218 research outputs found

    Results from the First Field Tests of the WISDOM GPR (2018 ExoMars Mission)

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    International audienceIntroduction: The WISDOM (Water Ice Subsur- face Deposit Observation on Mars) Ground Penetrating Radar (GPR) is one of the instruments that have been selected as part of the Pasteur payload of ESA’s 2018 ExoMars Rover mission[1]. The Pasteur payload actu- ally consists of two different sets of instruments: the Panoramic Instruments, which include a wide angle camera and the WISDOM radar, that will be used to perform large-scale scientific investigations of the landing site and the Analytical Laboratory Instruments that will analyze the core samples obtained by the sub- surface drill. WISDOM will help identify the location of sedimentary layers, where organic molecules are the most likely to be found and well-preserved. WISDOM has been designed to investigate the near subsurface environment down to a depth of ~2-3 m with a vertical resolution of a few centimeters [2]. WISDOM is a step frequency radar operating over a wide frequency band between 0.5 and 3 GHz. Particular attention was paid to the design of the antenna system, which needs to be able to conduct polarimetric measurements over the whole bandwidth without significant distortion [3]

    The Adenosinergic Signaling: A Complex but Promising Therapeutic Target for Alzheimer’s Disease

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    Alzheimer’s disease (AD) is the most common neurodegenerative disorder in elderly people. AD is characterized by a progressive cognitive decline and it is neuropathologically defined by two hallmarks: extracellular deposits of aggregated β-amyloid (Aβ) peptides and intraneuronal fibrillar aggregates of hyper- and abnormally phosphorylated Tau proteins. AD results from multiple genetic and environmental risk factors. Epidemiological studies reported beneficial effects of caffeine, a non-selective adenosine receptors antagonist. In the present review, we discuss the impact of caffeine and of adenosinergic system modulation on AD, in terms of pathology and therapeutics

    Increased Cardiovascular Reactivity to Acute Stress and Salt-Loading in Adult Male Offspring of Fat Fed Non-Obese Rats

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    Diet-induced obesity in rat pregnancy has been shown previously to be associated with consistently raised blood pressure in the offspring, attributed to sympathetic over-activation, but the relative contributions to this phenotype of maternal obesity versus raised dietary fat is unknown. Sprague-Dawley female rats were fed either a control (4.3% fat, n = 11) or lard-enriched (23.6% fat, n = 16) chow 10 days prior to mating, throughout pregnancy and lactation. In conscious adult (9-month-old) offspring cardiovascular parameters were measured (radiotelemetry). The short period of fat-feeding did not increase maternal weight versus controls and the baseline blood pressure was similar in offspring of fat fed dams (OF) and controls (OC). However, adult male OF showed heightened cardiovascular reactivity to acute restraint stress (p<0.01; Δ systolic blood pressure (SBP) and Δheart rate (HR)) with a prolonged recovery time compared to male OC. α1/β-adrenergic receptor blockade normalised the response. Also, after dietary salt-loading (8%-NaCl ad libitum for 1 week) male OF demonstrated higher SBP (p<0.05) in the awake phase (night-time) and increased low/high frequency ratio of power spectral density of HR variability versus OC. Baroreflex gain and basal power spectral density components of the heart rate or blood pressure were similar in male OF and OC. Minor abnormalities were evident in female OF. Fat feeding in the absence of maternal obesity in pregnant rats leads to altered sympathetic control of cardiovascular function in adult male offspring, and hypertension in response to stressor stimuli

    Sex- and Diet-Specific Changes of Imprinted Gene Expression and DNA Methylation in Mouse Placenta under a High-Fat Diet

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    Changes in imprinted gene dosage in the placenta may compromise the prenatal control of nutritional resources. Indeed monoallelic behaviour and sensitivity to changes in regional epigenetic state render imprinted genes both vulnerable and adaptable

    Vieau, Henry; Interview and Materials

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    Roster Number: 100. Picture Location: Box 6 Folder 2. Interview Location: Box 1 Folder 2

    La dénutrition maternelle périnatale programme les systèmes neuroendocriniens impliqués dans la réponse au stress chez le rat mâle adulte : rôle dans la genèse du syndrome métabolique?

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    De nombreuses données ont montré que les perturbations périnatales, comme la dénutrition maternelle, sont associées au développement accru de pathologies métaboliques chez l’adulte. Les mécanismes physiopathologiques impliqués dans ce qui est appelé « programmation fœtale » ou plus justement « origine développementale de la santé et des maladies de l’adulte » sont encore très méconnus, mais des arguments suggèrent que des perturbations des systèmes neuroendocriniens impliqués dans l’adaptation au stress (système sympatho-surrénalien et axe hypothalamo-hypophyso-surrénalien, respectivement) pourraient jouer un rôle crucial. Notre équipe a mis au point un modèle de dénutrition maternelle périnatale (réduction de 50 % de l’apport calorique global de la dernière semaine de gestation jusqu’au sevrage, modèle FR50) chez le rat, à partir duquel nous avons analysé, chez la descendance mâle, les conséquences de cette dénutrition sur l’activité des axes neuroendocriniens du stress. Au niveau du système sympatho-surrénalien, les altérations morphologiques des îlots de cellules chromaffines noradrénergiques, observées dès le sevrage, sont persistantes chez le rat mâle FR50 âgé de 8 mois et se traduisent par une sécrétion amoindrie de catécholamines en conditions de base et exacerbée en réponse au stress. À l’inverse, l’activité de l’axe hypothalamo-hypophyso-surrénalien est fortement augmentée en conditions de bases chez les rats FR50 adultes, ce qui se traduit par un taux circulant de glucocorticoïdes très élevé, mais qui n’est pas augmentée en réponse au stress. Nos résultats montrent que la dénutrition maternelle modifie durablement, chez la descendance, l’activité des systèmes neuroendocriniens impliqués dans la réponse et l’adaptation au stress. Dans la mesure où ces systèmes, via la production de catécholamines et de glucocorticoïdes, contrôlent divers paramètres métaboliques (régulation de la pression artérielle et de la glycémie notamment), leur dysfonctionnement, en particulier dans les situations de stress chronique, pourrait contribuer au développement de maladies chroniques de l’adulte d’origine métabolique, cognitive ou inflammatoire

    Perinatal nutritional programming of health and metabolic adult disease

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    Data indicate that perinatal nutritional insults not onlyhave short-term consequences on the growth velocity of the fetus/neonate but also sensitize to the development of metabolic adult diseases. The pathophysiological mechanisms involved in the so-called “Developmental Origin of Health and Adult Diseases” are still largely unknown and depend on the type of alteration (nutritional, psychological, endocrine disruptors, etc.), its intensity and duration, species, sex and the time during which it is applied. Perinatal stress, via disturbances of both hypothalamo-pituitary-adrenal (HPA) axis and sympatho-adrenal-system (SAS), as well as brain-adipose axis and pancreas alterations could play a crucial role. Interestingly, it has been demonstrated that perinatal insults may be transmitted transgenerationally, suggesting that these long-term consequences may be inherited via epigenetic mechanisms. Finally, since the placenta has been demonstrated to be sensitive to perinatal nutritional manipulations, the identification of placental markers may thus represent an important new avenue to identify the more susceptible babies prone to developing metabolic diseases

    Proopiomelanocortine et marqueurs biochimiques de differenciation neuroendocrine (7B2 et Chromogranine B) en pathologie tumorale chez l'homme

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    SIGLEAvailable from INIST (FR), Document Supply Service, under shelf-number : T 78403 / INIST-CNRS - Institut de l'Information Scientifique et TechniqueFRFranc
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