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        Methanol to gasoline (MTG): Parametric study and validation of the process in a two-zone fluidized bed reactor (TZFBR)

        A. Sanz-Martínez,J. Lasobras,J. Soler,J. Herguido,M. Menéndez 한국공업화학회 2022 Journal of Industrial and Engineering Chemistry Vol.113 No.-

        Methanol to Gasoline (MTG) process transforms methanol to hydrocarbons within the boiling point rangeof gasoline. The result is a wide spectrum of products (olefins, paraffins, aromatics and naphthenics,among others), with the total conversion of methanol to hydrocarbons and water. Catalyst deactivationby coke is a main problem in this process. This work aims to determine the feasibility of carrying out theproduction of gasoline from methanol in a two-zone fluidized bed reactor (TZFBR). The hypothesis is thatthe formation of carbonaceous deposits (coke) on the catalyst particles can be counteracted by its combustionin the regeneration zone that this novel reactor presents, thus achieving stable and continuousoperation. In this way, both processes (reaction and regeneration) would be being carried out simultaneouslyin the same reactor (process intensification). The comparison of results between a conventional fluidizedbed reactor and a TZFBR shows that the second one actually provides a better stability over time.

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        Metformin treatment reduces motor and neuropsychiatric phenotypes in the zQ175 mouse model of Huntington disease

        Ana Sanchis,María Adelaida García-Gimeno,Antonio José Cañada-Martínez,María Dolores Sequedo,José María Millán,Pascual Sanz,Rafael P. Vázquez-Manrique 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-

        Huntington disease is a neurodegenerative condition for which there is no cure to date. Activation of AMP-activated protein kinase has previously been shown to be beneficial in in vitro and in vivo models of Huntington’s disease. Moreover, a recent cross-sectional study demonstrated that treatment with metformin, a well-known activator of this enzyme, is associated with better cognitive scores in patients with this disease. We performed a preclinical study using metformin to treat phenotypes of the zQ175 mouse model of Huntington disease. We evaluated behavior (motor and neuropsychiatric function) and molecular phenotypes (aggregation of mutant huntingtin, levels of brain-derived neurotrophic factor, neuronal inflammation, etc.). We also used two models of polyglutamine toxicity in Caenorhabditis elegans to further explore potential mechanisms of metformin action. Our results provide strong evidence that metformin alleviates motor and neuropsychiatric phenotypes in zQ175 mice. Moreover, metformin intake reduces the number of nuclear aggregates of mutant huntingtin in the striatum. The expression of brain-derived neurotrophic factor, which is reduced in mutant animals, is partially restored in metformin-treated mice, and glial activation in mutant mice is reduced in metformin-treated animals. In addition, using worm models of polyglutamine toxicity, we demonstrate that metformin reduces polyglutamine aggregates and restores neuronal function through mechanisms involving AMP-activated protein kinase and lysosomal function. Our data indicate that metformin alleviates the progression of the disease and further supports AMP-activated protein kinase as a druggable target against Huntington’s disease.

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