89 research outputs found

    First report about ants associated with Diaphorina citri Kuwayama in Mexican lime (Citrus aurantiifolia Swingle) in the Apatzingán Valley, Michoacán, México

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    Objective: To carry out taxonomic studies that determine which formicine species are associated with the cultivation of Mexican lime. Design/Methodology/Approach: The study was conducted in eight municipalities and 59 localities of the Apatzingán Valley region, Michoacán, Mexico, where Mexican lime (Citrus aurantiifolia Swingle) is produced. A randomized complete blocks design was used in the experiment, where each municipality represented a block. The repetitions were the number of collections, while the experimental unit was a lime sprout infested with Diaphorina citri and ants. The collections were direct and were made with an entomological aspirator. The values obtained were analyzed with the SAS University Edition software (2018). Results: The studied ants belong to the Dolichoderinae, Formicinae, Myrmicinae, Pseudomyrmecinae, and Ponerinae subfamilies, which represent 15 genera and the same number of species. The subfamilies with the greatest presence in the eight municipalities were: Myrmicinae, Dolichoderinae, and Formicinae. The species with the highest impact were Paratrechina longicornis, Forelius mccooki, and Atta mexicana, while Cardiocondyla minutior and Odontomachus sp. had a lower impact. Study limitations/implications: Social insecurity in the eight municipalities and the new form of coexistence. Findings/Conclusions: The studied species prefer dry, warm, and disturbed site

    Boletín NUESTRA AMÉRICA XXI - Desafíos y alternativas, num.27, Enero 2019

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    Una excelente iniciativa del Grupo de Trabajo Crisis y economía mundial, coordinado por María Josefina Morales y Gabriela Roffinelli

    p38γ and p38δ regulate postnatal cardiac metabolism through glycogen synthase 1

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    During the first weeks of postnatal heart development, cardiomyocytes undergo a major adaptive metabolic shift from glycolytic energy production to fatty acid oxidation. This metabolic change is contemporaneous to the up-regulation and activation of the p38γ and p38δ stress-activated protein kinases in the heart. We demonstrate that p38γ/δ contribute to the early postnatal cardiac metabolic switch through inhibitory phosphorylation of glycogen synthase 1 (GYS1) and glycogen metabolism inactivation. Premature induction of p38γ/δ activation in cardiomyocytes of newborn mice results in an early GYS1 phosphorylation and inhibition of cardiac glycogen production, triggering an early metabolic shift that induces a deficit in cardiomyocyte fuel supply, leading to whole-body metabolic deregulation and maladaptive cardiac pathogenesis. Notably, the adverse effects of forced premature cardiac p38γ/δ activation in neonate mice are prevented by maternal diet supplementation of fatty acids during pregnancy and lactation. These results suggest that diet interventions have a potential for treating human cardiac genetic diseases that affect heart metabolism.G.S. is a YIP EMBO member. B.G.T. was a fellow of the FPI Severo Ochoa CNIC program (SVP-2013-067639) and currently is funded by the AHA-CHF (AHA award number: 818798). V.M.R. is a FPI fellow (BES-2014-069332) and A.M.S. is a fellow of the FPI Severo Ochoa CNIC program (BES-2016-077635). This work was funded by the following grants: to G.S.: funding from the EFSD/Lilly European Diabetes Research Programme Dr Sabio, from Spanish Ministry of Science, Innovation and Universities (MINECO-FEDER SAF2016-79126-R and PID2019-104399RB-I00), Comunidad de Madrid (IMMUNOTHERCAN-CM S2010/BMD-2326 and B2017/BMD-3733) and Fundación Jesús Serra; to P.A.: Ayudas para apoyar grupos de investigación del sistema Universitario Vasco (IT971-16 to P.A.), MCIU/AEI/FEDER, funding from Spanish Ministry of Science, Innovation and Universities (RTI2018-095134-B-100); Excellence Network Grant from MICIU/AEI (SAF2016-81975-REDT and 2018-PN188) to PA and GS; to J.V.: funding from Spanish Ministry of Science, Innovation and Universities (PGC2018-097019-B-I00), the Instituto de Salud Carlos III (Fondo de Investigación Sanitaria grant PRB3 (PT17/0019/0003- ISCIII-SGEFI / ERDF, ProteoRed), and “la Caixa” Banking Foundation (project code HR17-00247); to J.P.B.: funding from Spanish Ministry of Science, Innovation and Universities (PID2019-105699RB-I00, RED2018‐102576‐T) and Escalera de Excelencia (CLU-2017-03); to J.A.E.: funding from Spanish Ministry of Science, Innovation and Universities MINECO (RED2018-102576-T, RTI2018-099357-B-I00), CIBERFES (CB16/10/00282), and HFSP (RGP0016/2018). RAP (XPC/BBV1602 and MIN/RYC1102). The CNIC is supported by the Ministry of Science, Innovation and Universities and the Pro CNIC Foundation, and is a Severo Ochoa Center of Excellence (SEV-2015-0505). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

    γ-Linolenic acid in maternal milk drives cardiac metabolic maturation.

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    Birth presents a metabolic challenge to cardiomyocytes as they reshape fuel preference from glucose to fatty acids for postnatal energy production1,2. This adaptation is triggered in part by post-partum environmental changes3, but the molecules orchestrating cardiomyocyte maturation remain unknown. Here we show that this transition is coordinated by maternally supplied γ-linolenic acid (GLA), an 18:3 omega-6 fatty acid enriched in the maternal milk. GLA binds and activates retinoid X receptors4 (RXRs), ligand-regulated transcription factors that are expressed in cardiomyocytes from embryonic stages. Multifaceted genome-wide analysis revealed that the lack of RXR in embryonic cardiomyocytes caused an aberrant chromatin landscape that prevented the induction of an RXR-dependent gene expression signature controlling mitochondrial fatty acid homeostasis. The ensuing defective metabolic transition featured blunted mitochondrial lipid-derived energy production and enhanced glucose consumption, leading to perinatal cardiac dysfunction and death. Finally, GLA supplementation induced RXR-dependent expression of the mitochondrial fatty acid homeostasis signature in cardiomyocytes, both in vitro and in vivo. Thus, our study identifies the GLA-RXR axis as a key transcriptional regulatory mechanism underlying the maternal control of perinatal cardiac metabolism.S

    L’origine fœtale de l’obésité et des maladies associées

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    L’origine fœtale de l’obésité et des maladies associées

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    Syndrome métabolique : une histoire d'empreinte nutritionnelle et d'épigénétique ?

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    National audienceThe concept of metabolic imprinting developed from the observation of a relationship between perinatal growth rate and the risk of late onset metabolic disease. According to this concept, early nutrition could influence a number of key metabolic pathways in the long term, and this influence could even be in some way transmitted to future generations. As demonstrated in animal models, nutrients could act on secondary genomic structure and expression through epigenetic mechanisms. Further studies of human populations are needed to confirm this hypothesis.L'observation d'un lien entre intensité de croissance périnatale et risque de développer des maladies métaboliques à l'âge adulte a fait émerger la notion dite « d'empreinte métabolique ». La nutrition, pendant les stades précoces de la vie, conditionnerait certaines fonctions métaboliques de façon durable et éventuellement transmissible aux générations suivantes. Les nutriments exerceraient une régulation directe de l'expression du génome par des modifications épigénétiques. Cependant, à ce jour, ces données expérimentales sont obtenues sur des modèles animaux et nécessitent d'être confirmées par des recherches chez l'homme
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