954 resultados para Siglos VI-V a.C.


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Young people are less explored in museum audience research; this is a paradoxical situation when considering its strategic location in the cultural reproduction and if considering the high performing cultural consumption compared with other sectors. The phenomenon of museums consumption by young Chileans who are self recognized as public and non-public museums is explored from a qualitative approach. It was conducted with focus groups in the three largest cities in Chile (Santiago, Valparaíso and Concepción). They identify the museum as a cultural institution in full force. However, in questioning museums activity youth reveal the specificity of their cultural matrix. This is referred to a social temporality based on the fragment, the discourse of familiarity, proximity and instead of breaking and critical. They claim a museum aesthetic / historical experience based on pleasure and enjoyment. An overview is proposed to further clarify the youth cultural consumption to characterize more precisely the place of the museum in the set, to design more effective policies museums.

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The HSP90 chaperone and immunophilin FKBPL is an estrogen-responsive gene that interacts with estogen receptor a (ERa) and regulates its levels. In this study, we explored the effects of FKBPL on breast cancer proliferation. Breast cancer cells stably overexpressing FKBPL became dependent on estrogen for their growth and were dramatically more sensitive to the antiestrogens tamoxifen and fulvestrant, whereas FKBPL knockdown reverses this phenotype. FKBPL knockdown also decreased the levels of the cell cycle inhibitor p21WAF1 and increased ERa phosphorylation on Ser118 in response to 17ß-estradiol and tamoxifen. In support of the likelihood that these effects explained FKBPL-mediated cell growth inhibition and sensitivity to endocrine therapies, FKBPL expression was correlated with increased overall survival and distant metastasis-free survival in breast cancer patients. Our findings suggest that FKBPL may have prognostic value based on its impact on tumor proliferative capacity and sensitivity to endocrine therapies, which improve outcome.

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The chemokine eotaxin/CCL11 is an important mediator of leukocyte migration, but its effect on inflammatory cytokine signaling has not been explored. In this study, we find that CCL11 induces suppressor of cytokine signaling (SOCS) 1 and SOCS3 expression in murine macrophages, human monocytes, and dendritic cells (DCs). We also discover that CCL11 inhibits GM-CSF-mediated STAT5 activation and IL-4-induced STAT6 activation in a range of hematopoietic cells. This blockade of cytokine signaling by CCL11 results in reduced differentiation and endocytic ability of DCs, implicating CCL11-induced SOCS as mediators of chemotactic inflammatory control. These findings demonstrate cross-talk between chemokine and cytokine responses, suggesting that myeloid cells tracking to the inflammatory site do not differentiate in the presence of this chemokine, revealing another role for SOCS in inflammatory regulation. J. Leukoc. Biol. 85: 289-297; 2009.

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Background: The insulin-degrading enzyme gene (IDE) is a strong functional and positional candidate for late onset Alzheimer's disease (LOAD).

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