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Casals G.,Service of Biochemistry and Molecular Genetics | Foj L.,Service of Biochemistry and Molecular Genetics | de Osaba M.J.M.,Service of Biochemistry and Molecular Genetics
Clinical Biochemistry | Year: 2011

Objectives: The study examines the components of biological variation of nocturnal salivary cortisol in healthy subjects. Design and methods: Eight repetitive measurements were performed in seven subjects during a 25-day time period (study A), and then, for comparison, two salivary specimens were taken during two consecutive days from 20 subjects (study B). Salivary cortisol was measured with the Salimetrics HS-Cortisol assay. Results: Mean salivary cortisol (1.27. nmol/L), analytical variation (CV. a= 15.4%), within-subject variation (CV. i= 34.1%), between-subject variation (CV. g= 35.3%), index of individuality (II = 1.06) and reference change value (RCV = 104%) were obtained for study A. Similar results were obtained from the set of samples of study B. Conclusion: The study results show a medium degree of individuality for salivary cortisol. Both conventional reference values and comparison of serial results may be equally used for clinical interpretation. A change greater of 104% between two successive measurements should be considered significant. © 2011 The Canadian Society of Clinical Chemists. Source


Reichenbach V.,Service of Biochemistry and Molecular Genetics | Reichenbach V.,Institute dInvestigacions Biomediques August Pi i Sunyer | Ros J.,Service of Biochemistry and Molecular Genetics | Ros J.,Institute dInvestigacions Biomediques August Pi i Sunyer | And 15 more authors.
Journal of Pharmacology and Experimental Therapeutics | Year: 2012

Endocannabinoids behave as antifibrogenic agents by interacting with cannabinoid CB2 receptors, whereas the apelin (AP) system acts as a proangiogenic and profibrogenic mediator in the liver. This study assessed the effect of long-term stimulation of CB2 receptors or AP receptor (APJ) blockade on fibrosis progression in rats under a non-discontinued fibrosis induction program. The study was performed in control and CCl 4-treated rats for 13 weeks. Fibrosis-induced rats received a CB2 receptor agonist (R,S)-3-(2-iodo-5-nitrobenzoyl)-1-(1-methyl-2-piperidinylmethyl)- 1H-indole (AM1241) (1 mg/kg b.wt.), an APJ antagonist [Ala 13]-apelin-13 sequence: Gln-Arg-Pro-Arg-Leu- Ser-His-Lys-Gly-Pro-Met-Pro-Ala (F13A) (75 μg/kg b.wt.), or vehicle daily during the last 5 weeks of the CCl 4 inhalation program. Mean arterial pressure (MAP), portal pressure (PP), hepatic collagen content, angiogenesis, cell infiltrate, and mRNA expression of a panel of fibrosis-related genes were measured in all animals. Fibrosis-induced rats showed increased hepatic collagen content, reduced MAP, portal hypertension, and increased expression of the assessed messengers in comparison with control rats. However, fibrotic rats treated with either AM1241 or F13A had reduced hepatic collagen content, improved MAP and PP, ameliorated cell viability, and reduced angiogenesis and cell infiltrate compared with untreated fibrotic rats. These results were associated with attenuated induction of platelet-derived growth factor receptor β, α-smooth muscle actin, matrix metalloproteinases, and tissue inhibitors of matrix metalloproteinase. CB2 receptor stimulation or APJ blockade prevents fibrosis progression in CCl 4-treated rats. The mechanisms underlying these phenomena are coincident despite the marked dissimilarities between the CB2 and APJ signaling pathways, thus opening new avenues for preventing fibrosis progression in liver diseases. Copyright © 2012 by The American Society for Pharmacology and Experimental Therapeutics. Source

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