Lipoatrofia semicircular de etiología laboral asociada a alteraciones séricas de adipocinas / Occupational semicircular lipoatrophy associated with serum adipokine abnormalities

Objetivos: El objetivo de este estudio es examinar la relación entre lipoatrofia semicircular (LS), marcadores de inflamación (proteína C reactiva ultrasensible, [PCRus]), adipocinas (leptina, quemerina y vaspina) y marcadores inmunitarios (factor reumatoide [FR], fracciones de complemento C3 y C4, anticuerpos antinucleares [ANA], HLA DR3 y DR4). La quemerina es una adipocina, pero también es un marcador de inmunidad. Métodos: Estudio de casos y controles realizado en mayo de 2013. Participaron 21 casos, y como control participó el empleado sano más cercano a cada caso. Se utilizaron test no paramétricos (Kruskal-Wallis). Resultados: Se observó una relación estadísticamente significativa (p < 0,05) entre LS y niveles séricos de PCRus elevados, de leptina elevados y de quemerina disminuidos. Conclusiones: i) Parece haber un componente inflamatorio subyacente (PCRus elevada) en la LS; ii) la alteración de las adipocinas (leptina elevada y quemerina disminuida) apoyan la teoría de que la diferenciación adipocítica esté afectada en la LS, y iii) no hemos encontrado ningún marcador inmunitario (FR, etc.) asociado con LS, excepto la misma quemerina, que podría explicar una posible asociación entre LS y autoinmunidad (AU)

Objectives: The aim of this study was to examine the relationship between semicircular lipoatrophy (SL), inflammation marker (high sensibility C-reactive protein [hs-CRP]), adipokines (leptine, chemerine and vaspine) and autoimmune markers (rheumatoid factor [RF], C3 and C4 complement fractions, antinuclear antibodies [ANA], HLA DR3, and DR4). Chemerine is an adipokine, but also is an immunity marker. Methods: A case-control study was performed in May 2013; 21 cases were included. The closest healthy coworker to each case was used as a control. We calculated Kruskal-Wallis nonparametric test. Results: We found statistical significance (P < .05) between SL and raised hs-CRP, raised leptine and low chemerine. Conclusions: i) There seems to be an underlying inflammatory component (raised hs-CRP) in SL; ii) adipokine alteration (raised leptine and low chemerine) supports the idea that adipocytic differentiation is affected in SL, and iii) we have not found any immune marker associated with SL, except chemerine itself, which could explain a possible association between SL and immunity (AU)

[Occupational semicircular lipoatrophy associated with serum adipokine abnormalities]. / Lipoatrofia semicircular de etiología laboral asociada a alteraciones séricas de adipocinas.

OBJECTIVES: The aim of this study was to examine the relationship between semicircular lipoatrophy (SL), inflammation marker (high sensibility C-reactive protein [hs-CRP]), adipokines (leptine, chemerine and vaspine) and autoimmune markers (rheumatoid factor [RF], C3 and C4 complement fractions, antinuclear antibodies [ANA], HLA DR3, and DR4). Chemerine is an adipokine, but also is an immunity marker. METHODS: A case-control study was performed in May 2013; 21 cases were included. The closest healthy coworker to each case was used as a control. We calculated Kruskal-Wallis nonparametric test. RESULTS: We found statistical significance (P<.05) between SL and raised hs-CRP, raised leptine and low chemerine. CONCLUSIONS: i) There seems to be an underlying inflammatory component (raised hs-CRP) in SL; ii) adipokine alteration (raised leptine and low chemerine) supports the idea that adipocytic differentiation is affected in SL, and iii) we have not found any immune marker associated with SL, except chemerine itself, which could explain a possible association between SL and immunity.

A probabilistic model of reserve design.

We develop a probabilistic approach to optimum reserve design based on the species-area relationship. Specifically, we focus on the distribution of areas among a set of reserves maximizing biodiversity. We begin by presenting analytic solutions for the neutral case in which all species have the same colonization probability. The optimum size distribution is determined by the local-to-regional species richness ratio k. There is a critical k(t) ratio defined by the number of reserves raised to the scaling exponent of the species-area relationship. Below k(t), a uniform area distribution across reserves maximizes biodiversity. Beyond k(t), biodiversity is maximized by allocating a certain area to one reserve and uniformly allocating the remaining area to the other reserves. We proceed by numerically exploring the robustness of our analytic results when departing from the neutral assumption of identical colonization probabilities across species.