3 research outputs found

    Unstructured mathematical model for biomass, lactic acid and bacteriocin productions by lactic acid bacteria in batch fermentation

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    6 páginas, 3 figuras, 2 tablasBACKGROUND: A simple macroscopical model was proposed to describe the fermentation kinetics of growth, bacteriocins and lactic acid production by Lactococcus lactis and Pediococcus acidilactici in a batch system. The equations used were: the logistic reparametrized for growth, the Luedeking–Piret model for bacteriocin production, the maintenance energy model for glucose consumption; and the homofermentative balance equation for lactic acid formation. RESULTS: In all the cultures, the mathematical models, consistents and robusts, adjusted, perfectly, the experimental kinetic profiles. Also, the corresponding kinetic parameters were significant, so much biological as statistically. CONCLUSIONS: The group of integrated equations used, besides showing high accuracy in predicting the studied bioproductions, established a useful tool for the control of lactic acid bacteria kinetics in bioreactors in terms of its statistical consistency. Copyright © 2007 Society of Chemical IndustryPeer reviewe

    Targeted deletion of the AAA-ATPase Ruvbl1 in mice disrupts ciliary integrity and causes renal disease and hydrocephalus

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    Ciliopathies comprise a large number of hereditary human diseases and syndromes caused by mutations resulting in dysfunction of either primary or motile cilia. Both types of cilia share a similar architecture. While primary cilia are present on most cell types, expression of motile cilia is limited to specialized tissues utilizing ciliary motility. We characterized protein complexes of ciliopathy proteins and identified the conserved AAA-ATPase Ruvbl1 as a common novel component. Here, we demonstrate that Ruvbl1 is crucial for the development and maintenance of renal tubular epithelium in mice: both constitutive and inducible deletion in tubular epithelial cells result in renal failure with tubular dilatations and fewer ciliated cells. Moreover, inducible deletion of Ruvbl1 in cells carrying motile cilia results in hydrocephalus, suggesting functional relevance in both primary and motile cilia. Cilia of Ruvbl1-negative cells lack crucial proteins, consistent with the concept of Ruvbl1-dependent cytoplasmic pre-assembly of ciliary protein complexes
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