Altérations du comportement alimentaire en environnements externes (intégration centrale)

L exposition à des environnements extrêmes est en général à l origine de perturbations de la prise alimentaire, chez l homme comme chez le rongeur. Nous avons étudié, chez le rat, l implication de la leptine et de ses cibles centrales dans l instauration des anorexies induites par le stress psychogène ou par l exposition à l altitude. Nos résultats ont montré que le stress psychogène induisait le facteur SOCS-3, modulait l expression du récepteur de la leptine dans l hypothalamus, et était, à long terme, susceptible d altérer la régulation de l homéostasie du poids corporel de l organisme. En utilisant une souche de rats génétiquement déficients en signalisation de la leptine, les rats Zucker obèses, nous avons démontré de façon irréfutable que l anorexie d altitude n était pas imputable à des signaux centraux anorexigènes induits par une augmentation de la production de leptine par le tissu adipeux. Enfin, une 3ème étude nous permet de suggérer que l AMPKinase hypothalamique pourrait jouer un rôle déterminant dans l initiation de l anorexie d altitude. L implication de ce système dans d autres situations anorexigènes, comme l exercice physique exhaustif, serait à envisagerExposure to extreme environments usually elicits alteration in feeding behavior in men and rodents. We studied the involvement of leptin and it s central targets in the development of anorexia induced by psychogenic stress or altitude exposure. Our results suggested that restraint stress elicited SOCS-3 induction, modulated leptin signalling in hypothalamus, and was therefore likely to alter the regulation of body weight homeostasis. Using a rat model of genetic leptin receptor deficiency, the obese Zucker rat, we unequivocally demonstrated that altitude-induced anorexia could not be ascribed to anorectic signals triggered by enhanced leptin production. A third experiment suggested that the hypothalamic AMPKinase system may play a determinant role in the early stage of altitude-induced anorexia. The involvement of this system in other anorexigenic situations such as sustained exercise needs to be examinedLYON1-BU.Sciences (692662101) / SudocSudocFranceF

Weakened watershed assembly for remote sensing image segmentation and change detection

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Leptin receptor-deficient obese Zucker rats reduce their food intake in response to hypobaric hypoxia.

International audienceExposure to hypoxia induces anorexia in humans and rodents, but the role of leptin remains under discussion and that of orexigenic and anorexigenic hypothalamic neuropeptides remains unknown. The present study was designed to address this issue by using obese (Lepr(fa)/Lepr(fa)) Zucker rats, a rat model of genetic leptin receptor deficiency. Homozygous lean (Lepr(FA)/Lepr(FA)) and obese (Lepr(fa)/Lepr(fa)) rats were randomly assigned to two groups, either kept at ambient pressure or exposed to hypobaric hypoxia for 1, 2, or 4 days (barometric pressure, 505 hPa). Food intake and body weight were recorded throughout the experiment. The expression of leptin and vascular endothelial growth factor (VEGF) genes was studied in adipose tissue with real-time quantitative PCR and that of selected orexigenic and anorexigenic neuropeptides was measured in the hypothalamus. Lean and obese rats exhibited a similar hypophagia (38 and 67% of initial values at day 1, respectively, P < 0.01) and initial decrease in body weight during hypoxia exposure. Hypoxia led to increased plasma leptin levels only in obese rats. This resulted from increased leptin gene expression in adipose tissue in response to hypoxia, in association with enhanced VEGF gene expression. Increased hypothalamic neuropeptide Y levels in lean rats 2 days after hypoxia exposure contributed to accounting for the enhanced food consumption. No significant changes occurred in the expression of other hypothalamic neuropeptides involved in the control of food intake. This study demonstrates unequivocally that altitude-induced anorexia cannot be ascribed to anorectic signals triggered by enhanced leptin production or alterations of hypothalamic neuropeptides involved in anabolic or catabolic pathways

Comparaison et évaluation de méthodes de segmentation avec contrainte en vue d’une classification du bâti et des routes

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Cyclosporin A inhibits hypoxia-induced pulmonary hypertension and right ventricle hypertrophy.

International audienceRATIONALE: Hypoxia-induced pulmonary hypertension involves hypoxia-inducible factor-1alpha (HIF-1alpha) activation as well as elevated resting calcium levels. Cyclosporin A (CsA) inhibits calcium-induced calcineurin activation and blocks the stabilization of HIF-1alpha in cultured cells. OBJECTIVES: We hypothesized that treatment of rats with CsA would prevent HIF-1-dependent gene transcription, lower specific responses to acute hypoxia, and prevent pulmonary hypertension and right ventricle hypertrophy resulting from prolonged exposure to hypoxia. METHODS: Acute and chronic responses to hypoxia were studied in rats treated or not treated with CsA (25 mg x kg(-1) x d(-1)). MEASUREMENTS: Transcript levels of genes encoding the serotonin transporter or four HIF-1 target genes, in rats exposed for 6 h to ambient hypoxia, treated or not by CsA, were measured. In vivo hemodynamics, hematocrit, and heart morphologic characteristics were assessed in rats subjected to hypoxia for 3 wk, treated or not treated with CsA. Changes in mRNA levels of the modulatory calcineurin-interacting protein-1 (MCIP-1) were used as a sensitive indicator of calcineurin activity in lung and heart. MAIN RESULTS: Acute exposure to hypoxia led to a marked increase in mRNA levels of serotonin transporter, modulatory calcineurin-interacting protein-1, and HIF-1 target genes, which was blunted by CsA treatment. Prolonged exposure to hypoxia raised right ventricle pressure, induced right ventricle hypertrophy, and activated cardiac calcineurin, effects that were fully prevented by CsA treatment. CONCLUSIONS: These results suggest that CsA prevents hypoxia-induced pulmonary hypertension and right ventricle hypertrophy, either by inhibiting HIF-1 transcriptional activity in lung, by decreasing calcineurin activity in lung and heart, by direct effects of CsA, or by a combination of these factors

Automatic Recognition for Map Update by Remote Sensing, final report.

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Detecting man-made structure changes to assist geographic data producers in planning their update strategy, ISPRS

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