Early changes in diaphragmatic function evaluated using ultrasound in cardiac surgery patients: a cohort study.

Little is known about the evolution of diaphragmatic function in the early post-cardiac surgery period. The main purpose of this work is to describe its evolution using ultrasound measurements of muscular excursion and thickening fraction (TF). Single-center prospective study of 79 consecutive uncomplicated elective cardiac surgery patients, using motion-mode during quiet unassisted breathing. Excursion and TF were measured sequentially for each patient [pre-operative (D1), 1 day (D2) and 5 days (D3) after surgery]. Pre-operative median for right and left hemidiaphragmatic excursions were 1.8 (IQR 1.6 to 2.1) cm and 1.7 (1.4 to 2.0) cm, respectively. Pre-operative median right and left thickening fractions were 28 (19 to 36) % and 33 (22 to 51) %, respectively. At D2, there was a reduction in both excursion (right: 1.5 (1.1 to 1.8) cm, p < 0.001, left: 1.5 (1.1 to 1.8), p = 0.003) and thickening fractions (right: 20 (15 to 34) %, p = 0.021, left: 24 (17 to 39) %, p = 0.002), followed by a return to pre-operative values at D3. A positive moderate correlation was found between excursion and thickening fraction (Spearman's rho 0.518 for right and 0.548 for left hemidiaphragm, p < 0.001). Interobserver reliability yielded a bias below 0.1 cm with limits of agreement (LOA) of ± 0.3 cm for excursion and - 2% with LOA of ± 21% for thickening fractions. After cardiac surgery, the evolution of diaphragmatic function is characterized by a transient impairment followed by a quick recovery. Although ultrasound diaphragmatic excursion and thickening fraction are correlated, excursion seems to be a more feasible and reproducible method in this population

Do patients with adenosquamous carcinoma of the lung need a more aggressive approach?

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Evaluation des voies de dissémination non hématogènes des cancers pulmonaires non à petites cellules

L extension lymphatique des cancers pulmonaires, facteur pronostique indépendant, reste d évaluation difficile compte tenu de la complexité des voies possibles de dissémination et du large fossé entre l imagerie morphologique, seule disponible en routine clinique, et les études plus fondamentales en biologie moléculaire, permettant de détecter des petites quantité de cellules tumorales dont l impact sur l évolution tumorale reste incertain. En effet, le profil évolutif de certains stades précoces (stades IA et IB), présentant des récidives tumorales métastatiques précoces, fait suspecter la possible existence de métastases occultes non détectées en histologie conventionnelle de routine et de modes de dissémination tumorale atypiques ou mal connus. Les travaux rapportés ici abordent plusieurs volets de cette dynamique tumorale analysant d une part les voies de propagation sous la forme de courants lymphatiques issus des organes intra-thoraciques avec leurs variantes et d autre part les moyens simples, par étude cytologique, ou plus complexes par biologie moléculaire, permettant de détecter ces progressions tumorales. L impact de ces résultats et de la connaissance des voies de dissémination se situe dans les options thérapeutiques pluridisciplinaires, à la fois au niveau de la chirurgie mais aussi du choix des traitements adjuvants, en apportant des éléments supplémentaires sur l état de la dissémination tumorale.PARIS-BIUSJ-Thèses (751052125) / SudocPARIS-BIUSJ-Physique recherche (751052113) / SudocSudocFranceF

Recovery of function after intracordal autologous fat injection for unilateral recurrent laryngeal nerve paralysis

International audienc

Is arginase a potential drug target in tobacco-induced pulmonary endothelial dysfunction?

International audienceBackgroundTobacco-induced pulmonary vascular disease is partly driven by endothelial dysfunction. The bioavailability of the potent vasodilator nitric oxide (NO) depends on competition between NO synthase-3 (NOS3) and arginases for their common substrate (L-arginine). We tested the hypothesis whereby tobacco smoking impairs pulmonary endothelial function via upregulation of the arginase pathway.MethodsEndothelium-dependent vasodilation in response to acetylcholine (Ach) was compared ex vivo for pulmonary vascular rings from 29 smokers and 10 never-smokers. The results were expressed as a percentage of the contraction with phenylephrine. We tested the effects of L-arginine supplementation, arginase inhibition (by N(omega)-hydroxy-nor-l-arginine, NorNOHA) and NOS3 induction (by genistein) on vasodilation. Protein levels of NOS3 and arginases I and II in the pulmonary arteries were quantified by Western blotting.ResultsOverall, vasodilation was impaired in smokers (relative to controls; p < 0.01). Eleven of the 29 smokers (the ED+ subgroup) displayed endothelial dysfunction (defined as the absence of a relaxant response to Ach), whereas 18 (the ED− subgroup) had normal vasodilation. The mean responses to 10−4 M Ach were −23 ± 10% and 31 ± 4% in the ED+ and ED− subgroups, respectively (p < 0.01). Supplementation with L- arginine improved endothelial function in the ED+ subgroup (−4 ± 10% vs. -32 ± 10% in the presence and absence of L- arginine, respectively; p = 0.006), as did arginase inhibition (18 ± 9% vs. -1 ± 9%, respectively; p = 0.0002). Arginase I protein was overexpressed in ED+ samples, whereas ED+ and ED− samples did not differ significantly in terms of NOS3 expression. Treatment with genistein did not significantly improve endothelial function in ED+ samples.ConclusionOverexpression and elevated activity of arginase I are involved in tobacco-induced pulmonary endothelial dysfunction