Degradación biológica de lignina presente en residuos de nopal para la obtención de celulosa

El presente trabajo tuvo como objetivo el desarrollo de un proceso biotecnológico para la obtención de celulosa. A partir de la fermentación de espinas de Opuntia ficus-indica proveniente del Residuo Agroindustrial generado en la Delegación Milpa Alta, Ciudad de México. El microorganismo Fycnoporus cinnabarinus realizó la fermentación en un biorreactor homogéneo. En este trabajo se evalúo la eficiencia de la deslignificación, bajo diferentes condiciones de operación: pH de 4 y 6, temperatura de 30 ºC y 50 ºC, y un tamaño de partícula de 0.075 mm y 0.25 mm. La deslignificación de la materia prima se evaluó mediante espectroscopia IR. Además se determinaron durante las fermentaciones las concentraciones de biomasa y azúcares reductores totales, empleando el reactivo de Bradford y el método del ácido 3, 5- Dinitrosalicílico (DNS) respectivamente.The objective of this work was the development of a biotechnological process to obtain cellulose. From the fermentation of Opuntiajicus-indica thorns from the Agroindustrial Residue generated in the Milpa Alta Delegation, Mexico City. The microorganism Fycnoporus cinnabarinus carried out the fermentation in a homogeneous bioreactor. In this work the efficiency of the delignification was evaluated, under different operating conditions: pH of 4 and 6, temperature of 30 ºC and 50 ºC, and a particle size ofü.074 mm and 0.25 mm. The delignification ofthe waste was evaluated by IR spectroscopy. In addition, the concentrations of biomass and total reducing carbohydrates were determined during the fermentations, using the Bradford reagent and the 3, 5- Dinitrosalicylic acid (DNS) method, respectively

Pleiotrophin as a central nervous system neuromodulator, evidences from the hippocampus

Pleiotrophin (PTN) is a secreted growth factor, and also a cytokine, associated with the extracellular matrix, which has recently starting to attract attention as a significant neuromodulator with multiple neuronal functions during development. PTN is expressed in several tissues, where its signals are generally related with cell proliferation, growth, and differentiation by acting through different receptors. In Central Nervous System (CNS), PTN exerts post-developmental neurotrophic and -protective effects, and additionally has been involved in neurodegenerative diseases and neural disorders. Studies in Drosophila shed light on some aspects of the different levels of regulatory control of PTN invertebrate homologs. Specifically in hippocampus, recent evidence from PTN Knock-out (KO) mice involves PTN functioning in learning and memory. In this paper, we summarize, discuss, and contrast the most recent advances and results that lead to proposing a PTN as a neuromodulatory molecule in the CNS, particularly in hippocampus

Voluntary Exercise Promotes Beneficial Anti-aging Mechanisms in SAMP8 Female Brain

© 2014, Springer Science+Business Media New York. Regular physical exercise mediates health and longevity promotion involving Sirtuin 1 (SIRT1)-regulated pathways. The anti-aging activity of SIRT1 is achieved, at least in part, by means of fine-tuning the adenosine monophosphate (AMP)-activated protein kinase (AMPK) pathway by preventing the transition of an originally pro-survival program into a pro-aging mechanism. Additionally, SIRT1 promotes mitochondrial function and reduces the production of reactive oxygen species (ROS) through regulating peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), the master controller of mitochondrial biogenesis. Here, by using senescence-accelerated mice prone 8 (SAMP8) as a model for aging, we determined the effect of wheel-running as a paradigm for long-term voluntary exercise on SIRT1-AMPK pathway and mitochondrial functionality measured by oxidative phosphorylation (OXPHOS) complex content in the hippocampus and cortex. We found differential activation of SIRT1 in both tissues and hippocampal-specific activation of AMPK. These findings correlated well with significant changes in OXPHOS in the hippocampal, but not in the cerebral cortex, area. Collectively, the results revealed greater benefits of the exercise in the wheel-running intervention in a murine model of senescence, which was directly related with mitochondrial function and which was mediated through the modulation of SIRT1 and AMPK pathways.This study was supported by grants SAF2010-15050 (PK), PSI2008-06417-C03-03 (RME), and SAF-2012-39852 (MP) from the “Ministerio de Educación y Ciencia” and 2009/SGR00893 from the “Generalitat de Catalunya.” S.B. was supported by a predoctoral fellowship (APIF) from the University of Barcelona. J.F.L. was supported by a predoctoral fellowship from the Generalitat de Catalunya (FI-DGR 2011)Peer Reviewe

Prenatal Alcohol Exposure in Rats Diminishes Postnatal Cxcl16 Chemokine Ligand Brain Expression

Maternal ethanol consumption during pregnancy is one of the main causes of Neurodevelopmental disorders (NDD). Prenatal alcohol exposure (PAE) produces several adverse manifestations. Even low or moderate intake has been associated with long-lasting behavioral and cognitive impairment in offspring. In this study we examined the gene expression profile in the rat nucleus accumbens using microarrays, comparing animals exposed prenatally to ethanol and controls. Microarray gene expression showed an overall downward regulatory effect of PAE. Gene cluster analysis reveals that the gene groups most affected are related to transcription regulation, transcription factors and homeobox genes. We focus on the expression of the C-X-C motif chemokine ligand 16 (Cxcl16) which was differentially expressed. There is a significant reduction in the expression of this chemokine throughout the brain under PAE conditions, evidenced here by quantitative polymerase chain reaction qPCR and immunohistochemistry. Chemokines are involved in neuroprotection and implicated in alcohol-induced brain damage and neuroinflammation in the developing central nervous system (CNS), therefore, the significance of the overall decrease in Cxcl16 expression in the brain as a consequence of PAE may reflect a reduced ability in neuroprotection against subsequent conditions, such as excitotoxic damage, inflammatory processes or even hypoxic-ischemic insult