1,721,213 research outputs found
Cox-2 polymorphisms and cardiovascular disease: elucidating the hidden side of the disease.
No full textIn the last years, the role of individual genetic background is considered
critical in several aspects of medicine, such as susceptibility
to diseases, disease progression, and responses to drug treatment
[1].
Genomes from different individuals are 99.9 percent identical,
with only 0.1 percent of the genome showing mutations
[2]. Nevertheless, the constant improvement in genome analysis
has contributed to produce a huge search for biologically active
genomic polymorphisms, particularly single-nucleotide polymorphisms
(SNPs), which consist of substitutions of one nucleotide
for another in a DNA sequence [1]. The possibility that SNPs
may contribute to identify genes responsible for common diseases
as well as individuals at risk of disease had led to large
studies focused on discovery and organization of SNPs into public
databases
EP Receptors and Coxibs: Seeing the Light at the End of the Tunnel
No full textFew chemical compounds have demonstrated a controver- sial association with a specific disease such as arachidonic acid with atherothrombosis. Arachidonic acid metabolism is deeply linked to atherothrombosis because compounds gener- ated by this cascade, the eicosanoids, are key regulators of several pathophysiological processes critically involved in vessel homeostasis and blood clotting. After its release from membrane-bound phospholipids, arachidonic acid is metabo- lized by 4 main pathways: (1) prostaglandin (PG) endoperoxi- dase synthase, usually referred as cyclooxygenase (COX); (2) lipoxygenase; (3) P450 epoxygenase; and (4) nonenzymatic isoprostane biosynthesis..
Elevated circulating levels of monocyte chemoattractant protein-1 in patients with restenosis after coronary angioplasty: A response
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Letter by Santovito et al regarding article, "rhythm versus rate control therapy and subsequent stroke or transient ischemic attack in patients with atrial fibrillation".
No full textTo the Editor:
We have read with interest the article by Tsadok et al1 regarding the incidence of stroke or transient ischemic attack in patients with atrial fibrillation under rhythm or rate control, recently published on Circulation. The authors found that patients undergoing initial rhythm control may have lower rates of stroke and transient ischemic attack when compared with patients under rate-control strategy (hazard ratio, 0.80). However, it should be noted that patients were greatly different in terms of risk factors for stroke between the 2 groups. In fact, patients in the rate-control group were significantly older (>70% of them were aged ≥75 years), with higher prevalence of hypertension, diabetes mellitus, and previous cerebrovascular events..
New insights on the molecular mechanisms of type-1 angiotensin II receptor blockers and their contribution to atherosclerotic plaque stabilization
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Oxidative stress, inflammation and atherosclerotic plaque development
No full textAlthough the pathophysiological mechanisms underlying atherosclerosis are not completely understood, it is widely recognized that both inflammation and oxidative stress play important roles in all of the phases of atherosclerosis evolution. The oxidative modification hypothesis of atherosclerosis supports the concept that oxidation of circulating low density lipoprotein (LDL) plays a key role in the early phases of atherogenesis. However, in addition to LDL oxidation, other oxidative events are worth noting in the setting of atherosclerosis, such as the generation of oxygen reactive species. These compounds are crucial mediators in the signaling pathways underlying vascular inflammation, from the initial phases of fatty streak formation to atherosclerotic plaque evolution toward instability and rupture. In this manuscript, we summarize the newest evidence linking oxidative signaling to inflammation and atherosclerosis evolution. © 2007 Elsevier B.V. All rights reserved
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