17 research outputs found

    Producci贸n de hidr贸geno a partir de etanol y purificaci贸n con un catalizador de Au/TiO2

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    Uno de los principales objetivos de la ciencia y la ingenier铆a es el desarrollo de nuevas tecnolog铆as para la obtenci贸n de energ铆a de forma limpia y eficiente, es en ese sentido que el desarrollo de celdas de combustible ha cobrado un gran valor en los 煤ltimos a帽os, ya que provocan un m铆nimo impacto sobre el ambiente debido a su alta eficiencia y su baja emisi贸n de contaminantes. El etanol, materia prima en el presente proyecto, es una de las sustancias m谩s atractivas para ser utilizada en sistemas equipados con una celda de combustible, pues a diferencia de otros combustibles como el hidr贸geno y el metanol, es f谩cil de almacenar, manipular y obtener por medio de fermentaciones biol贸gicas (bioetanol). Hoy en d铆a la fuente m谩s importante para la producci贸n de hidr贸geno se encuentra en los combustibles f贸siles, fuentes de energ铆a no renovables. Sin embargo la producci贸n de etanol, combustible renovable que puede obtenerse por v铆as biol贸gicas, es simple, barata y su uso para la producci贸n de hidr贸geno presenta un elevado atractivo. El presente proyecto estudia la obtenci贸n de hidr贸geno a trav茅s de un catalizador de Au/TiO2 en un reactor. Se estudia tanto la reacci贸n de reformado con vapor como la oxidaci贸n parcial para producir hidr贸geno que pueda ser transferido a una celda de combustible para generar posteriormente electricidad, variando par谩metros como la temperatura, el tiempo de residencia, el flujo de aire... y encontrando as铆 las condiciones 贸ptimas de funcionamiento. Tambi茅n se ha realizado un estudio con el mismo catalizador sobre la eliminaci贸n de CO, puesto que 茅ste supone un veneno para las pilas de combustible de baja temperatura. Este proyecto abarca la preparaci贸n y caracterizaci贸n del catalizador, el montaje del reactor y la elecci贸n y puesta a punto de la periferia necesaria para el correcto funcionamiento del mismo. El comportamiento catal铆tico del reactor con respecto a la actividad, selectividad y estabilidad se cuantifican y valoran a trav茅s de los datos obtenidos a lo largo de 200 horas de pruebas de reacci贸n

    Producci贸n de hidr贸geno a partir de etanol y purificaci贸n con un catalizador de Au/TiO2

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    Uno de los principales objetivos de la ciencia y la ingenier铆a es el desarrollo de nuevas tecnolog铆as para la obtenci贸n de energ铆a de forma limpia y eficiente, es en ese sentido que el desarrollo de celdas de combustible ha cobrado un gran valor en los 煤ltimos a帽os, ya que provocan un m铆nimo impacto sobre el ambiente debido a su alta eficiencia y su baja emisi贸n de contaminantes. El etanol, materia prima en el presente proyecto, es una de las sustancias m谩s atractivas para ser utilizada en sistemas equipados con una celda de combustible, pues a diferencia de otros combustibles como el hidr贸geno y el metanol, es f谩cil de almacenar, manipular y obtener por medio de fermentaciones biol贸gicas (bioetanol). Hoy en d铆a la fuente m谩s importante para la producci贸n de hidr贸geno se encuentra en los combustibles f贸siles, fuentes de energ铆a no renovables. Sin embargo la producci贸n de etanol, combustible renovable que puede obtenerse por v铆as biol贸gicas, es simple, barata y su uso para la producci贸n de hidr贸geno presenta un elevado atractivo. El presente proyecto estudia la obtenci贸n de hidr贸geno a trav茅s de un catalizador de Au/TiO2 en un reactor. Se estudia tanto la reacci贸n de reformado con vapor como la oxidaci贸n parcial para producir hidr贸geno que pueda ser transferido a una celda de combustible para generar posteriormente electricidad, variando par谩metros como la temperatura, el tiempo de residencia, el flujo de aire... y encontrando as铆 las condiciones 贸ptimas de funcionamiento. Tambi茅n se ha realizado un estudio con el mismo catalizador sobre la eliminaci贸n de CO, puesto que 茅ste supone un veneno para las pilas de combustible de baja temperatura. Este proyecto abarca la preparaci贸n y caracterizaci贸n del catalizador, el montaje del reactor y la elecci贸n y puesta a punto de la periferia necesaria para el correcto funcionamiento del mismo. El comportamiento catal铆tico del reactor con respecto a la actividad, selectividad y estabilidad se cuantifican y valoran a trav茅s de los datos obtenidos a lo largo de 200 horas de pruebas de reacci贸n

    Producci贸n de hidr贸geno a partir de etanol y purificaci贸n con un catalizador de Au/TiO2

    No full text
    Uno de los principales objetivos de la ciencia y la ingenier铆a es el desarrollo de nuevas tecnolog铆as para la obtenci贸n de energ铆a de forma limpia y eficiente, es en ese sentido que el desarrollo de celdas de combustible ha cobrado un gran valor en los 煤ltimos a帽os, ya que provocan un m铆nimo impacto sobre el ambiente debido a su alta eficiencia y su baja emisi贸n de contaminantes. El etanol, materia prima en el presente proyecto, es una de las sustancias m谩s atractivas para ser utilizada en sistemas equipados con una celda de combustible, pues a diferencia de otros combustibles como el hidr贸geno y el metanol, es f谩cil de almacenar, manipular y obtener por medio de fermentaciones biol贸gicas (bioetanol). Hoy en d铆a la fuente m谩s importante para la producci贸n de hidr贸geno se encuentra en los combustibles f贸siles, fuentes de energ铆a no renovables. Sin embargo la producci贸n de etanol, combustible renovable que puede obtenerse por v铆as biol贸gicas, es simple, barata y su uso para la producci贸n de hidr贸geno presenta un elevado atractivo. El presente proyecto estudia la obtenci贸n de hidr贸geno a trav茅s de un catalizador de Au/TiO2 en un reactor. Se estudia tanto la reacci贸n de reformado con vapor como la oxidaci贸n parcial para producir hidr贸geno que pueda ser transferido a una celda de combustible para generar posteriormente electricidad, variando par谩metros como la temperatura, el tiempo de residencia, el flujo de aire... y encontrando as铆 las condiciones 贸ptimas de funcionamiento. Tambi茅n se ha realizado un estudio con el mismo catalizador sobre la eliminaci贸n de CO, puesto que 茅ste supone un veneno para las pilas de combustible de baja temperatura. Este proyecto abarca la preparaci贸n y caracterizaci贸n del catalizador, el montaje del reactor y la elecci贸n y puesta a punto de la periferia necesaria para el correcto funcionamiento del mismo. El comportamiento catal铆tico del reactor con respecto a la actividad, selectividad y estabilidad se cuantifican y valoran a trav茅s de los datos obtenidos a lo largo de 200 horas de pruebas de reacci贸n

    Transcriptome analysis in prenatal IGF1-deficient mice identifies molecular pathways and target genes involved in distal lung differentiation

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    This is an open-access article distributed under the terms of the Creative Commons Attribution License.[Background]: Insulin-like Growth Factor 1 (IGF1) is a multifunctional regulator of somatic growth and development throughout evolution. IGF1 signaling through IGF type 1 receptor (IGF1R) controls cell proliferation, survival and differentiation in multiple cell types. IGF1 deficiency in mice disrupts lung morphogenesis, causing altered prenatal pulmonary alveologenesis. Nevertheless, little is known about the cellular and molecular basis of IGF1 activity during lung development. [Methods/Principal Findings]: Prenatal Igf1-/- mutant mice with a C57Bl/6J genetic background displayed severe disproportional lung hypoplasia, leading to lethal neonatal respiratory distress. Immuno-histological analysis of their lungs showed a thickened mesenchyme, alterations in extracellular matrix deposition, thinner smooth muscles and dilated blood vessels, which indicated immature and delayed distal pulmonary organogenesis. Transcriptomic analysis of Igf1-/- E18.5 lungs using RNA microarrays identified deregulated genes related to vascularization, morphogenesis and cellular growth, and to MAP-kinase, Wnt and cell-adhesion pathways. Up-regulation of immunity-related genes was verified by an increase in inflammatory markers. Increased expression of Nfib and reduced expression of Klf2, Egr1 and Ctgf regulatory proteins as well as activation of ERK2 MAP-kinase were corroborated by Western blot. Among IGF-system genes only IGFBP2 revealed a reduction in mRNA expression in mutant lungs. Immuno-staining patterns for IGF1R and IGF2, similar in both genotypes, correlated to alterations found in specific cell compartments of Igf1-/- lungs. IGF1 addition to Igf1-/- embryonic lungs cultured ex vivo increased airway septa remodeling and distal epithelium maturation, processes accompanied by upregulation of Nfib and Klf2 transcription factors and Cyr61 matricellular protein. [Conclusions/Significance]: We demonstrated the functional tissue specific implication of IGF1 on fetal lung development in mice. Results revealed novel target genes and gene networks mediators of IGF1 action on pulmonary cellular proliferation, differentiation, adhesion and immunity, and on vascular and distal epithelium maturation during prenatal lung development.This work was partially supported by the Fundaci贸n Rioja Salud (Logro帽o) and Ministerio de Ciencia e Innovaci贸n (BFU200501437) (Spain). R.S.P. was a pre-doctoral fellow from Fundaci贸n Rioja Salud, N.M.-B. was a doctoral fellow from the Ministerio de Ciencia e Innovaci贸n and I.H.-P. was a JAE fellow from the Consejo Superior de Investigaciones Cient铆ficas (Spain).Peer Reviewe

    Transcriptome Analysis in Prenatal IGF1-Deficient Mice Identifies Molecular Pathways and Target Genes Involved in Distal Lung Differentiation

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    <div><p>Background</p><p>Insulin-like Growth Factor 1 (IGF1) is a multifunctional regulator of somatic growth and development throughout evolution. IGF1 signaling through IGF type 1 receptor (IGF1R) controls cell proliferation, survival and differentiation in multiple cell types. IGF1 deficiency in mice disrupts lung morphogenesis, causing altered prenatal pulmonary alveologenesis. Nevertheless, little is known about the cellular and molecular basis of IGF1 activity during lung development.</p><p>Methods/Principal Findings</p><p>Prenatal <i>Igf1<sup>鈭/鈭</sup></i> mutant mice with a C57Bl/6J genetic background displayed severe disproportional lung hypoplasia, leading to lethal neonatal respiratory distress. Immuno-histological analysis of their lungs showed a thickened mesenchyme, alterations in extracellular matrix deposition, thinner smooth muscles and dilated blood vessels, which indicated immature and delayed distal pulmonary organogenesis. Transcriptomic analysis of <i>Igf1<sup>鈭/鈭</sup></i> E18.5 lungs using RNA microarrays identified deregulated genes related to vascularization, morphogenesis and cellular growth, and to MAP-kinase, Wnt and cell-adhesion pathways. Up-regulation of immunity-related genes was verified by an increase in inflammatory markers. Increased expression of Nfib and reduced expression of Klf2, Egr1 and Ctgf regulatory proteins as well as activation of ERK2 MAP-kinase were corroborated by Western blot. Among IGF-system genes only IGFBP2 revealed a reduction in mRNA expression in mutant lungs. Immuno-staining patterns for IGF1R and IGF2, similar in both genotypes, correlated to alterations found in specific cell compartments of <i>Igf1<sup>鈭/鈭</sup></i> lungs. IGF1 addition to <i>Igf1<sup>鈭/鈭</sup></i> embryonic lungs cultured <i>ex vivo</i> increased airway septa remodeling and distal epithelium maturation, processes accompanied by up-regulation of Nfib and Klf2 transcription factors and Cyr61 matricellular protein.</p><p>Conclusions/Significance</p><p>We demonstrated the functional tissue specific implication of IGF1 on fetal lung development in mice. Results revealed novel target genes and gene networks mediators of IGF1 action on pulmonary cellular proliferation, differentiation, adhesion and immunity, and on vascular and distal epithelium maturation during prenatal lung development.</p></div

    Expression of IGF system genes in the E18.5 lung.

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    <p>(<b>A</b>) mRNA expression levels of <i>Igf2, Igf1r, Igf2r, Insr</i> (splice variants A and B), <i>Igfbp2</i>, <i>Igfbp4</i> and <i>Igfbp6</i> analyzed by qRT-PCR in <i>Igf1<sup>+/+</sup></i> and <i>Igf1<sup>鈭/鈭</sup></i> lungs (n鈥=鈥4 per genotype). <i>Gapdh</i> was the endogenous control gene. Only <i>Igfbp2</i> mRNA levels were significantly reduced in <i>Igf1<sup>鈭/鈭</sup></i> lungs (*<i>p</i><0.05) (Mann-Whitney <i>U</i>-test), however note the slightly increased <i>Igf2</i>, <i>Igf1r</i>, <i>Igf2r</i>, <i>InsrA</i> and <i>InsrB</i> and slightly reduced <i>Igfbp4</i> and <i>Igfbp6</i> mRNA mean levels in <i>Igf1<sup>鈭/鈭</sup></i> lungs. (<b>B鈥揔</b>) Immuno-staining of IGF1R (green labeling) counterstained in red with lung cell-type specific markers. IGF1R staining was high in the bronchiolar epithelium (green arrows), but also found scattered throughout the distal parenchyma (asterisks). No major differences were noted between genotypes. (B鈥揅) Bronchiolar epithelium showed strong staining for IGF1R (green arrows), with the highest levels co-localizing in CCSP<sup>+</sup> Clara cells (yellow arrows). (D鈥揈) IGF1R stained vascular endothelial cells (green arrowheads) and co-localized with SMA (smooth muscle actin, clone 1A1 antigen) in peribronchiolar and perivascular smooth muscle (yellow arrows), and in scattered cells of lung parenchyma (yellow arrowheads). (F鈥揋) Co-stain with Pro-SPC (SPC) showed IGF1R co-localization in many type 2 pneumocytes (yellow arrows), more randomly distributed in controls (F) and with a more acinar-like organization in <i>Igf1<sup>鈭/鈭</sup></i> lungs. (H鈥揑) Type 1 epithelial cells, stained with Aqp5, did not co-stain with IGF1R (red arrows). (J鈥揔) CD31 endothelial marker co-localized with IGF1R in some parenchymal endothelial cells of <i>Igf1<sup>+/+</sup></i> lungs (yellow arrow in J), but not in <i>Igf1<sup>鈭/鈭</sup></i> (white arrow in K). (<b>L鈥揗</b>) Immuno-staining for IGF2 expression (red labeling) was positive in bronchiolar epithelial cells of both genotypes (red arrows). EDTA antigen retrieval for IGF2 caused unspecific refringent signal on red blood cells (orange arrowheads). All confocal images in B鈥揗 are representative of samples analyzed from independent experiments. as, airway space; br, bronchiole; bv, blood vessel. Scale bars: 25 碌m in B鈥揅 and F鈥揋, 17 碌m in D鈥揈 and L鈥揗, 12 碌m in H鈥揑 and 8 碌m in J鈥揔.</p

    IGF1 induces alveolar morphogenesis and expression of target genes in prenatal lungs cultured <i>ex vivo</i>.

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    <p>E16.5 <i>Igf1<sup>+/+</sup></i> and <i>Igf1<sup>鈭/鈭</sup></i> lung lobes were cultured in defined medium for 96 h in the presence or absence of recombinant IGF1 (100 ng/mL). (<b>A鈥揇</b>) Images of cultured lobes showing the effect on explant morphogenesis induced by addition of IGF1. Note the differences in morphology shown by <i>Igf1<sup>鈭/鈭</sup></i> explants treated with IGF1 (D) (n鈥=鈥10 per condition). Purple dashed lines indicate sectioning planes in E to L. (<b>E鈥揌</b>) H&E staining on sections of the cultured lungs (n鈥=鈥4 per condition). Untreated explants show compact tissue with undefined septa and reduced spaces mainly lined by cuboidal epithelium (arrows in E鈥揊). IGF1 treatment opens tissue spaces, narrows septa and flattens the epithelium (arrows in G鈥揌), with a more pronounced effect on <i>Igf1<sup>鈭/鈭</sup></i> explants (H). Insets in E鈥揌 are high magnifications of lung epithelium (arrows), demonstrating that it becomes thinner and flatter in both genotypes of IGF1-treated cultures. (<b>I鈥揕</b>) Immuno-histochemical staining for Pro-SPC on lung explants. The high proportion of cubic positive cells lining the reduced aerial spaces in non IGF1-treated explants (asterisks in I鈥揓), decrease in proportion in the epithelium of IGF1-treated tissues (arrowheads in K鈥揕) (n鈥=鈥2 per condition). All images in A鈥揕 are representative of samples analyzed from independent experiments. (<b>M</b>) Immunoblots for IGF1 target gene expressions in explanted lungs. (<b>N</b>) Densitometric representation of gene expression levels after total protein loading normalization with 脽-Tubulin (脽-Tub). In parentheses, quantified Western blots. IGF1 addition to explants increased levels of Nfib and laminin in lungs of both genotypes, Ctgf in <i>Igf1<sup>+/+</sup></i>explants, and Klf2 and Cyr61 in <i>Igf1<sup>鈭/鈭</sup></i> samples, but it reduced levels of IGF1R in both genotypes. (*<i>p</i><0.05; **<i>p</i><0.01) (Mann-Whitney <i>U</i>-test). as, air space; s, septum. Scale bar corresponds to 500 碌m in A鈥揇; 50 碌m in E鈥揌, and 7 碌m in their insets; 20 碌m in I鈥揕.</p

    Disproportionately smaller fetal lungs in <i>Igf1<sup>鈭/鈭</sup></i> mice and decreased proliferation during early pulmonary organogenesis.

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    <p>(<b>A</b>) Graphical representation of lung-to-body weight ratio in normal (+/+) and <i>Igf1<sup>鈭/鈭</sup></i> (鈭/鈭) E18.5 fetuses (shown as mean % 卤 SEM). ***<i>p</i><0.001 (Mann-Whitney <i>U</i> test). In parentheses, number of samples determined. Note that absence of IGF1 during embryonic development disproportionately reduces lung growth. (<b>B鈥揇</b>) Growth deficiency in E12.5 explanted lungs after 6 h of <i>ex vivo</i> culture. Microphotographs of lung explants in (B) show a reduced number of terminal lung buds, represented in (C) (mean number 卤 SEM), and smaller surface, represented in (D) (mean surface 卤 SEM), of the <i>Igf1<sup>鈭/鈭</sup></i> explants. *<i>p</i><0.05; ***<i>p</i><0.001 (Mann-Whitney <i>U</i> test). In parentheses, number of samples determined. (<b>E鈥揊</b>) Cell proliferation in E12.5 explanted lungs cultured in defined medium for 48 h and pulse-chased with BrdU. Representative confocal images of whole-mount lungs analyzed from independent experiments immuno-labeled for BrdU in red (yellow arrowheads) and counterstained in green with Sytox, show more BrdU-labeled cells in <i>Igf1<sup>+/+</sup></i> (E), than do <i>Igf1<sup>鈭/鈭</sup></i> explanted lungs (F) (n鈥=鈥5 per genotype). as, airway space. Scale bar: 250 碌m in B and 30 碌m in E鈥揊.</p

    Levels of IGF signaling mediators in prenatal <i>Igf1<sup>鈭/鈭</sup></i> lungs.

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    <p>(<b>A</b>) Representative Western blots of total protein extracts for total IGF1R, phosphor-(p)-Akt and total Akt, pSTAT3 and total STAT3, pERK1/2 and total ERK1/2, pp38 and total p38-alpha and pJNK and total JNK (p46), using two representative samples from both normal and <i>Igf1<sup>鈭/鈭</sup></i> E18.5 lungs. Activation levels were determined using phosphor-specific antibodies. 尾-Tubulin was additionally used as a protein loading control (bottom panels). (<b>B</b>) Western blot band densitometric measurements of after total protein loading normalization, using either 脽-Tubulin or total content of each protein when evaluating phosphorylation levels with phosphor-specific antibodies. <i>Igf1<sup>+/+</sup></i> relative values were taken as 100%. In parentheses, number of Western blots quantified per genotype. Increased levels of pERK2 with respect to total ERK2 was found to be significant (*<i>p</i><0.05) (Mann-Whitney <i>U</i>-test). 脽-Tub or b-Tub, 脽-Tubulin.</p

    Protein levels of selected regulatory genes found with differential expression in microarrays of RNA.

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    <p>(<b>A</b>) Representative Western blots for Nfib, Klf2, Egr1 and c-Jun transcription factors as well as Ctgf and Cyr61 matricellular growth factors in E18.5 <i>Igf1<sup>+/+</sup></i> and <i>Igf1<sup>鈭/鈭</sup></i> lungs. 尾-Tubulin was used as a loading control. (<b>B</b>) Graphical representation of densitometric measurements of specific band signals after total protein loading normalization with 脽-Tubulin. <i>Igf1<sup>+/+</sup></i> relative values were taken as 100%. In parentheses, number of samples determined. Increased levels of Nfib in <i>Igf1<sup>鈭/鈭</sup></i> lungs were statistically significant (**<i>p</i><0.01), and decreased levels of Klf2, Egr1 and Ctgf were also found to be significant (*<i>p</i><0.05) (Mann-Whitney <i>U</i>-test). (<b>C鈥揇</b>) Representative immuno-staining for Nfib in lung cross-sections analyzed from independent experiments. Note high levels of Nfib nuclear expression in subsets of mesenchymal cells surrounding blood vessels (arrows) and bronchioles (arrowheads), more evident and with a flattened morphology in <i>Igf1<sup>鈭/鈭</sup></i> (n鈥=鈥4) than in <i>Igf1<sup>+/+</sup></i> (n鈥=鈥3) lungs. as, saccular space; br, bronchiole; bv, blood vessel; 脽-Tub, 脽-Tubulin; s, septum. Scale bar: 20 碌m.</p
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