Diversidad de enemigos naturales de pulgones en cultivos de lechuga

Este trabajo ha sido subvencionado por la beca predoctoral del Ministerio de Ciencia y Tecnología: AGL2003-0753-C03-01 y forma parte de la Tesis Doctoral de I. Morales (BES-2004-5217)

DocStories: @foto_historias_

Se trata de un proyecto de innovación docente del grupo de investigación Fotodoc enmarcado en la convocatoria Innova-Docencia 2021/2022 del Vicerrectorado de Calidad de la Universidad Complutense de Madrid. Está formado por 12 personas en total, 9 profesores investigadores (PDI), 2 alumnas y una persona de administración y servicios (PAS). Es un proyecto que reúne a personal de la Facultad de Ciencias de la Información y de la Facultad de Ciencias de la Documentación, e interdisciplinar, ya que está formado por personas expertas en diferentes ámbitos de la comunicación y la documentación: patrimonio fotográfico, ética, comunicación audiovisual, etc. A partir de una plataforma de Instagram @foto_historias_ se pretende trabajar con el alumnado de las asignaturas de Documentación Audiovisual: Perspectivas y Métodos, Documentación fotográfica y audiovisual, Documentación Informativa y Ética y deontología profesional la concienciación sobre la importancia del patrimonio fotográfico, especialmente el doméstico (aquellas fotografías contenidas en álbumes familiares). Se espera que los alumnos y alumnas elijan una fotografía familiar, la escaneen, rastreen su historia y la compartan en la cuenta de Instagram conformando una constelación de foto historias. Las clases magistrales y prácticas (digitalización, conservación, ética y derechos de la imagen) ayudarán a conseguir el objetivo esperado. Además, también se les enseñará a hacer un buen uso de las redes sociales y se intentará fomentar la creatividad y el espíritu crítico

DocStories: @foto_historias_ The Photo Stories exhibition and intergenerational meetings

A partir de las fotografías recogidas en Instagram (@foto_historias_ ) se organizará una exposición fotográfica itinerante comisariada por el alumnado y se llevarán a cabo encuentros intergeneracionales entre estudiantes y escuelas de adultos.Unidad Deptal. de Biblioteconomía y DocumentaciónFac. de Ciencias de la InformaciónFALSEsubmitte

p38α blocks brown adipose tissue thermogenesis through p38δ inhibition

<div><p>Adipose tissue has emerged as an important regulator of whole-body metabolism, and its capacity to dissipate energy in the form of heat has acquired a special relevance in recent years as potential treatment for obesity. In this context, the p38MAPK pathway has arisen as a key player in the thermogenic program because it is required for the activation of brown adipose tissue (BAT) thermogenesis and participates also in the transformation of white adipose tissue (WAT) into BAT-like depot called beige/brite tissue. Here, using mice that are deficient in p38α specifically in adipose tissue (p38α^Fab-KO), we unexpectedly found that lack of p38α protected against high-fat diet (HFD)-induced obesity. We also showed that p38α^Fab-KO mice presented higher energy expenditure due to increased BAT thermogenesis. Mechanistically, we found that lack of p38α resulted in the activation of the related protein kinase family member p38δ. Our results showed that p38δ is activated in BAT by cold exposure, and lack of this kinase specifically in adipose tissue (p38δ ^Fab-KO) resulted in overweight together with reduced energy expenditure and lower body and skin surface temperature in the BAT region. These observations indicate that p38α probably blocks BAT thermogenesis through p38δ inhibition. Consistent with the results obtained in animals, p38α was reduced in visceral and subcutaneous adipose tissue of subjects with obesity and was inversely correlated with body mass index (BMI). Altogether, we have elucidated a mechanism implicated in physiological BAT activation that has potential clinical implications for the treatment of obesity and related diseases such as diabetes.</p></div

p38α^Fab-KO mice are protected against diet-induced obesity and diabetes.

<p>(A) Body weight time course in Fab-Cre and p38α^Fab-KO male (8–10-wk-old) mice fed an HFD over 8 weeks. Data are presented as the increase above initial weight (left panel) or as total weight comparing mice fed an HDF with mice fed an ND (right panel). HFD-induced weight gain was significantly higher in Fab-Cre than p38α^Fab-KO mice (mean ± SEM; Fab-Cre HFD <i>n =</i> 10 mice; p38α^Fab-KO HFD <i>n =</i> 11 mice; Fab-Cre ND <i>n =</i> 9 mice; p38α^Fab-KO ND <i>n =</i> 8 mice). (B) NMR analysis of fat mass in p38α^Fab-KO and Fab-Cre mice after 8 weeks of HFD (mean ± SEM; Fab-Cre <i>n =</i> 10 mice; p38α^Fab-KO <i>n =</i> 8 mice). (C) Representative haematoxylin–eosin and oil red O staining of liver sections (Fab-Cre <i>n =</i> 6 mice; p38α^Fab-KO <i>n =</i> 6 mice; and 3 pictures from each mouse). Scale bar: 50 μm. (D) Fasting and fed blood glucose in Fab-Cre and p38α^Fab-KO mice fed the HFD (8 weeks) (mean ± SEM; Fab-Cre <i>n =</i> 10 mice; p38α^Fab-KO <i>n =</i> 11 mice). (E) GTT and ITT in Fab-Cre and p38α^Fab-KO mice fed the HFD for 8 weeks. Mice were fasted overnight (for GTT) or 1 hour (for ITT), and blood glucose concentration was measured in mice given intraperitoneal injections of glucose (1 g/kg of total body weight) or insulin (0.75 U/kg of total body weight) (mean ± SEM; Fab-Cre <i>n =</i> 10 mice; p38α^Fab-KO <i>n =</i> 11 mice). (F) Immunohistochemistry of eWAT sections using anti-GLUT4 (green), anti-Cav-1 (red) antibodies, and the nuclear dye DAPI (blue). Location of GLUT4 was analysed in mice treated without or with insulin (1.5 IU/kg) for 15 minutes after overnight fasting. Scale bar: 20 μm. (G) Representative haematoxylin–eosin BAT and eWAT sections (Fab-Cre <i>n =</i> 6 mice; p38α^Fab-KO <i>n =</i> 6 mice; and 3 pictures from each mouse). Scale bar: 50 μm. *<i>p</i> < 0.05, ***<i>p</i> < 0.001 Fab-Cre versus p38α^Fab-KO. ‘&&’ indicates <i>p</i> < 0.01, ‘&&&’ indicates <i>p</i> < 0.001 Fab-Cre ND versus Fab-Cre HFD (2-way ANOVA coupled with Bonferroni’s post-tests or <i>t</i> test or Welch’s test when variances were different). See also <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2004455#pbio.2004455.s015" target="_blank">S1 Data</a>. BAT, brown adipose tissue; Cav-1, caveolin-1; eWAT, epididymal fat; GLUT4, glucose transporter type 4; GTT, glucose tolerance test; HFD, high-fat diet; ITT, insulin tolerance test; ND, normal-chow diet; WAT, white adipose tissue.</p

p38s regulate respiratory capacity of brown adipocytes.

<p>Primary adipocytes isolated from intercapsular BAT were differentiated in vitro. (A) qRT-PCR analysis of browning genes mRNA expression from primary adipocytes isolated from WT or p38δ^−/− mice. mRNA expression was normalised to the amount of <i>Gapdh</i> mRNA (mean ± SEM; WT <i>n =</i> 5 wells; p38δ^−/− <i>n =</i> 5 wells). (B) Analysis of mitochondrial DNA content with respect to nuclear DNA by RT-PCR in adipocytes isolated from BAT of Fab-cre or p38α^Fab-KO mice (mean ± SEM; Fab-Cre <i>n =</i> 3 wells; p38α^Fab-KO <i>n =</i> 5 wells) and of (C) WT or p38δ^−/− mice (mean ± SEM; WT <i>n =</i> 3 wells; p38δ^−/− <i>n =</i> 4 wells). (D–E) OCR to NE (1 μM) and ISO (1 μM) in differentiated brown adipocytes from Fab-Cre and p38α^Fab-KO mice (mean ± SEM; Fab-Cre <i>n =</i> 7 or p38α^Fab-KO <i>n =</i> 7 wells treated with NE; and Fab-Cre <i>n =</i> 8 or p38α^Fab-KO <i>n =</i> 8 wells treated with ISO) (panel D) or from WT or p38δ^−/− mice (mean ± SEM; WT <i>n =</i> 22 or p38δ^−/− <i>n =</i> 12 wells treated with NE; and WT <i>n =</i> 12 or p38δ^−/− <i>n =</i> 12 wells treated with ISO) (panel E) analysed by Seahorse assay. Nonmitochondrial respiration was subtracted from OCR values, and all values were normalised to protein content. Upper panels show OCR over time upon different drugs injections: oligomycin (1 μM), FCCP (1 μM), and antimycin A (1 μM) with rotenone (1 μM). Lower panels show basal and NE/ISO-induced OCR. (F) OCR induced by NE and ISO in differentiated brown adipocytes from Fab-Cre and p38α^Fab-KO mice was abolished by pretreatment with BIRB796 (10 μM) for 1 hour (mean ± SEM; Fab-Cre <i>n =</i> 6 or p38α^Fab-KO <i>n =</i> 7 wells treated with NE; and Fab-Cre <i>n =</i> 7 or p38α^Fab-KO <i>n =</i> 8 wells treated with ISO). See also <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2004455#pbio.2004455.s015" target="_blank">S1 Data</a>. BAT, brown adipose tissue; FCCP, carbonyl cyanide-4-(trifluoromethoxy)phenylhydrazone; ISO, isoproterenol; NE, norepinephrine; OCR, oxygen consumption rate; qRT-PCR, quantitative real-time polymerase chain reaction; WT, wild-type.</p

p38α^Fab-KO mice are protected against diet-induced obesity and diabetes.

<p>(A) Body weight time course in Fab-Cre and p38α^Fab-KO male (8–10-wk-old) mice fed an HFD over 8 weeks. Data are presented as the increase above initial weight (left panel) or as total weight comparing mice fed an HDF with mice fed an ND (right panel). HFD-induced weight gain was significantly higher in Fab-Cre than p38α^Fab-KO mice (mean ± SEM; Fab-Cre HFD <i>n =</i> 10 mice; p38α^Fab-KO HFD <i>n =</i> 11 mice; Fab-Cre ND <i>n =</i> 9 mice; p38α^Fab-KO ND <i>n =</i> 8 mice). (B) NMR analysis of fat mass in p38α^Fab-KO and Fab-Cre mice after 8 weeks of HFD (mean ± SEM; Fab-Cre <i>n =</i> 10 mice; p38α^Fab-KO <i>n =</i> 8 mice). (C) Representative haematoxylin–eosin and oil red O staining of liver sections (Fab-Cre <i>n =</i> 6 mice; p38α^Fab-KO <i>n =</i> 6 mice; and 3 pictures from each mouse). Scale bar: 50 μm. (D) Fasting and fed blood glucose in Fab-Cre and p38α^Fab-KO mice fed the HFD (8 weeks) (mean ± SEM; Fab-Cre <i>n =</i> 10 mice; p38α^Fab-KO <i>n =</i> 11 mice). (E) GTT and ITT in Fab-Cre and p38α^Fab-KO mice fed the HFD for 8 weeks. Mice were fasted overnight (for GTT) or 1 hour (for ITT), and blood glucose concentration was measured in mice given intraperitoneal injections of glucose (1 g/kg of total body weight) or insulin (0.75 U/kg of total body weight) (mean ± SEM; Fab-Cre <i>n =</i> 10 mice; p38α^Fab-KO <i>n =</i> 11 mice). (F) Immunohistochemistry of eWAT sections using anti-GLUT4 (green), anti-Cav-1 (red) antibodies, and the nuclear dye DAPI (blue). Location of GLUT4 was analysed in mice treated without or with insulin (1.5 IU/kg) for 15 minutes after overnight fasting. Scale bar: 20 μm. (G) Representative haematoxylin–eosin BAT and eWAT sections (Fab-Cre <i>n =</i> 6 mice; p38α^Fab-KO <i>n =</i> 6 mice; and 3 pictures from each mouse). Scale bar: 50 μm. *<i>p</i> < 0.05, ***<i>p</i> < 0.001 Fab-Cre versus p38α^Fab-KO. ‘&&’ indicates <i>p</i> < 0.01, ‘&&&’ indicates <i>p</i> < 0.001 Fab-Cre ND versus Fab-Cre HFD (2-way ANOVA coupled with Bonferroni’s post-tests or <i>t</i> test or Welch’s test when variances were different). See also <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2004455#pbio.2004455.s015" target="_blank">S1 Data</a>. BAT, brown adipose tissue; Cav-1, caveolin-1; eWAT, epididymal fat; GLUT4, glucose transporter type 4; GTT, glucose tolerance test; HFD, high-fat diet; ITT, insulin tolerance test; ND, normal-chow diet; WAT, white adipose tissue.</p

Regulation of browning and BAT activation by p38 pathway.

<p>Graphical abstract summarising the role of p38 isoforms in adipose tissue. In eWAT, p38α activates browning through the phosphorylation of Creb and ATF2 increasing UCP1 expression. In iWAT and BAT, p38α activation inhibits p38γ and p38δ and in consequence reduces browning and BAT activation, respectively, by down-regulation of UCP1. ATF2, activating transcription factor 2; BAT, brown adipose tissue; Creb, cAMP response element-binding; eWAT, epididymal fat; iWAT, inguinal fat; UCP1, uncoupling protein 1.</p

p38α in human visceral fat inversely correlated with BMI and directly correlated with UCP1 in human visceral fat and sWAT.

<p>(A) mRNA levels of <i>Mapk14</i> (p38α) in visceral fat from lean individuals and individuals with obesity—mRNA expression was normalised to the amount of <i>Gapdh</i> mRNA. (B) Correlation between mRNA levels of <i>Mapk14</i> (p38α) and BMI (r² = −0,365; <i>p</i> = 0.001) or (C) <i>Ucp1</i> in visceral fat (r² = 0.316; <i>p</i> = 0.007). The mRNA levels of <i>Mapk14</i> (p38α) and <i>Ucp1</i> were determined by qRT-PCR (<i>n</i> = 71). (D) mRNA levels of <i>Mapk14</i> (p38α) in sWAT from lean individuals and individuals with obesity. mRNA expression was normalised to the amount of <i>Gapdh</i> mRNA. (E) Correlation between mRNA levels of <i>Mapk14</i> (p38α) and <i>Ucp1</i> in sWAT (r² = 0.320; <i>p</i> < 0.0001). Graph correlating mRNA <i>Mapk14</i> and log mRNA <i>Ucp1</i> is also shown. The mRNA levels of <i>Mapk14</i> (p38α) and <i>Ucp1</i> were determined by qRT-PCR (<i>n</i> = 168). See also <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2004455#pbio.2004455.s015" target="_blank">S1 Data</a>. Linear relationships between variables were tested using Pearson’s correlation coefficient. BMI, body mass index; qRT-PCR, quantitative real-time polymerase chain reaction; UCP1, uncoupling protein 1.</p