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listelement.badge.dso-typeItem, Implementação de suporte à alta disponibilidade em ambientes NFV usando OSM(Universidade Federal de São Carlos, 2018-05-23) Saito, Alexis Seiki; Verdi, Fábio Luciano; https://lattes.cnpq.br/9143186843657940; https://lattes.cnpq.br/4608719952884975High Availability is the most important aspect when discussing resiliency over telecommunications systems in the context of the adoption of the cloud computing paradigm, a big challenge for telecommunications service providers. Initiatives of NFV platform implementations like OpenMANO (strongly based on NFV standardization from ETSI) serve as base to run experiments like the one proposed in this master project, in which we describe our contribution to an implementation of management for high availability on top of platform proposed by Open Source MANO (OSM). The high availability implementation presented in this project is adherent to ETSI standardization and contributes to one of the most important NFV frameworks that up to now has not presented support to such feature. In this project, we present an experimentation over OSM implementation which involves the whole environment with its technological complexity. In concrete terms, our contribution addresses two main aspects: a proposal for information modeling based on ETSI standardization on high availability and its implementation in the OSM framework. Such implementation consists in the detection of failure by the orchestrator implying in a network reconfiguration as a mechanism to support redundancy in an active-active scenario. The experiment was tested and evaluated in a real minimalist environment to demonstrate the implementation performed to manage high availability information and re-orchestrate data flows between redundant VNFs.listelement.badge.dso-typeItem, Inibição do cross-talk entre alfa (v) beta (3) e VEGFR2 na angiogênese pela desintegrina DisBa-01(Universidade Federal de São Carlos, 2018-05-23) Danilucci, Taís Marolato; Araújo, Heloísa Sobreiro Selistre de; https://lattes.cnpq.br/4065824911933203; https://lattes.cnpq.br/8809608503567793Angiogenesis, a process by which new capillaries are formed from pre-existing vasculature, is essential in both physiological and pathological conditions. Inadequate balance between pro and antiangiogenic factors can contribute to the progression of tumors and development of metastases. The αvβ3 integrin is considered an angiogenic regulatory receptor due to its cross-talk with vascular endothelial growth factor receptor 2 (VEGFR2). Understanding how these components functionally interact as angiogenic repressors is crucial for the identification of new therapeutic strategies. Disintegrins comprise a family of low molecular weight, cystein-rich peptides from snake venoms that specifically bind to integrins, inhibiting their functions. DisBa-01, a recombinant RGD (Arginine - Glycine - Aspartic acid)-disintegrin from Bothrops alternatus venom, has high affinity for αvβ3, exhibiting anti-metastatic and anti-angiogenic properties. However, its role in the cross-talk between β3 integrin and VEGFR2 in addition to its involvement in downstream signaling pathways, has not been explored. The present study has shown in vitro evidences regarding the direct association between DisBa-01 and the β3/VEGFR2 complex in human umbilical endothelial cells. DisBa-01 inhibited VEGF-induced viability, migration, invasion, adhesion to vitronectin and tubulogenesis, thus decreasing the angiogenic response. DisBa-01 treatment did not affect β3 expression, however, it decreased VEGFR2 protein expression. VEGF-mediated phosphorylation of both receptors was inhibited, causing downregulation of ERK1/2 and PI3K signaling pathways. DisBa-01 positively regulated FAK/Src/Paxillin downstream signal, affecting actin cytoskeleton reorganization, cell migration and adhesion. In conclusion, DisBa-01 impairs the β3/VEGFR2 cross-talk in HUVECs, which interferes in the signaling pathways of ERK1/2, PI3K, FAK, Src and Paxillin, resulting in anti-angiogenic action and cellular morphological alterations. Moreover, these results indicate a strong regulatory role of αvβ3 integrin on VEGF-induced angiogenesis.