¿Pueden núcleos de galaxias enanas dar origen a cúmulos globulares?

Las galaxias elípticas gigantes pueden tener una población del orden de miles de cúmulos globulares, tal como M87 en el centro del cúmulo de Virgo, mientras que otras galaxias, como la Vía Láctea, solo poseen unos cientos de ellos. Una posible explicación del origen de sistemas de cúmulos globulares tan numerosos es que parte de los mismos sean núcleos de galaxias enanas nucleadas, que originariamente pertenecían al cúmulo de Virgo y luego fueron capturadas por M87, perdiendo durante el proceso sus capas exteriores. Se realizaron simulaciones numéricas con la finalidad de comprobar si dicho mecanismo es factible y los resultados indican que los núcleos de las galaxias enanas nucleadas logran sobrevivir mientras que las galaxias enanas no nucleadas se desintegran completamente después de algunos pasajes pericéntricos. Para obtener remanentes similares a cúmulos globulares, tanto en tamaño como en luminosidad, se necesitan distancias pericéntricas cortas, pues los pasajes distantes dan como resultado remanentes al menos un orden de magnitud mayores. Para poder dirimir la cuestión sería útil realizar una búsqueda de remanentes grandes en los alrededores de M87.Asociación Argentina de Astronomí

Función luminosidad de cúmulos globulares de galaxias elípticas

Se está llevando a cabo un estudio de función luminosidad de galaxias elípticas en diferentes entornos. Se busca correlacionar observaciones con resultados obtenidos mediante simulaciones numéricas (Muzzio et al. 1984, Rabolli, 1990). En este caso se presentan observaciones de cuatro galaxias elípticas del cúmulo de Fornax (d = 22.9 Mpc): NGC 1379 y NGC 1399, que se sabe tienen abundante cantidad de cúmulos globulares (Harris, 1988), y NGC 1351 y NGC 1427, ubicadas a distancias mayores del centro del cúmulo. Las observaciones fueron realizadas utilizando el EFOSC (Faint Object Spectrograph and Camera) en el telescopio de 3.6m del ESO (La Silla, Chile). Se tomaron campos alrededor de cada una de las galaxias en tres colores (B, V y R). Se obtuvieron cuatro exposiciones para cada color, de modo que el tiempo total de integración para cada filtro y campo es de 60 min. Se deriva la función luminosidad de los cúmulos globulares. Para NGC 1399, se observa un exceso de objetos cerca del centro de la galaxia que se supone se debe a los cúmulos globulares asociados a la misma. Teniendo en cuenta una función luminosidad promedio para las galaxias débiles del background, se encuentra un claro "turnover" de la función luminosidad de los cúmulos globulares de NGC 1399 en m(B) = 24.8 mag, m(V) = 24.0 mag y m(R) = 23.4 mag.Asociación Argentina de Astronomí

Interacción entre una galaxia gigante y una enana

Se realizan simulaciones numéricas del encuentro de dos galaxias con el propósito de estudiar la posibilidad que los núcleos de galaxias enanas pasen a formar parte del sistema de cúmulos globulares de galaxias gigantes, de acuerdo con los resultados observacionales de Zinnecker et al. (1988).Asociación Argentina de Astronomí

Exercise induces new cardiomyocyte generation in the adult mammalian heart.

Loss of cardiomyocytes is a major cause of heart failure, and while the adult heart has a limited capacity for cardiomyogenesis, little is known about what regulates this ability or whether it can be effectively harnessed. Here we show that 8 weeks of running exercise increase birth of new cardiomyocytes in adult mice (~4.6-fold). New cardiomyocytes are identified based on incorporation of 15N-thymidine by multi-isotope imaging mass spectrometry (MIMS) and on being mononucleate/diploid. Furthermore, we demonstrate that exercise after myocardial infarction induces a robust cardiomyogenic response in an extended border zone of the infarcted area. Inhibition of miR-222, a microRNA increased by exercise in both animal models and humans, completely blocks the cardiomyogenic exercise response. These findings demonstrate that cardiomyogenesis can be activated by exercise in the normal and injured adult mouse heart and suggest that stimulation of endogenous cardiomyocyte generation could contribute to the benefits of exercise

Innate immune activation by inhaled lipopolysaccharide, independent of oxidative stress, exacerbates silica-induced pulmonary fibrosis in mice

Acute exacerbations of pulmonary fibrosis are characterized by rapid decrements in lung function. Environmental factors that may contribute to acute exacerbations remain poorly understood. We have previously demonstrated that exposure to inhaled lipopolysaccharide (LPS) induces expression of genes associated with fibrosis. To address whether exposure to LPS could exacerbate fibrosis, we exposed male C57BL/6 mice to crystalline silica, or vehicle, followed 28 days later by LPS or saline inhalation. We observed that mice receiving both silica and LPS had significantly more total inflammatory cells, more whole lung lavage MCP-1, MIP-2, KC and IL-1β, more evidence of oxidative stress and more total lung hydroxyproline than mice receiving either LPS alone, or silica alone. Blocking oxidative stress with N-acetylcysteine attenuated whole lung inflammation but had no effect on total lung hydroxyproline. These observations suggest that exposure to innate immune stimuli, such as LPS in the environment, may exacerbate stable pulmonary fibrosis via mechanisms that are independent of inflammation and oxidative stress. © 2012 Brass et al

In Vivo Quantitative Study of Sized-Dependent Transport and Toxicity of Single Silver Nanoparticles Using Zebrafish Embryos

Nanomaterials possess distinctive physicochemical properties (e.g., small sizes and high surface area-to-volume ratios) and promise a wide variety of applications, ranging from the design of high quality consumer products to effective disease diagnosis and therapy. These properties can lead to toxic effects, potentially hindering advances in nanotechnology. In this study, we have synthesized and characterized purified and stable (nonaggregation) silver nanoparticles (Ag NPs, 41.6 ± 9.1 nm in average diameter) and utilized early developing (cleavage-stage) zebrafish embryos (critical aquatic and eco- species) as in vivo model organisms to probe the diffusion and toxicity of Ag NPs. We found that single Ag NPs (30-72 nm diameters) passively diffused into the embryos through chorionic pores via random Brownian motion and stayed inside the embryos throughout their entire development (120 hours-post-fertilization, hpf). Dose-and size-dependent toxic effects of the NPs on embryonic development were observed, showing the possibility of tuning biocompatibility and toxicity of the NPs. At lower concentrations of the NPs (≤0.02 nM), 75-91% of embryos developed into normal zebrafish. At the higher concentrations of NPs (≥0.20 nM), 100% of embryos became dead. At the concentrations in between (0.02-0.2 nM), embryos developed into various deformed zebrafish. Number and sizes of individual Ag NPs embedded in tissues of normal and deformed zebrafish at 120 hpf were quantitatively analyzed, showing deformed zebrafish with higher number of larger NPs than normal zebrafish and size-dependent nanotoxicity. By comparing with our previous studies of smaller Ag NPs (11.6 ± 3.5 nm), we found striking size-dependent nanotoxicity that, at the same molar concentration, the larger Ag NPs (41.6 ± 9.1 nm) are more toxic than the smaller Ag NPs (11.6 ± 3.5 nm)

Regulation of Macrophage Motility by the Water Channel Aquaporin-1: Crucial Role of M0/M2 Phenotype Switch

The water channel aquaporin-1 (AQP1) promotes migration of many cell types. Although AQP1 is expressed in macrophages, its potential role in macrophage motility, particularly in relation with phenotype polarization, remains unknown. We here addressed these issues in peritoneal macrophages isolated from AQP1-deficient mice, either undifferentiated (M0) or stimulated with LPS to orientate towards pro-inflammatory phenotype (classical macrophage activation; M1). In non-stimulated macrophages, ablation of AQP1 (like inhibition by HgCl2) increased by 2-3 fold spontaneous migration in a Src/PI3K/Rac-dependent manner. This correlated with cell elongation and formation of lamellipodia/ruffles, resulting in membrane lipid and F4/80 recruitment to the leading edge. This indicated that AQP1 normally suppresses migration of resting macrophages, as opposed to other cell types. Resting Aqp1-/- macrophages exhibited CD206 redistribution into ruffles and increased arginase activity like IL4/IL13 (alternative macrophage activation; M2), indicating a M0-M2 shift. In contrast, upon M1 orientation by LPS in vitro or peritoneal inflammation in vivo , migration of Aqp1-/- macrophages was reduced. Taken together, these data indicate that AQP1 oppositely regulates macrophage migration, depending on stimulation or not by LPS, and that macrophage phenotypic and migratory changes may be regulated independently of external cues