IW, Heyndrickx GR. Pretreatment of adult bone marrow mesenchymal stem cells with cardiomyogenic growth factors and repair of the chronically infarcted myocardium.

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AimsRecent studies indicate that brain natriuretic peptide (BNP 1 -32 ) may be truncated into BNP 3 -32 by dipeptidyl peptidase IV (DPP4) and that BNP 3 -32 has reduced biological activities compared with BNP 1 -32 . We investigated if DPP4 contributes to the cardiorenal alterations and to the attenuated response to BNP seen in heart failure. Methods and resultsHaemodynamic and renal assessment was performed in 12 pigs at baseline, 4 weeks after pacing-induced heart failure, and during BNP infusion. They were randomized to either placebo or treatment with a DPP4 inhibitor, sitagliptin. After 4 weeks of pacing, heart rate was reduced compared with baseline in the sitagliptin group (60 + 2 vs. 95 + 16 b.p.m., P , 0.01), and an increase in stroke volume was observed in the sitagliptin group compared with placebo (+24 + 6% vs. -17 + 7%, P , 0.01). Glomerular filtration rate declined at week 4 compared with baseline in the placebo group (1.3 + 0.4 vs. 2.3 + 0.3 mL/kg/min, P , 0.01) but remained preserved in the sitagliptin group [1.8 + 0.2 vs. 2.0 + 0.3 mL/kg/min, P ¼ NS (non-significant)]. In the sitagliptin group, BNP infusion improved end-systolic elastance (68 + 5 vs. 31 + 4 mmHg/kg/mL, P , 0.05), ventricular-arterial coupling, and mechanical efficiency. Compared with controls (n ¼ 6), myocardial gene expression of BNP, interleukin-6, Na + -Ca 2+ exchanger, and calmodulin was up-regulated in the placebo group, but not in the sitagliptin group. ConclusionIn pacing-induced heart failure, DPP4 inhibition preserves the glomerular filtration rate, modulates stroke volume and heart rate, and potentiates the positive inotropic effect of exogenous BNP at no energy expense.--

Résumé:Les politiques de sécurité routière utilisent souvent des mécanismes incitatifs basés sur les infractions pour améliorer le comportement des conducteurs. Ces mécanismes sont par exemple des amendes, des primes d'assurance ou des permis à points. Nous analysons l'efficacité incitative de ces mécanismes. Nous obtenons leurs propriétés théoriques par rapport au nombre de points associés aux infractions et par rapport au temps contrat. Ces propriétés sont ensuite testées empiriquement avec des données issues du système public d'assurance au Québec. Nous concluons à la présence d'aléa moral dans les données, qui traduit le fait que les conducteurs qui accumulent les points deviennent plus prudents car ils sont plus sous risque de perdre leur permis. Par ailleurs, la prime indicée sur les points introduite en 1992 a réduit de 15% la fréquence d'infractions. Nous utilisons ce résultat pour calculer des équivalents monétaires pour les infractions et les retraits de permis. Abstract:Road safety policies often use incentive mechanisms based on traffic violations to promote safe driving. Examples of mechanisms are fines, experience rating and point-record driving licenses. We analyse the effectiveness of these mechanisms in promoting safe driving. We derive their theoretical properties with respect to contract time and accumulated demerit points. These properties are tested empirically with data from the Quebec public insurance plan. We find evidence of moral hazard, which means that drivers who accumulate demerit points become more careful because they are at threat of losing their license. The insurance rating scheme introduced in 1992 reduced the frequency of traffic violations by 15%. We use this result to derive monetary equivalents for traffic violations and license suspensions. Mots clés :Mécanismes incitatifs, permis à points, sécurité routière

In a canine model of chronic myocardial infarction, bone marrow mononuclear cell transfer is superior to mesenchymal stem cell transfer in improvement of cardiac contractility and regional systolic function and reduction in infarct size and plasma N-terminal B-type natriuretic propeptide level. Functional improvement is associated with a favorable angiogenic environment and neovascularization.