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E J Field

Publications and source records attributed to E J Field.

At least 19 recordsLinked to original sources
PubMed1997

Inhibition of apolipoprotein B secretion by IL-6 is mediated by EGF or an EGF-like molecule in CaCo-2 cells.

Small intestinal mucosal inflammation observed in celiac disease is associated with the local release of growth factors and various cytokines. In a previous study, we investigated the effect of various cytokines on triacylglycerol and apoB secretion by CaCo-2 cells and observed that TNF-alpha, IL-1 beta, and particularly IL-6, decreased apolipoprotein (apo) B and triacylglycerol secretion. In this study, we explored possible mechanisms to explain the inhibitory effect of IL-6 on apoB secretion. IL-6, 10 ng/mL, added to the basolateral medium of CaCo-2 cells grown on semi-permeable filters, decreased apoB secretion by 42%. Adding a blocking monoclonal antibody (mAb 528) to the EGF receptor completely prevented this effect. IL-6 decreased the amount of EGF receptor protein and the binding of iodinated EGF to its receptor by 50% and 30%, respectively. Incubation of cells with various ligands to the EGF receptor, such as EGF, TGF-alpha, HB-EGF, and amphiregulin, also decreased apoB secretion. Inhibition of apoB secretion by EGF was prevented by the mAb 528 or an EGF neutralizing antibody. In a dose-dependent manner, the neutralizing antibody to EGF prevented the decrease in secretion of apoB, triacylglycerol mass, and cell-surface binding of labeled EGF caused by IL-6. Similar to the effects of IL-6, EGF decreased the secretion of triacylglycerol mass and the synthesis and secretion on newly synthesized apoB. The results suggest that, in CaCo-2 cells, IL-6 causes the release of EGF or an EGF-like molecule. By binding to cell surface EGF receptors, the molecule then causes a decrease in triacylglycerol and apoB secretion.

Antibodies, Monoclonal↗
PubMed1990

Darwin's illness.

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Encephalomyelitis↗
PubMed1987

Duchenne muscular dystrophy: do both parents contribute genetically to the disease?

By observing the effect of 0.08 and 0.02 mg/ml linoleic acid (LA on the electrophoretic mobility of fresh red blood cells derived from the parents of a subject with DMD, it has been shown that all of 16 fathers as well as 15 mothers, consistently differ from normal. In normal subjects, whilst 0.08 mg/ml LA causes increased mobility, 0.02 mg/ml causes reduced mobility (P less than 0.001). In both parents this reversal is abolished and 0.02 mg/ml LA gives the same increased electrophoretic mobility of the RBC as does 0.08 mg/ml. This indicates that there is qualitative alteration of the RBC membrane in both, apparently genetically determined. Only when such an abnormal male mates with an abnormal female can DMD occur in a male offspring; other children appear either normal or showing the same abnormality as do the parents, thus continuing the production of DMD parents, the chance mating of whom produces further DMD. The evidence supports the hypothesis that in DMD there is a widespread membrane disturbance. Other relatives have also been explored. It would appear that the common DMD of children is of autosomal recessive origin with strong limitation to the male.

Adolescent↗
PubMed1986

Use of plasma for immediate diagnosis of multiple sclerosis (plasma-erythrocyte unsaturated fatty acid test): comparison with the erythrocyte-unsaturated fatty acid (E-UFA) test.

A labile factor in plasma (but not serum) of MS subjects confers MS like properties vis à vis effect of linoleic acid (LA) and arachidonic acid (AA), on the electrophoretic mobility of washed red blood cells (RBC) irrespective of their provenance. Plasma from anomalous MS relatives and other neurological diseases (OND) likewise confer corresponding properties on washed RBC. The magnitude of results produced by LA and AA on plasma coated cells is equal to that produced by LA and AA directly on the original cells and approximately twice that reported with latex particles.

Arachidonic Acid↗
PubMed1983

Multiple sclerosis: effect of gamma linolenate administration upon membranes and the need for extended clinical trials of unsaturated fatty acids.

Electrophoretic mobility studies of red blood cells from subjects with multiple sclerosis indicate that treatment with unsaturated fatty acids must continue for at least 2 years before normal reactivity is restored by currently available tests. If this applies to myelin also, then clinical trials aimed at treating the recognized multiple sclerosis subject by polyunsaturated fatty acids really begin after 2 years, and this should be recognized when a trial program is drawn up.

Adolescent↗
PubMed1981

Simplified E-UFA test for multiple sclerosis (MS): some sources of "false" results.

A simple modification of the Erythrocyte-Unsaturated Fatty Acid (E-UFA) Test for Multiple Sclerosis is described, whereby well washed erythrocytes (RBC) are allowed to stand in Hanks medium 199, for about 21 days at 4 degrees C. The control-experimental difference in electrophoretic mobility of RBC rises to nearly 20%. Precautions in interpretation and wider implications of the SE-UFA test, recently uncovered, are briefly indicated.

Adrenocorticotropic Hormone↗
PubMed1980

Further observations with the erythrocyte-unsaturated fatty acid test. A contribution to the genetics of multiple sclerosis.

The absolute electrophoretic mobility of RBC of near relatives of multiple sclerosis (MS) patients has been studied in the presence of 0.08 mg/ml linoleic (LA) or arachidonic acid (AA). 42.9% of near relatives show anomalous results (slow with LA, fast with AA), chiefly females, and mothers always. The effect of LA is greater in clinical MS than in 'anomalous' relatives. Silent MS is recorded in 1 in 45 of near relatives, so that the 'disease' is much more common than the usual 5--20 times described in clinical surveys but corresponds with clinical occurrence in the Orkney Islands. Children (below the age of 14 years) with MS have been picked out with the same frequency as in adults. The sibship position of anomalous relatives has been studied where possible.

Adolescent↗