308 results on '"Legrand, Alexandre"'
Search Results
102. Accuracy of Medical Oxygen Flowmeters: A Multicentric Field Study
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Duprez, Frédéric, primary, Barile, Maria, additional, Bonus, Thierry, additional, Cuvelier, Grégory, additional, Ollieuz, Sandra, additional, Mashayekhi, Shahram, additional, and Legrand, Alexandre, additional
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- 2014
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103. Structure–property relationships of water adsorption in metal–organic frameworks
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Canivet, Jérôme, primary, Bonnefoy, Jonathan, additional, Daniel, Cécile, additional, Legrand, Alexandre, additional, Coasne, Benoit, additional, and Farrusseng, David, additional
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- 2014
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104. Influence de l'environnement sur la productivité des péneïdes (crevettes)
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Legrand, Alexandre
- Abstract
Les ressources aquatiques, quoique renouvelables, ne sont pas infinies et doivent être convenablement gérées si l'on veut maintenir leur contribution au bien-être nutritionnel, économique et social d'une population mondiale croissante. La pêche et l'aquaculture apportent une contribution fondamentale à l'alimentation, à l'emploi, aux loisirs, au commerce et à l'économie des populations du monde entier, qu'il s'agisse des générations présentes ou futures, et devraient par conséquent, être conduites de manière responsable. Selon la FAO (1995), plus de 20% des ressources en produits de la mer de la biosphère proviennent aujourd'hui de l'élevage. Certaines formes d'aquaculture, comme celles des crevettes de mer, ont connu un développement important aux cours des deux dernières décennies. En effet, l'aquaculture de crevettes représente aujourd'hui près de 25% de la production mondiale de crevettes (incluant la pêche) et le développement de cette activité concerne plus de 50 pays, situés pour l'essentiel en zone tropicale. La production mondiale repose principalement sur trois espèces Penaeus monodon, Penaeus stylirostris et Peneaus vannamei, qui concernent cette étude. Il est aujourd'hui largement démontré que le maintien d'une certaine intégrité de l'environnement est la seule approche fiable sur le long terme pour garantir la "durabilité" de l'activité aquacole. Une mise en valeur excessive et désorganisée ou la mise en pratique de solutions techniques mal adaptées, peuvent entraîner des situations de surexploitation, d'autopollution, de dégradations environnementales et conduire à des catastrophes environnementales, ainsi qu'à de graves conflits sociaux. Le développement harmonieux de la crevetticulture doit donc passer en tout premier lieu par une sélection rigoureuse des sites et des techniques adaptées, réalisée dans le cadre d'une approche scientifique prudente, intégrant de très nombreux paramètres. C'est en effet, l'évaluation correcte du potentiel de production d'une zone qui va déterminer le niveau de développement "soutenable", c'est à dire acceptable pour l'environnement, permettant la mise en place de structures de production optimale fiable sur le long terme. Le cycle de vie des Péneïdés est très hétérogène, puisque les crevettes passent dans des milieux très divers. Les éleveurs se doivent donc de connaître leur capacité biologique afin de maximiser la production; optimums variant en fonction des phases de développement, mais aussi des espèces. Ces dernières années, des pathologies ont décimé de nombreux élevages. Pour étendre la production, il est nécessaire de lutter contre ces dernières. De nouvelles biotechnologies se développent: la production d'espèces résistantes (par sélection génétique par exemple) semble être une des solutions des années futures. Il est nécessaire dans le futur, de maximiser les productions, de lutter contre les maladies, mais aussi de connaître et de mettre en évidence les paramètres optimums de la productivité et de tenir compte de leurs interactions possibles.
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- 2001
105. A New Device to Mimic Intermittent Hypoxia in Mice
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Chodzyński, Kamil J., primary, Conotte, Stephanie, additional, Vanhamme, Luc, additional, Van Antwerpen, Pierre, additional, Kerkhofs, Myriam, additional, Legros, J. L., additional, Vanhaeverbeek, Michel, additional, Van Meerhaeghe, Alain, additional, Coussement, Gregory, additional, Boudjeltia, Karim Zouaoui, additional, and Legrand, Alexandre, additional
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- 2013
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106. Determination of a shear rate threshold for thrombus formation in intracranial aneurysms.
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Ribeiro de Sousa, Daniel, Vallecilla, Carolina, Chodzynski, Kamil, Corredor Jerez, Ricardo, Malaspinas, Orestis, Faruk Eker, Omer, Ouared, Rafik, Vanhamme, Luc, Legrand, Alexandre, Chopard, Bastien, Courbebaisse, Guy, and Zouaoui Boudjeltia, Karim
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ANEURYSMS ,BLOOD circulation ,CEREBRAL embolism & thrombosis ,DIGITAL subtraction angiography ,FINITE element method ,INTRACRANIAL aneurysms ,SURGICAL stents ,THROMBOSIS ,CROSS-sectional method - Abstract
Background Particular intra-aneurysmal blood flow conditions, created naturally by the growth of an aneurysm or induced artificially by implantation of a flow diverter stent (FDS), can potentiate intra-aneurysmal thrombosis. The aim of this study was to identify hemodynamic indicators, relevant to this process, which could be used as a prediction of the success of a preventive endovascular treatment. Method A cross sectional study on 21 patients was carried out to investigate the possible association between intra-aneurysmal spontaneous thrombus volume and the dome to neck aspect ratio (AR) of the aneurysm. The mechanistic link between these two parameters was further investigated through a Fourier analysis of the intra-aneurysmal shear rate (SR) obtained by computational fluid dynamics (CFD). This analysis was first applied to 10 additional patients (4 with and 6 without spontaneous thrombosis) and later to 3 patients whose intracranial aneurysms only thrombosed after FDS implantation. Results The cross sectional study revealed an association between intra-aneurysmal spontaneous thrombus volume and the AR of the aneurysm (R²=0.67, p<0.001). Fourier analysis revealed that in cases where thrombosis occurred, the SR harmonics 0, 1, and 2 were always less than 25/s, 10/s, and 5/s, respectively, and always greater than these values where spontaneous thrombosis was not observed. Conclusions Our study suggests the existence of an SR threshold below which thrombosis will occur. Therefore, by analyzing the SR on patient specific data with CFD techniques, it may be potentially possible to predict whether or the intra-aneurysmal flow conditions, after FDS implantation, will become prothrombotic. [ABSTRACT FROM AUTHOR]
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- 2016
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107. Do segmental reflexes play a role in the distribution of external intercostal EMG activity in the rabbit?
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Bonaert, Adeline, primary, Voisin, Virginie, additional, Caron, Nathalie, additional, and Legrand, Alexandre, additional
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- 2012
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108. Electron Transfers Induced by t-Stilbene Sorption in Acidic Aluminum, Gallium, and Boron Beta (BEA) Zeolites
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Lobo, Raul F., primary, Moissette, Alain, additional, Hureau, Matthieu, additional, Carré, Sonia, additional, Vezin, Hervé, additional, and Legrand, Alexandre, additional
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- 2012
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109. Chemical Control of Photoinduced Charges under Confinement in Zeolites
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Hureau, Matthieu, primary, Moissette, Alain, additional, Legrand, Alexandre, additional, Luchez, Florence, additional, Sliwa, Michel, additional, and Bremard, Claude, additional
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- 2012
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110. Monoclonal Antibody to CD31 (PECAM-1) Inhibits Tubular Regeneration after Ischemia Reperfusion Injury in the Rat
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Valentini, Xavier, primary, Gossiaux, Annabel, additional, Caron, Nathalie, additional, Nonclercq, Denis, additional, Legrand, Alexandre, additional, and Toubeau, Gérard, additional
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- 2011
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111. Expression of Nestin, Vimentin, and NCAM by Renal Interstitial Cells after Ischemic Tubular Injury
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Vansthertem, David, primary, Gossiaux, Annabel, additional, Declèves, Anne-Emilie, additional, Caron, Nathalie, additional, Nonclercq, Denis, additional, Legrand, Alexandre, additional, and Toubeau, Gérard, additional
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- 2010
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112. Neuromechanical matching of drive in the scalene muscle of the anesthetized rabbit
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Legrand, Alexandre, primary, Majcher, Melanie, additional, Joly, Emma, additional, Bonaert, Adeline, additional, and Gevenois, Pierre Alain, additional
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- 2009
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113. Schwannoma of the accessory phrenic nerve
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De Bie, Gersende, Legrand, Alexandre, Mahillon, Virginie, Lemort, Marc, Gilles, André, and Saussez, Sven
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- 2007
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114. Dynamics of hyaluronan, CD44, and inflammatory cells in the rat kidney after ischemia/reperfusion injury
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Declèves, Anne-Emilie, primary, Caron, Nathalie, additional, Nonclercq, Denis, additional, Legrand, Alexandre, additional, Toubeau, Gérard, additional, Kramp, Ronald, additional, and Flamion, Bruno, additional
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- 2006
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115. Physiological response of the blue shrimp Litopenaeus stylirostris to short-term confinement on a pond bottom
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Mugnier, Chantal, primary, Lemonnier, Hugues, additional, and Legrand, Alexandre, additional
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- 2006
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116. Respiratory effects of the scalene and sternomastoid muscles in humans
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Legrand, Alexandre, primary, Schneider, Emmanuelle, additional, Gevenois, Pierre-Alain, additional, and De Troyer, André, additional
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- 2003
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117. Auteurs
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Abdellaoui, Aldjia, Adam, Jean-François, Adler, Dan, Aubriot, Anne-Sophie, Beaumont, Marc, Bialais, Émilie, Bodart, Eddy, Bulpa, Pierre, Cabillic, Michel, Caty, Gilles, Colbrant, Coralie, Contal, Olivier, Coppens, Thibault, de Biourge, Ingrid, Debouche, Sophie, Delguste, Pierre, Denef, Jean-François, Desuter, Gauthier, Detaille, Thierry, Dethy, Caroline, Devroey, Marianne, Dousse, Nicolas, Dubus, Jean-Christophe, Dugernier, Jonathan, Duplaquet, Fabrice, Duprez, Frédéric, Gaudin, Corinne, Gouilly, Pascal, Guérot, Emmanuel, Henin, Pauline, Infante, Vito, Janssens, Jean-Paul, Latiers, Anne-Claire, Lamotte, Michel, Legrand, Alexandre, Lemaire, Muriel, Lengelé, Benoît, Lessire, Fred, Liistro, Giuseppe, Luts, Alain, Many, Marie-Christine, Marchand, Éric, Menten, Renaud, Michotte, Jean-Bernard, Moerman, Damien, Monnin, Dominique, Mouthuy, Jonathan, Norrenberg, Michelle, Nyssen-Behets, Catherine, Opdekamp, Christian, Pieters, Thierry, Pitance, Laurent, Poncin, William, Portuesi, Vito, Reychler, Gregory, Roeseler, Jean, Wittebole, Xavier, Saey, Didier, Scheiff, Jean-Marie, Selleron, Bertrand, Sottiaux, Thierry, Soudon, Philippe, Thys, Frédéric, Toussaint, Michel, Troosters, Thierry, Van Caeneghem, Olivier, Vanpee, Dominique, Vecellio, Laurent, Vermeulen, François, and Zech, Francis
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- 2014
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118. Heterogeneity of metabolic activity in the canine parasternal intercostals during breathing
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Legrand, Alexandre, primary, Goldman, Serge, additional, Damhaut, Philippe, additional, and De Troyer, André, additional
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- 2001
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119. Respiratory effects of the external and internal intercostal muscles in humans
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Wilson, Theodore A., primary, Legrand, Alexandre, additional, Gevenois, Pierre‐Alain, additional, and Troyer, André, additional
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- 2001
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120. Muscle kinematics for minimal work of breathing
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Wilson, Theodore A., primary, Angelillo, Maurizio, additional, Legrand, Alexandre, additional, and de Troyer, André, additional
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- 1999
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121. Respiratory mechanical advantage of the canine external and internal intercostal muscles
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De Troyer, André, primary, Legrand, Alexandre, additional, and Wilson, Theodore A., additional
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- 1999
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122. Spatial distribution of external and internal intercostal activity in dogs
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Legrand, Alexandre, primary and De Troyer, André, additional
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- 1999
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123. Mechanical advantage of the human parasternal intercostal and triangularis sterni muscles
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De Troyer, André, primary, Legrand, Alexandre, additional, Gevenois, Pierre-Alain, additional, and Wilson, Theodore A., additional
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- 1998
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124. Rib cage muscle interaction in airway pressure generation
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Legrand, Alexandre, primary, Wilson, Theodore A., additional, and De Troyer, André, additional
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- 1998
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125. Mechanical advantage of the canine triangularis sterni
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De Troyer, André, primary and Legrand, Alexandre, additional
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- 1998
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126. Mechanical advantage of sternomastoid and scalene muscles in dogs
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Legrand, Alexandre, primary, Ninane, Vincent, additional, and De Troyer, André, additional
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- 1997
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127. Response of the inspiratory intercoastal muscles to increased inertial loads
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Legrand, Alexandre, primary, Cappello, Matteo, additional, and De Troyer, André, additional
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- 1995
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128. Respiratory mechanical advantage of the canine external and internal intercostal muscles.
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Troyer, André, Legrand, Alexandre, and Wilson, Theodore A.
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- 1999
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129. Mechanical advantage of the human parasternal intercostal and triangularis sterni muscles.
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Troyer, André, Legrand, Alexandre, Gevenois, Pierre-Alain, and Wilson, Theodore A.
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- 1998
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130. Mediolateral gradient of mechanical advantage in the canine parasternal intercostals.
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LEGRAND, ALEXANDRE, WILSON, THEODORE A., and DE TROYER, ANDRÉ
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- 1996
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131. On the mechanism of the mediolateral gradient of parasternal activation.
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DE TROYER, ANDRÉ, LEGRAND, ALEXANDRE, GAYAN-RAMIREZ, GHISLAINE, CAPPELLO, MATTEO, and DECRAMER, MARC
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- 1996
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132. Inhomogeneous activation of the parasternal intercostals during breathing.
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DE TROYER, ANDRÉ and LEGRAND, ALEXANDRE
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- 1995
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133. Chronic hypoxaemia and gender status modulate adiponectin plasmatic level and its multimer proportion in severe COPD patients: new endotypic presentation?
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Pierard, Mélany, Tassin, Alexandra, Legrand, Antoine, and Legrand, Alexandre
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OBSTRUCTIVE lung diseases ,BLOOD testing ,GENDER ,CARDIOVASCULAR diseases ,ADIPONECTIN - Abstract
Background: Disease progression in COPD patient is associated to lung function decline, leading to a higher risk of hypoxaemia and associated comorbidities, notably cardiovascular diseases (CVD). Adiponectin (Ad) is an adipokine with cardio-protective properties. In COPD patients, conflicting results were previously reported regarding Ad plasmatic (Adpl) level, probably because COPD is a heterogeneous disease with multifactorial influence. Among these factors, gender and hypoxaemia could interact in a variety of ways with Ad pathway. Therefore, we postulated that these components could influence Adpl level and its multimers in COPD patients and contribute to the appearance of a distinct endotype associated to an altered CVD risk.Methods: One hundred COPD patients were recruited: 61 were men and 39 were women. Patients who were not severely hypoxemic were allocated to non-hypoxemic group which included 46 patients: 27 men and 19 women. Hypoxemic group included 54 patients: 34 men and 20 women. For all patients, Adpl level and proportion of its different forms were measured. Differences between groups were evaluated by Rank-Sum tests. The relationship between these measures and BMI, blood gas analysis (PaO2, PaCO2), or lung function (FEV1, FEV1/FVC, TLCO, TLC, RV) were evaluated by Pearson correlation analysis.Results: Despite similar age, BMI and obstruction severity, women had a higher TLC and RV (median: TLC = 105%; RV = 166%) than men (median: TLC = 87%; RV = 132%). Adpl level was higher in women (median = 11,152 ng/ml) than in men (median = 10,239 ng/ml) and was negatively associated with hyperinflation (R = - 0,43) and hypercapnia (R = - 0,42). The proportion of the most active forms of Ad (HMW) was increased in hypoxemic women (median = 10%) compared with non-hypoxemic women (median = 8%) but was not modulated in men.Conclusion: COPD pathophysiology seemed to be different in hypoxemic women and was associated to Ad modulations. Hyperinflation and air-trapping in association with hypercapnia and hypoxaemia, could contribute to a modulation of Adpl level and of its HMW forms. These results suggest the development of a distinct endotypic presentation, based on gender. [ABSTRACT FROM AUTHOR]- Published
- 2020
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134. Repeated KI Prophylaxis in Case of Prolonged Exposure to Iodine Radioisotopes: Pharmacokinetic Studies in Adult Rats.
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Phan, Guillaume, Chioukh, Rym, Suhard, David, Legrand, Alexandre, Moulin, Charlotte, Sontag, Thibaud, Rebière, François, Bouvier-Capely, Céline, Agarande, Michelle, Renaud-Salis, Valérie, and Jourdain, Jean-René
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PREVENTIVE medicine ,IODINE radioisotopes ,PHARMACOKINETICS ,THYROID diseases ,RADIOACTIVE dating - Abstract
Purpose: To propose a new and effective dose regimen for stable potassium iodide (KI) repeated prophylaxis in case of prolonged exposure to radioactive iodine.Methods: The pharmacokinetics of iodine was determined in rats by compartmental analyses after intravenous and oral administrations of the optimal dose of 1 mg/kg KI, which was previously selected in a dose-effect study. The thyroid protection against iodine-125 incorporation was followed during 24 h after a single oral dosing of KI. A repeated KI prophylaxis was modeled using initial estimates of iodine pharmacokinetic parameters.Results: A dose regimen consisting in administrations of 1 mg/kg daily for 8 days was selected and studied. Plasma iodine concentrations predicted by simulation were verified by experimental data and varied after the third dose of KI between 174 and 1190 μg/l. The inhibition study of iodine-125 binding in the thyroid as a function of the time showed that the protection effect of KI could be correlated to stable iodine plasma concentrations. Hence, a theoretical decrease in iodine-125 thyroid uptake from 63 to 88% could be achieved in a 24 h-interval between two KI doses.Conclusion: Given the satisfactory levels of thyroid protection, this dose regimen could be envisaged in order to extent KI indications for repeated prophylaxis. [ABSTRACT FROM AUTHOR]
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- 2018
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135. The DUX4–HIF1α Axis in Murine and Human Muscle Cells: A Link More Complex Than Expected.
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Nguyen, Thuy-Hang, Limpens, Maelle, Bouhmidi, Sihame, Paprzycki, Lise, Legrand, Alexandre, Declèves, Anne-Emilie, Heher, Philipp, Belayew, Alexandra, Banerji, Christopher R. S., Zammit, Peter S., and Tassin, Alexandra
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MUSCLE cells , *FACIOSCAPULOHUMERAL muscular dystrophy , *SKELETAL muscle , *CELL death , *TRANSCRIPTION factors , *LABORATORY mice - Abstract
FacioScapuloHumeral muscular Dystrophy (FSHD) is one of the most prevalent inherited muscle disorders and is linked to the inappropriate expression of the DUX4 transcription factor in skeletal muscles. The deregulated molecular network causing FSHD muscle dysfunction and pathology is not well understood. It has been shown that the hypoxia response factor HIF1α is critically disturbed in FSHD and has a major role in DUX4-induced cell death. In this study, we further explored the relationship between DUX4 and HIF1α. We found that the DUX4 and HIF1α link differed according to the stage of myogenic differentiation and was conserved between human and mouse muscle. Furthermore, we found that HIF1α knockdown in a mouse model of DUX4 local expression exacerbated DUX4-mediated muscle fibrosis. Our data indicate that the suggested role of HIF1α in DUX4 toxicity is complex and that targeting HIF1α might be challenging in the context of FSHD therapeutic approaches. [ABSTRACT FROM AUTHOR]
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- 2024
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136. The use of time‐of‐flight camera to assess respiratory rates and thoracoabdominal depths in patients with chronic respiratory disease.
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Van Hove, Olivier, Andrianopoulos, Vasileios, Dabach, Ali, Debeir, Olivier, Van Muylem, Alain, Leduc, Dimitri, Legrand, Alexandre, Ercek, Rudy, Feipel, Véronique, and Bonnechère, Bruno
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CHRONICALLY ill , *CHRONIC obstructive pulmonary disease , *VENTILATION monitoring , *PULMONARY fibrosis , *COGNITIVE load - Abstract
Introduction: Over the last 5 years, the analysis of respiratory patterns presents a growing usage in clinical and research purposes, but there is still currently a lack of easy‐to‐use and affordable devices to perform such kind of evaluation. Objectives: The aim of this study is to validate a new specifically developed method, based on Kinect sensor, to assess respiratory patterns against spirometry under various conditions. Methods: One hundred and one participants took parts in one of the three validations studies. Twenty‐five chronic respiratory disease patients (14 with chronic obstructive pulmonary disease (COPD) [65 ± 10 years old, FEV1 = 37 (15% predicted value), VC = 62 (20% predicted value)], and 11 with lung fibrosis (LF) [64 ± 14 years old, FEV1 = 55 (19% predicted value), VC = 62 (20% predicted value)]) and 76 healthy controls (HC) were recruited. The correlations between the signal of the Kinect (depth and respiratory rate) and the spirometer (tidal volume and respiratory rate) were computed in part 1. We then included 66 HC to test the ability of the system to detect modifications of respiratory patterns induced by various conditions known to modify respiratory pattern (cognitive load, inspiratory load and combination) in parts 2 and 3. Results: There is a strong correlation between the depth recorded by the Kinect and the tidal volume recorded by the spirometer: r = 0.973 for COPD patients, r = 0.989 for LF patients and r = 0.984 for HC. The Kinect is able to detect changes in breathing patterns induced by different respiratory disturbance conditions, gender and oral task. Conclusions: Measurements performed with the Kinect sensors are highly correlated with the spirometer in HC and patients with COPD and LF. Kinect is also able to assess respiratory patterns under various loads and disturbances. This method is affordable, easy to use, fully automated and could be used in the current clinical context. Respiratory patterns are important to assess in daily clinics. However, there is currently no affordable and easy‐to‐use tool to evaluate these parameters in clinics. We validated a new system to assess respiratory patterns using the Kinect sensor in patients with chronic respiratory diseases. [ABSTRACT FROM AUTHOR]
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- 2023
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137. Induction of a local muscular dystrophy using electroporation in vivo: an easy tool for screening therapeutics.
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Derenne, Aline, Tassin, Alexandra, Nguyen, Thuy Hang, De Roeck, Estelle, Jenart, Vincianne, Ansseau, Eugénie, Belayew, Alexandra, Coppée, Frédérique, Declèves, Anne-Emilie, and Legrand, Alexandre
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MUSCULAR dystrophy , *PLASMIDS , *INTRAMUSCULAR injections , *ELECTROPORATION , *MEDICAL screening , *THERAPEUTICS - Abstract
Intramuscular injection and electroporation of naked plasmid DNA (IMEP) has emerged as a potential alternative to viral vector injection for transgene expression into skeletal muscles. In this study, IMEP was used to express the DUX4 gene into mouse tibialis anterior muscle. DUX4 is normally expressed in germ cells and early embryo, and silenced in adult muscle cells where its pathological reactivation leads to Facioscapulohumeral muscular dystrophy. DUX4 encodes a potent transcription factor causing a large deregulation cascade. Its high toxicity but sporadic expression constitutes major issues for testing emerging therapeutics. The IMEP method appeared as a convenient technique to locally express DUX4 in mouse muscles. Histological analyses revealed well delineated muscle lesions 1-week after DUX4 IMEP. We have therefore developed a convenient outcome measure by quantification of the damaged muscle area using color thresholding. This method was used to characterize lesion distribution and to assess plasmid recirculation and dose–response. DUX4 expression and activity were confirmed at the mRNA and protein levels and through a quantification of target gene expression. Finally, this study gives a proof of concept of IMEP model usefulness for the rapid screening of therapeutic strategies, as demonstrated using antisense oligonucleotides against DUX4 mRNA. [ABSTRACT FROM AUTHOR]
- Published
- 2020
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138. The use of time-of-flight camera to assess respiratory rates and thoracoabdominal depths in patients with chronic respiratory disease
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Olivier Van Hove, Vasileios Andrianopoulos, Ali Dabach, Olivier Debeir, Alain Van Muylem, Dimitri Leduc, Alexandre Legrand, Rudy Ercek, Véronique Feipel, Bruno Bonnechère, Van Hove, Olivier, Andrianopoulos, Vasileios, Dabach, Ali, Debeir, Olivier, Van Muylem, Alain, Leduc, Dimitri, Legrand, Alexandre, Ercek, Rudy, Feipel, Véronique, and BONNECHERE, Bruno
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Pulmonary and Respiratory Medicine ,validation ,breathing ,respiratory diseases ,assessment ,Immunology and Allergy ,Kinect sensor ,Genetics (clinical) - Abstract
Introduction: Over the last 5 years, the analysis of respiratory patterns presents a growing usage in clinical and research purposes, but there is still
- Published
- 2023
139. Nigella sativa, a traditional Tunisian herbal medicine, attenuates bleomycin-induced pulmonary fibrosis in a rat model.
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Abidi, Anouar, Robbe, Alexandre, Kourda, Nadia, Ben Khamsa, Saloua, and Legrand, Alexandre
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BLACK cumin , *LUNG diseases , *FIBROSIS , *INFLAMMATION , *BRONCHOALVEOLAR lavage - Abstract
The present study investigated the effects of Nigella sativa oil (NSO) on bleomycin (BLM)-induced lung fibrosis in rats. The rat model of pulmonary fibrosis (PF) was established by intratracheal instillation of BLM, and the effect of 1 ml/kg oral NSO treatment once daily observed. The effect of NSO was studied over a period of 50 days using 1 H RMN analysis on the urine and broncho alveolar lavage fluid (Balf) of the rats. Histopathological (inflammation and fibrosis) and immunohistochemical (TGF-β1 density) changes were evaluated. Results found that the BLM group showed a significant increase in inflammatory index (II), fibrosis score (FS) and TGF-β1 distribution in the lung inflammatory infiltrate, accompanied by a decreased urinary secretion of Krebs cycle intermediates, including acetate, pyruvate, carnitine, trimethylamine-N-oxide and succinate. However, at the same time point, NSO treated rats had a reduced II and FS, and had an increased urinary secretion of histidine, fumarate, allantoin and malate. In conclusion, NSO treatment attenuated the effects of BLM-induced PF, by supporting lung, liver and kidney activity in resisting PF. These findings provide an insight into the preventive and therapeutic potential of NSO in the treatment of PF. [ABSTRACT FROM AUTHOR]
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- 2017
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140. Mechanisms of altitude-related cough
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Mason, Nicholas, Naeije, Robert, Gevenois, Pierre-Alain, Richalet, Jean-Paul, Milledge, James J.S., Legrand, Alexandre, De Troyer, André, De Vuyst, Paul, and Decaux, Guy
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Anoxemia ,Altitude, Influence de l' ,environmental pathophysiology ,Oedème pulmonaire ,Cough -- Pathophysiology ,Anoxémie ,hypoxia ,Appareil respiratoire -- Physiologie ,œdème pulmonaire ,Médecine pathologie humaine ,hypoxie ,respiratory system ,respiratory tract diseases ,pulmonary oedema ,Toux -- Physiopathologie ,système respiratoire ,Pulmonary edema ,Altitude, Influence of ,pathophysiologie de l’environnement ,Respiratory organs -- Physiology - Abstract
The original work presented in this thesis investigates some of the mechanisms that may be responsible for the aetiology of altitude-related cough. Particular attention is paid to its relationship to the long recognised, but poorly understood, changes in lung volumes that occur on ascent to altitude. The literature relevant to this thesis is reviewed in Chapter 1.Widespread reports have long existed of a debilitating cough affecting visitors to high altitude that can incapacitate the sufferer and, on occasions, be severe enough to cause rib fractures (22, 34, 35). The prevalence of cough at altitude has been estimated to be between 22 and 42% at between 4200 and 4900 m in the Everest region of Nepal (10, 29). Traditionally the cough was attributed to the inspiration of the cold, dry air characteristic of the high altitude environment (37) but no attempts were made to confirm this aetiology. In the first formal study of cough at high altitude, nocturnal cough frequency was found to increase with increasing altitude during a trek to Everest Base Camp (5300 m) and massively so in 3 climbers on whom recordings were made up to 7000 m on Everest (8). After 9 days at 5300 m the citric acid cough threshold, a measure of the sensitivity of the cough reflex arc, was significantly reduced compared with both sea level and arrival at 5300 m.During Operation Everest II, a simulated climb of Mount Everest in a hypobaric chamber, the majority of the subjects were troubled above 7000 m by pain and dryness in the throat and an irritating cough despite the chamber being maintained at a relative humidity of between 72 and 82% and a temperature of 23ºC (18). This argued against the widely held view that altitude-related cough was due to the inspiration of cold, dry air. In the next major hypobaric chamber study, Operation Everest III, nocturnal cough frequency and citric acid cough threshold were measured on the 8 subjects in the study. The chamber temperature was maintained between 18 and 24ºC and relative humidity between 30 and 60% (24). This work is presented in Chapter 2 and, demonstrated an increase in nocturnal cough frequency with increasing altitude which immediately returned to control values on descent to sea level. Citric acid cough threshold was reduced at 8000 m compared to both sea level and 5000 m values. Changes in citric acid cough threshold at lower altitudes may not have been detected because of the constraints on subject numbers in the chamber. The study still however demonstrated an increase in clinical cough and a reduction in the citric acid cough threshold at extreme altitude, despite controlled environmental conditions, and thus refuted the long held belief that altitude-related cough is solely due to the inspiration of cold, dry air. If altitude-related cough is not simply due to the inspiration of cold, dry air, other possible aetiologies are:•\, Doctorat en Sciences médicales, info:eu-repo/semantics/nonPublished
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- 2012
141. Mechanisms of Altitude-Related Cough/Mécanismes de la Toux Liée à l’Altitude
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Mason, Nicholas, Naeije, Robert, Gevenois, Pierre-Alain, Richalet, Jean-Paul, Milledge, James, Legrand, Alexandre, De Troyer, André, De Vuyst, Paul, and Decaux, Guy
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pulmonary oedema ,environmental pathophysiology ,système respiratoire ,hypoxia ,pathophysiologie de l’environnement ,œdème pulmonaire ,hypoxie ,respiratory system - Abstract
The original work presented in this thesis investigates some of the mechanisms that may be responsible for the aetiology of altitude-related cough. Particular attention is paid to its relationship to the long recognised, but poorly understood, changes in lung volumes that occur on ascent to altitude. The literature relevant to this thesis is reviewed in Chapter 1. Widespread reports have long existed of a debilitating cough affecting visitors to high altitude that can incapacitate the sufferer and, on occasions, be severe enough to cause rib fractures (22, 34, 35). The prevalence of cough at altitude has been estimated to be between 22 and 42% at between 4200 and 4900 m in the Everest region of Nepal (10, 29). Traditionally the cough was attributed to the inspiration of the cold, dry air characteristic of the high altitude environment (37) but no attempts were made to confirm this aetiology. In the first formal study of cough at high altitude, nocturnal cough frequency was found to increase with increasing altitude during a trek to Everest Base Camp (5300 m) and massively so in 3 climbers on whom recordings were made up to 7000 m on Everest (8). After 9 days at 5300 m the citric acid cough threshold, a measure of the sensitivity of the cough reflex arc, was significantly reduced compared with both sea level and arrival at 5300 m. During Operation Everest II, a simulated climb of Mount Everest in a hypobaric chamber, the majority of the subjects were troubled above 7000 m by pain and dryness in the throat and an irritating cough despite the chamber being maintained at a relative humidity of between 72 and 82% and a temperature of 23ºC (18). This argued against the widely held view that altitude-related cough was due to the inspiration of cold, dry air. In the next major hypobaric chamber study, Operation Everest III, nocturnal cough frequency and citric acid cough threshold were measured on the 8 subjects in the study. The chamber temperature was maintained between 18 and 24ºC and relative humidity between 30 and 60% (24). This work is presented in Chapter 2 and, demonstrated an increase in nocturnal cough frequency with increasing altitude which immediately returned to control values on descent to sea level. Citric acid cough threshold was reduced at 8000 m compared to both sea level and 5000 m values. Changes in citric acid cough threshold at lower altitudes may not have been detected because of the constraints on subject numbers in the chamber. The study still however demonstrated an increase in clinical cough and a reduction in the citric acid cough threshold at extreme altitude, despite controlled environmental conditions, and thus refuted the long held belief that altitude-related cough is solely due to the inspiration of cold, dry air. If altitude-related cough is not simply due to the inspiration of cold, dry air, other possible aetiologies are: • Acute mountain sickness (AMS). • Sub-clinical high altitude pulmonary oedema. • Changes in the central control of cough. • Respiratory tract infections. • Loss of water from the respiratory tract. • Bronchoconstriction and asthma. • Vasomotor-rhinitis and post-nasal drip. • Gastro-oesophageal reflux. It is unlikely that cough at altitude is due to AMS. Despite both AMS and cough occurring commonly at high altitude no relationship has ever been demonstrated between them in any study of altitude-related cough (8, 24, 27, 38) and cough has not been reported as a symptom in over 20 papers studying AMS (9). There is considerable indirect evidence that the majority of subjects ascending to high altitude may develop sub-clinical pulmonary oedema. This evidence includes changes in lung volumes and in particular forced vital capacity (FVC) and changes in the nitrogen washout curve and closing volume. The conflicting literature on this topic, and other possible mechanisms underlying the fall in FVC on ascent to altitude, are reviewed fully in Chapter 1. Chapter 3 presents a field study investigating the changes in FVC, forced expiratory volume in one second (FEV1) and peak expiratory flow (PEF) in 55 subjects ascending to Everest Base Camp at 5300 m and addressing some of the methodological shortcomings of previous studies (25). Forced vital capacity fell significantly on ascent to 5300 m. Peak expiratory flow increased, as predicted by the fall in gas density with increasing altitude, while FEV1 was unchanged. If sub-clinical pulmonary oedema is responsible for the fall in FVC on ascent to altitude then it might also be an aetiological factor in altitude-related cough. Animal work has demonstrated that even small changes in left atrial pressure can be sufficient to produce pulmonary venous congestion sufficient to stimulate airway rapidly adapting receptors (RAR) that form part of the afferent limb of the cough reflex arc (15-17). It is therefore possible that sub-clinical pulmonary oedema occurring at altitude could stimulate airway RARs and provoke cough. Two possible mechanisms could be responsible for sub-clinical pulmonary oedema at high altitude: pulmonary hypertension secondary to hypoxic pulmonary vasoconstriction or a reduction in respiratory epithelial fluid clearance. Chapter 4 presents a study investigating these two mechanisms during a 14 day stay at 3800 m in 20 lowland volunteers (26). Forced vital capacity fell on ascent to 3800m as did the normalized change in lung electrical impedance tomography suggestive of an increase in extravascular lung water. There was a positive correlation between FVC and the change in lung electrical impedance tomography. Respiratory epithelial ion transport was studied using nasal potential difference measurements. Nasal potential difference hyperpolarised at altitude which would be consistent with either increased transepithelial sodium absorption or anion secretion, or a combination of both. If anion secretion predominated over sodium reabsorption, it would be associated with the secretion of water into the respiratory lumen as occurs in the fetal lung (4) and could cause sub-clinical pulmonary oedema. The increase in pulmonary artery pressure estimated by echo-Doppler was insufficient to cause clinical pulmonary oedema. Cough is a recognised side effect of angiotensin converting enzyme (ACE) inhibitors and is thought to be due to the sensitisation of airway RARs by increased levels of bradykinin and substance P (21). Bradykinin is degraded by kininases of which the most important in human serum is ACE. Little or nothing was known about the effects of hypoxia on ACE and bradykinin. Chapter 5 presents further work done on the 20 lowland subjects during their 2 week stay at 3800 m (27). Citric acid cough threshold was reduced throughout the stay at altitude compared to low altitude baseline measurements. Serum ACE activity was unchanged on ascent to 3800 m, although plasma bradykinin fell significantly making it unlikely that bradykinin plays a role in the change in citric acid cough threshold seen on ascent to altitude. Respiratory control undergoes profound changes with acclimatisation (39) and the central control of cough is complex and poorly understood (12, 13). A relationship has been demonstrated between the hypercapnic ventilatory response (HCVR) and the cough threshold to hypotonic saline (1). Those subjects who responded to the hypotonic saline challenge had a higher HCVR than the subjects who did not respond. In addition post-hoc analysis of data from the 1994 British Mount Everest Medical Expedition also demonstrated a relationship between the citric acid cough threshold and the dynamic ventilatory response to CO2 (5). Chapter 6 presents work which investigated the relationship between the citric acid cough threshold and HCVR in 25 healthy subjects during a 9 day stay at 5200 m (38). Citric acid cough threshold fell significantly on ascent to altitude and the HCVR increased significantly on ascent to 5200 m. There was, however, no demonstrable relationship between the citric acid cough threshold and HCVR, or any change in these parameters on ascent to altitude. These findings argue against altitude-related cough being mediated through changes in central control mechanisms. Respiratory tract infections are the commonest cause of acute cough at sea level (20, 28, 32) and occur commonly in visitors to altitude (11, 29). There is also evidence of impairment of mucociliary transport, a crucial respiratory defence mechanism, at altitude (6). While there was no clinical evidence of respiratory infection observed in any of the subjects during Operation Everest III (24), cough associated with the production of purulent sputum is, anecdotally, a common finding at altitude, particularly following prolonged vigorous exertion. It is still possible, despite the controlled environmental conditions during Operation Everest III (24), that water loss from the respiratory tract plays a role in the aetiology of altitude-related cough. Hyperpnoea with cold air, in subjects susceptible to exercise-induced cough, and at respiratory rates similar to those occurring with strenuous exercise, has been shown to be associated with an increase in cough frequency (2). However increased coughing associated with hypernoea appears to depend upon water loss rather than heat loss. Hypernoea with warm dry air produced more coughing than hypernoea with cold air despite causing less heat loss (3). Hyperpnoea with ambient air also produced an increase in cough frequency because it was associated with water loss. Increased minute ventilation is a feature of the body’s response to hypobaric hypoxia and will increase further with exercise (23). In addition there is evidence of subjective nasal blockage and an increase in nasal resistance at altitude which may result in increased mouth breathing (6, 7) which will increase water loss compared to nasal breathing (36). Cough may be the only symptom of asthma (28) and bronchoconstriction can occur at altitude and after hyperpnoea with cold air (14). However there was no demonstrable relationship between FEV1 or PEF and the change in the citric acid cough threshold at 5300 m altitude (8) or FEV1 and the citric acid threshold during Operation Everest III (24). In addition no evidence of bronchoconstriction could be found in healthy, non-asthmatic, subjects at Mount Everest Base Camp (30). Nasal blockage could also be a symptom of vasomotor rhinitis and post-nasal drip (recently redesignated upper airway cough syndrome) and which is reported in some series to be one of the most common causes of chronic cough at sea level (28, 31). Gastro-oesophageal reflux disease has been reported in up to 40% of patients with chronic cough at sea level (19, 33). Nothing is known about the relationship between post-nasal drip and cough, or the prevalence of gastro-oesophageal reflux, at high altitude. Conclusions and Future Perspectives: This thesis has investigated some of the potential aetiologies of altitude-related cough and demonstrates that, contrary to the popularly held view, it may not solely be due to the inspiration of the cold, dry air characteristic of the high-altitude environment. Data is presented that confirms the fall in vital capacity on ascent to altitude and possible causes for this reduction are discussed. One possible cause would be sub-clinical pulmonary oedema. This could also be a potential cause for altitude-related cough and data is presented that suggests that this may be the result of changes in respiratory epithelial ion and water transport. Evidence is presented that argues against altitude-related cough being due to changes in bradykinin or in the central control of cough. While sub-clinical pulmonary oedema may be an aetiological factor in altitude-related cough, and merits further study, it is likely that it is not the only cause and it is probable that cough at altitude is a symptom of a number of unrelated conditions. Future work should focus on the role of water loss from the respiratory tract at altitude, particularly during exercise as well as the association of upper respiratory tract infection with cough and the place of vasomotor rhinitis and gastro-oesophageal reflux in the aetiology of this fascinating condition. RESUME DE LA THESE L’étude d’une partie des mécanismes à l’origine de la toux liée à l’altitude, constitue un travail original, présenté dans cette thèse. La relation entre cette toux et les modifications de volumes pulmonaires survenant lors de la montée en altitude sont connues de longue date mais mal élucidées ;elle fait l’objet d’une attention particulière. Une revue de la littérature pertinente est exposée dans le chapitre 1. Des rapports largement diffusés évoquent une toux fatigante, possiblement invalidante, qui touche les personnes en haute altitude et qui, quand elle est suffisamment sévère, peut entraîner des fractures de côtes (22, 34, 35). La prévalence de la toux en altitude a été estimée entre 22 et 42 % à une altitude comprise entre 4 200 et 4 900 m dans la région de l’Everest népalais (10, 29). Traditionnellement, la toux est attribuée à l’inspiration d’air froid et sec, caractéristique de l’environnement à haute altitude (37), mais aucun essai n’a été réalisé pour confirmer cette étiologie. Dans la première étude formelle sur la toux en haute altitude, il a été montré, au cours d’un trek vers le camp de base de l’Everest (5 300 m), que la fréquence de la toux nocturne augmentait avec l’altitude et, de façon massive, pour 3 alpinistes chez lesquels les enregistrements ont été effectués jusqu’à 7 000 m sur l’Everest (8). Après 9 jours à 5 300 m, le seuil de toux à l’acide citrique, mesurant la sensibilité de l’arc réflexe de la toux, était significativement diminué comparé à celui, à la fois, du niveau de la mer et de l’arrivée à 5 300 m. Au cours de l’Opération Everest II (ascension simulée du Mont Everest réalisée en chambre hypobare), la majorité des sujets ont présenté des troubles à type de douleur et de sécheresse au niveau de la gorge ainsi qu’une toux irritative, malgré une humidité relative comprise entre 72 % et 82 % et une température à 23° C (18). Ce résultat plaide contre l’idée largement répandue que l’air froid et sec serait à l’origine de la toux liée à l’altitude. Dans l’étude majeure suivante en chambre hypobare, Opération Everest III, la fréquence de la toux nocturne et le seuil de toux à l’acide citrique ont été mesurés chez 8 sujets. La température de la chambre et l’humidité relative ont été maintenues respectivement entre 18 et 24°C et entre 30 et 60% (24). Dans ce travail, présenté au chapitre 2, la fréquence de la toux nocturne s’élève avec l’altitude revenant immédiatement aux valeurs de base en descendant vers le niveau de la mer. Le seuil de toux à l’acide citrique est abaissé à 8 000 m par rapport aux valeurs à la fois au niveau de la mer et à 5 000 m. Les modifications du seuil de toux à l’acide citrique à de plus basses altitudes peuvent ne pas avoir été détectées du fait de la limitation du nombre de sujets dans la chambre. Néanmoins, l’étude montre un accroissement de la toux clinique et une réduction du seuil de la toux à l’acide citrique à une altitude extrême, malgré des conditions environnementales contrôlées, et réfute, par conséquence, la vieille croyance selon laquelle la toux liée à l’altitude est uniquement due à l’inspiration d’air froid et sec. Si la toux liée à l’altitude n’est pas simplement la conséquence de l’inspiration d’air froid et sec, quelles sont les autres étiologies possibles ?Il existe plusieurs mécanismes potentiels comprenant : • mal aigu des montagnes (MAM) • sub-œdème pulmonaire de haute altitude • modifications du contrôle central de la toux • infections des voies aériennes • perte d’eau des voies aériennes • bronchoconstriction et asthme • rhinite vasomotrice et secrétions post-nasales • reflux gastro-œsophagien. Il est peu probable que ce type de toux soit dû au MAM. Bien que toux et MAM surviennent tous deux, à haute altitude, aucune relation n’a jamais été démontrée entre eux, dans quelque étude que soit sur la toux liée à l’altitude (8, 24, 27, 38). Dans plus d’une vingtaine d’articles sur le MAM, la toux n’a jamais été signalée comme un symptôme (9). Il a largement été prouvé, de façon indirecte, que la majorité des personnes montant en haute altitude peuvent développer un sub-œdème pulmonaire. Cette preuve comporte des modifications des volumes pulmonaires, en particulier de la capacité vitale forcée, de la courbe de rinçage de l’azote et du volume de fermeture. La littérature contradictoire sur le sujet, et d’autres mécanismes possibles à l’origine de la baisse de la capacité vitale forcée lors de la montée en altitude, sont largement examinés au chapitre 1. Le chapitre 3 présente un travail de terrain étudiant les modifications de la capacité vitale forcée, du volume expiratoire forcé sur une seconde (VEF1) et du débit expiratoire de pointe (DEP) de 55 sujets en ascension vers le Camp de Base de l’Everest à 5 300 m. Ce travail répond à certaines des insuffisances méthodologiques des études précédentes (25). La capacité vitale forcée a chuté, de façon significative, en montant à 5 300 m. Le débit expiratoire de pointe a augmenté, comme attendu puisque la densité d’un gaz baisse quand l’altitude s’élève, tandis que VEF1 restait inchangé. Si le sub-œdème pulmonaire est responsable de la baisse de capacité vitale forcée en montant en altitude, il pourrait être aussi un facteur étiologique de la toux liée à l’altitude. Des travaux chez l’animal, ont montré que même de faibles modifications de la pression de l’oreillette gauche suffisaient à produire une congestion veineuse pulmonaire entraînant une stimulation des récepteurs ventilatoires à adaptation rapide qui constituent une partie de la branche afférente de l’arc réflexe de la toux (15-17). C’est pourquoi, il est possible que ce sub-œdème pulmonaire survenant en altitude stimule les récepteurs ventilatoires à adaptation rapide et provoque la toux. Deux mécanismes pourraient être responsables du sub-oedème pulmonaire en haute altitude :l’HTAP secondaire à la vasoconstriction pulmonaire hypoxique ou la diminution de la clairance du liquide alvéolaire. Le travail présenté dans le chapitre 4 analyse ces deux mécanismes pendant un séjour de 14 jours à 3 800 m, chez 20 volontaires venus des plaines (26). En montant à 3 800 m, la capacité vitale forcée a diminué tout comme la modification normalisée de la tomographie pulmonaire d’impédance électrique, évocatrice d’une élévation de liquide pulmonaire extravasculaire. Il existe une corrélation positive entre la capacité vitale forcée et la modification de tomographie d’impédance électrique du poumon. Le transport ionique dans l’épithélium respiratoire a été étudié en utilisant des mesures de différence de potentiel nasale. Cette dernière s’hyperpolarise en altitude, ce qui pourrait être compatible avec soit une absorption sodique transépithéliale augmentée, soit une sécrétion d’anions soit une combinaison des deux. Si la sécrétion d’anions prédominait sur la réabsorption sodique, elle aurait été associée à la sécrétion d’eau dans la lumière respiratoire comme c’est le cas dans le poumon fœtal (4) et pourrait causer un sub-œdème pulmonaire. L’augmentation de pression artérielle pulmonaire estimée par échodoppler, n’a pas été suffisante pour déclencher un sub-œdème pulmonaire. La toux est un effet secondaire connu des inhibiteurs de l’enzyme de conversion de l’angiotensine qui serait due à la sensibilisation des récepteurs ventilatoires à adaptation rapide par des taux élevés de bradykinine et de substance P (21). La bradykinine est dégradée par des kinases dont la plus importante est l’enzyme de conversion de l’angiotensine dans le sérum humain. Très peu de données sont disponibles concernant les effets de l’hypoxie sur l’enzyme de conversion de l’angiotensine et la bradykinine. Dans le chapitre 5, est présenté un autre travail, réalisé sur les 20 sujets venus des plaines, pendant leur séjour de 2 semaines à 3 800 m (27). Le seuil de toux à l’acide citrique était réduit tout au long du séjour en altitude comparé aux mesures de référence en basse altitude. L’activité sérique de l’enzyme de conversion de l’angiotensine n’était pas modifiée en montant à 3 800 m, alors que la bradykinine plasmatique a chuté de façon significative. Il est donc improbable que la bradykinine joue un rôle dans la modification du seuil de la toux à l’acide citrique relevée lors de la montée en altitude. Le contrôle respiratoire subit de profonds changements en s’adaptant au climat (39) et le contrôle central de la toux est d’une part complexe, d’autre part mal élucidé (12, 13). On note une relation entre la réponse ventilatoire à l’hypercapnie et le seuil de la toux au sérum hypotonique (1). Ces sujets qui répondent au test de provocation au sérum hypotonique ont une réponse ventilatoire à l’hypercapnie supérieure à ceux qui ne répondent pas. De plus, l’analyse post-hoc des données de l’expédition britannique médicale de 1994 sur le Mont Everest a aussi montré une relation entre le seuil de toux à l’acide citrique et la réponse ventilatoire dynamique au CO2 (5). Le travail présenté dans le chapitre 6 analyse la relation entre le seuil de la toux à l’acide citrique et la réponse ventilatoire à l’hypercapnie chez 25 sujets en bonne santé, au cours d’un séjour de 9 jours à 5 200 m (38). Le seuil de toux à l’acide citrique a chuté, de façon significative, lors de la montée en altitude et la réponse ventilatoire à l’hypercapnie a augmenté, de façon significative, lors de l’ascension à 5 200 m. Pourtant, il n’existait aucune relation évidente entre le seuil de la toux à l’acide citrique et la relation ventilatoire hypercapnique ou quelque modification de ces paramètres lors de la montée en altitude. Ces résultats plaident contre la toux liée à l’altitude impliquant des modifications des mécanismes centraux de contrôle. Les infections des voies aériennes sont la cause la plus fréquente de toux aiguë, au niveau de la mer (20, 28, 32) et survient généralement en altitude chez les touristes (11, 29). Un dysfonctionnement du transport mucociliaire, mécanisme de défense respiratoire crucial, en altitude est prouvé également (6). Bien qu’il n’ait pas été relevé de preuve clinique d’infection respiratoire chez les sujets pendant l’Opération Everest III (24), la toux associée à la production d’expectoration purulente a été fréquemment constatée en altitude, en particulier à la suite d’un effort vigoureux prolongé. Il est toujours possible, malgré des conditions environnementales contrôlées au cours de l’opération Everest III (9), que la perte d’eau des voies aériennes joue un rôle dans l’étiologie de la toux liée à l’altitude. Il a été montré que l’hyperpnée due à l’air froid, à une fréquence ventilatoire similaire de celle survenant lors d’un effort énergique, était associée à une élévation de la fréquence de la toux (2). Néanmoins, l’élévation de la toux associée à l’hyperpnée semble plus dépendre de la perte d’eau que de la perte de chaleur. L’hyperpnée liée à l’air chaud et sec a entraîné plus de toux que l’hyperpnée liée à l’air froid bien qu’entraînant moins de perte de chaleur (3). L’hyperpnée en air ambiant a également eu pour conséquence une augmentation de la fréquence de la toux car associée à une perte d’eau. L’augmentation de la ventilation-minute est une réponse à l’hypoxie hypobare qui augmente un peu plus avec l’exercice (23). De plus, il est démontré un blocage nasal subjectif et une augmentation de la résistance nasale en altitude qui peuvent entraîner une respiration buccale (6, 7) et donc une élévation de la perte d’eau comparé à la respiration nasale (36). La toux peut être le seul symptôme de l’asthme (28) et la bronchoconstriction peut survenir en altitude et après hyperpnée liée à l’air froid (14). Pourtant, il n’existait pas de relation évidente entre le volume expiratoire forcé en une seconde ou le débit expiratoire de pointe et la modification du seuil de toux à l’acide citrique, à 5 300 m d’altitude (8), ni entre le volume expiratoire forcé en une seconde et le seuil de toux à l’acide citrique au cours de l’Opération Everest III (24). De plus, aucune preuve de bronchoconstriction n’a été retrouvée chez les sujets en bonne santé, non asthmatiques, au camp de base du Mont Everest (30). Le blocage nasal pourrait être aussi un symptôme de rhinite vasomotrice et de, considéré, dans quelques séries, comme l’une des plus fréquentes causes de toux chronique au niveau de la mer (28, 31). Le reflux gastro-œsophagien est retrouvé chez presque 40 % des patients présentant une toux chronique, au niveau de la mer (19, 33). On ne connait ni la relation entre les secrétions post-nasales et la toux, ni la prévalence du reflux gastro-œsophagien à haute altitude. Conclusions et perspectives futures: Cette thèse a passé en revue quelques causes potentielles de toux liée à l’altitude et a montré que, contrairement à une idée populaire répandue, elle n’est pas seulement due à l’inspiration d’air froid et sec, caractéristique de l’environnement en haute altitude. Les données présentées confirment la chute de la capacité vitale lors de la montée en altitude et les causes possibles de cette chute sont discutées. Une cause possible pourrait être le sub-œdème pulmonaire. Cela pourrait être aussi une cause potentielle à la toux liée à l’altitude et les données présentées suggèrent qu’il résulte de modifications du transfert ionique et d’eau à travers l’épithélium respiratoire. Il est également prouvé que la toux liée à l’altitude n’est la conséquence des modifications ni des taux de bradykinine ou ni du centre de contrôle de la toux. Alors que le sub-œdème pulmonaire peut être un facteur étiologique de la toux liée à l’altitude, et mérite des études complémentaires, il est vraisemblable qu’il ne s’agit pas de la seule cause, la toux étant un symptôme retrouvé dans bon nombre de situations sans rapport avec l’altitude. Un travail futur devrait se concentrer sur le rôle de la perte d’eau des voies aériennes en altitude, particulièrement au cours de l’exercice, mais aussi sur l’association infections des voies aériennes supérieures et toux, et envisager la place de la rhinite vasomotrice et du reflux gastro-œsophagien dans l’étiologie de cette passionnante situation. REFERENCES 1. Banner AS. Relationship between cough due to hypotonic aerosol and the ventilatory response to CO2 in normal subjects. Am Rev Respir Dis 137: 647-650, 1988. 2. Banner AS, Chausow A, and Green J. The tussive effect of hyperpnea with cold air. Am Rev Respir Dis 131: 362-367, 1985. 3. Banner AS, Green J, and O'Connor M. Relation of respiratory water loss to coughing after exercise. N Engl J Med 311: 883-886, 1984. 4. Barker PM and Olver RE. Invited Review: Clearance of lung liquid during the perinatal period. J Appl Physiol 93: 1542-1548. 2002. 5. Barry P, Mason N, Nickol A, Datta A, Milledge J, Wolffe C, and Collier D. Cough receptor sensitivity and dynamic ventilatory response to carbon dioxide in man acclimatised to high altitude (Abstract). J Physiol: 497P: 429-430, 1996. 6. Barry PW, Mason NP, and O'Callaghan C. Nasal mucociliary transport is impaired at altitude. Eur Respir J 10: 35-37, 1997. 7. Barry PW, Mason NP, and Richalet JP. Nasal peak inspiratory flow at altitude. Eur Respir J 19: 16-19. 2002. 8. Barry PW, Mason NP, Riordan M, and O'Callaghan C. Cough frequency and cough-receptor sensitivity are increased in man at altitude. Clin Sci (Colch) 93: 181-186, 1997. 9. Bartsch P and Roach R. Acute Mountain Sickness and High-Altitude Cerebral Edema. In: High Altitude: an exploration of human adaptation, edited by Hornbein T and Schoene R. New York: Marcel Dekker, 2001, p. 732-740. 10. Basnyat B, Gertsch JH, Johnson EW, Castro-Marin F, Inoue Y, and Yeh C. Efficacy of low-dose acetazolamide (125 mg BID) for the prophylaxis of acute mountain sickness: a prospective, double-blind, randomized, placebo-controlled trial. High Alt Med Biol 4: 45-52, 2003. 11. Basnyat B and Litch JA. Medical problems of porters and trekkers in the Nepal Himalaya. Wilderness Environ Med 8: 78-81, 1997. 12. Bolser DC and Davenport PW. Functional organization of the central cough generation mechanism. Pulm Pharmacol Ther 15: 221-225, 2002. 13. Bonham AC, Sekizawa SI, Chen CY, and Joad JP. Plasticity of brainstem mechanisms of cough. Respir Physiol Neurobiol, 2006. 14. Cogo A, Basnyat B, Legnani D, and Allegra L. Bronchial asthma and airway hyperresponsiveness at high altitude. Respiration 64: 444-449, 1997. 15. Gunawardena S, Bravo E, and Kappagoda CT. Effect of chronic mitral valve damage on activity of pulmonary rapidly adapting receptors in the rabbit. J Physiol 511: 79-88. 1998. 16. Gunawardena S, Bravo E, and Kappagoda CT. Rapidly adapting receptors in a rabbit model of mitral regurgitation. J Physiol 521 Pt 3: 739-748. 1999. 17. Hargreaves M, Ravi K, and Kappagoda CT. Responses of slowly and rapidly adapting receptors in the airways of rabbits to changes in the Starling forces. J Physiol 432: 81-97. 1991. 18. Houston CS, Sutton JR, Cymerman A, and Reeves JT. Operation Everest II: man at extreme altitude. J Appl Physiol 63: 877-882, 1987. 19. Irwin RS. Chronic cough due to gastroesophageal reflux disease: ACCP evidence-based clinical practice guidelines. Chest 129: 80S-94S, 2006. 20. Irwin RS, Rosen MJ, and Braman SS. Cough. A comprehensive review. Arch Intern Med 137: 1186-1191, 1977. 21. Israili ZH and Hall WD. Cough and angioneurotic edema associated with angiotensin-converting enzyme inhibitor therapy. A review of the literature and pathophysiology. Ann Intern Med 117: 234-242, 1992. 22. Litch JA and Tuggy M. Cough induced stress fracture and arthropathy of the ribs at extreme altitude. Int J Sports Med 19: 220-222, 1998. 23. Mason NP. The physiology of high altitude: an introduction to the cardiorespiratory changes occurring on ascent to altitude. Current anaesthesia and critical care 11: 34-41, 2000. 24. Mason NP, Barry PW, Despiau G, Gardette B, and Richalet JP. Cough frequency and cough receptor sensitivity to citric acid challenge during a simulated ascent to extreme altitude. Eur Respir J 13: 508-513, 1999. 25. Mason NP, Barry PW, Pollard AJ, Collier DJ, Taub NA, Miller MR, and Milledge JS. Serial changes in spirometry during an ascent to 5,300 m in the Nepalese Himalayas. High Alt Med Biol 1: 185-195. 2000. 26. Mason NP, Petersen M, Melot C, Imanow B, Matveykine O, Gautier MT, Sarybaev A, Aldashev A, Mirrakhimov MM, Brown BH, Leathard AD, and Naeije R. Serial changes in nasal potential difference and lung electrical impedance tomography at high altitude. J Appl Physiol 94: 2043-2050, 2003. 27. Mason NP, Petersen M, Melot C, Kim EV, Aldashev A, Sarybaev A, Mirrakhimov MM, and Naeije R. Changes in plasma bradykinin concentration and citric acid cough threshold at altitude. Wilderness and Environmental Medicine (in press) 20: 353-358, 2009. 28. McGarvey LP and Morice AH. Clinical cough and its mechanisms. Respir Physiol Neurobiol 152: 363-371, 2006. 29. Murdoch DR. Symptoms of infection and altitude illness among hikers in the Mount Everest region of Nepal. Aviat Space Environ Med 66: 148-151, 1995. 30. Pollard AJ, Barry PW, Mason NP, Collier DJ, Pollard RC, Pollard PF, Martin I, Fraser RS, Miller MR, and Milledge JS. Hypoxia, hypocapnia and spirometry at altitude [published erratum appears in Clin Sci (Colch) 1997 Dec;93(6):611]. Clin Sci (Colch) 92: 593-598, 1997. 31. Pratter MR. Chronic upper airway cough syndrome secondary to rhinosinus diseases (previously referred to as postnasal drip syndrome): ACCP evidence-based clinical practice guidelines. Chest 129: 63S-71S, 2006. 32. Pratter MR. Cough and the common cold: ACCP evidence-based clinical practice guidelines. Chest 129: 72S-74S, 2006. 33. Pratter MR. Overview of common causes of chronic cough: ACCP evidence-based clinical practice guidelines. Chest 129: 59S-62S, 2006. 34. Somervell T. After Everest. London: Hodder and Stoughton, 1936. 35. Steele P. Medicine on Mount Everest 1971. Lancet 2: 32-39, 1971. 36. Svensson S, Olin AC, and Hellgren J. Increased net water loss by oral compared to nasal expiration in healthy subjects. Rhinology 44: 74-77, 2006. 37. Tasker J. Everest the Cruel Way. London: Eyre Methuen Ltd. 1981. 38. Thompson AA, Baillie JK, Bates MG, Schnopp MF, Simpson A, Partridge RW, Drummond GB, and Mason NP. The citric acid cough threshold and the ventilatory response to carbon dioxide on ascent to high altitude. Respir Med 103: 1182-1188, 2009. 39. Ward M, Milledge JS, and West JB. Ventilatory response to hypoxia and carbon dioxide. In: High altitude medicine and physiology (3rd ed.). London: Arnold, 2000, p. 50-64., Doctorat en Sciences médicales, info:eu-repo/semantics/published
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- 2012
142. Quantification de l'emphysème pulmonaire en tomodensitométrie hélicoïdale multi-coupes
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Madani, Afarine, Gevenois, Pierre-Alain, Ninane, Vincent, Louryan, Stéphane, Sculier, Jean-Paul, Avni, Efraim, Verschakelen, Johny, and Legrand, Alexandre
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Imagerie ,Emphysème pulmonaire ,Médecine pathologie humaine ,thoracique ,Emphysema, Pulmonary ,Spiral computed tomography ,emphysème ,Tomodensitométrie hélicoïdale - Abstract
L’emphysème pulmonaire est, avec la bronchite chronique à laquelle il est généralement associé, une bronchopathie chronique obstructive (BPCO). Ce groupe de maladie a été la sixième cause de mortalité au monde en 1990 et pourrait devenir la troisième en 2020.L’emphysème pulmonaire est défini par un élargissement anormal et permanent des espaces aériens en amont des bronchioles terminales avec destruction des parois alvéolaires sans fibrose évidente. Compte tenu de cette définition, son diagnostic devrait idéalement être basé sur l’histopathologie. Cependant, en pratique clinique, si les EFR sont à la base de la définition de la BPCO, elles ne suffisent pas au diagnostic de l’emphysème pulmonaire.La tomodensitométrie (TDM) est une méthode diagnostique d’obtention in vivo de coupes anatomiques qui, formées de milliers de pixels, en font la méthode morphologique la plus précise pour investiguer la structure pulmonaire. Si la juxtaposition de ces pixels – dont la tonalité de gris est fonction de l’atténuation – est à la base de l’image TDM, la même information peut être représentée par la distribution de fréquence de ces atténuations. En présence d’emphysème, la destruction du tissu pulmonaire (et la plus grande proportion d’air) déterminent le déplacement de cette distribution vers les atténuations plus négatives. Plusieurs index TDM dérivés de cette distribution – notamment l’atténuation moyenne, la surface pulmonaire occupée par des valeurs d’atténuation inférieures à un seuil, un percentile particulier de la distribution – sont de possibles mesures de l’étendue de l’emphysème pulmonaire. L’émergence de la technique hélicoïdale, permettant notamment d’explorer tout le parenchyme pulmonaire en une seule apnée, justifie de déterminer les seuils et percentiles adéquats par comparaison à une mesure histologique de référence.Au cours de nos études, nous avons montré que les index TDM dérivés de la distribution de fréquence d’atténuation tels que les surfaces relatives de poumon occupées par les coefficients d’atténuation inférieures à -960 UH (RA960) ou -970 UH (RA970) et le premier percentile (p1) sont les index les plus appropriés. En revanche, toujours sur base de comparaisons histo-morphométriques, d’autre index qui reflètent la géométrie des espaces emphysémateux – tels que la distribution de la taille des groupes de pixels adjacents occupés par des coefficients d’atténuation inférieurs à un seuil ou à un percentile – ne sont pas des index valables.La dose d’irradiation peut être abaissée à 20 mAs effectifs. Cette réduction est particulièrement appropriée dans une pathologie susceptible de concerner des patients jeunes et l’objet d’examens répétés. Cependant, la dose d’irradiation influençant ces index, elle doit être maintenue constante au cours de suivis longitudinaux.En TDM multi-coupes, ces index sont les plus appropriés quelque soit l’épaisseur des coupes. Cependant, cette épaisseur influençant ces index, elle doit aussi être maintenue constante au cours de suivis longitudinaux.L’inspiration incomplète induit une sous-estimation statistiquement significative mais cliniquement insignifiante de l’étendue de l’emphysème pulmonaire. La destruction du tissu pulmonaire et l’hyperinflation ont des influences séparées sur les index TDM, faisant recommander leur ajustement aux valeurs prédites de la CPT., Doctorat en Sciences médicales, info:eu-repo/semantics/nonPublished
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- 2010
143. SAMD9L acts as an antiviral factor against HIV-1 and primate lentiviruses by restricting viral and cellular translation.
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Legrand A, Dahoui C, De La Myre Mory C, Noy K, Guiguettaz L, Versapuech M, Loyer C, Pillon M, Wcislo M, Guéguen L, Berlioz-Torrent C, Cimarelli A, Mateo M, Fiorini F, Ricci EP, and Etienne L
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- Humans, Animals, HEK293 Cells, Protein Biosynthesis, Antiviral Restriction Factors, Intracellular Signaling Peptides and Proteins metabolism, Intracellular Signaling Peptides and Proteins genetics, HIV Infections virology, HIV Infections drug therapy, Tumor Suppressor Proteins, HIV-1 genetics, HIV-1 physiology, Virus Replication, Lentiviruses, Primate genetics, Lentiviruses, Primate metabolism
- Abstract
Sterile alpha motif domain-containing proteins 9 and 9-like (SAMD9/9L) are associated with life-threatening genetic diseases in humans and are restriction factors of poxviruses. Yet, their cellular function and the extent of their antiviral role are poorly known. Here, we found that interferon-stimulated human SAMD9L restricts HIV-1 in the late phases of replication, at the posttranscriptional and prematuration steps, impacting viral translation and, possibly, endosomal trafficking. Surprisingly, the paralog SAMD9 exerted an opposite effect, enhancing HIV-1. More broadly, we showed that SAMD9L restricts primate lentiviruses, but not a gammaretrovirus (MLV), nor 2 RNA viruses (arenavirus MOPV and rhabdovirus VSV). Using structural modeling and mutagenesis of SAMD9L, we identified a conserved Schlafen-like active site necessary for HIV-1 restriction by human and a rodent SAMD9L. By testing a gain-of-function constitutively active variant from patients with SAMD9L-associated autoinflammatory disease, we determined that SAMD9L pathogenic functions also depend on the Schlafen-like active site. Finally, we found that the constitutively active SAMD9L strongly inhibited HIV, MLV, and, to a lesser extent, MOPV. This suggests that the virus-specific effect of SAMD9L may involve its differential activation/sensing and the virus ability to evade from SAMD9L restriction. Overall, our study identifies SAMD9L as an HIV-1 antiviral factor from the cell autonomous immunity and deciphers host determinants underlying the translational repression. This provides novel links and therapeutic avenues against viral infections and genetic diseases., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2024 Legrand et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)
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- 2024
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144. Quasi-Homogeneous Photocatalysis in Ultrastiff Microporous Polymer Aerogels.
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Su Y, Li B, Wang Z, Legrand A, Aoyama T, Fu S, Wu Y, Otake KI, Bonn M, Wang HI, Liao Q, Urayama K, Kitagawa S, Huang L, Furukawa S, and Gu C
- Abstract
The development of efficient and low-cost catalysts is essential for photocatalysis; however, the intrinsically low photocatalytic efficiency as well as the difficulty in using and recycling photocatalysts in powder morphology greatly limit their practical performance. Herein, we describe quasi-homogeneous photocatalysis to overcome these two limitations by constructing ultrastiff, hierarchically porous, and photoactive aerogels of conjugated microporous polymers (CMPs). The CMP aerogels exhibit low density but high stiffness beyond 10
5 m2 s-2 , outperforming most low-density materials. Extraordinary stiffness ensures their use as robust scaffolds for scaled photocatalysis and recycling without damage at the macroscopic level. A challenging but desirable reaction for direct deaminative borylation is demonstrated using CMP aerogel-based quasi-homogeneous photocatalysis with gram-scale productivity and record-high efficiency under ambient conditions. Combined terahertz and transient absorption spectroscopic studies unveil the generation of high-mobility free carriers and long-lived excitonic species in the CMP aerogels, underlying the observed superior catalytic performance.- Published
- 2024
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145. Hypoxia enhances human myoblast differentiation: involvement of HIF1α and impact of DUX4, the FSHD causal gene.
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Nguyen TH, Paprzycki L, Legrand A, Declèves AE, Heher P, Limpens M, Belayew A, Banerji CRS, Zammit PS, and Tassin A
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- Humans, Cell Differentiation, Gene Expression Regulation, Muscle Fibers, Skeletal metabolism, Muscle, Skeletal metabolism, Myoblasts metabolism, Homeodomain Proteins genetics, Homeodomain Proteins metabolism, Muscular Dystrophy, Facioscapulohumeral metabolism, Hypoxia-Inducible Factor 1, alpha Subunit genetics, Hypoxia-Inducible Factor 1, alpha Subunit metabolism
- Abstract
Background: Hypoxia is known to modify skeletal muscle biological functions and muscle regeneration. However, the mechanisms underlying the effects of hypoxia on human myoblast differentiation remain unclear. The hypoxic response pathway is of particular interest in patients with hereditary muscular dystrophies since many present respiratory impairment and muscle regeneration defects. For example, an altered hypoxia response characterizes the muscles of patients with facioscapulohumeral dystrophy (FSHD)., Methods: We examined the impact of hypoxia on the differentiation of human immortalized myoblasts (LHCN-M2) cultured in normoxia (PO
2 : 21%) or hypoxia (PO2 : 1%). Cells were grown in proliferation (myoblasts) or differentiation medium for 2 (myocytes) or 4 days (myotubes). We evaluated proliferation rate by EdU incorporation, used myogenin-positive nuclei as a differentiation marker for myocytes, and determined the fusion index and myosin heavy chain-positive area in myotubes. The contribution of HIF1α was studied by gain (CoCl2 ) and loss (siRNAs) of function experiments. We further examined hypoxia in LHCN-M2-iDUX4 myoblasts with inducible expression of DUX4, the transcription factor underlying FSHD pathology., Results: We found that the hypoxic response did not impact myoblast proliferation but activated precocious myogenic differentiation and that HIF1α was critical for this process. Hypoxia also enhanced the late differentiation of human myocytes, but in an HIF1α-independent manner. Interestingly, the impact of hypoxia on muscle cell proliferation was influenced by dexamethasone. In the FSHD pathological context, DUX4 suppressed HIF1α-mediated precocious muscle differentiation., Conclusion: Hypoxia stimulates myogenic differentiation in healthy myoblasts, with HIF1α-dependent early steps. In FSHD, DUX4-HIF1α interplay indicates a novel mechanism by which DUX4 could interfere with HIF1α function in the myogenic program and therefore with FSHD muscle performance and regeneration., (© 2023. The Author(s).)- Published
- 2023
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146. [Cold Spring Harbor Laboratory Retroviruses Meeting: major advancements in retrovirus research].
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Legrand A
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- 2023
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147. Porous Metal-Organic Cages Based on Rigid Bicyclo[2.2.2]oct-7-ene Type Ligands: Synthesis, Structure, and Gas Uptake Properties.
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Doñagueda Suso B, Legrand A, Weetman C, Kennedy AR, Fletcher AJ, Furukawa S, and Craig GA
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- Ligands, Porosity, Biological Transport, Crystallography, X-Ray, Metals
- Abstract
Three new ligands containing a bicyclo[2.2.2]oct-7-ene-2,3,5,6-tetracarboxydiimide unit have been used to assemble lantern-type metal-organic cages with the general formula [Cu
4 L4 ]. Functionalisation of the backbone of the ligands leads to distinct crystal packing motifs between the three cages, as observed with single-crystal X-ray diffraction. The three cages vary in their gas sorption behaviour, and the capacity of the materials for CO2 is found to depend on the activation conditions: softer activation conditions lead to superior uptake, and one of the cages displays the highest BET surface area found for lantern-type cages so far., (© 2023 The Authors. Chemistry - A European Journal published by Wiley-VCH GmbH.)- Published
- 2023
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148. Tunable acetylene sorption by flexible catenated metal-organic frameworks.
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Bonneau M, Lavenn C, Zheng JJ, Legrand A, Ogawa T, Sugimoto K, Coudert FX, Reau R, Sakaki S, Otake KI, and Kitagawa S
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The safe storage of flammable gases, such as acetylene, is essential for current industrial purposes. However, the narrow pressure (P) and temperature range required for the industrial use of pure acetylene (100 < P < 200 kPa at 298 K) and its explosive behaviour at higher pressures make its storage and release challenging. Flexible metal-organic frameworks that exhibit a gated adsorption/desorption behaviour-in which guest uptake and release occur above threshold pressures, usually accompanied by framework deformations-have shown promise as storage adsorbents. Herein, the pressures for gas uptake and release of a series of zinc-based mixed-ligand catenated metal-organic frameworks were controlled by decorating its ligands with two different functional groups and changing their ratio. This affects the deformation energy of the framework, which in turn controls the gated behaviour. The materials offer good performances for acetylene storage with a usable capacity of ~90 v/v (77% of the overall amount) at 298 K and under a practical pressure range (100-150 kPa)., (© 2022. The Author(s), under exclusive licence to Springer Nature Limited.)
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- 2022
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149. Rhodium-Based Metal-Organic Polyhedra Assemblies for Selective CO 2 Photoreduction.
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Ghosh AC, Legrand A, Rajapaksha R, Craig GA, Sassoye C, Balázs G, Farrusseng D, Furukawa S, Canivet J, and Wisser FM
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Heterogenization of molecular catalysts via their immobilization within extended structures often results in a lowering of their catalytic properties due to a change in their coordination sphere. Metal-organic polyhedra (MOP) are an emerging class of well-defined hybrid compounds with a high number of accessible metal sites organized around an inner cavity, making them appealing candidates for catalytic applications. Here, we demonstrate a design strategy that enhances the catalytic properties of dirhodium paddlewheels heterogenized within MOP (Rh-MOP) and their three-dimensional assembled supramolecular structures, which proved to be very efficient catalysts for the selective photochemical reduction of carbon dioxide to formic acid. Surprisingly, the catalytic activity per Rh atom is higher in the supramolecular structures than in its molecular sub-unit Rh-MOP or in the Rh-metal-organic framework (Rh-MOF) and yields turnover frequencies of up to 60 h
-1 and production rates of approx. 76 mmole formic acid per gram of the catalyst per hour, unprecedented in heterogeneous photocatalysis. The enhanced catalytic activity is investigated by X-ray photoelectron spectroscopy and electrochemical characterization, showing that self-assembly into supramolecular polymers increases the electron density on the active site, making the overall reaction thermodynamically more favorable. The catalyst can be recycled without loss of activity and with no change of its molecular structure as shown by pair distribution function analysis. These results demonstrate the high potential of MOP as catalysts for the photoreduction of CO2 and open a new perspective for the electronic design of discrete molecular architectures with accessible metal sites for the production of solar fuels.- Published
- 2022
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150. Improvement of arterial oxygenation using the double trunk mask above low flow nasal cannula: a pilot study.
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Duprez F, Cocu S, Legrand A, Brimioulle S, Mashayekhi S, Bodur G, Bruyneel A, Roeseler J, Cuvelier G, and Reychler G
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- Double-Blind Method, Humans, Masks, Oxygen Inhalation Therapy, Pilot Projects, Cannula, Respiratory Physiological Phenomena
- Published
- 2021
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