Deposição de nutrientes na carcaça de girinos de rã-touro

O objetivo deste trabalho foi determinar a deposição de nutrientes na carcaça de girinos de rã-touro (Lithobates catesbeianus) por meio de modelo não linear. Foram utilizados 2.700 girinos com peso médio inicial de 0,039 g. Ração comercial farelada com 55% de proteína bruta foi fornecida ad libitum. Os animais foram pesados e avaliados a cada dez dias para análise dos conteúdos de proteína bruta, extrato etéreo, água e sais minerais. Os parâmetros do modelo Gompertz foram estimados pelo método de Gauss-Newton modificado, e as taxas de deposição (g por dia) em função do tempo foram calculadas por meio da derivada da equação. Os valores encontrados para os parâmetros da equação de Gompertz, para descrever a deposição dos nutrientes na carcaça de girinos, apresentaram interpretação biológica. A taxa máxima (t*) de deposição foi observada aos 36,2331 dias para proteína, aos 37,1420 dias para água, aos 35,2971 dias para sais minerais, e aos 41,3547 dias para gordura. O consumo de nutrientes da dieta é maior do que a taxa de deposição na carcaça dos girinos.

Legal issues in promoting FOSS in R+D projects - Policy, Organisation and Management

Creating and using FLOSS in R+D projects raises several legal issues, which need to be managed as soon as possible - preferably during the project planning stage. Challenges in the areas of project structure and policy, licenses and licensing, exploitation strategies, community management, and FLOSS-friendliness in general all have their legal aspects, which are commented here. Some recommendations are made for assisting in the use of FLOSS in R+D projects, especially in multiple party consortiums.

Licensing Review in R+D Projects

FOSS packages are becoming ever more present in R&D projects carried out a variety of entities, including large corporations. I will focus on how legal risks associated with the use of FOSS licenses can be assessed and discuss measures directed to risk mitigation.

Are R&D collaborative agreements persistent at the firm level? Empirical evidence for the Spanish case

We provide evidence on the dynamics in firms’ R&D cooperation behaviour. Our main objective is to analyse if R&D collaborative agreements are persistent at the firm level, and in such a case, to study what are the main drivers of this phenomenon. R&D cooperation activities at the firm level can be persistent due to true state dependence, this implying that cooperating in a given period enhances the probability of doing it in the subsequent period and it can also be a consequence of firms’ individual heterogeneity, so that certain firms have certain characteristics that make them more likely to carry out technological alliances.

Are R&D collaborative agreements persistent at the firm level? Empirical evidence for the Spanish case

We provide evidence on the dynamics in firms’ R&D cooperation behaviour. Our main objective is to analyse if R&D collaborative agreements are persistent at the firm level, and in such a case, to study what are the main drivers of this phenomenon. R&D cooperation activities at the firm level can be persistent due to true state dependence, this implying that cooperating in a given period enhances the probability of doing it in the subsequent period and it can also be a consequence of firms’ individual heterogeneity, so that certain firms have certain characteristics that make them more likely to carry out technological alliances.

IAP antagonists target cIAP1 to induce TNFalpha-dependent apoptosis.

XIAP prevents apoptosis by binding to and inhibiting caspases, and this inhibition can be relieved by IAP antagonists, such as Smac/DIABLO. IAP antagonist compounds (IACs) have therefore been designed to inhibit XIAP to kill tumor cells. Because XIAP inhibits postmitochondrial caspases, caspase 8 inhibitors should not block killing by IACs. Instead, we show that apoptosis caused by an IAC is blocked by the caspase 8 inhibitor crmA and that IAP antagonists activate NF-kappaB signaling via inhibtion of cIAP1. In sensitive tumor lines, IAP antagonist induced NF-kappaB-stimulated production of TNFalpha that killed cells in an autocrine fashion. Inhibition of NF-kappaB reduced TNFalpha production, and blocking NF-kappaB activation or TNFalpha allowed tumor cells to survive IAC-induced apoptosis. Cells treated with an IAC, or those in which cIAP1 was deleted, became sensitive to apoptosis induced by exogenous TNFalpha, suggesting novel uses of these compounds in treating cancer.