23 research outputs found

    Energy recovery methodology in industrial processes

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    International audienceThrough the CERES -2 project, supported by the French Research National Agency (ANR), we have developed an open source software platform, called CERES, to optimize heat recovery in continuous industrial processes. This platform is based on a multi-scale and multi critera methodology for heat recovery optimisation. This methodology is based on the following calculation steps:1. Minimum Energy Requirement identification2. Minimum Exergy Requirement and utilities identification3. Exchanger network constructionAt each step we solve a linear mono-objective problem. The first step allows, from a set of heat flows, to build the composite curves and to determine the minimum heating and cooling energy requirements. With the set of heat flows and a solution of the first step, the second step proposes the introduction of utilities, such as heat pumps or organic Rankine cycle (ORC), to minimize the exergy destruction. The last step is based on an algorithm of heat exchanger network design (HEN) including utilities and heat recovery technologies sizing, based on economic criteria. The set of heat flows are constructed in the platform CERES from industrial processes Modelica models. CERES has been validated with 3 industrial case studies

    Estrogen- and Progesterone (P4)-Mediated Epigenetic Modifications of Endometrial Stromal Cells (EnSCs) and/or Mesenchymal Stem/Stromal Cells (MSCs) in the Etiopathogenesis of Endometriosis

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    Endometriosis is a common chronic inflammatory condition in which endometrial tissue appears outside the uterine cavity. Because ectopic endometriosis cells express both estrogen and progesterone (P4) receptors, they grow and undergo cyclic proliferation and breakdown similar to the endometrium. This debilitating gynecological disease affects up to 15% of reproductive aged women. Despite many years of research, the etiopathogenesis of endometrial lesions remains unclear. Retrograde transport of the viable menstrual endometrial cells with retained ability for attachment within the pelvic cavity, proliferation, differentiation and subsequent invasion into the surrounding tissue constitutes the rationale for widely accepted implantation theory. Accordingly, the most abundant cells in the endometrium are endometrial stromal cells (EnSCs). These cells constitute a particular population with clonogenic activity that resembles properties of mesenchymal stem/stromal cells (MSCs). Thus, a significant role of stem cell-based dysfunction in formation of the initial endometrial lesions is suspected. There is increasing evidence that the role of epigenetic mechanisms and processes in endometriosis have been underestimated. The importance of excess estrogen exposure and P4 resistance in epigenetic homeostasis failure in the endometrial/endometriotic tissue are crucial. Epigenetic alterations regarding transcription factors of estrogen and P4 signaling pathways in MSCs are robust in endometriotic tissue. Thus, perspectives for the future may include MSCs and EnSCs as the targets of epigenetic therapies in the prevention and treatment of endometriosis. Here, we reviewed the current known changes in the epigenetic background of EnSCs and MSCs due to estrogen/P4 imbalances in the context of etiopathogenesis of endometriosis

    Reciprocal Interactions between Wakefulness and Sleep Influence Global and Regional Brain Activity.

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    Reciprocal interactions between wakefulness and sleep substantially influence human brain function in both states of vigilance. On the one hand, there is evidence that regionally-specialized brain activity during wakefulness is modulated by the interaction between a local use-dependent buildup of homeostatic sleep pressure and circadian signals. On the other hand, brain activity during sleep, although mainly constrained by genuine sleep oscillations, shows wake-dependent regionally-specific modulations, which are involved in the dissipation of local homeostatic sleep pressure and memory consolidation

    Reciprocal Interactions between Wakefulness and Sleep Influence Global and Regional Brain Activity.

    No full text
    Reciprocal interactions between wakefulness and sleep substantially influence human brain function in both states of vigilance. On the one hand, there is evidence that regionally-specialized brain activity during wakefulness is modulated by the interaction between a local use-dependent buildup of homeostatic sleep pressure and circadian signals. On the other hand, brain activity during sleep, although mainly constrained by genuine sleep oscillations, shows wake-dependent regionally-specific modulations, which are involved in the dissipation of local homeostatic sleep pressure and memory consolidation

    Altered white matter architecture in BDNF Met carriers

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    Brain-derived neurotrophic factor (BDNF) modulates the pruning of synaptically-silent axonal arbors. The Met allele of the BDNF gene is associated with a reduction in the neurotrophin's activity-dependent release. We used di ffusion-weighted imaging to construct structural brain networks for 36 healthy subjects with known BDNF genotypes. Through permutation testing we discovered clear di fferences in connection strength between subjects carrying the Met allele and those homozygotic for the Val allele. We trained a Gaussian process classi fier capable of identifying the subjects' allelic group with 86% accuracy and high predictive value. In Met carriers structural connectivity was greatly increased throughout the forebrain, particularly in connections corresponding to the anterior and superior corona radiata as well as corticothalamic and corticospinal projections from the sensorimotor, premotor and prefrontal portions of the internal capsule. Interhemispheric connectivity was also increased via the corpus callosum and anterior commissure, and extremely high connectivity values were found between inferior medial frontal polar regions via the anterior forceps. We propose that the decreased availability of BDNF leads to de cifits in axonal maintenance in carriers of the Met allele, and that this produces mesoscale changes in white matter architecture
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