Journal: Scientific Reports

Article Title: Decompensated liver cirrhosis and neural regulation of mesenteric vascular tone in rats: role of sympathetic, nitrergic and sensory innervations

doi: 10.1038/srep31076

Figure Lengend Snippet: Effect of liver cholestasis (LC) on EFS-induced NA, ATP, nitrite and CGRP release.

Article Snippet: To measure the release of NA, ATP, nitrite and CGRP, we used a Noradrenaline research EIA (Labor Diagnostica Nord, Gmbh & Co., KG), an ATP Colorimetric/Fluorometric Assay kit (Abcam, Cambridge, UK), Nitric Oxide Assay Kit (Abcam, Cambridge, UK) and a rat CGRP enzyme immunoassay kit (Spibio, Bertin group), following the manufacturers’ instructions.

Techniques:

Journal: Scientific Reports

Article Title: Decompensated liver cirrhosis and neural regulation of mesenteric vascular tone in rats: role of sympathetic, nitrergic and sensory innervations

doi: 10.1038/srep31076

Figure Lengend Snippet: Effect of preincubation with 0.5 μmol/L CGRP (8-37) on the vasoconstrictor response induced by EFS in mesenteric segments from Sham-operated (SO, A ) and liver cholestasis (LC, B ) rats. Results (mean ± S.E.M.) are expressed as a percentage of the previous contraction elicited by KCl. n = 8 animals per group. *P < 0.05 (Fisher post hoc test) ( B ) Vasodilator response to exogenous CGRP in NA-precontracted mesenteric segments from SO and LC rats. Results (mean ± S.E.M.) are expressed as a percentage of the previous tone elicited by exogenous NA. n = 6 animals per group.

Article Snippet: To measure the release of NA, ATP, nitrite and CGRP, we used a Noradrenaline research EIA (Labor Diagnostica Nord, Gmbh & Co., KG), an ATP Colorimetric/Fluorometric Assay kit (Abcam, Cambridge, UK), Nitric Oxide Assay Kit (Abcam, Cambridge, UK) and a rat CGRP enzyme immunoassay kit (Spibio, Bertin group), following the manufacturers’ instructions.

Techniques:

Journal: The Journal of Experimental Medicine

Article Title: Tau deletion promotes brain insulin resistance

doi: 10.1084/jem.20161731

Figure Lengend Snippet: Tau deficiency inhibits an anorexigenic effect of brain insulin administration leading to metabolic disturbances. (A) Cumulative food intake for 24 h measured using metabolic cages in tau KO and littermate controls intracerebroventricularly injected first with vehicle and then 2 µl insulin (5 mg/ml; ***, P < 0.001 vs. WT-PBS; °°°, P < 0.001 vs. tau KO/insulin; two-way ANOVA). (B) Cumulated food intake in WT and tau KO mice 24 h after vehicle or insulin brain injection (same animals as in A; *, P < 0.05; **, P < 0.01 vs. WT-PBS; #, P < 0.05 vs. WT/insulin; °°°, P < 0.001 vs. tau KO/insulin; one-way ANOVA, LSD Fisher’s post-hoc test). (C) 48-h body weight variation after vehicle or insulin brain injection in tau KO and WT littermates (same animals as in A; °°°, P < 0.001 vs. tau KO/insulin; two-way ANOVA). Data in A–C show mean ± SEM from 5–10 mice per group from three independent experiments. (D) Mean food intake (*, P < 0.05, two-way ANOVA). (E) Ambulatory activity (*, P < 0.05, two-way ANOVA). (F) Body weight gain (***, P < 0.05, two-way ANOVA). (G) Plasma leptin levels (**, P < 0.01, Student’s t test). (H and I) Adipose tissue weight (*, P < 0.05; **, P < 0.01, Student’s t test). (J) Glycemia. (K) Insulinemia (*, P < 0.05, Student’s t test). (L) Intraperitoneal glucose tolerance test (***, P < 0.05, two-way ANOVA) in tau KO mice and littermate controls. Quantifications represent mean ± SEM. Controls are indicated as open circles/bars, tau KO as black circles/bars. Dashed lines/bars represent insulin-treated animals. Mice were 6–8 mo old at time of experiments and sacrifice. Metabolic data in C–L show mean ± SEM from 10–12 (D), 9–12 (E), 13–27 (F), 4–5 (G), 11–14 (H and I), 15–17 (J), 20–23 (K), and 12–14 (L) mice per group acquired from three independent experiments.

Article Snippet: Plasma insulin and leptin were measured using ultrasensitive insulin ELISA (Mercodia AB) and a mouse/rat leptin enzyme immunoassay kit (Spibio), respectively.

Techniques: Injection, Activity Assay, Clinical Proteomics