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Bisi Melissa Cláudia do Prado Aline Defaveri Piovesan Deise Marcela Bredemeier Markus da Silveira Inês Guimarães Mendonça José Alexandre Staub Henrique Luiz 《Clinical rheumatology》2018,37(3):855-855
Clinical Rheumatology - The original version of this article, unfortunately, contained an error. One of the author's name on this article was incorrectly spelled as “José Alexandre... 相似文献
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Eduardo Alexandre Loth Samia Khalil Biazim José Henrique Fermino Ferreira dos Santos Rosana Puccia Rosimeire Costa Brancalh?o Lucinéia de Fátima Chasco Rinaldo Ferreira Gandra Rita de Cássia Garcia Sim?o Marcello Fabiano de Franco 《Revista do Instituto de Medicina Tropical de S?o Paulo》2014,56(3):259-264
Paracoccidioidomycosis (PCM) is caused by the dimorphic fungus
Paracoccidioides brasiliensis (Pb) and corresponds to prevalent
systemic mycosis in Latin America. The aim of the present work was to evaluate the
dose response effect of the fungal yeast phase for the standardization of an
experimental model of septic arthritis. The experiments were performed with groups of
14 rats that received doses of 103, 104 or 105
P. brasiliensis (Pb18) cells. The fungi were injected in 50 µL of
phosphate-buffered saline (PBS) directly into the knee joints of the animals. The
following parameters were analyzed in this work: the formation of swelling in knees
infused with yeast cells and the radiological and anatomopathological alterations,
besides antibody titer by ELISA. After 15 days of infection, signs of inflammation
were evident. At 45 days, some features of damage and necrosis were observed in the
articular cartilage. The systemic dissemination of the fungus was observed in 11% of
the inoculated animals, and it was concluded that the experimental model is able to
mimic articular PCM in humans and that the dose of 105 yeast cells can be
used as standard in this model. 相似文献
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Arnaud Jabouille Maylis Delugin Rapha?l Pineau Alexandre Dubrac Fabienne Soulet Stéphanie Lhomond Nestor Pallares-Lupon Hervé Prats Andreas Bikfalvi Eric Chevet Christian Touriol Michel Moenner 《Oncotarget》2015,6(28):24922-24934
IRE1α is an endoplasmic reticulum (ER)-resident transmembrane signaling protein and a cellular stress sensor. The protein harbors a cytosolic dual kinase/endoribonuclease activity required for adaptive responses to micro-environmental changes. In an orthotopic xenograft model of human glioma, invalidation of IRE1α RNase or/and kinase activities generated tumors with remarkably distinct phenotypes. Contrasting with the extensive angiogenesis observed in tumors derived from control cells, the double kinase/RNase invalidation reprogrammed mesenchymal differentiation of cancer cells and produced avascular and infiltrative glioblastomas with blood vessel co-option. In comparison, selective invalidation of IRE1α RNase did not compromise tumor angiogenesis but still elicited invasive features and vessel co-option. In vitro, IRE1α RNase deficient cells were also endowed with a higher ability to migrate. Constitutive activation of both enzymes led to wild-type-like lesions. The presence of IRE1α, but not its RNase activity, is therefore required for glioblastoma neovascularization, whereas invasion results only from RNase inhibition. In this model, two key mechanisms of tumor progression and cancer cell survival are functionally linked to IRE1α. 相似文献