ANÁLISE DAS MUDANÇAS DOS FATORES DETERMINANTES DA ESTRUTURA DE CAPITAL EM FUNÇÃO DO CICLO DE VIDA DAS EMPRESAS BRASILEIRAS SÃO BERNARDO DO CAMPO

As várias teorias acerca da estrutura de capital despertam interesse motivando diversos estudos sobre o assunto sem, no entanto, ter um consenso. Outro tema aparentemente pouco explorado refere-se ao ciclo de vida das empresas e como ele pode influenciar a estrutura de capital. Este estudo teve como objetivo verificar quais determinantes possuem maior relevância no endividamento das empresas e se estes determinantes alteram-se dependendo do ciclo de vida da empresa apoiada pelas teorias Trade Off, Pecking Order e Teoria da Agência. Para alcançar o objetivo deste trabalho foi utilizado análise em painel de efeito fixo sendo a amostra composta por empresas brasileiras de capital aberto, com dados secundários disponíveis na Economática® no período de 2005 a 2013, utilizando-se os setores da BM&FBOVESPA. Como resultado principal destaca-se o mesmo comportamento entre a amostra geral, alto e baixo crescimento pelo endividamento contábil para o determinante Lucratividade apresentando uma relação negativa, e para os determinantes Oportunidade de Crescimento e Tamanho, estes com uma relação positiva. Para os grupos de alto e baixo crescimento alguns determinantes apresentaram resultados diferentes, como a singularidade que resultou significância nestes dois grupos, sendo positiva no baixo crescimento e negativa no alto crescimento, para o valor colateral dos ativos e benefício fiscal não dívida apresentaram significância apenas no grupo de baixo crescimento. Para o endividamento a valor de mercado foi observado significância para o Benefício fiscal não dívida e Singularidade. Este resultado reforça o argumento de que o ciclo de vida influência a estrutura de capital

Transglutaminase 2 null macrophages respond to lipopolysaccharide stimulation by elevated proinflammatory cytokine production due to an enhanced αvβ3 integrin-induced Src tyrosine kinase signaling

Transglutaminase 2 (TG2) is a protein crosslinking enzyme with several additional biochemical functions. Loss of TG2 in vivo results in impaired phagocytosis of apoptotic cells and altered proinflammatory cytokine production by macrophages engulfing apoptotic cells leading to autoimmunity. It has been proposed that TG2 acts as an integrin ß(3) coreceptor in the engulfment process, while altered proinflammatory cytokine production is related to the lack of latent TGFß activation by TG2 null macrophages. Here we report that TG2 null macrophages respond to lipopolysaccharide treatment by elevated IL-6 and TNFa production. Though TGFß has been proposed to act as a feed back regulator of proinflammatory cytokine production in LPS-stimulated macrophages, this phenomenon is not related to the lack of active TGFß production. Instead, in the absence of TG2 integrin ß(3) maintains an elevated basal Src family kinase activity in macrophages, which leads to enhanced phosphorylation and degradation of the I?Ba. Low basal levels of I?Ba explain the enhanced sensitivity of TG2 null macrophages to signals that regulate NF-?B. Our data suggest that TG2 null macrophages bear a proinflammatory phenotype, which might contribute to the enhanced susceptibility of these mice to develop autoimmunity and atherosclerosis.

Problems with formative and higher-order reflective variables

Cadogan and Lee (this issue) discuss the problems inherent in modeling formative latent variables as endogenous. In response to the commentaries by Rigdon (this issue) and Finn and Wang (this issue), the present article extends the discussion on formative measures. First, the article shows that regardless of whether statistical identification is achieved, researchers are unable to illuminate the nature of a formative latent variable. Second, the study clarifies issues regarding formative indicator weighting, highlighting that the weightings of formative components should be specified as part of the construct definition. Finally, the study shows that higher-order reflective constructs are invalid, highlights the damage their use can inflict on theory development and knowledge accumulation, and provides recommendations on a number of alternative models which should be used in their place (including the formative model). © 2012 Elsevier Inc.

Impaired sensitivity to dynamic stimuli in poor readers of a regular orthography

The mappings from grapheme to phoneme are much less consistent in English than they are for most other languages. Therefore, the differences found between English-speaking dyslexics and controls on sensory measures of temporal processing might be related more to the irregularities of English orthography than to a general deficit affecting reading ability in all languages. However, here we show that poor readers of Norwegian, a language with a relatively regular orthography, are less sensitive than controls to dynamic visual and auditory stimuli. Consistent with results from previous studies of English-readers, detection thresholds for visual motion and auditory frequency modulation (FM) were significantly higher in 19 poor readers of Norwegian compared to 22 control readers of the same age. Over two-thirds (68.4%) of the children identified as poor readers were less sensitive than controls to either or both of the visual coherent motion or auditory 2Hz FM stimuli. © 2003 Elsevier Science (USA). All rights reserved.