1,721,295 research outputs found
Brain protection and cognitive function. cocoa flavonoids as nutraceuticals
No full textCognitive decline and dementia are major public health social problems, suggesting the specific need to provide research into risk factors for cognitive decline as priority topic. Increasing evidence supports the hypothesis that oxidative stress and neuroinflammation might play a crucial role in the pathophysiology of cognitive decline. Further, cognitive dysfunction and dementia in Alzheimer's disease as well as in vascular dementia seem to be also the consequence of cerebral blood flow decrease and deregulation, also suggesting a putative pathophysiological convergence of mechanisms between atherosclerosis and Alzheimer's disease. In keeping with this, a growing interest has been addressed to flavonoids as potential nutraceuticals with neuroprotective effects. Of interest, cocoa beans have been described as a fundamental source of anti-oxidant flavonoids with the flavan-3-ols and their derivatives being present in high concentrations. Therefore, recent studies specifically focused on the favorable effects of flavonoid-rich cocoa and chocolate on cerebrovascular risk factors and cognitive function. Aim of this review is to summarize new findings concerning the cocoa effects on cognitive function, particularly focusing on some putative mechanisms of vascular and antioxidant action involved in preventing dementia
Brain Protection and Cognitive Function: Cocoa Flavonoids as Nutraceuticals
No full textCognitive decline and dementia are major public health social problems, suggesting the specific need to provide research into risk factors for cognitive decline as priority topic. Increasing evidence supports the hypothesis that oxidative stress and neuroinflammation might play a crucial role in the pathophysiology of cognitive decline. Further, cognitive dysfunction and dementia in Alzheimer's disease as well as in vascular dementia seem to be also the consequence of cerebral blood flow decrease and deregulation, also suggesting a putative pathophysiological convergence of mechanisms between atherosclerosis and Alzheimer's disease. In keeping with this, a growing interest has been addressed to flavonoids as potential nutraceuticals with neuroprotective effects. Of interest, cocoa beans have been described as a fundamental source of anti-oxidant flavonoids with the flavan-3-ols and their derivatives being present in high concentrations. Therefore, recent studies specifically focused on the favorable effects of flavonoid-rich cocoa and chocolate on cerebrovascular risk factors and cognitive function. Aim of this review is to summarize new findings concerning the cocoa effects on cognitive function, particularly focusing on some putative mechanisms of vascular and antioxidant action involved in preventing dementia
New insight into urate-related mechanism of cardiovascular damage
No full textSeveral experimental and clinical studies reported that hyperuricemia may trigger hypertension, metabolic syndrome, vascular damage and renal disease. Furthermore, a substantial proportion of epidemiological studies are compatible with the hypothesis that hyperuricemia may be an indipendent risk factor for cardiovascular disease as well as for an increased cardiovascular mortality. Xanthine oxidase is a critical source of reactive oxygen species contributing to vascular inflammation and endothelial dysfunction. Although a causal relationship between these conditions has not been clearly clarified, the capacity of uric acid to negatively affect vascular function by pro-oxidant effects and by decreasing nitric oxide bioavailability and consequently induce endothelial dysfunction may explain the association among hyperuricemia, hypertension, metabolic syndrome, and cardiovascular disease, also by a common mechanicistic point of view
New Insight into Urate-Related Mechanism of Cardiovascular Damage
No full textSeveral experimental and clinical studies reported that hyperuricemia may trigger hypertension, metabolic syndrome, vascular damage and renal disease. Furthermore, a substantial proportion of epidemiological studies are compatible with the hypothesis that hyperuricemia may be an indipendent risk factor for cardiovascular disease as well as for an increased cardiovascular mortality. Xanthine oxidase is a critical source of reactive oxygen species contributing to vascular inflammation and endothelial dysfunction. Although a causal relationship between these conditions has not been clearly clarified, the capacity of uric acid to negatively affect vascular function by pro-oxidant effects and by decreasing nitric oxide bioavailability and consequently induce endothelial dysfunction may explain the association among hyperuricemia, hypertension, metabolic syndrome, and cardiovascular disease, also by a common mechanicistic point of view
Forme testuali e strategie retoriche di elogio della lingua portoghese nei secoli XVI e XVII
No full textPeople living with human immunodeficiency virus: Ccardiovascular risk screening for an early and effective risk management
No full textExercise training improves cardiopulmonary and endothelial function in women with breast cancer: findings from the Diana-5 study
No full textEffects of a Novel Fixed Combination of Nutraceuticals on Serum Uric Acid Concentrations and the Lipid Profile in Asymptomatic Hyperuricemic Patients : Results from the PICONZ-UA Study
No full textAsymptomatic hyperuricemia is not a current indication for therapy as the definite role of serum uric acid elevation as a cardiovascular risk factor is extremely likely but still controversial
Therapeutic approaches to chronic hyperuricemia and gout
No full textGout is currently one of the most common causes of inflammatory arthritis in most industrialised countries. Apart from its high frequency, gout is associated with disability, poor quality of life and increased mortality and therefore represents an ever increasing public health concern. Substantial experimental and epidemiological evidence exists supporting the link between elevated levels of serum uric acid and several comorbidities including cardiovascular and kidney diseases. The cornerstone of effective gout management is long-term serum urate lowering below saturation concentrations (<6 mg/dL or <360 μmol/L) in order to promote crystal dissolution and prevent monosodium urate crystals formation. The management of gout includes not only pharmacological approaches, but also a number of nonpharmacologic interventions aiming at lessening attack risk, lowering uric acid levels and promoting general health while preventing the development of comorbidities. It is of great address whether urate lowering strategies can also lower cardiovascular risk and some preliminary studies in both animal and human subjects suggest that they might. Patient education and appropriate lifestyle advice are core aspects of management of hyperuricemia and gout. The two xanthine oxidase inhibitors currently available are effective as long-term urate lowering therapy although the greater efficacy and good tolerability of febuxostat as urate lowering agent has to be adequately considered especially when the reduction of serum uric acid levels to achieve the target is particularly ambitious and/or the presence of comorbidities increases the risk of adverse effects. Associated comorbidities and cardiovascular risk factors should be also addressed as an important part of the management of chronic hyperuricemia and gou
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