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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence from observational studies suggests that elevated levels of homocysteine are associated with an increased risk of cardiovascular diseases. We assessed whether moderate alcohol intake in healthy social drinkers, suggested to be cardioprotective according to the 'French paradox', influences the cardiovascular risk factor homocysteine. A total of 60 normal nourished subjects who had no evidence of vascular disease or other risk factors for hyperhomocysteinaemia were assigned to receive mineral water or 30 g of alcohol per day (as beer, red wine or spirits) for a period of 6 weeks. Homocysteine levels of social drinkers, independent of which beverage was consumed, increased during the observation. We postulate that elevated levels of homocysteine in social drinkers with regular moderate alcohol intake are at risk of developing cardiovascular diseases, which contradicts the suggested cardioprotection of alcohol according to the 'French paradox'.
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PMID:Moderate alcohol consumption in social drinkers raises plasma homocysteine levels: a contradiction to the 'French Paradox'? 1137 52

A pandemic of obesity is contributing importantly to the prevalence of the metabolic syndrome characterized by hypertension, insulin resistance, and hyperlipidemia. In turn, the metabolic syndrome is contributing to vascular disease and the accelerating epidemic of chronic renal failure. Currently, pharmacological approaches to attenuate obesity and its cardiovascular/renal sequelae are limited. The purpose of this study was to determine the effects of 2-hydroxyestradiol, a metabolite of 17beta-estradiol with minimal estrogenic activity, on the development of obesity, the metabolic syndrome, and heart, vascular, and renal dysfunction in obese ZSF1 rats, a well-characterized genetic model of obesity and the metabolic syndrome with concomitant heart, vascular, and kidney disease. ZSF1 rats were treated, beginning at 12 weeks of age, for 26 weeks with vehicle or 2-hydroxyestradiol (10 microg/kg/h). At baseline and after 24 weeks of treatment, animals were placed in metabolic cages, and food intake, water intake, urine output, and urinary excretion of proteins and glucose were determined. Next, in fasting animals, plasma cholesterol was measured, an oral glucose tolerance test was conducted, and total glycated hemoglobin levels were determined. At the end of the study, animals were anesthetized and instrumented for assessment of heart performance, renal hemodynamics, and mesenteric vascular reactivity. 2-Hydroxyestradiol attenuated the development of obesity and improved endothelial function, decreased nephropathy, decreased the severity of diabetes, lowered arterial blood pressure, and reduced plasma cholesterol. 2-Hydroxyestradiol may be an important lead for the development of safe and effect drugs to attenuate obesity and its metabolic, vascular, and renal sequelae.
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PMID:2-Hydroxyestradiol attenuates the development of obesity, the metabolic syndrome, and vascular and renal dysfunction in obese ZSF1 rats. 1171 85

Hypertension (HTN) is ubiquitous in the renal failure patient. It has long been thought that renal disease interferes with salt excretion, leading to volume overload and consequent hypertension. This theory gives prominence to the kidney in long-term regulation of blood pressure (BP). It is assumed that the excess salt and water retention increases the blood flow to the tissues, which sets in motion the phenomenon of autoregulation. The tissue arterioles vasoconstrict to decrease the excessive blood flow. The resulting vasoconstriction raises the peripheral vascular resistance, which is the cardinal most consistent findings in HTN (whether essential or renal in origin). Recently, more light has been shed on the multitude of factors and pathophysiologic mechanisms that lead to HTN in the renal disease patient. The level of BP is most likely determined by the level of the peripheral vascular resistance and volume status in combination. If the peripheral vascular resistance is not appropriately lowered in the face of hypervolemia, HTN results. This primary role of the blood vessel in HTN is consistent with the close correlation of vascular disease to HTN (because HTN is a manifestation of vessel disease). In this review, evidence for and against the different pathophysiologic mechanisms that have been postulated to explain renal HTN is presented.
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PMID:Pathophysiology of hypertension in renal failure. 1178 65

Drinking water contaminated by arsenic remains a major public health problem. Long-term arsenic exposure has been found to be associated with peripheral vascular diseases in a variety of studies. Reports of vascular effects of arsenic in drinking water, which span almost 100 years, have been published in Taiwan, Chile, Mexico, and China. This paper reviewed the association of peripheral vascular diseases resulting from arsenic exposure to drinking water from the clinical and pathological points of view. An endemic peripheral vascular disorder called "blackfoot disease" has been noticed in a limited area in Taiwan. This disease results in gangrene in the extremities. It has been associated with the ingestion of high concentrations of arsenic-tainted artesian well water. Epidemiological studies confirmed a dose-response relationship between long-term arsenic exposure and the occurrence of blackfoot disease. Whereas arsenic has induced various clinical manifestations of vascular effects in Chile, Mexico and China, they do not compare in magnitude or severity to the blackfoot disease found in Taiwan. The pathogenesis of vascular effects induced by arsenic is still controversial. The possible mechanisms include endothelial cell destruction, arsenic-associated atherogenesis, carotene and zinc deficiency, and/or some immunological mechanism. Microcirculatory assessments revealed that deficits of capillary blood flow and permeability exist in clinically normal skin of patients with chronic arsenical poisoning. The vascular effects of chronic arsenic poisoning may involve cardiovascular and cerebrovascular systems as well. In view of the increasing public health problems caused by arsenic exposure, vascular effects should be included in the future study of health effects of arsenic.
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PMID:Peripheral vascular diseases resulting from chronic arsenical poisoning. 1199 Feb 46

Generation of new blood vessels from pre-existing vasculature (angiogenesis) is accompanied in almost all states by increased vascular permeability. This is true in physiological as well as pathological angiogenesis, but is more marked during disease states. Physiological angiogenesis occurs during tissue growth and repair in adult tissues, as well as during development. Pathological angiogenesis is seen in a wide variety of diseases, which include all the major causes of mortality in the west: heart disease, cancer, stroke, vascular disease and diabetes. Angiogenesis is regulated by vascular growth factors, particularly the vascular endothelial growth factor family of proteins (VEGF). These act on two specific receptors in the vascular system (VEGF-R1 and 2) to stimulate new vessel growth. VEGFs also directly stimulate increased vascular permeability to water and large-molecular-weight proteins. We have shown that VEGFs increase vascular permeability in mesenteric microvessels by stimulation of tyrosine auto-phosphorylation of VEGF-R2 on endothelial cells, and subsequent activation of phospholipase C (PLC). This in turn causes increased production of diacylglycerol (DAG) that results in influx of calcium across the plasma membrane through store-independent cation channels. We have proposed that this influx is through DAG-mediated TRP channels. It is not known how this results in increased vascular permeability in endothelial cells in vivo. It has been shown, however, that VEGF can stimulate formation of a variety of pathways through the endothelial cell, including transcellular gaps, vesiculovacuolar organelle formation, and fenestrations. A hypothesis is outlined that suggests that these all may be part of the same process.
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PMID:Regulation of microvascular permeability by vascular endothelial growth factors. 1216 26

Inadequate folate status is associated with an increased risk for chronic diseases that may have a negative impact on the health of the aging population. Folate, a water-soluble vitamin, includes naturally occurring food folate and synthetic folic acid in supplements and fortified foods. Inadequate folate status may result in hyperhomocysteinemia, a significant risk factor for atherosclerotic vascular disease, changes in DNA that may result in pro-carcinogenic effects and increased risk for cognitive dysfunction. Folate status may be negatively influenced by inadequate intake, genetic polymorphisms and interactions with various drugs. In the US, folic acid is now added to enriched grain products and continues to be included in the majority of ready-to-eat breakfast cereals. Recent data indicate that the folate status in the US population has improved significantly, presumably due to the effects of fortification. Folic acid (not food folate) intake in excess of the Tolerable Upper Intake Level may mask the diagnosis of a vitamin B(12) deficiency, which is more prevalent in the elderly than younger individuals. When folic acid supplements are recommended, a multivitamin that includes vitamin B(12) should also be advised. To safely and effectively increase folate intake in the elderly, naturally occurring folate-rich food sources should be promoted. Folate-rich foods include orange juice, dark green leafy vegetables, asparagus, strawberries and legumes. These foods are also excellent sources of other health-promoting nutrients associated with chronic disease risk reduction.
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PMID:Folate: a key to optimizing health and reducing disease risk in the elderly. 1256 9

Flow-mediated dilation (FMD) measures the ability of an artery to relax in response to increases in blood velocity. FMD, primarily of the brachial artery, has been used as a noninvasive method of assessing vascular health. The purpose of this study was to assess FMD in the lower legs of humans. Six healthy subjects (27 PlusMinus; 6 yrs) were tested. Doppler ultrasound images of the posterior tibial artery were taken before, during, and after 5 minutes of proximal cuff occlusion. FMD was measured as the percent increase in diameter after cuff release. Vascular tone was calculated using the resting diameter as a percentage of the vessel's vasoactive range. Minimum diameter occurred during ischemia and maximal diameter occurred following reactive hyperemia with local heating. The lower leg was heated with 10 minutes of immersion in 44 degrees C water. Mean diameters at rest, cuff, and during release were 0.267 PlusMinus; 0.062, 0.162 PlusMinus; 0.036, 0.302 PlusMinus; 0.058 cm, respectively. FMD was 13.5 PlusMinus; 6.6 % and vascular tone was 29 PlusMinus; 16.3%. We also found that retesting on a second day produced mean diameter values within 8% of the first day. Larger resting diameter (decreased tone) correlated with decreased FMD (r2 = 0.73). These results suggest that FMD and vascular tone can be measured in the posterior tibial artery. This is a potentially powerful tool to non-invasively measure vascular health in the lower legs of people at risk for vascular disease.
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PMID:Noninvasive assessment of vascular function in the posterior tibial artery of healthy humans. 1262 21

Bronchiolitis obliterans combined organizing pneumonia (BOOP), now called organizing pneumonia, is a multi-etiologic disease. It can present as a solitary lesion, or as multinodular or diffuse interstitial lung disease. It is speculated if solitary BOOP may evolve into inflammatory pseudotumor of the lung. BOOP can be seen after non-resolving infectious bronchopneumonia as well as acute interstitial pneumonia with diffuse alveolar damage. BOOP can be the early morphologic pattern in toxic inhalation, especially water-soluble substances, but also in drug induced lung disease. BOOP can be the late stage of extrinsic allergic alveolitis, but also a morphologic sequel of collagen vascular disease. Even Wegener's granulomatosis can be preceded by a BOOP pattern. In many cases a careful analysis of BOOP, including changes of the pneumocytes, macrophages, myofibroblasts and endothelial cells, can establish the correct etiologic diagnosis. For example virus-induced pneumocyte proliferation can be seen months after the onset of interstitial pneumonia, and can be found within BOOP. A small percentage of BOOP, however, has to be labeled as idiopathic, which is important too, because of different modalities of therapy. Idiopathic BOOP also is different with respect to prognosis. In the overview different BOOP etiologies will be discussed, and the etiologic background will be analyzed. The pathogenesis will be discussed with respect to the understanding of the causing mechanisms. The role of bronchoalveolar lavage and the optimal tissue sample for establishing the diagnosis will be discussed and demonstrated by examples. A part of the presentation will deal with the differential diagnosis, such as usual interstitial pneumonia, non-specific interstitial pneumonia, constrictive, and respiratory bronchiolitis combined interstitial lung disease.
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PMID:Bronchiolitis obliterans. Organizing pneumonia. 1264 57

Many plants emit isoprene, a hydrocarbon that has important influences on atmospheric chemistry. Pathogens may affect isoprene fluxes, both through damage to plant tissue and by changing the abundance of isoprene-emitting species. Live oaks (Quercus fusiformis (Small) Sarg. and Q. virginiana Mill) are major emitters of isoprene in the southern United States, and oak populations in Texas are being dramatically reduced by oak wilt, a widespread fungal vascular disease. We investigated the effects of oak wilt on isoprene emissions from live oak leaves (Q. fusiformis) in the field, as a first step in exploring the physiological effects of oak wilt on isoprene production and the implications of these effects for larger-scale isoprene fluxes. Isoprene emission rates per unit dry leaf mass were 44% lower for actively symptomatic leaves than for leaves on healthy trees (P = 0.033). Isoprene fluxes were significantly negatively correlated with rankings of disease activity in the host tree (fluxes in leaves on healthy trees > healthy leaves on survivor trees > healthy leaves on the same branch as symptomatic leaves > symptomatic leaves; isoprene per unit dry mass: Spearman's rho = -0.781, P = 0.001; isoprene per unit leaf area: Spearman's rho = -0.652, P = 0.008). Photosynthesis and stomatal conductance were reduced by 57 and 63%, respectively, in symptomatic relative to healthy leaves (P < 0.05); these reductions were proportionally greater than the reductions in isoprene emissions. Low isoprene emission rates in symptomatic leaves are most simply explained by physiological constraints on isoprene production, such as water stress as a result of xylem blockage, rather than direct effects of the oak wilt fungus on isoprene synthesis. The effects of oak wilt on leaf-level isoprene emission rates are probably less important for regional isoprene fluxes than the reduction in oak leaf area across landscapes.
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PMID:Reduction of isoprene emissions from live oak (Quercus fusiformis) with oak wilt. 1265 96

Increased vascular permeability is one of the first stages in both physiological and pathological angiogenesis-the generation of new blood vessels from preexisting vasculature. Although this has been hypothesised to be true in physiological angiogenesis, it is clearly a mark of blood vessel growth in disease. Normal, healthy blood vessel growth (physiological angiogenesis) occurs throughout development as well as during tissue repair and growth in adult tissues. Angiogenesis is also seen in a wide variety of diseases, which include all the major causes of mortality in the West-heart disease, cancer, stroke, vascular disease, and diabetes. Much of this angiogenesis is significantly different from normal blood vessel growth and is termed pathological angiogenesis. Angiogenesis is regulated by vascular growth factors, the most notable being the vascular endothelial growth factor family of proteins (VEGF). These act on specific receptors in the vascular system to stimulate new vessel growth by a number of mechanisms. VEGFs also directly stimulate increased vascular permeability to water and large molecular weight proteins and vasodilatation. These two effects result in a large flux of water and macromolecules from the vasculature to the interstitium, often resulting in oedema. This review will outline the mechanisms by which VEGFs do this and discuss some of the difficulties in interpreting data from VEGF studies due to the conflicting and synergistic effects of these actions.
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PMID:Regulation of vascular permeability by vascular endothelial growth factors. 1274 62


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