Primely generated refinement monoids

We extend both Dobbertin's characterization of primely generated regular refinement monoids and Pierce's characterization of primitive monoids to general primely generated refinement monoids.The first-named author was partially supported by DGI MINECO MTM2011-28992-C02-01, by FEDER UNAB10-4E-378 "Una manera de hacer Europa", and by the Comissionat per Universitats i Recerca de la Generalitat de Catalunya. The second-named author was partially supported by the DGI and European Regional Development Fund, jointly, through Project MTM2011-28992-C02-02, and by PAI III grants FQM-298 and P11-FQM-7156 of the Junta de Andalucía

Are coronary event rates declining slower in women than in men – evidence from two population-based myocardial infarction registers in Finland?

<p>Abstract</p> <p>Background</p> <p>Studies have suggested that the prevention and treatment of coronary heart disease may not have been as effective in women as in men. Therefore, we aimed to examine whether the incidence, attack rate and mortality of myocardial infarction (MI) events have declined less in women than in men.</p> <p>Methods</p> <p>Two large population-based MI registers, the FINAMI register and the Finnish Cardiovascular Disease Register (CVDR) were used for comparing the event rates among men and women aged ≥35 years in two time periods, 1994–1996 and 2000–2002.</p> <p>Results</p> <p>In the FINAMI register a total of 5,252 events were recorded in men and 4,898 in women. Corresponding numbers in the CVDR were 78,709 and 70,464. Both FINAMI and CVDR data suggested smaller declines in incidence and attack rate of MI events in women than in men. In CVDR data the decline in mortality was also smaller in women than in men, while in FINAMI data this difference did not reach statistical significance. In the large CVDR data set, negative binomial regression models revealed smaller declines in incidence (p = 0.006), attack rate (p = 0.008) and mortality (p = 0.04) in women than in men aged <55 years. In persons ≥55 years no difference was observed between women and men.</p> <p>Conclusion</p> <p>The incidence and attack rate of MI events have declined less in women aged <55 than in men of similar age. In older persons no significant differences were observed. Further studies are warranted to find out the reasons why the development has been less favourable for young women than for men.</p

Modulation of vascular reactivity by perivascular adipose tissue (PVAT)

Purpose of Review: In this review we discuss the role of perivascular adipose tissue (PVAT) in the modulation of vascular contractility and arterial pressure, focusing on the role of the renin-angiotensin-aldosterone system and oxidative stress/inflammation. Recent Findings: PVAT possesses an relevant endocrine-paracrine activity, which may be altered in several pathophysiological and clinical conditions. During the last two decades it has been shown PVAT may modulate vascular reactivity. It has also been previously demonstrated that inflammation in adipose tissue may be implicated in vascular dysfunction. In particular, adipocytes secrete a number of adipokines with various functions, as well as several vasoactive factors, together with components of the renin-angiotensin system which may act at local or at systemic level. It has been shown that the anticontractile effect of PVAT is lost in obesity, probably as a consequence of the development of adipocyte hypertrophy, inflammation, and oxidative stress. Summary: Adipose tissue dysfunction is interrelated with inflammation and oxidative stress, thus contributing to endothelial dysfunction observed in several pathological and clinical conditions such as obesity and hypertension. Decreased local adiponectin level, macrophage recruitment and infiltration, and activation of renin-angiotensin-aldosterone system could play an important role in this regards

Epigenetic regulation of caloric restriction in aging

The molecular mechanisms of aging are the subject of much research and have facilitated potential interventions to delay aging and aging-related degenerative diseases in humans. The aging process is frequently affected by environmental factors, and caloric restriction is by far the most effective and established environmental manipulation for extending lifespan in various animal models. However, the precise mechanisms by which caloric restriction affects lifespan are still not clear. Epigenetic mechanisms have recently been recognized as major contributors to nutrition-related longevity and aging control. Two primary epigenetic codes, DNA methylation and histone modification, are believed to dynamically influence chromatin structure, resulting in expression changes of relevant genes. In this review, we assess the current advances in epigenetic regulation in response to caloric restriction and how this affects cellular senescence, aging and potential extension of a healthy lifespan in humans. Enhanced understanding of the important role of epigenetics in the control of the aging process through caloric restriction may lead to clinical advances in the prevention and therapy of human aging-associated diseases