Hose-induced current enhancement associated with beam propagation.
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Biomedical subjects
Publications and source records attributed to G Joyce.
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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.
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.
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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.
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The absolute electrophoretic mobility of erythrocytes from MS patients is reduced in the presence of 0.08 mg/ml of linoleic or arachidonic acid, whilst that of normal or other neurological disease patients is increased in the presence of these acids. When an MS patient ingests gamma-linolenate (in capsule form equivalent to 413.4 mg of gamma-linolenic acid and 2.664 g of linoleic acid per day) the reaction of MS erythrocytes begins to change. After 3 or 4 months the reaction becomes normal with arachidonic acid (i.e. mobility is speeded up) and 2 months or so later this occurs also with linoleic acid. Very prolonged administration of gamma-linolenate leads to a markedly increased sensitivity to the effect of prostaglandins (PGE2) on RBC mobility. The observations are interpreted to mean the induction of a biochemical-biophysical change in the membranes, and the significance of this in the aetiology and treatment of multiple sclerosis is discussed.
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Erythrocytes from patients with Multiple Sclerosis (MS) show a highly significant reduction in their absolute electrophoretic mobility in the presence of linoleic and arachidonic acids (LA; AA). Patients with other (destructive) neurological disease (OND) and normal subjects show an increased absolute mobility of their erythrocytes in the presence of LA and AA. About 40 per cent of blood relatives of MS patients show an intermediate type of reaction - being slowed by LA and speeded up by AA. Administration of LA (or gamma linolenate) to an MS patient for some months leads to change in the mobilities from the MS to normal type, the AA result altering first. The effect of LA and AA on the absolute mobility of RBC may thus be used as a simple laboratory test involving a long established technique and eliminating the animal and other needs of the macrophage electrophoretic mobility (MEM) test. The implications of these findings for our understanding and handling of MS are briefly discussed.
This study has shown that while some liposomes are highly toxic to the central nervous system, others, of different composition, are tolerated well in the dosage used (0.02-0.05 ml = 4-12 mg of lipid/inoculum). Those composed of lecithin-cholesterol-dicetyl phosphate or lecithin-cholesterol-stearylamine produced generalised epileptic seizures and some deaths due to respiratory failure immediately after injection,and a subsequent widespread tissue necrosis. However liposomes composed of lecithin-cholesterol-phosphatidic acid, or dipalmitoyl lecithin only, produced minimal morphological changes and by the sixth day post-injection the pathology was limited to the mechanical trauma caused by the injection. It is concluded that liposomes of appropriate composition may be sufficiently benign to use as carriers of therapeutic agents into the CNS.
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Lymphocytes from patients with multiple sclerosis are much more susceptible to the inhibitory activity of linoleic acid (0.08 mg/ml) when tested for sensitization to thyroid by the macrophage electrophoretic mobility test (91% inhibition) than are those from normal subjects (57% inhibition). Cells from patients with a variety of other neurological diseases give 47% inhibition with linoleic acid. These differences are specific for multiple sclerosis and can be used as an in-vitro diagnostic test for the disease. Nearly 43% of clinically normal near relatives of patients with multiple sclerosis show an "anomalous" figure of about 77%; in the remainder the figure is the same as in the general population (57%). An anomalous result is compatible with lifelong freedom from M.S. Possibly a congenital anomalous handling of unsaturated fatty acids is a constant feature of the disease.
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