplementation of the diet with linoleic acid on the severity of experimental allergic encephalomyelitis (EAE) in guinea pigs. Clinical signs of disease (e.g. paresis, paraplegia, urinary incontinence), weight loss, frequency of perivascular lesions in the central nervous system and ability of isolated lymph node cells to respond to myelin basic protein in vitro were all reduced by linoleic acid supplementation. Linoleic acid was effective when fed at a dose of 0.5 ml/day from 7 to 21 days after sensitization of the animals with basic protein, i.e., before and during the time in which clinical signs normally appeared. The same daily dose fed from 7 days before to 7 days after sensitization, i.e., ceasing about 7 days before the normal time of appearance of clinical signs, produced no significant effect. Feeding linoleic acid to normal guinea pigs significantly altered the fatty acid composition of their serum and lymph nodes, but not of their brain. Of several possible explantations for the protective effect of lineolic acid in EAE, we considered action by this essential fatty acid on the immune system most likely.

Animals↗