Forecasting Air Quality Data with the Gamma Classifier

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MECHANISTIC STUDY OF A RUTHENIUM HYDRIDE COMPLEX OF TYPE [RuH(CO)(N-N)(PR3)2]+ AS CATALYST PRECURSOR FOR THE HYDROFORMYLATION REACTION OF 1-HEXENE

Indexación: Web of Science; Scopus; Scielo.The catalytic activity of systems of type [RuH(CO)(N-N)(PR3)(2)](+) was evaluated in the hydroformylation reaction of 1-hexene. The observed activity is explained through a reaction mechanism on the basis of the quantum theory. The mechanism included total energy calculations for each of the intermediaries of the elemental steps considered in the catalytic cycle. The deactivation of the catalyst precursors takes place via dissociation of the polypyridine ligand and the subsequent formation of thermodynamically stable species, such as RuH(CO)(3)(PPh3)(2) and RuH3(CO)(PPh3)(2), which interrupt the catalytic cycle. In addition, the theoretical study allows to explain the observed regioselectivity which is defined in two steps: (a) the hydride migration reaction with an anti-Markovnikov orientation to produce the alkyl-linear-complex (3.1a), which is more stable by 19.4 kJ/mol than the Markovnikov orientation (alkyl-branched-complex) (3.1b); (b) the carbon monoxide insertion step generates the carbonyl alkyl-linear specie (4.1a) which is more stable by 9.5 kJ/mol than the alternative species (4.1b), determining the preferred formation of heptanal in the hydroformylation of 1-hexene. Palabras clavehttp://ref.scielo.org/db4yc

Effect of Sunflower and Marine Oils on Ruminal Microbiota, In vitro Fermentation and Digesta Fatty Acid Profile

Funding This work has been funded by Consejería de Educación, Junta de Castilla y León (research project LE007A07). Acknowledgments We acknowledge support of the publication fee by the CSIC Open Access Publication Support Initiative through its Unit of Information Resources for Research (URICI). Support received from CICYT project AGL2005-04760-C02-02 is gratefully acknowledged.Peer reviewedPublisher PD

Detecting neuroinflammation with molecular MRI

The work in this thesis is focused on the study of neuroinflammation with molecular magnetic resonance imaging (MRI) methods. Neuroinflammation is a response of the central nervous system to pathological insult and it is present in many neurological disorders, such as Alzheimer’s disease. Being able to image neuroinflammation non-invasively with MRI techniques would have an important clinical value for diagnosis and assessment of therapy effectiveness. The aim of this work is to develop and validate an MR biomarker of neuroinflammation using MR Spectroscopy (MRS) and chemical exchange saturation transfer imaging (CEST). First, intravenous administration of lipopolysaccharide (LPS) is used as a mild inflammatory stimulus in wild type mice and in a mouse model of Alzheimer’s disease (AD). Elevated levels of the osmolyte myo-inositol, measured with MRS and microglia activation are found in AD mice after LPS administration. Due to the inherent low spatial resolution of MRS, a CEST MRI method is developed next. A myo-inositol CEST protocol is optimised, using Matlab simulations based on the Bloch-McConnell equations for a three pool model, in order to maximize the contrast and to estimate the amount of signal that can be expected in vivo. In vitro and in vivo tests are presented and a fast CEST sequence is developed, while the experimental difficulties and limitations of the technique are discussed. A CEST protocol is finally applied to evaluate the metabolite response to an LPS inflammatory challenge using MRS and histology as validation. A correlation is described between CEST and MRS myo-inositol levels, as well as between CEST and microglia concentration (Iba1 immunostaining), which highlight the potential of CEST as a non-invasive in vivo neuroinflammatory biomarker

Detecting neuroinflammation with molecular MRI

The work in this thesis is focused on the study of neuroinflammation with molecular magnetic resonance imaging (MRI) methods. Neuroinflammation is a response of the central nervous system to pathological insult and it is present in many neurological disorders, such as Alzheimer’s disease. Being able to image neuroinflammation non-invasively with MRI techniques would have an important clinical value for diagnosis and assessment of therapy effectiveness. The aim of this work is to develop and validate an MR biomarker of neuroinflammation using MR Spectroscopy (MRS) and chemical exchange saturation transfer imaging (CEST). First, intravenous administration of lipopolysaccharide (LPS) is used as a mild inflammatory stimulus in wild type mice and in a mouse model of Alzheimer’s disease (AD). Elevated levels of the osmolyte myo-inositol, measured with MRS and microglia activation are found in AD mice after LPS administration. Due to the inherent low spatial resolution of MRS, a CEST MRI method is developed next. A myo-inositol CEST protocol is optimised, using Matlab simulations based on the Bloch-McConnell equations for a three pool model, in order to maximize the contrast and to estimate the amount of signal that can be expected in vivo. In vitro and in vivo tests are presented and a fast CEST sequence is developed, while the experimental difficulties and limitations of the technique are discussed. A CEST protocol is finally applied to evaluate the metabolite response to an LPS inflammatory challenge using MRS and histology as validation. A correlation is described between CEST and MRS myo-inositol levels, as well as between CEST and microglia concentration (Iba1 immunostaining), which highlight the potential of CEST as a non-invasive in vivo neuroinflammatory biomarker

Magnetic Resonance Spectroscopy discriminates the response to microglial stimulation of wild type and Alzheimer's disease models.

Microglia activation has emerged as a potential key factor in the pathogenesis of Alzheimers disease. Metabolite levels assessed by magnetic resonance spectroscopy (MRS) are used as markers of neuroinflammation in neurodegenerative diseases, but how they relate to microglial activation in health and chronic disease is incompletely understood. Using MRS, we monitored the brain metabolic response to lipopolysaccharides (LPS)-induced microglia activation in vivo in a transgenic mouse model of Alzheimers disease (APP/PS1) and healthy controls (wild-type (WT) littermates) over 4 hours. We assessed reactive gliosis by immunohistochemistry and correlated metabolic and histological measures. In WT mice, LPS induced a microglial phenotype consistent with activation, associated with a sustained increase in macromolecule and lipid levels (ML9). This effect was not seen in APP/PS1 mice, where LPS did not lead to a microglial response measured by histology, but induced a late increase in the putative inflammation marker myoinositol (mI) and metabolic changes in total creatine and taurine previously reported to be associated with amyloid load. We argue that ML9 and mI distinguish the response of WT and APP/PS1 mice to immune mediators. Lipid and macromolecule levels may represent a biomarker of activation of healthy microglia, while mI may not be a glial marker