Decrease in plasma high density lipoprotein cholesterol with weight loss.
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Biomedical subjects
Publications and source records attributed to M Ruggiero.
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Serum alpha-tocopherol, lipids, potassium and creatine phosphokinase levels we-remeasured in 20 adult male control patients and 120 malabsorption patients. The malabsorption group had significantly lower serum alpha-tocopherol levels than the control group. The change was independent of serum total lipid levels that were not significantly different among the two groups. Serum potassium and creatine phosphokinase did not correlate with serum alpha-tocopherol levels in either control and malabsorption group. Body mass indices that are directly relate to adiposity increased with increase of serum alpha-tocopherol and total lipids of serum.
Proteins (casein) heat treated, frozen and heat retreated show a net decrease of digestibility and utilization as results of synthesis of Maillard compounds, directly related to the total time of heat treatment.
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The AA. reports that lysine deficiency in rats results in poor growth, low weight of heart and liver, anemia, hypoproteinemia and low concentration of haemoglobin. Rats fed supplemented lysine diet did not have any pathological condition in comparison with normal rats receiving standard laboratory diet.
Male rats weanling fed 20% gluten diet for 90 days of demonstrate to have about one-third lower level of carnitine per gram of skeletal muscle and heart muscle than the group which received the same diet supplemented with 1% of lysine. The carnitine level of the liver, however, was significantly higher in the unsupplemented versus the lysine supplemented groups.
The AA. reports the possibility to prepare special sugar mixtures at various degree of complexity (mono-di-oligo-polisaccharides). These have high solubility and neutral taste. These supply to athletes disposable amounts of glucose for muscular contraction during the play time.
The AA, reports the variations of collagen of carcass and skin of overnourished and proteic and caloric malnourished rats. The level of collagen is higher in malnourished when compared with normal and overnourished rats. The insoluble hydroxyproline concentration is higher in malnourished than in overnourished rats. This is reported to a variation of metabolic enzymatic patterns related to the catabolism of collagen.
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Metabolic rate of obese patients is reported, recorded to cellular active mass. The metabolic rate is higher in obese patients and the value is diucthy related to individual actual weight. The dinamic-specific action of proteins is normal.
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Hemorrhagic disorders are common in patients with liver cirrhosis and result from several factors including impaired platelet function. We evaluated platelet aggregation and arachidonic acid metabolism in response to standard agonists in platelet-rich plasma from 12 cirrhotic patients with mild impairment of liver function (Child A), 12 patients with severe liver dysfunction (Child B and C) and 12 healthy subjects. Platelet aggregation and thromboxane A2 production were consistently reduced in patients with severe liver impairment. To determine whether the platelet dysfunction is due to an intrinsic platelet defect or a circulating inhibitor, we measured platelet aggregation and thromboxane A2 synthesis on washed platelets in healthy subjects and in Child B and C patients. The aggregating response of washed platelets in response to thrombin, collagen and arachidonic acid was markedly reduced, suggesting an intrinsic platelet defect. The biochemical events underlying platelet aggregation were investigated by prelabeling platelets with [1-14C]arachidonic acid. Thrombin-induced activation of phospholipase C (measured as the release of [1-14C]phosphatidic acid) and phospholipase A2 (measured as the release of [1-14C]arachidonic acid and its metabolites) was greatly impaired in platelets from patients with severe liver impairment. We conclude that in advanced cirrhosis there is a severe reduction in platelet aggregatory response to physiologic agonists due to an intrinsic platelet defect which is related to an impairment of the platelet transmembrane signaling mechanism induced by receptor stimulation.
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