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Biomedical subjects

N McIntyre

Publications and source records attributed to N McIntyre.

At least 127 records · Page 7Linked to original sources
PubMed1979

Lecithin-cholesterol acyltransferase and the lipoprotein abnormalities of parenchymal liver disease.

1. Detailed studies have been made of the plasma lipoprotein abnormalities in parenchymal liver disease to test the hypothesis that the abnormalities would correlate with plasma lecithin-cholesterol acyltransferase (LCAT) activity. 2. When LCAT was high, very-low-density-lipoproteins (VLDL) were normal in composition and had a normal pre-beta electrophoretic mobility. When LCAT was low, VLDL concentrations were greatly reduced. 3. With high LCAT low-density lipoproteins (LDL) were normal. The LDL particles found with low LCAT activity were of normal size but of abnormal composition, being triglyceride rich and cholesteryl ester poor. Regardless of LCAT activity LDL were present in normal amounts. 4. High-density lipoproteins (HDL) were normal in composition and electron-microscopic appearance when LCAT activity was high. When LCAT activity was low HDL were abnormal in composition and 'stacked discs' were seen on electron microscopy. 5. These results suggest that low LCAT activity may be the cause of at least some of the lipoprotein changes of parenchymal liver disease.

Adult↗
PubMed1978

Erythrocyte lipid composition and sodium transport in human liver disease.

In patients with liver disease there are usually increases in erythrocyte cholesterol and phosphatidylcholine concentrations. This increase in membrane lipid changes the shape of the erythrocyte and "spur" or "target" cells may be present. Sodium fluxes were measured in erythrocytes from 17 patients with a variety of liver diseases and from 17 normal subjects and the values related to the lipid content of the membrane. Ouabain-insensitive and ouabain-sensitive effluxes were lower in patients than in normal subjects and the reduction in ouabain-insensitive efflux was more marked. Sodium influx was also significantly lower in erythrocytes from patients than controls. Ouabain-sensitive and ouabain-insensitive effluxes and sodium influx did not correlate with the cholesterol content of erythrocytes from patients. Significant negative correlations were noted between ouabain-insensitive sodium efflux (r=--0.63, P less than 0.01), sodium influx (r=--0.61, P less than 0.01) and intracellular sodium concentration (r=--0.66, P less than 0.01) and the cholesterol : phospholipid molar ratio of the cell but there was no significant correlation between this ratio and the ouabain-sensitive sodium efflux (r=0.41, P less than 0.05). These results support the hypothesis that an altered lipid composition may affect the permeability of the erythrocyte membrane in patients with liver disease.

Biological Transport↗
PubMed1978

Lecithin--cholesterol acyltransferase and the lipoprotein abnormalities of obstructive jaundice.

1. We have studied the plasma lipoprotein abnormalities in obstructive jaundice to test the hypothesis that the abnormalities would correlate with plasma lecithin--cholesterol acyltransferase activity. 2. Very-low-density lipoproteins (VLDL) were normal in composition and had a normal pre-beta electrophoretic mobility when lecithin--cholesterol acyltransferase activity was high. When it was low VLDL had abnormal composition and ran in the beta position. 3. With high lecithin--cholesterol acyltransferase activity, low-density lipoprotein (LDL) was normal and cholestatic LDL (LP-X) was not found. With low lecithin--cholesterol acyltransferase activity up to three LDL fractions were found: (i) large triglyceride-rich particles, (ii) LP-X and (iii) a triglyceride-rich cholesteryl ester-poor particle of normal dimensions. 4. High-density lipoprotein (HDL) concentrations correlated with lecithin--cholesterol acyltransferase activity and HDL were normal in composition and electron-microscopic appearance when the activity was high. When lecithin--cholesterol acyltransferase activity was low HDL was abnormal in composition and 'stacked discs' were seen on electron microscopy as well as normal spherical particles. 5. These results suggest that low lecithin-cholesterol acyltransferase activity may cause at least some of the lipoprotein changes of obstructive jaundice.

Adult↗
PubMed1978

The quality and educational value of medical records--a survey of student opinion.

In July 1975 clinical students at the Royal Free Hospital School of Medicine were asked to complete a questionnaire, including questions on medical records. Full and accurate recording of clinical information was considered an important characteristic of the good physician, but less important for success as a medical student. Students felt they should be given more instruction on the writing of medical records and that teachers should pay more attention to students' notes. Review of students' notes is a valuable method of teaching clinical medicine; teachers can ensure that patients are the focus of learning and can encourage students to simulate real clinical practice.

Attitude of Health Personnel↗
PubMed1978

Plasma lipids and lipoproteins in liver disease.

There are many changes in the plasma, lipids, and lipoproteins in patients with liver disease. They have proved difficult to study but our understanding of these changes has increased greatly during recent years. In obstructive jaundice hyperlipidaemia is a fairly constant finding and this appears to be due to the regurgitation of phospholipid from the obstructed biliary tree. The plasma lipids tend to fall with parenchymal liver disease. The composition of the lipoproteins depends on the activity of the plasma enzyme lecithin: cholesterol acyl transferase. When LCAT activity is high the individual lipoprotein fractions are normal. When it is reduced all of the lipoprotein fractions are affected but the pattern found with obstruction is quite different from that found with parenchymal disease. The changes in plasma lipoproteins appear to be associated with change in the lipid composition of cellular membranes and this may have important functional implications.

Cholestasis↗
PubMed1977

Signals for insulin secretion.

Glucose is an effective stimulus for the release of insulin from pancreatic beta-cells but its pre-eminence for the physiological control of insulin secretion is now challenged. The insulin response to oral glucose is much greater than the response to intravenous glucose because an intestinal factor, or factors, has a powerful stimulant effect on insulin secretion. Conversely, the hyperglycaemia which accompanies sympathetic overactivity is accompanied by reduced plasma insulin levels because adrenaline inhibits pancreatic insulin by an alpha-adrenergic mechanism. Other hormonal and chemical factors also modify pancreatic insulin release. Plasma insulin levels will be determined not only by the interplay of signals which stimulate or inhibit insulin release but also by the rate at which insulin leaves the circulation. Because insulin is secreted into the portal circulation the concentration of insulin to which hepatocytes are exposed is normally greater than that affecting peripheral tissues. This ratio will be affected by portal venous diversion and might be altered by hepatic damage. Both factors might also influence the intestinal control of insulin secretion, as the gut 'hormone' would not have to traverse the liver, which might remove some of it, before it arrived at the pancreatic islets. If insulin is the key 'hepatotrophic factor' stimulating hepatic growth and regeneration, as well as preventing atrophy, we might expect it to induce hepatic growth in otherwise normal liver and we would expect it to be secreted in larger amounts when regeneration is active.

Acetylcholine↗