Antiguo testamento

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Llamamiento eclesial y vocación sacerdotal

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La Biblia: su mundo y problemas

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La Biblia: comentarios y teología

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Pastoral

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The X-ray Emission from the Nucleus of the Dwarf Elliptical Galaxy NGC 3226

We present the first high resolution X-ray image of the dwarf elliptical galaxy NGC 3226. The data were obtained during an observation of the nearby Seyfert Galaxy NGC 3227 using the Chandra X-ray Observatory. We detect a point X-ray source spatially consistent with the optical nucleus of NGC 3226 and a recently-detected, compact, flat-spectrum, radio source. The X-ray spectrum can be measured up to ~10 keV and is consistent with a power law with a photon index 1.7 <~ Gamma <~ 2.2, or thermal bremmstrahlung emission with 4 <~ kT <~ 10 keV. In both cases the luminosity in the 2--10 keV band ~10^{40} h_{75}^{-1} erg/s. We find marginal evidence that the nucleus varies within the observation. These characteristics support evidence from other wavebands that NGC 3226 harbors a low-luminosity, active nucleus. We also comment on two previously-unknown, fainter X-ray sources <~ 15 arcsec from the nucleus of NGC 3226. Their proximity to the nucleus (with projected distances <~ 1.3/h_{75} kpc) suggests both are within NGC 3226, and thus have luminosities (~few x 10^{38} -- few x 10^{39} erg/s) consistent with black-hole binary systems.Comment: Accepted for publication in ApJ. Figures in colo

Sagrada escritura

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A functional IL1RL1 variant regulates corticosteroid-induced sST2 expression in ulcerative colitis

Indexación: Web of Science; Scopus.The ST2/IL33 signalling pathway has been associated with ulcerative colitis (UC). ST2, encoded by the IL1RL1 gene, is expressed as both a membrane-anchored receptor (ST2L) activated by IL33 and as a soluble receptor (sST2) with anti-inflammatory properties. In UC patients, sST2 is further increased by corticosteroid treatment; however, the glucocorticoid-mediated molecular regulation remains unknown. We therefore tested whether genetic variants in the IL1RL1 distal promoter are involved in UC and affect glucocorticoid-mediated ST2 expression. Serum ST2 levels and genetic variants in the IL1RL1 distal promoter were examined by ELISA and PCR sequencing in UC patients receiving corticosteroids. Glucocorticoid-mediated ST2 production was evaluated in intestinal mucosa cultures. Molecular regulation of glucocorticoid-mediated ST2 was assessed by RT-qPCR, ChIP assay and luciferase reporter assay. Dexamethasone effect on ST2 transcript expression was analyzed in leukocytes and related to IL1RL1 variants. Sequencing of a distal IL1RL1 promoter region demonstrated that SNPs rs6543115(C) and rs6543116(A) are associated with increased sST2 in UC patients on corticosteroids. Dexamethasone up-regulated sST2 transcription through interaction with the glucocorticoid-response element (GRE) carrying rs6543115(C) variant. Our data indicate that IL1RL1 SNPs rs6543115(C) confer susceptibility to UC and is contained in the GRE, which may modulate glucocorticoid-induced sST2 expression.https://www.nature.com/articles/s41598-017-10465-

Regulation of mammary gland branching morphogenesis by the extracellular matrix and its remodeling enzymes.

A considerable body of research indicates that mammary gland branching morphogenesis is dependent, in part, on the extracellular matrix (ECM), ECM-receptors, such as integrins and other ECM receptors, and ECM-degrading enzymes, including matrix metalloproteinases (MMPs) and their inhibitors, tissue inhibitors of metalloproteinases (TIMPs). There is some evidence that these ECM cues affect one or more of the following processes: cell survival, polarity, proliferation, differentiation, adhesion, and migration. Both three-dimensional culture models and genetic manipulations of the mouse mammary gland have been used to study the signaling pathways that affect these processes. However, the precise mechanisms of ECM-directed mammary morphogenesis are not well understood. Mammary morphogenesis involves epithelial 'invasion' of adipose tissue, a process akin to invasion by breast cancer cells, although the former is a highly regulated developmental process. How these morphogenic pathways are integrated in the normal gland and how they become dysregulated and subverted in the progression of breast cancer also remain largely unanswered questions