Gastric stimulation: influence of electrical parameters on gastric emptying in control and diabetic rats

BACKGROUND: The aim of this study was to test the effect of different pulse frequencies and amplitudes during gastric stimulation (GS) on gastric emptying in the rat. METHODS: GS was performed in 2 groups of laparotomized rats: healthy control animals, and rats with acute diabetes. The effects of four pulse frequencies (0.5, 1, 10, 20 Hz) and three pulse amplitudes (5, 20, 40 mA) were tested. The volumes emptied from the stomach after the oro-gastric instillation of a nutrient solution were compared to those obtained in animals without GS. Intragastric pH values were assessed under basal conditions and after GS. RESULTS: In both groups, GS increased emptied volumes compared to conditions without stimulation (p < 0.05) for pulse frequencies above 0.5 Hz. Increases in pulse frequencies accelerated gastric emptying (p < 0.01) with a plateau at around 10 Hz. The increase in pulse amplitudes resulted in larger emptied volumes only when the pulse frequency was 1 Hz (p < 0.04) while the opposite effect was observed at 20 Hz (p < 0.04). The most effective combinations to enhance gastric emptying compared to baseline conditions were 10 Hz with 5 or 20 mA. The overall effect of GS on gastric emptying compared to baseline conditions without stimulation, was greater in diabetic than in controls rats (p < 0.05). During stimulation, intragastric pH values were not different from basal conditions during fasting or after a meal in control and diabetic rats. CONCLUSIONS: Although both pulse frequency and amplitude should be considered during GS, frequency appears to be the most critical point. The possibility of increasing gastric emptying by electrical stimulation in diabetic rats suggests potential clinical applications for this method

The "saisie-appréhension"

La saisie-appréhension, en dépit de sa nouveauté, reste de nos jours largement ignorée par la doctrine. Pourtant, en venant assurer l’exécution forcée en nature de certaines obligations de faire (celles de livraison/délivrance et restitution de biens meubles corporels), cette mesure offre de nouvelles perspectives et ce, tant dans les procédures civiles d’exécution que dans le droit des obligations. En effet, son objectif repose sur une logique différente de celle qui gouverne traditionnellement les saisies et cette nouvelle logique qu’elle incarne conduit à une résolution des problèmes touchant la classification des obligations selon leur objet.Cette étude se propose ainsi de cerner cette mesure et de montrer les intérêts qu’elle présente, ce qui amènera à des analyses à la fois dans les voies d’exécution et dans le droit substantiel. Au terme de celle-ci, la saisie-appréhension se révèlera comme l’autre figure de l’exécution forcée en nature.The saisie-appréhension, in spite of its newness, stays nowadays widely unknown by the doctrine. However, in so far as it stands ensure for specific performance of some obligations to do like delivery or restitution of tangible movables, this measure offers new prospects concerning the civil proceedings of execution as well as Law of obligations. Its aim is based indeed on a logical different from the one which controls traditionally the other executions all, this new logical allows to resolve problems about the classification of obligation in accordance with their object.This study has so in view to determine this measure and to show its interests, what induces to analysis in Law of seizures and in substantial law. At the end of this one, the saisie-appréhension will come to light as the other face of specific performance

L'entreprise en restructuration

Cet ouvrage explore les dynamiques institutionnelles et les mobilisations à l’œuvre dans les restructurations d’entreprise. Celles-ci apparaissent, actuellement, comme des processus diffus, récurrents et complexes de réorganisation affectant l’entreprise dans sa recherche de flexibilité et d’avantages compétitifs. Dans un contexte de crise, elles prennent un relief particulier en raison de leur ampleur, de l’intensité des conflits auxquels elles donnent lieu et de leurs conséquences sociales notamment en termes d’emplois. Loin de s’imposer comme des adaptations inéluctables à une évolution économique qui leur échapperait, les restructurations se caractérisent par de nombreuses initiatives des acteurs concernés, tant les directions d’entreprise, que les salariés et leurs représentants. Prenant appui sur tout un ensemble d’équipements institutionnels et des mobilisations collectives, un débat argumenté et contradictoire s’instaure entre les différentes parties prenantes. Il ne se réduit pas aux reclassements des salariés et à la compensation financière des pertes d’emploi. Il porte également sur la formulation même des problèmes à résoudre et peut parfois conduire à la construction concertée de stratégies économiques alternatives permettant de préserver les emplois. L’ouvrage envisage les restructurations au croisement des pratiques managériales et de l’intervention des salariés et de leurs représentants dans l’entreprise. Il explore des dynamiques institutionnelles à partir de l’analyse des dispositifs juridiques européens et nationaux et d’enquêtes de terrain dans les entreprises, en adoptant une perspective transnationale et pluridisciplinaire liant histoire, économie, droit et sociologie. Cet ouvrage se compose des contributions présentées lors d’un colloque réunissant des acteurs parties prenantes des restructurations et des chercheurs. Il propose un nouveau regard sur une question sociale brûlante

Coenzyme Q10 supplementation lowers hepatic oxidative stress and inflammation associated with diet-induced obesity in mice.

BACKGROUND: Diabetes and obesity are metabolic disorders induced by an excessive dietary intake of fat, usually related to inflammation and oxidative stress. AIMS: The aim of the study is to investigate the effect of the antioxidant coenzyme Q10 (CoQ10) on hepatic metabolic and inflammatory disorders associated with diet-induced obesity and glucose intolerance. METHODS: C57bl6/j mice were fed for 8 weeks, either a control diet (CT) or a high fat diet plus 21% fructose in the drinking water (HFF). CoQ10 supplementation was performed in this later condition (HFFQ). RESULTS: HFF mice exhibit increased energy consumption, fat mass development, fasting glycemia and insulinemia and impaired glucose tolerance. HFF treatment promoted the expression of genes involved in reactive oxygen species production (NADPH oxidase), inflammation (CRP, STAMP-2) and metabolism (CPT1alpha) in the liver. CoQ10 supplementation decreased the global hepatic mRNA expression of inflammatory and metabolic stresses markers without changing obesity and tissue lipid peroxides compared to HFF mice. HFF diets paradoxically decreased TBARS (reflecting lipid peroxides) levels in liver, muscle and adipose tissue versus CT group, an effect related to vitamin E content of the diet. CONCLUSION: In conclusion, HFF model promotes glucose intolerance and obesity by a mechanism independent on the level of tissue peroxides. CoQ10 tends to decrease hepatic stress gene expression, independently of any modulation of lipid peroxidation, which is classically considered as its most relevant effect

PPARα inhibits vascular smooth muscle cell proliferation underlying intimal hyperplasia by inducing the tumor suppressor p16(INK4a)

Vascular SMC proliferation is a crucial event in occlusive cardiovascular diseases. PPARα is a nuclear receptor controlling lipid metabolism and inflammation, but its role in the regulation of SMC growth remains to be established. Here, we show that PPARα controls SMC cell-cycle progression at the G(1)/S transition by targeting the cyclin-dependent kinase inhibitor and tumor suppressor p16(INK4a) (p16), resulting in an inhibition of retinoblastoma protein phosphorylation. PPARα activates p16 gene transcription by both binding to a canonical PPAR-response element and interacting with the transcription factor Sp1 at specific proximal Sp1-binding sites of the p16 promoter. In a carotid arterial–injury mouse model, p16 deficiency results in an enhanced SMC proliferation underlying intimal hyperplasia. Moreover, PPARα activation inhibits SMC growth in vivo, and this effect requires p16 expression. These results identify an unexpected role for p16 in SMC cell-cycle control and demonstrate that PPARα inhibits SMC proliferation through p16. Thus, the PPARα/p16 pathway may be a potential pharmacological target for the prevention of cardiovascular occlusive complications of atherosclerosis

Breast cancer and obesity: in vitro interferences between adipokines and proangiogenic features and/or antitumor therapies?

International audienceObesity is now considered as a risk factor for breast cancer in postmenopausal women. Adipokine levels are modulated in obesity, and may play a role in carcinogenesis. Moreover, obesity increases risk of cancer mortality. Here, we hypothesized that this increase could be due to a modification in angiogenesis, capital event in the development of metastases, and/or in effectiveness of cancer treatments. To test these assumptions, following a same experimental design and simultaneously the effects of leptin and adiponectin on angiogenesis were investigated, and the impact of hyperleptinemia on anticancer drug effectiveness was measured in physiological and obesity situations. Focusing on angiogenesis, the proliferation of endothelial cells (HUVEC), which expressed leptin and adiponectin receptors, was stimulated by leptin and inhibited by adiponectin. Both adipokines globally reduced apoptosis and caspase activity. Leptin increased migration whereas adiponectin decreased migration, and leptin enhanced the area of the tubes formed by HUVEC cells while adiponectin inhibited their formation. MCF7 and MDA-MB-231 cells treated with leptin secreted more VEGF than untreated cells, whereas adiponectin treatment inhibited VEGF secretion. Finally, MCF7 cells pre-treated with leptin were more invasive than untreated cells. This effect was not reproduced in MDA-MB-231 cells. In the MCF7 breast cancer cell line, leptin could induce cell proliferation and reduced the efficacy of all breast cancer therapies (tamoxifen, 5-fluorouracil, taxol and vinblastin). These results suggest that, in obesity situation, leptin-in contrast to adiponectin - may promote tumor invasion and angiogenesis, leading to metastases 'apparition, and reduce treatment efficacy, which could explain the increased risk of cancer mortality in cases of overweight. The evidence suggests adipokines influence breast cancer issue and could play a significant role, especially in obese patients for which hyperleptinemia, hypoadiponectinemia and increased metastatic potential are described