Antagonism by deanol of some behavioral effects of hemicholinium.
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Biomedical subjects
Publications and source records attributed to M Roch.
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The significance of these synapses is considered as part of a dynamic pattern of relations between neurons and neuroglia: transmission of a rapid message leading to an adjustment of the oligodendroglial cells to the functional changes of the neurons of which they are satellites.
The numerous synapses in the normal human brain cortex display various aspects. The authors have also observed some electronic type synapses which are more numerous around the pericaryons. The cortical synapses are classed according to their synaptic vesicle richness : synapses with very few vesicles, synapses very rich in vesicles and synapses with a middling vesicular density. With the help of observations on these aspects and on variations of the synaptic cleft and that of the postsynaptic density, the authors advance an hypothesis on synaptic plasticity, the synaptic structures going from a simple intercellular contact (probably non functional) to a completly formed synapse and vice versa.
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BACKGROUND: Previous studies have shown that plasma and urinary free choline concentrations decrease significantly during a marathon, and that these decreases may be associated with decreased performance. OBJECTIVE: In a pilot study, we sought to determine whether lecithin supplementation prior to a marathon would maintain plasma free and urinary choline concentrations and improve performance versus placebo. METHODS: 12 accomplished marathon runners, males (7) and females (5), 21 to 50 years of age were randomized to receive lecithin (4 capsules BID; PhosChol 900) or placebo beginning one day prior to the 2000 Houston-Methodist Health Care Marathon. The lecithin supplement provided approximately 1.1 g of choline on a daily basis (2.2 g total). Runners estimated finish time based on recent performance and training. Fasting, pre- and post-marathon plasma and a five-hour urine collection were analyzed for free choline and plasma for phospholipid-bound choline. Pre-race predicted, as well as the actual finish time, were recorded. RESULTS: All subjects completed the marathon. Plasma free choline decreased significantly in the placebo group and increased significantly in the lecithin group (9.6 +/- 3.6 to 7.0 +/- 3.6 nmol/mL vs. 8.0 +/- 1.2 to 11.7 +/- 3.6 nmol/mL, p = 0.001 for the delta between groups). No significant changes in plasma phospholipid-bound choline concentration were observed. There was a non-significant decrease in urine free choline in both groups. Actual finish time was 256.3 +/- 46.3 minutes for the lecithin group vs. 240.8 +/- 62.0 for the placebo group and the actual:predicted time was 1.03 +/- 0.06 (lecithin) and 1.07 +/- 0.08 (placebo), p = 0.36. CONCLUSION: Short-term lecithin supplementation prior to a marathon maintains normal plasma free choline concentration during the race, but failed to improve performance.
BACKGROUND: Previous investigations have demonstrated that choline deficiency, manifested in low plasma-free choline concentration and hepatic injury, may develop in patients who require long-term total parenteral nutrition (TPN). Preliminary studies have suggested lecithin or choline supplementation might lead to improved visual memory in the elderly and reverse abnormal neuropsychological development in children. We sought to determine if choline-supplemented TPN would lead to improvement in neuropsychological test scores in a group of adult, choline-deficient outpatients receiving TPN. METHODS: Eleven subjects (8 males, 3 females) who received nightly TPN for more than 80% of their nutritional needs for at least 12 weeks before entry in the study were enrolled. Exclusion criteria included active drug abuse, mental retardation, cerebral vascular accident, head trauma, hemodialysis or peritoneal dialysis, (prothrombin time [PT] >2x control), or acquired immune deficiency syndrome (AIDS). Patients were randomly assigned to receive their usual TPN regimen (n = 6, aged 34.0 +/- 12.6 years) over a 12-hour nightly infusion or their usual TPN regimen plus choline chloride (2 g) (n = 5, aged 37.3 +/- 7.3 years). The following neuropsychological tests were administered at baseline and after 24 weeks of choline supplementation (or placebo): Weschler Adult Intelligence Scale-Revised (WAIS-R, intellectual functioning), Weschler Memory Scale-Revised (WMS-R, two subtests, verbal and visual memory), Rey-Osterrieth Complex Figure Test (visuospatial functioning and perceptual organization), Controlled Oral Word Association Test (verbal fluency), Grooved Pegboard (manual dexterity and motor speed), California Verbal Learning Test (CVLT, rote verbal learning ability), and Trail Making Parts A & B (visual scanning, psychomotor speed and set shifting). Scores were reported in terms of standard scores including z scores and percentile ranks. Mean absolute changes in raw scores were compared between groups using the Wilcoxon rank sum test, where p values < .05 constituted statistical significance. RESULTS: Significant improvements were found in the delayed visual recall of the WMS-R (7.0 +/- 2.7 vs -.33 +/- 5.7, p = .028), and borderline improvements in the List B subset of the CVLT (1.0 +/- 0.8 vs -2.0 +/- 2.4, p = .06) and the Trails A test (-3.8 +/- 8.1 vs 3.7 +/- 4.5 seconds, p = .067). No other statistically significant changes were seen. CONCLUSIONS: This pilot study indicates both verbal and visual memory may be impaired in patients who require long-term TPN and both may be improved with choline supplementation.
BACKGROUND: Previous studies have shown that plasma free choline concentrations are significantly decreased in many long-term home total parenteral nutrition (TPN) patients. Furthermore, low choline status has been associated with both hepatic morphologic and hepatic aminotransferase abnormalities. A preliminary pilot study suggested choline-supplemented TPN may be useful in reversal of these hepatic abnormalities. METHODS: Fifteen patients (10 M, 5 F) who had required TPN for > or =80% of their nutritional needs were randomized to receive their usual TPN (n = 8), or TPN to which 2 g choline chloride had been added (n = 7) for 24 weeks. Baseline demographic data were similar between groups. Patients had CT scans of the liver and spleen, and blood for plasma free and phospholipid-bound choline, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, gamma glutamyl transferase (GGT), bilirubin, serum lipids, complete blood count (CBC), and chemistry profile obtained at baseline, and weeks 2, 4, 6, 12, 16, 20, 24, and 34. CT scans were analyzed for Hounsfield unit (HU) densities. RESULTS: There were no significant differences in any measured parameters after 2 weeks. However, at 4 weeks, a significant difference in liver HU between groups was observed (13.3+/-5.0 HU [choline] vs 5.8+/-5.2 HU [placebo], p = .04). This significant trend continued through week 24. Recurrent hepatic steatosis and decreased HU were observed at week 34, 10 weeks after choline supplementation had been discontinued. A significant increase in the liver-spleen differential HU was also observed in the choline group (10.6+/-6.2 HU [choline] vs 1.3+/-3.3 HU [placebo], p = .01). Serum ALT decreased significantly (p = .01 to .05) in the choline group vs placebo at weeks 6,12, 20, and 24. Serum AST was significantly decreased in the choline group by week 24 (p = .02). The serum alkaline phosphatase was significantly reduced in the choline group at weeks 2, 12, 20, 24, and 34 (p = .02 to 0.07). Total bilirubin was normal in these patients and remained unchanged during the study. Serum GGT tended to decrease more in the choline group, but the greater decrease was not statistically significant. CONCLUSIONS: Choline deficiency is a significant contributor to the development of TPN-associated liver disease. The data suggest choline is a required nutrient for long-term home TPN patients.
BACKGROUND: Low plasma free choline concentration has been associated with elevated serum hepatic aminotransferase concentrations and hepatic steatosis in adults who need home parenteral nutrition (HPN). We sought to determine if plasma free choline is similarly reduced in children who need home total parenteral nutrition (TPN). METHODS: We compared the plasma free choline concentration in 21 children who required long-term HPN with 31 normal controls. Patients had received HPN for 75 +/- 13 (SD) months (range 3-206 months). All control children ingested a normal, mixed, nonvegetarian diet. RESULTS: The mean plasma free choline concentration in the children receiving HPN was significantly lower than normal children (6.6 +/- 4.3 vs 8.0 +/- 2.3 nmol/mL, p = .002). Plasma free choline concentration was correlated with age (r = -0.43, p = .049). Using multiple linear regression analysis for age, sex, and squared age (considered in order to account for possible nonlinearity between choline and age), HPN children showed a steady and significant decline in plasma free choline concentration with increased age at the rate of 0.03 nmol/mL per month. Plasma lipid bound choline concentration did not vary with age. No relationship was seen between either plasma free and lipid bound choline concentration and amount of daily IV lipid infusion. A significant negative correlation was observed between plasma free choline concentration and aspartate aminotransferase (AST) and alanine aminostransferase (ALT) (r = -0.72, p = .04 and r = -0.80, p = .02, respectively). CONCLUSION: Our data support the notion that patients who need long-term HPN without significant enteral feeding have a significant risk for the development of choline deficiency with its associated hepatic dysfunction.