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Montevideo, Uruguay

Okada D.Y.,University of Sao Paulo | Delforno T.P.,University of Sao Paulo | Etchebehere C.,Instituto Clemente Estable | Varesche M.B.A.,University of Sao Paulo
International Biodeterioration and Biodegradation | Year: 2014

The microbial communities from two upflow anaerobic sludge blanket (UASB) reactors treating synthetic wastewater supplemented with linear alkylbenzene sulfonate (LAS) (RS) and laundry wastewater (RL) were analyzed by pyrosequencing of 16S rRNA genes. A higher LAS degradation rate was observed in RL (82±9%) than RS (45±16%). A high proportion of the LAS removal rate (55-90%) was observed in the PS region for both reactors, most likely due to the low concentration of co-substrates and oxygen diffusion in this region. A microbiological analysis of samples taken at 112 days of operation from the sludge blanket (SB) and the phase-separator (PS) region of both reactors confirmed these findings. The distinct microbial communities found in each reactor resulting from the different wastewaters used were related to the LAS degradation rates obtained. The microbial community from reactor RL was more capable of degrading LAS, most likely because of the presence of xenobiotics. © 2014 Elsevier Ltd. Source


Olivera-Bravo S.,Instituto Clemente Estable | Barbeito L.,Institute Pasteur Montevideo
FEBS Letters | Year: 2015

Astrocytes are crucial for postnatal development of neuronal networks, axon myelination and neurovascular structures. Defects in astrocyte generation or maturation are associated with severe neurological developmental disorders. Glutaric acidemia type I (GAI), an inherited neurometabolic disorder characterized by accumulation of glutaric (GA) and 3-hydroxyglutaric acids, shows a paradigmatic postnatal neuropathology characterized by massive degeneration of neurons in the striatum. While the disorder is caused by genetic mutations on glutaryl-CoA dehydrogenase, the neurological defects usually start months after birth. Pathogenesis of GAI has remained largely unknown, and specifically, it is unclear how accumulation of GAI metabolites may result in neurodegeneration. Recent evidence supports a GAI model involving primary defective astrocyte maturation leading to a co-morbid spectrum of neurologic symptoms similar to those of patients. Astrocytes are vulnerable to GAI metabolites, but instead of dying, they follow long-lasting phenotypic changes leading to striatal neuron degeneration as well as defective myelination and blood brain barrier maturation. Here, we summarized recent findings on the pathogenic role of GA-damaged astrocytes in GAI and discuss if astrocyte dysfunction may be a target of therapeutic interventions. © 2015 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved. Source


Aebischer J.,French Institute of Health and Medical Research | Aebischer J.,Aix - Marseille University | Cassina P.,Instituto Clemente Estable | Otsmane B.,French Institute of Health and Medical Research | And 10 more authors.
Cell Death and Differentiation | Year: 2011

Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disease that primarily affects motoneurons in the brain and spinal cord. Dominant mutations in superoxide dismutase-1 (SOD1) cause a familial form of ALS. Mutant SOD1-damaged glial cells contribute to ALS pathogenesis by releasing neurotoxic factors, but the mechanistic basis of the motoneuron-specific elimination is poorly understood. Here, we describe a motoneuron-selective death pathway triggered by activation of lymphotoxin-Β receptor (LT-ΒR) by LIGHT, and operating by a novel signaling scheme. We show that astrocytes expressing mutant SOD1 mediate the selective death of motoneurons through the proinflammatory cytokine interferon-γ (IFNγ), which activates the LIGHT-LT-ΒR death pathway. The expression of LIGHT and LT-ΒR by motoneurons in vivo correlates with the preferential expression of IFNγ by motoneurons and astrocytes at disease onset and symptomatic stage in ALS mice. Importantly, the genetic ablation of Light in an ALS mouse model retards progression, but not onset, of the disease and increases lifespan. We propose that IFNγ contributes to a cross-talk between motoneurons and astrocytes causing the selective loss of some motoneurons following activation of the LIGHT-induced death pathway. © 2011 Macmillan Publishers Limited All rights reserved. Source


Mansilla S.F.,CONICET | Soria G.,CONICET | Soria G.,National University of Cordoba | Vallerga M.B.,CONICET | And 4 more authors.
Nucleic Acids Research | Year: 2013

Although many genotoxic treatments upregulate the cyclin kinase inhibitor p21, agents such as UV irradiation trigger p21 degradation. This suggests that p21 blocks a process relevant for the cellular response to UV. Here, we show that forced p21 stabilization after UV strongly impairs damaged-DNA replication, which is associated with permanent deficiencies in the recruitment of DNA polymerases from the Y family involved in translesion DNA synthesis), with the accumulation of DNA damage markers and increased genomic instability. Remarkably, such noxious effects disappear when disrupting the proliferating cell nuclear antigen (PCNA) interacting motif of stable p21, thus suggesting that the release of PCNA from p21 interaction is sufficient to allow the recruitment to PCNA of partners (such as Y polymerases) relevant for the UV response. Expression of degradable p21 only transiently delays early replication events and Y polymerase recruitment after UV irradiation. These temporary defects disappear in a manner that correlates with p21 degradation with no detectable consequences on later replication events or genomic stability. Together, our findings suggest that the biological role of UV-triggered p21 degradation is to prevent replication defects by facilitating the tolerance of UV-induced DNA lesions. © The Author(s) 2013. Published by Oxford University Press. Source


Infante I.,Instituto Clemente Estable | Morel M.A.,Instituto Clemente Estable | Ubalde M.C.,Instituto Clemente Estable | Martinez-Rosales C.,Instituto Clemente Estable | And 3 more authors.
World Journal of Microbiology and Biotechnology | Year: 2010

Wool is a natural animal fiber commonly used in fabrics, but requires physical and chemical processing treatment for such applications. With the aim of developing new woollen textile products using environmentally friendly treatments, proteolytic bacteria were isolated from raw wool samples of Merino sheep and screened for wool-degrading activity. Two isolates were identified as Bacillus megaterium L4 and Bacillus thuringiensis L11 by 16S rRNA gene sequence analysis. Both isolates grew on a minimal medium using wool-fiber or wool-fabric as sole carbon and nitrogen sources. Bacterial growth was correlated with extracellular protease activity, and maximal protease production was in early stationary phase. The exoprotease produced by L11 was found to be a thermo-tolerant metalloprotease stabilized by calcium or magnesium, and had optimum activity at pH 7. 0 and temperature at 40°C. During bacterial growth the wool-fiber lost weight, but it did not show changes in diameter. When wool-fabric was used instead of wool-fiber weight loss and non-shrinking was found. These are encouraging results for textile processing that should be useful for development of new textile products by direct microbial processing. A potential alternative that could be suggested from our study would be to treat wool with wool-degrading microorganisms in order to develop environmentally friendly processes. © Springer Science+Business Media B.V. 2009. Source

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