There is, I think, something ethereal about i —the square root of minus one. I remember first hearing about it at school. It seemed an odd beast at that time—an intruder hovering on the edge of reality.

Usually familiarity dulls this sense of the bizarre, but in the case of i it was the reverse: over the years the sense of its surreal nature intensified. It seemed that it was impossible to write mathematics that described the real world in …

I and i

http://www.dietcan.net/docs/Polifenoles%20en%20alimentos%20y%20biodisponibilidad.pdf

Polyphenols: food sources and bioavailability

Polyphenols constitute one of the most numerous and ubiquitous groups of plant metabolites and are an integral part of both human and animal diets. Ranging from simple phenolic molecules to highly polymerized compounds with molecular weights of greater than 30,000 Da, the occurrence of this complex group of substances in plant foods is extremely variable. Polyphenols traditionally have been considered antinutrients by animal nutritionists, because of the adverse effect of tannins, one type of polyphenol, on protein digestibility. However, recent interest in food phenolics has increased greatly, owing to their antioxidant capacity (free radical scavenging and metal chelating activities) and their possible beneficial implications in human health, such as in the treatment and prevention of cancer, cardiovascular disease, and other pathologies. Much of the literature refers to a single group of plant phenolics, the flavonoids. This review offers an overview of the nutritional effects of the main groups of polyphenolic compounds, including their metabolism, effects on nutrient bioavailability, and antioxidant activity, as well as a brief description of the chemistry of polyphenols and their occurrence in plant foods.

Polyphenols: Chemistry, Dietary Sources, Metabolism, and Nutritional Significance

This report is the continuation of two earlier reports that defined human arterial intima and precursors of advanced atherosclerotic lesions in humans. This report describes the characteristic components and pathogenic mechanisms of the various advanced atherosclerotic lesions. These, with the earlier definitions of precursor lesions, led to the histological classification of human atherosclerotic lesions found in the second part of this report. The Committee on Vascular Lesions also attempted to correlate the appearance of lesions noted in clinical imaging studies with histological lesion types and corresponding clinical syndromes. In the histological classification, lesions are designated by Roman numerals, which indicate the usual sequence of lesions progression. The initial (type I) lesion contains enough atherogenic lipoprotein to elicit an increase in macrophages and formation of scattered macrophage foam cells. As in subsequent lesion types, the changes are more marked in locations of arteries with adaptive intimal thickening. (Adaptive thickenings, which are present at constant locations in everyone from birth, do not obstruct the lumen and represent adaptations to local mechanical forces). Type II lesions consist primarily of layers of macrophage foam cells and lipid-laden smooth muscle cells and include lesions grossly designated as fatty streaks. Type III is the intermediate stage between type II and type IV (atheroma, a lesion that is potentially symptom-producing). In addition to the lipid-laden cells of type II, type III lesions contain scattered collections of extracellular lipid droplets and particles that disrupt the coherence of some intimal smooth muscle cells. This extracellular lipid is the immediate precursor of the larger, confluent, and more disruptive core of extracellular lipid that characterizes type IV lesions. Beginning around the fourth decade of life, lesions that usually have a lipid core may also contain thick layers of fibrous connective tissue (type V lesion) and/or fissure, hematoma, and thrombus (type VI lesion). Some type V lesions are largely calcified (type Vb), and some consist mainly of fibrous connective tissue and little or no accumulated lipid or calcium (type Vc).

A Definition of Advanced Types of Atherosclerotic Lesions and a Histological Classification of Atherosclerosis A Report From the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association

Resveratrol, a constituent of red wine, has long been suspected to have cardioprotective effects. Interest in this compound has been renewed in recent years, first from its identification as a chemopreventive agent for skin cancer, and subsequently from reports that it activates sirtuin deacetylases and extends the lifespans of lower organisms. Despite scepticism concerning its bioavailability, a growing body of in vivo evidence indicates that resveratrol has protective effects in rodent models of stress and disease. Here, we provide a comprehensive and critical review of the in vivo data on resveratrol, and consider its potential as a therapeutic for humans.

Therapeutic potential of resveratrol: the in vivo evidence.

Fourteen patients with established hypertension followed a double-blind crossover-styled trial to study the effects of 100 mg/day atenolol compared to placebo. Atenolol was found to be an effective antihypertensive agent, reducing both systolic and diastolic blood pressure. Hypertensive patients appear to have increased in vitro platelet adhesion and aggregation. Atenolol significantly reduced platelet adhesion, but had little effect on aggregation. This may be important in contributing towards the now-recognised cardio-protective effect of the beta-adrenoceptor blocking agents. Blood chemistry and haematological parameters were unchanged; but whereas plasma cholesterol and plasma triglyceride levels remained normal, there was a significant fall in plasma high-density lipoprotein cholesterol levels. Side effects were very few.

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Increased platelet adhesion and aggregation in hypertensive patients: effect of atenolol.

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Oxidative Stress in Cardiovascular Disease: Role of Oxidized Lipoproteins in Macrophage Foam Cell Formation and Atherosclerosis

Plasma lipoprotein concentration and composition of 6 healthy subjects were studied before and 3 h after a fatty meal (900 kcal) consisting of either cream (mainly saturated fatty acids) or cod liver oil (CLO; rich in n-3 polyunsaturated fatty acids). The plasma triglyceride concentration was increased after both meals. This was caused by an increase in both chylomicron and very-low-density lipoprotein (VLDL) triglycerides. Plasma total cholesterol was unchanged. The cholesterol content was also increased in low-density lipoproteins and in VLDL after cream intake, but was reduced in high-density lipoproteins (HDL), whereas no changes were observed in these fractions after CLO. The fatty acid composition of the diet was reflected in the plasma and in the chylomicron fraction. Both fatty meals reduced the relative concentration of plasma linoleic acid. Fatty acid composition in HDL suggested dietary fatty acid transfer from the chylomicrons and VLDL to the HDL after CLO, but not after the cream diet. The results suggest that in the postprandial state the fatty acid transfer between the triglyceride-rich lipoproteins and HDL depends on the quality of the fatty acids and that the n-3 polyunsaturated fatty acid may increase such transfer.

Acute effects of dietary cod liver oil and cream on plasma lipoproteins.

Human carotid plaque phosphatidylcholine specifically interacts with paraoxonase 1, increases its activity, and enhances its uptake by macrophage at the expense of its binding to HDL.

Michael Aviram

Papers

Increased platelet adhesion and aggregation in hypertensive patients: effect of atenolol.

Comprar The Paraoxonases: Their Role in Disease Development and Xenobiotic Metabolism | Mackness, Bharti | 9781402065606 | Springer

Oxidative Stress in Cardiovascular Disease: Role of Oxidized Lipoproteins in Macrophage Foam Cell Formation and Atherosclerosis

Acute effects of dietary cod liver oil and cream on plasma lipoproteins.

Human carotid plaque phosphatidylcholine specifically interacts with paraoxonase 1, increases its activity, and enhances its uptake by macrophage at the expense of its binding to HDL.