13 resultados para downstream drift

em Universidade do Minho


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The increasing interest for greener and biological methods of synthesis has led to the development of non-toxic and comparatively more bioactive nanoparticles. Unlike physical and chemical methods of nanoparticle synthesis, microbial synthesis in general and mycosynthesis in particular is cost-effective and environment-friendly. However, different aspects, such as the rate of synthesis, monodispersity and downstream processing, need to be improved. Many fungal-based mechanisms have been proposed for the formation of silver nanoparticles (AgNPs), mainly those involving the presence of nitrate reductase, which has been detected in filtered fungus cell used for AgNPs production. There is a general acceptance that nitrate reductase is the main responsible for the reduction of Ag ions for the formation of AgNPs. However, this generally accepted mechanism for fungal AgNPs production is not totally understood. In order to elucidate the molecules participating in the mechanistic formation of metal nanoparticles, the current study is focused on the enzymes and other organic compounds involved in the biosynthesis of AgNPs. The use of each free fungal mycelium of both Stereum hirsutum and Fusarium oxysporum will be assessed. In order to identify defective mutants on the nitrate reductase structural gene niaD, fungal cultures of S.hirsutum and F.oxysporum will be selected by chlorate resistance. In addition, in order to verify if each compound identified as key-molecule influenced on the production of nanoparticles, an in vitro assay using different nitrogen sources will be developed. Lately, fungal extracellular enzymes will be measured and an in vitro assay will be done. Finally, The nanoparticle formation and its characterization will be evaluated by UV-visible spectroscopy, electron microscopy (TEM), X-ray diffraction analysis (XRD), Fourier transforms infrared spectroscopy (FTIR), and LC-MS/MS.

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For years, silk fibroin of a domestic silkworm, Bombyx mori, has been recognized as a valuable material and extensively used. In the last decades, new application fields are emerging for this versatile material. Those final, specific applications of silk dictate the way it has been processed in industry and research. This review focuses on the description of various approaches for silk downstream processing in a laboratory scale, that fall within several categories. The detailed description of workflow possibilities from the naturally found material to a finally formulated product is presented. Considerable attention is given to (bio-) chemical approaches of silk fibroin transformation, particularly, to its enzyme-driven modifications. The focus of the current literature survey is exclusively on the methods applied in research and not industry.

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FOSTER aims to support different stakeholders, especially young researchers, in adopting open access in the context of the European Research Area (ERA) and in complying with the open access policies and rules of participation set out for Horizon 2020 (H2020). FOSTER establish a European-wide training programme on open access and open data, consolidating training activities at downstream level and reaching diverse disciplinary communities and countries in the ERA. The training programme includes different approaches and delivery options: elearning, blearning, self-learning, dissemination of training materials/contents, helpdesk, face-to-face training, especially training-the-trainers, summer schools, seminars, etc.

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The current study describes the in vitro phosphorylation of a human hair keratin, using protein kinase for the first time. Phosphorylation of keratin was demonstrated by 31P NMR (Nuclear Magnetic Resonance) and Diffuse Reflectance Infrared Fourier Transform (DRIFT) techniques. Phosphorylation induced a 2.5 fold increase of adsorption capacity in the first 10 minutes for cationic moiety like Methylene Blue (MB). Thorough description of MB adsorption process was performed by several isothermal models. Reconstructed fluorescent microscopy images depict distinct amounts of dye bound to the differently treated hair. The results of this work suggest that the enzymatic phosphorylation of keratins might have significant implications in hair shampooing and conditioning, where short application times of cationic components are of prime importance.

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Dissertação de mestrado em Marketing e Estratégia

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Tese de Doutoramento em Biologia de Plantas.

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Tese de Doutoramento em Ciências da Saúde.

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Em 2008, o Governo português anunciou a iniciativa ‘e.escolinha’ que contemplou a distribuição de computadores ‘Magalhães’ aos alunos do 1º ciclo do ensino básico, durante três anos letivos consecutivos. Atualmente suspenso, o programa foi bandeira do XVII Governo Constitucional, liderado por José Sócrates, mas alvo de controvérsias por parte da oposição política e da comunidade escolar, sobretudo pela aparente tónica no acesso à tecnologia em vez de uma maior preocupação com a formação e as práticas pedagógicas. Ao abrigo do Plano Tecnológico da Educação, o ‘e.escolinha’ inseria-se numa política mais ampla para o desenvolvimento de uma economia competitiva e dinâmica, através das metas estabelecidas pela União Europeia na Estratégia de Lisboa 2000. A iniciativa foi apresentada ao país com objetivos ambiciosos, no que diz respeito às esperadas mudanças ao nível das práticas pedagógicas dos professores, do processo de aprendizagem das crianças e do sucesso escolar em geral. Porém, a face mais visível da política, embora possa compreender outros matizes, poderá ter ficado reduzida à questão do acesso, apostando pouco nas outras dimensões da literacia digital. Com base em entrevistas realizadas a atores-chave envolvidos no processo de conceção e implementação do ‘e.escolinha’, e nos documentos oficiais que enquadram o programa, o presente artigo pretende dar a conhecer a forma como decisores políticos e empresas enunciam e avaliam os objetivos desta iniciativa. Pretende-se, em particular, conhecer se partilham a ideia de uma deriva tecnológica desta medida governamental ou se entreveem, na mesma, objetivos de literacia digital. Este trabalho decorre do projeto de investigação “Navegando com o Magalhães: Estudo sobre o Impacto dos Media Digitais nas Crianças”, em curso no Centro de Estudos de Comunicação e Sociedade da Universidade do Minho, financiado pela Fundação para a Ciência e Tecnologia ((PTDC/CCI-COM/101381/2008) ) e co-financiado pelo FEDER (COMPETE: FCOMP-01-0124-FEDER-009056).

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Dissertação de mestrado integrado em Engenharia Civil

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Spinocerebellar ataxia type 3 (SCA3), also known as Machado-Joseph disease (MJD), is an untreatable autosomal dominant neurodegenerative disease, and the most common such inherited ataxia worldwide. The mutation in SCA3 is the expansion of a polymorphic CAG tri-nucleotide repeat sequence in the C-terminal coding region of the ATXN3 gene at chromosomal locus 14q32.1. The mutant ATXN3 protein encoding expanded glutamine (polyQ) sequences interacts with multiple proteins in vivo, and is deposited as aggregates in the SCA3 brain. A large body of literature suggests that the loss of function of the native ATNX3-interacting proteins that are deposited in the polyQ aggregates contributes to cellular toxicity, systemic neurodegeneration and the pathogenic mechanism in SCA3. Nonetheless, a significant understanding of the disease etiology of SCA3, the molecular mechanism by which the polyQ expansions in the mutant ATXN3 induce neurodegeneration in SCA3 has remained elusive. In the present study, we show that the essential DNA strand break repair enzyme PNKP (polynucleotide kinase 3'-phosphatase) interacts with, and is inactivated by, the mutant ATXN3, resulting in inefficient DNA repair, persistent accumulation of DNA damage/strand breaks, and subsequent chronic activation of the DNA damage-response ataxia telangiectasia-mutated (ATM) signaling pathway in SCA3. We report that persistent accumulation of DNA damage/strand breaks and chronic activation of the serine/threonine kinase ATM and the downstream p53 and protein kinase C-d pro-apoptotic pathways trigger neuronal dysfunction and eventually neuronal death in SCA3. Either PNKP overexpression or pharmacological inhibition of ATM dramatically blocked mutant ATXN3-mediated cell death. Discovery of the mechanism by which mutant ATXN3 induces DNA damage and amplifies the pro-death signaling pathways provides a molecular basis for neurodegeneration due to PNKP inactivation in SCA3, and for the first time offers a possible approach to treatment.

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Dissertação de mestrado integrado em Engenharia Civil

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Tese de Doutoramento em Ciências da Saúde

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Tese de Doutoramento em Ciência e Engenharia de Polímeros e Compósitos.