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W McConathy

Publications and source records attributed to W McConathy.

5 recordsLinked to original sources
PubMed2000

Apolipoprotein D in the aging brain and in Alzheimer's dementia.

Apolipoprotein D (apoD) levels were examined in the temporal cortex as well as an assessment of the location of apoD positive cells within the brain by immunohistochemical and biochemical methods in young control (YC), aged control (AC), and Alzheimer's demented (AD) probands. Scattered apoD positive astrocytes and oligodendrocytes were found throughout the white matter by immunohistochemistry. ApoD immunoreactivity was also observed in the cerebellar oligodendrocytes of the YC group. There was faint positive apoD staining in scattered cortical astrocytes and a few neurons in the same group. In contrast, some of the AC and all of the AD probands had intense and frequent apoD immunostained cortical astrocytes and pyramidal neurons. The cortical senile plaques and neurofibrillary tangles were apoD immunonegative. No quantitative differences were found between the cortical apoD levels in the AC and AD groups, determined by immunoblotting. ApoD detected in the brain tissue was different in molecular weight (29 kDal) from that seen in CSF or in the serum (32 kDal). Our results indicate apoD is present in the human brain, especially in glial cells, and has increased abundance in the elderly and AD subjects.

Adult↗
PubMed1993

Effect of gemfibrozil on fatty acids in lipid fractions of plasma from patients with hypertriglyceridemia.

The fatty acid composition of plasma triglycerides, phospholipids, and cholesterol esters have been studied during gemfibrozil (G)-induced lipid-lowering treatment in six patients with hypertriglyceridemia. Gemfibrozil caused significant plasma triglyceride reductions from 776 +/- 573 to 226 +/- 82 mg/dL (P < .001). Gemfibrozil therapy also caused significant changes in the plasma lipid fatty acid composition, mainly by increasing palmitoleic acid (16:1) in triglycerides (2.1-5.6%) and cholesterol esters (2.2-3.7%), concomitant with the significant decrease in the content of the linoleic acid (18:2) in phospholipids (20.1-16.0%) and triglycerides (18.0-15.2%). The ratio of unsaturated fatty acids (20:3 + 20:4/18:2) was increased in the phospholipid fraction. These findings support a G effect on the desaturation of fatty acids in patients with hypertriglyceridemia. Because fatty acid composition was significantly altered by G, those biologic systems dependent on the pattern of fatty acids may be modified in clinical important ways.

Fatty Acids↗
PubMed1988

Plasma lipoprotein abnormalities in heterozygotes for familial lecithin:cholesterol acyltransferase deficiency.

Measurement of plasma lecithin:cholesterol acyltransferase (LCAT) activity was used to segregate unaffected family members (n = 8) from heterozygotes (n = 8) and homozygotes (n = 2) in a large LCAT-deficient kindred. The activity was absent in the homozygotes and was decreased to 50% of normal in the heterozygotes. Endogenous cholesterol esterification rate measurements did not differentiate the heterozygotes from the unaffected family members or normal subjects. The heterozygotes had significantly higher fasting plasma triglycerides, apo B, and lower HDL-cholesterol and apo AI than the unaffected family members. The HDL of the heterozygotes had the same mass of free cholesterol and triglyceride, but the mass of cholesteryl ester was reduced by 47%. The differences were not related to abnormal postheparin lipolytic activities. However, cholesteryl ester transfer activity in the lipoprotein-free (d greater than 1.21 bottom) fraction of plasma was significantly (P less than .05) decreased in the heterozygotes when compared to unaffected members. We conclude that the low LCAT activity is the likely cause of the qualitative and quantitative differences in the plasma lipoproteins of the heterozygotes in this family with LCAT deficiency. However, the low HDL and apo A-I levels are not associated with either a family or personal history of premature atherosclerosis.

Adult↗
PubMedDate not supplied

Effect of probucol therapy on plasma fatty acid composition during postprandial lipemia in hypertriglyceridemia.

OBJECTIVE: To determine the effect of probucol (PR) on fatty acid composition of plasma lipids in patients with hypertriglyceridemia during the fasting and postprandial states. DESIGN: Open-label, single-center, 6-week treatment, baseline-controlled trial. SETTING: Outpatient clinical research center. PATIENTS: Six patients with established hypertriglyceridemia and no complicating medical conditions. INTERVENTION: Step 1 American Heart Association diet and no lipid-lowering medications for at least 4 weeks. Lead to a baseline standarized meal ingestion with postprandial blood samplings. After 6 weeks of treatment with 500-mg of PR twice daily and diet, the meal tests were repeated. MEASUREMENTS: The clinical status, 3-day food records, postprandial blood samplings (0, 2, 4, 6, and 8 hours) for lipid and fatty acids in whole plasma, triglyceride (TG), phospholipid (PL), and cholesteryl ester (CE) fractions. RESULTS: PR had the following effects: (1) In plasma, cholesterol, high-density lipoprotein cholesterol, apolipoprotein (Apo) A1, and ApoB were decreased postprandially. ApoC111 ratio (heparin-treated plasma versus precipitate) was decreased in the fasting state. (2) The saturated/unsaturated (S/U) fatty acid ratios in the PL, TG, and CE fractions were elevated postprandially and increased in CE in the fasting state. In the PL fraction it was due to an increase in the percentage of myristic, palmitic, stearic, and oleic acids and a decrease in linolenic, eicosatrienoic, and arachidonic acids. In the TG and CE fractions the changes were not due to any particular patterns of fatty acids. The ratio of arachidonic/eicosatrienoic acid was decreased postprandially in PL and CE fractions. The ratio of eicosatrienoic/linoleic acid was decreased in PL and increased in CE fractions. (3) The S/U ratio in the lipoprotein (Lp) B and LP(a) lipid components decreased in PL and CE. Lp(a) was more saturated with respect to fatty acids than LpB. CONCLUSION: PR treatment for 6 weeks increased postprandial S/U fatty acid ratios. This was due to a combination of an increase in saturated and monounsaturated levels and a decrease in polyunsaturated levels. The effect was most notable in the PL fraction. In those systems dependent on the pattern of fatty acids, the fatty acid compositional change could modify biological responses in clinically important ways during lipid-lowering therapy. The change toward saturation of fatty acids in the postprandial state may contribute to the antioxidant properties of probucol.

Anticholesteremic Agents↗