Belges pour, Français contre Richard Wagner en 1890 (Documents inédits)

Beaufrère Marie-France. Belges pour, Français contre Richard Wagner en 1890 (Documents inédits) . In: Littératures 14, septembre 1967. pp. 65-75

FDG PET-CT as a powerful tool for diagnosing and monitoring treatment outcomes of relapsing polychondritis

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Does long-term intermittent treatment with glutamine improve the well-being of fed and fasted very old rats?

International audienceBACKGROUND: Glutamine is known to have a specific role in very old rats (>25 months of age). For this reason, we have orally supplemented female rats with glutamine (20% of diet protein) intermittently. The treatment started before animals became very old and lasted 5 months. Very old rats were studied in fed state or after 5-day fasting after the last glutamine cure. The aim of this study was to determine whether this in vivo pretreatment improves the well-being of very old rats (muscle sarcopenia decrease, gut integrity improvement, decrease of the known up-regulated glutamine synthetase observed regardless of nutrition state). METHODS: Protein turnover was measured in epitrochlearis muscle, whereas glutamine synthetase (GS) activities were assessed in tibialis anterior muscle from fed and 5-days-fasted female Wistar adult (6 months) and very old (27 months) rats, pretreated or not with glutamine. Furthermore, gut was dissected and weighed. RESULTS: Long-term treatment with glutamine had positive effects on very old rats: (1) it prevented the loss of body weight, but, (2) it did not prevent the inevitable sarcopenia regardless of nutrition state, and (3) it maintained the gut mass. Surprisingly, the muscle up-regulated GS activity observed in fed and fasted very old rats was only decreased in the fed state when rats were supplemented, without change in plasma and muscle glutamine concentrations. CONCLUSIONS: Long-term treatment with glutamine started before advanced age had essentially a beneficial role on the gut. It may play a role in maintaining intestine integrity and intestinal immune function. Further investigations would be warranted to explore these mechanisms

Slow and fast dietary proteins differently modulate postprandial protein accretion

The speed of absorption of dietary amino acids by the gut varies according to the type of ingested dietary protein. This could affect postprandial protein synthesis, breakdown, and deposition. To test this hypothesis, two intrinsically (13)C-leucine-labeled milk proteins, casein (CAS) and whey protein (WP), of different physicochemical properties were ingested as one single meal by healthy adults. Postprandial whole body leucine kinetics were assessed by using a dual tracer methodology. WP induced a dramatic but short increase of plasma amino acids. CAS induced a prolonged plateau of moderate hyperaminoacidemia, probably because of a slow gastric emptying. Whole body protein breakdown was inhibited by 34% after CAS ingestion but not after WP ingestion. Postprandial protein synthesis was stimulated by 68% with the WP meal and to a lesser extent (+31%) with the CAS meal. Postprandial whole body leucine oxidation over 7 h was lower with CAS (272 ± 91 μmol⋅kg(−1)) than with WP (373 ± 56 μmol⋅kg(−1)). Leucine intake was identical in both meals (380 μmol⋅kg(−1)). Therefore, net leucine balance over the 7 h after the meal was more positive with CAS than with WP (P < 0.05, WP vs. CAS). In conclusion, the speed of protein digestion and amino acid absorption from the gut has a major effect on whole body protein anabolism after one single meal. By analogy with carbohydrate metabolism, slow and fast proteins modulate the postprandial metabolic response, a concept to be applied to wasting situations

Validation de l'impédancemétrie bi-fréquence lors de la sclérose latérale amyotrophique.

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Glutamate and CO2 production from glutamine in incubated enterocytes of adult and very old rats

International audienceGlutamine is the major fuel for enterocytes and promotes the growth of intestinal mucosa. Although oral glutamine exerts a positive effect on intestinal villus height in very old rats, how glutamine is used by enterocytes is unclear. Adult (8 months) and very old (27 months) female rats were exposed to intermittent glutamine supplementation for 50% of their age lifetime. Treated rats received glutamine added to their drinking water, and control rats received water alone. Jejunal epithelial cells (similar to 300x10(6) cells) were incubated in oxygenated Krebs-Henseleit buffer for 30 min containing [1-C-13] glutamine (similar to 17 M) for analysis of glutamine metabolites by C-13 nuclear magnetic resonance (C-13 NMR). An aliquot fraction was incubated in the presence of [U-C-14] glutamine to measure produced CO2. Glutamine pretreatment increased glutamate production and decreased CO2 production in very old rats. The ratio CO2/glutamate, which was very high in control very old rats, was similar at both ages after glutamine pretreatment, as if enterocytes from very old rats recovered the metabolic abilities of enterocytes from adult rats. Our results suggest that long-term treatment with glutamine started before advanced age (a) prevented the loss of rat body weight without limiting sarcopenia and (b) had a beneficial effect on enterocytes from very old rats probably by favoring the role of glutamate as a precursor for glutathione, arginine and proline biosynthesis, which was not detected in 13C NMR spectra in our experimental condition

Lessons on SpA pathogenesis from animal models

International audienceUnderstanding the complex mechanisms underlying a disorder such as spondyloarthritis (SpA) may benefit from studying animal models. Several suitable models have been developed, in particular to investigate the role of genetic factors predisposing to SpA, including HLA-B27, ERAP1, and genes related to the interleukin (IL)-23/IL-17 axis. One of the best examples of such research is the HLA-B27 transgenic rat model that fostered the emergence of original theories regarding HLA-B27 pathogenicity, including dysregulation of innate immunity, contribution of the adaptive immune system to chronic inflammation, and influence of the microbiota on disease development. Very recently, a new model of HLA-B27 transgenic Drosophila helped to expand further some of those theories in an unexpected direction involving the TGFβ/BMP family of mediators. On the other hand, several spontaneous, inducible, and/or genetically modified mouse models-including SKG mouse, TNFΔARE mouse and IL-23-inducible mouse model of SpA-have highlighted the importance of TNFα and IL-23/IL-17 axis in the development of SpA manifestations. Altogether, those animal models afford not only to study disease mechanism but also to investigate putative therapeutic targets