Annals of medicine
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Selected inflammatory conditions increase the risk of cancer. An inflammatory component is present also in the micro-environment of tumours epidemiologically unrelated to inflammation. ⋯ Emerging evidence also suggests that cancer-related inflammation promotes genetic instability. Thus, cancer-related inflammation represents a target for innovative diagnostic and therapeutic strategies.
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Abstract Suicide is a major public health concern. The etiology and pathogenic mechanisms associated with suicidal behavior are poorly understood. Recent research on the biological perspective of suicide has gained momentum and appears to provide a promising approach for identifying potential risk factors associated with this disorder. ⋯ Recent studies also demonstrate abnormalities in the functioning of BDNF, because its cognate receptors (tropomycin receptor kinase B and pan75 neurotrophin receptor) are abnormally active and/or expressed in the post-mortem brains of suicide subjects. There is further evidence of the role of BDNF in suicide as numerous studies show a strong association of suicidal behavior with BDNF functional polymorphism. Overall, it appears that abnormalities in BDNF signaling may serve as an important biological risk factor in the etiology and pathogenesis of suicide.
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The increasing awareness of cost issues in health care has led to the increasing use of policy-driven substitution of branded for generic medications, particularly relative to statin treatment for cardiovascular diseases. While there are potential short-term health care savings, the consequences for primary care are under-researched. Our objective was to review data on intensive statin therapy and generic substitution in patients at high cardiovascular risk. ⋯ Substitution of generic statins may be cost-saving, particularly at the primary prevention level. However, statin substitution policies have not been adequately studied on a population level. Data raise concern that mandated statin substitution may lead to unfavourable treatment choices at the level of the individual high-risk patient.
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Review
Vascular endothelial responses to altered shear stress: pathologic implications for atherosclerosis.
Atherosclerosis preferentially develops at branches and curvatures of the arterial tree, where blood flow is disturbed from a laminar pattern, and wall shear stress is non-uniform and has an irregular distribution. Vascular endothelial cells (ECs), which form an interface between the flowing blood and the vessel wall, are exposed to blood flow-induced shear stress. ⋯ The aim of this review article is to summarize current findings on the effects of shear stress on ECs, in terms of their signal transduction, gene expression, structure, and function. These endothelial cellular responses have important relevance to understanding the pathophysiological effects of altered shear stress associated with atherosclerosis and thrombosis and their complications.
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Atrial fibrillation (AF) is associated with an increased risk of mortality and morbidity from stroke and thromboembolism. Endothelial damage or dysfunction may contribute to this increased risk of thromboembolism via the mediation of a prothrombotic or hypercoagulable state. However, the precise pathophysiological mechanism(s) relating endothelial (dys)function to AF and thromboembolism are yet to be fully elucidated. This review article aims to provide a comprehensive overview of endothelial (dys)function and AF, as well as the merits and limitations of the different methods used to assess endothelial function in AF.