Estudo do processo de abertura de capital : análise temporal dos IPO’s no Brasil de 2008 a 2012

Orientadora : Paula Mussi Szabo CherobimMonografia (especialização) - Universidade Federal do Paraná, Setor de Ciências Sociais Aplicadas. Curso de Especialização em Contabilidade e FinançasInclui referênciasResumo : O crescimento das empresas é acompanhado da necessidade crescente de recursos, seja para ampliação da capacidade instalada e incremento da produção, investimento em pesquisa e desenvolvimento, ou reforço no capital de giro para fazer frente às novas despesas. Este estudo trata, portanto, da Oferta Pública Inicial (IPO, na sigla em inglês), modalidade de captação de recursos financeiros junto ao mercado, seu conceito e funcionamento, bem como faz um levantamento do desempenho das empresas que realizaram IPO de 2008 a 2012, apontando os cinco maiores e menores desempenho. É um trabalho qualitativo o quantitativo quanto aos procedimentos, descritivo quanto aos objetivos e fundamentado em revisão teórica. Como amostragem obteve-se 33 (trinta e três) empresas que abriram o capital no período compreendido entre 2008 e 2012. O levantamento dos maiores e menores resultados foi elaborado com base na valorização ou desvalorização das ações das empresas. O trabalho concluiu que o IPO é uma importante forma de captação de recursos para as empresas, desde que se observe custos e legislação, como também se compare com outras fontes de financiamento

A relação entre independência do Conselho de administração e maturidade da dívida em empresas com ações listadas na BM&FBOVESPA

Orientador : Prof. Dr. Ademir ClementeDissertação (mestrado) - Universidade Federal do Paraná, Setor de Ciências Sociais Aplicadas, Programa de Pós-Graduação em Contabilidade. Defesa: Curitiba, 2016Inclui referências : f. 64-75Área de concentração : Contabilidade e finançasResumo: A presente pesquisa tem como objetivo estudar e identificar a existência de relação entre independência do conselho de administração e maturidade da dívida nas empresas com ações listadas na BM&FBOVESPA, considerando o período de 2010 a 2014. Com embasamento em importantes trabalhos aplicados no mercado norte-americano, este trabalho empregará abordagem descritiva, explicativa e documental com análise de dados em painel, procurando constatar a ocorrência da relação no âmbito das empresas brasileiras de capital aberto, além de levantar algumas explicações para a ocorrência ou não do fenômeno neste ambiente. Devido a possibilidade de ocorrência de endogeneidade entre decisões de maturidade da dívida e endividamento, conforme descrito na literatura pertinente, foram realizados testes de simultaneidade, onde não se constatou o fenômeno supracitado. Houve relação significativa entre maturidade da dívida e variáveis explicativas, porém o mesmo efeito não foi percebido entre maturidade da dívida e independência do conselho de administração. Tal fato pode sugerir que, embora o tema Governança Corporativa ganhe cada vez mais força no mundo contemporâneo, e uma "cadeira" no conselho de administração seja muito disputada entre acionistas, não há uma preocupação pontual do conselho independente com maturidade da dívida, e que dados de crescimento e rentabilidade ainda ocupem as principais pautas das reuniões. Cabe ressaltar que as objeções conclusivas desta pesquisa se aplicam apenas ao conjunto de empresas estudas, haja vista se tratar de amostra não-probabilística. Palavras-chave: Maturidade da Dívida. Independência do Conselho de Administração. Análise de dados em painel.Abstract: This research aims to study and identify the existence of relationship between independence of the board and maturity of the debt of companies with shares listed on BM & FBOVESPA, considering the period from 2010 to 2014. With background in important works applied in the North American market this work will use descriptive, explanatory and documentary approach with panel data analysis, trying to prove the occurrence of the relationship in the context of Brazilian public companies, as well as raise some explanations for the presence or absence of the phenomenon in this environment. Because of the possibility of endogeneity between debt and debt maturity decisions, as described in the relevant literature, concurrency tests were performed, where there was not found the above phenomenon. There was a significant relationship between debt maturity and explanatory variables, but the same effect was not seen between debt maturity and independence of the board. This may suggest that although the topic Corporate Governance will become even stronger in the contemporary world, and a "chair" on the board is much disputed among shareholders, there isn't a specific concern of independent advice with debt maturity, and data growth and profitability still occupy the main agendas of meetings. It notes that the conclusive objections of this research apply only to the set of companies studied, considering the case of non-probabilistic sample. Keywords: Debt Maturity. Independence of the Board of Directors. Panel Data Analysis

Investigation of the interaction between Ebola virus and the host

Ebola viruses cause viral haemorrhagic fever in humans and non human primates. Due to the severity of their symptoms, the lack of an approved treatment or vaccine, and the mechanism of transmission, these viruses have been classified as containment level 4 (CL4) pathogens. In December 2013, an Ebola virus outbreak initiated in West Africa, which lasted more than two years, and has been considered the worst outbreak in the history of the Ebola viruses. More than twenty-seven thousand people had a positive diagnosis of infection with more than eleven thousand confirmed dead. This outbreak highlights not only the urgent necessity for new treatments and vaccines against this virus but also that there is still a large knowledge gap for Ebola viruses compared to other pathogens. This thesis focuses on using high resolution approaches to characterise the interaction between the Zaire ebolavirus species (EBOV) and the host. The work focuses on using high resolution sequencing to characterise the evolution of EBOV throughout the outbreak in West Africa and also in adapting to grow in a novel host. The work also focuses on two viral proteins that are critical to the virus life cycle. The VP24 protein that is an interferon antagonist and the nucleoprotein (NP) which encapsidates the viral genome. Quantitative proteomics was used to identify host cell proteins that interacted with these viral proteins and inhibitors were used to ablate cellular protein function and monitor the effect on viral biology. The thesis is written in the style of ‘by publication’ and the publications associated with this work are reproduced in the Appendix

EMISSÕES DE GASES DO EFEITO ESTUFA DA QUEIMA DE PELLETS DE MADEIRA

As previsões indicam crescimento do uso da biomassa florestal como recurso energético nos próximos anos, sobretudo depois dos recentes acordos firmados pela Cúpula do Clima em Paris (COP21), que apontam a necessidade de substituir combustíveis fósseis por fontes renováveis e de baixas emissões de gases do efeito estufa (GEE). Há poucos estudos relacionando a combustão dos pellets de madeira com os limites dessas emissões estabelecidos para a biomassa florestal. Este estudo comparou as emissões da combustão dos pellets com os limites máximos estabelecidos na Resolução nº 436 do CONAMA. Utilizou-se quatro amostras de pellets de madeira e três biomassas florestais (casca de pinus, cavacos de pinus e serragem de eucalipto). Para a combustão foi utilizado um queimador de biomassa vegetal, com alimentação automática e consumo de 14 kg por hora. As análises das emissões foram realizadas com o analisador eletroquímico Unigas 3000 MKIII, que determinou a composição química dos gases da combustão. Os resultados mostraram que os pellets de madeira têm baixas emissões de CO, NOx e SOx. Assim, conclui-se que as biomassas florestais atendem aos limites de emissões gasosas estabelecidos pela legislação vigente, com exceção da serragem de eucalipto e a casca de pinus

Identification of a small molecule inhibitor of Ebolavirus genome replication and transcription using in silico screening.

Ebola virus (EBOV) causes a severe haemorrhagic fever in humans and has a mortality rate over 50%. With no licensed drug treatments available, EBOV poses a significant threat. Investigations into possible therapeutics have been severely hampered by the classification of EBOV as a BSL4 pathogen. Here, we describe a drug discovery pathway combining in silico screening of compounds predicted to bind to a hydrophobic pocket on the nucleoprotein (NP); with a robust and rapid EBOV minigenome assay for inhibitor validation at BSL2. One compound (MCCB4) was efficacious (EC50 4.8 μM), exhibited low cytotoxicity (CC50 > 100 μM) and was specific, with no effect on either a T7 RNA polymerase driven firefly luciferase or a Bunyamwera virus minigenome. Further investigations revealed that this small molecule inhibitor was able to outcompete established replication complexes, an essential aspect for a potential EBOV treatment

A comparison of host gene expression signatures associated with infection in vitro by the Makona and Ecran (Mayinga) variants of Ebola virus

The Ebola virus (EBOV) variant Makona (which emerged in 2013) was the causative agent of the largest outbreak of Ebola Virus Disease recorded. Differences in virus-host interactions between viral variants have potential consequences for transmission, disease severity and mortality. A detailed profile of the cellular changes induced by the Makona variant compared with other Ebola virus variants was lacking. In this study, A549 cells, a human cell line with a robust innate response, were infected with the Makona variant or with the Ecran variant originating from the 1976 outbreak in Central Africa. The abundance of viral and cellular mRNA transcripts was profiled using RNASeq and differential gene expression analysis performed. Differences in effects of each virus on the expression of interferon-stimulated genes were also investigated in A549 NPro cells where the type 1 interferon response had been attenuated. Cellular transcriptomic changes were compared with those induced by human respiratory syncytial virus (HRSV), a virus with a similar genome organisation and replication strategy to EBOV. Pathway and gene ontology analysis revealed differential expression of functionally important genes; including genes involved in the inflammatory response, cell proliferation, leukocyte extravasation and cholesterol biosynthesis. Whilst there was overlap with HRSV, there was unique commonality to the EBOV variants

African Swine Fever Virus Ubiquitin-Conjugating Enzyme Is an Immunomodulator Targeting NF-kappa B Activation

African swine fever virus (ASFV) is an acute and persistent swine virus with a high economic burden that encodes multiple genes to evade host immune response. In this work, we have revealed that early viral protein UBCv1, the only known conjugating enzyme encoded by a virus, modulates innate immune and inflammatory signaling. Transient overexpression of UBCv1 impaired activation of NF-κB and AP-1 transcription factors induced by several agonists of these pathways. In contrast, activation of IRF3 and ISRE signaling upon stimulation with TRIFΔRIP, cGAS/STING or RIG-I-CARD remained unaltered. Experiments aimed at mapping UBCv1 inhibitory activity indicated that this viral protein acts upstream or at the level step of IKKβ. In agreement with this, UBCv1 was able to block p65 nuclear translocation upon cytokine stimulation, a key event in NF-ĸB signaling. Additionally, A549 stably transduced for UBCv1 showed a significant decrease in the levels of NF-ĸB dependent genes. Interestingly, despite the well-defined capacity of UBCv1 to conjugate ubiquitin chains, a mutant disabled for ubiquitylation activity retained similar immunomodulatory activity as the wild-type enzyme, suggesting that the two functions are segregated. Altogether these data suggest that ASFV UBCv1 manipulates the innate immune response targeting the NF-κB and AP-1 pathways and opens new questions about the multifunctionality of this enzyme

Expression of the Ebola Virus VP24 Protein Compromises the Integrity of the Nuclear Envelope and Induces a Laminopathy- Like Cellular Phenotype

ABSTRACT Ebola virus (EBOV) VP24 protein is a nucleocapsid-associated protein that inhibits interferon (IFN) gene expression and counteracts the IFN-mediated antiviral response, preventing nuclear import of signal transducer and activator of transcription 1 (STAT1). Proteomic studies to identify additional EBOV VP24 partners have pointed to the nuclear membrane component emerin as a potential element of the VP24 cellular interactome. Here, we have further studied this interaction and its impact on cell biology. We demonstrate that VP24 interacts with emerin but also with other components of the inner nuclear membrane, such as lamin A/C and lamin B. We also show that VP24 diminishes the interaction between emerin and lamin A/C and compromises the integrity of the nuclear membrane. This disruption is associated with nuclear morphological abnormalities, activation of a DNA damage response, the phosphorylation of extracellular signal-regulated kinase (ERK), and the induction of interferon-stimulated gene 15 (ISG15). Interestingly, expression of VP24 also promoted the cytoplasmic translocation and downmodulation of barrier-to-autointegration factor (BAF), a common interactor of lamin A/C and emerin, leading to repression of the BAF-regulated CSF1 gene. Importantly, we found that EBOV infection results in the activation of pathways associated with nuclear envelope damage, consistent with our observations in cells expressing VP24. In summary, here we demonstrate that VP24 acts at the nuclear membrane, causing morphological and functional changes in cells that recapitulate several of the hallmarks of laminopathy diseases. IMPORTANCE The Ebola virus (EBOV) VP24 protein is a nucleocapsid-associated protein with multiple functions. Proteomic studies have identified the cellular nuclear membrane component emerin as a potential VP24 interactor. Here, we demonstrate that VP24 not only interacts with emerin but also with lamin A/C and lamin B, prompting nuclear membrane disruption. This disruption is associated with nuclear morphological abnormalities, activation of a DNA damage response, the phosphorylation of extracellular signal-regulated kinase (ERK), and the induction of interferon-stimulated gene 15 (ISG15). Interestingly, VP24 also promotes the cytoplasmic translocation and downmodulation of barrier-to-autointegration factor (BAF), leading to repression of the BAF-regulated CSF1 gene. Finally, we show that EBOV infection also results in the activation of pathways associated with nuclear envelope damage, consistent with our observations in cells expressing VP24. These results reveal novel activities of EBOV VP24 protein, resulting in a cell phenotype similar to that of most laminopathies, with potential impact on EBOV replication