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1. Using Good Vibrations: Melting and Controlled Shear Jamming of Dense Granular Suspensions

Author

C. Garat, S. Kiesgen de Richter, P. Lidon, A. Colin, G. Ovarlez, Laboratory of Future (LOF), Université de Bordeaux (UB)-Solvay (France)-Centre National de la Recherche Scientifique (CNRS), Laboratoire Énergies et Mécanique Théorique et Appliquée (LEMTA ), Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS), Matériaux Innovants pour l'Energie (MIE), Chimie-Biologie-Innovation (UMR 8231) (CBI), Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Ecole Superieure de Physique et de Chimie Industrielles de la Ville de Paris (ESPCI Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Ecole Superieure de Physique et de Chimie Industrielles de la Ville de Paris (ESPCI Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL), ANR-17-CE07-0040,FLUIDIDENSE,Suspensions concentrées : vers des matériaux plus fluides et plus denses(2017), Ovarlez, Guillaume, and Suspensions concentrées : vers des matériaux plus fluides et plus denses - - FLUIDIDENSE2017 - ANR-17-CE07-0040 - AAPG2017 - VALID

Subjects
Physics::Fluid Dynamics, Condensed Matter::Soft Condensed Matter, Mechanics of Materials, Mechanical Engineering, [SPI.MECA.MEFL] Engineering Sciences [physics]/Mechanics [physics.med-ph]/Fluids mechanics [physics.class-ph], General Materials Science, Condensed Matter Physics, [PHYS.COND.CM-SCM]Physics [physics]/Condensed Matter [cond-mat]/Soft Condensed Matter [cond-mat.soft], [PHYS.COND.CM-SCM] Physics [physics]/Condensed Matter [cond-mat]/Soft Condensed Matter [cond-mat.soft], [SPI.MECA.MEFL]Engineering Sciences [physics]/Mechanics [physics.med-ph]/Fluids mechanics [physics.class-ph]
Abstract

Flows of suspensions can be blocked when the suspended particles are densely packed. This makes their formulation and their transport challenging in the industry. In this paper, we study the impact of vibrations on the behavior of dense granular suspensions prepared at volume fraction above their jamming volume fraction, but below the particle assembly random close packing. Vibrations are shown to have a strong effect on their rheological properties and to tune their transition from solid-like to liquid-like behavior. We study suspensions of rough silica particles in a Newtonian fluid. In the absence of vibrations, they have a solid-like behavior: they flow only above a yield stress. Particles are confined by the liquid interface and the yield stress is of frictional origin. When vibrations are applied, the yield stress vanishes to give rise to a liquid-like pseudo-Newtonian behavior at low shear rate. Using shear-reversal experiments, we show that these liquid-like vibrated suspensions of frictional particles behave like nonvibrated suspensions of frictionless particles. As the shear rate is increased, we observe a shear thickening of the vibrated suspensions, eventually leading to shearjamming: the yield stress behavior is recovered and vibrations have no more impact. We show that this shear thickening can be tuned by changing the vibration energy injected into the system. We finally propose a physical picture based on the competition between contact opening by vibration and contact formation by shear to account for these behaviors. In the framework of the Wyart and Cates (2014) model, vibrations can be seen as introducing a thermal-like repulsive force, yielding a critical stress proportional to the vibration stress introduced by Hanotin et al. (2015).

Published
2021

2. The Solar Orbiter Solar Wind Analyser (SWA) suite

Author

C. Brockley-Blatt, Mark Phillips, G. Dirks, A. Malpus, J. Ford, Michael R. Collier, M. Hailey, C. Loeffler, G. Terrier, S. Myers, Iannis Dandouras, D. Rust, G. Capuano, L. M. Kistler, Gethyn R. Lewis, S. Clemens, R. Baruah, John A. Trevino, R. Ascolese, Jean-André Sauvaud, S. Persyn, K. Ruane, C. Urdiales, E. Penou, G. Davison, Timothy J. Stubbs, A. Barthe, J. Yardley, Vincent Génot, A. Lawrenson, R. Thibodeaux, B. Hancock, Glyn Collinson, Jason A. Gilbert, C. Anekallu, C. Jacquey, Robert F. Wimmer-Schweingruber, I. Čermák, S. Gradone, L. Přech, J. Coker, P. Louarn, V. de Giosa, Berend Winter, Timothy S. Horbury, W. Marty, M. Salatti, Daniel Verscharen, Jim M. Raines, P. Devoto, E. Edlund, C. Brysbaert, M. Johnson, J. Rubiella, T. Hunt, Frederic Allegrini, M. Ferris, Roberto Bruno, Matthieu Berthomier, M. Petiot, Christopher J. Owen, K. L. Arnett, A. Rousseau, D. Davies, V. Arciuli, P. Bland, Peter Wurz, J. W. Thomas, G. Mele, R. Calvanese, G. Watson, F. Monti, C. Bancroft, Dennis J. Chornay, P. Wheeler, Andrew Walsh, Jason L. Stange, K. Al Janabi, Dhiren Kataria, V. Fortunato, Keiichi Ogasawara, A. Spencer, Rossana DeMarco, Susan T. Lepri, C. Amoros, Milan Maksimovic, D. Heirtzler, Stefano Livi, N. André, Antoinette B. Galvin, Mark A. Popecki, Benoit Lavraud, A. Alapide, W. Gibson, Leonardo Amoruso, W. Lockhart, Raffaella D'Amicis, G. Willis, C. Mazelle, F. Marcucci, S. Rogacki, A. Pacros, A. P. Rouillard, F. Leblanc, K. Rees, J.-D. Techer, Javier Rodriguez-Pacheco, I. Fratter, Ali Varsani, I. Zouganelis, M. Orlandi, C. Garat, T. Taylor, Marco Castronuovo, C. Frost, G. Fruit, A. De Los Santos, A. Mayall, M. Reden, Andrew Fazakerley, R. Mathon, I. Phillips, A. Fedorov, T. Nguyen, H. Seran, M. Brysch, R. Darnley, Mark Stakhiv, S. Bordon, Institut de recherche en astrophysique et planétologie (IRAP), Centre National de la Recherche Scientifique (CNRS)-Observatoire Midi-Pyrénées (OMP), Météo France-Centre National d'Études Spatiales [Toulouse] (CNES)-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Météo France-Centre National d'Études Spatiales [Toulouse] (CNES)-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Institut national des sciences de l'Univers (INSU - CNRS), Mullard Space Science Laboratory (MSSL), University College of London [London] (UCL), Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut national des sciences de l'Univers (INSU - CNRS)-Observatoire Midi-Pyrénées (OMP), Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut national des sciences de l'Univers (INSU - CNRS)-Centre National d'Études Spatiales [Toulouse] (CNES)-Centre National de la Recherche Scientifique (CNRS)-Météo-France -Institut de Recherche pour le Développement (IRD)-Institut national des sciences de l'Univers (INSU - CNRS)-Centre National d'Études Spatiales [Toulouse] (CNES)-Centre National de la Recherche Scientifique (CNRS)-Météo-France -Centre National de la Recherche Scientifique (CNRS), Laboratoire de Physique des Plasmas (LPP), Observatoire de Paris, Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-École polytechnique (X)-Sorbonne Université (SU)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS), Laboratoire d'études spatiales et d'instrumentation en astrophysique = Laboratory of Space Studies and Instrumentation in Astrophysics (LESIA), Institut national des sciences de l'Univers (INSU - CNRS)-Observatoire de Paris, Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Institut national des sciences de l'Univers (INSU - CNRS)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Observatoire Midi-Pyrénées (OMP), Météo France-Centre National d'Études Spatiales [Toulouse] (CNES)-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Météo France-Centre National d'Études Spatiales [Toulouse] (CNES)-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Centre National de la Recherche Scientifique (CNRS), Laboratoire d'études spatiales et d'instrumentation en astrophysique (LESIA (UMR_8109)), and Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP)

Subjects
010504 meteorology & atmospheric sciences, Analyser, Astrophysics, 7. Clean energy, 01 natural sciences, law.invention, Orbiter, law, Sun: particle emission, 0103 physical sciences, Thermal, Astrophysics::Solar and Stellar Astrophysics, Aerospace engineering, Sun: heliosphere, 010303 astronomy & astrophysics, ComputingMilieux_MISCELLANEOUS, 0105 earth and related environmental sciences, Physics, Spacecraft, business.industry, instrumentation: detectors, [SDU.ASTR.SR]Sciences of the Universe [physics]/Astrophysics [astro-ph]/Solar and Stellar Astrophysics [astro-ph.SR], Astronomy and Astrophysics, Plasma, plasmas, [SDU.ASTR.IM]Sciences of the Universe [physics]/Astrophysics [astro-ph]/Instrumentation and Methods for Astrophysic [astro-ph.IM], Solar wind, solar wind, Space and Planetary Science, [SDU]Sciences of the Universe [physics], Physics::Space Physics, Astrophysical plasma, Astrophysics::Earth and Planetary Astrophysics, business, Heliosphere
Abstract

The Solar Orbiter mission seeks to make connections between the physical processes occurring at the Sun or in the solar corona and the nature of the solar wind created by those processes which is subsequently observed at the spacecraft. The mission also targets physical processes occurring in the solar wind itself during its journey from its source to the spacecraft. To meet the specific mission science goals, Solar Orbiter will be equipped with both remote-sensing and in-situ instruments which will make unprecedented measurements of the solar atmosphere and the inner heliosphere. A crucial set of measurements will be provided by the Solar Wind Analyser (SWA) suite of instruments. This suite consists of an Electron Analyser System (SWA-EAS), a Proton and Alpha particle Sensor (SWA-PAS), and a Heavy Ion Sensor (SWA-HIS) which are jointly served by a central control and data processing unit (SWA-DPU). Together these sensors will measure and categorise the vast majority of thermal and suprathermal ions and electrons in the solar wind and determine the abundances and charge states of the heavy ion populations. The three sensors in the SWA suite are each based on the top hat electrostatic analyser concept, which has been deployed on numerous space plasma missions. The SWA-EAS uses two such heads, each of which have 360° azimuth acceptance angles and ±45° aperture deflection plates. Together these two sensors, which are mounted on the end of the boom, will cover a full sky field-of-view (FoV) (except for blockages by the spacecraft and its appendages) and measure the full 3D velocity distribution function (VDF) of solar wind electrons in the energy range of a few eV to ∼5 keV. The SWA-PAS instrument also uses an electrostatic analyser with a more confined FoV (−24° to +42° × ±22.5° around the expected solar wind arrival direction), which nevertheless is capable of measuring the full 3D VDF of the protons and alpha particles arriving at the instrument in the energy range from 200 eV/q to 20 keV/e. Finally, SWA-HIS measures the composition and 3D VDFs of heavy ions in the bulk solar wind as well as those of the major constituents in the suprathermal energy range and those of pick-up ions. The sensor resolves the full 3D VDFs of the prominent heavy ions at a resolution of 5 min in normal mode and 30 s in burst mode. Additionally, SWA-HIS measures 3D VDFs of alpha particles at a 4 s resolution in burst mode. Measurements are over a FoV of −33° to +66° × ±20° around the expected solar wind arrival direction and at energies up to 80 keV/e. The mass resolution (m/Δm) is > 5. This paper describes how the three SWA scientific sensors, as delivered to the spacecraft, meet or exceed the performance requirements originally set out to achieve the mission’s science goals. We describe the motivation and specific requirements for each of the three sensors within the SWA suite, their expected science results, their main characteristics, and their operation through the central SWA-DPU. We describe the combined data products that we expect to return from the suite and provide to the Solar Orbiter Archive for use in scientific analyses by members of the wider solar and heliospheric communities. These unique data products will help reveal the nature of the solar wind as a function of both heliocentric distance and solar latitude. Indeed, SWA-HIS measurements of solar wind composition will be the first such measurements made in the inner heliosphere. The SWA data are crucial to efforts to link the in situ measurements of the solar wind made at the spacecraft with remote observations of candidate source regions. This is a novel aspect of the mission which will lead to significant advances in our understanding of the mechanisms accelerating and heating the solar wind, driving eruptions and other transient phenomena on the Sun, and controlling the injection, acceleration, and transport of the energetic particles in the heliosphere.

Published
2020

3. Instilación intrapleural de estreptoquinasa en el tratamiento del empiema paraneumónico complicado

Author

M C Garat Gómez, M A Vero Acevedo, M. C. Pírez García, C. Castillo Casati, G. Giannini Fernández, J. Pastorini Correa, L. Servente Luquetti, A. Fernández Fernández, G. Giachetto Larraz, and A M Ferrari Castilla

Subjects
Gynecology, medicine.medical_specialty, business.industry, Recien nacido, Pediatrics, Perinatology and Child Health, Treatment outcome, medicine, Streptokinase, business, Empyema, Children, Pediatrics, RJ1-570
Abstract

Introducción: En el Hospital Pediátrico del Centro Hospitalario Pereira Rossell el empiema paraneumónico constituye un motivo de hospitalización frecuente. En enero de 2005 se implementó un protocolo de tratamiento del empiema complicado que incluía la instilación de estreptoquinasa intrapleural como alternativa del tratamiento quirúrgico. Objetivos: Describir los resultados de la instilación de estreptoquinasa intrapleural en niños hospitalizados con empiema paraneumónico complicado y compararlos con los resultados de la toracotomía precoz. Pacientes y métodos: Se incluyeron los niños con empiema paraneumónico complicado que ingresaron entre el 1 de enero de 2004 y el 1 de octubre de 2005. Se dividieron en dos cohortes: Histórica, niños hospitalizados entre el 1 de enero y el 31 de diciembre de 2004, tratados con toracotomía convencional antes de los 8 días de colocado el drenaje de tórax; Prospectiva, niños hospitalizados entre el 1 de enero y el 1 de octubre de 2005, tratados con estreptoquinasa intrapleural antes de los 8 días de colocado el drenaje de tórax. Se comparó la evolución y complicaciones del tratamiento mediante las siguientes variables: duración del drenaje posprocedimiento, complicaciones, reingresos, duración de la estancia hospitalaria y muerte. Resultados: Ambos grupos fueron comparables. La estancia hospitalaria no mostró diferencias significativas. La duración del drenaje de tórax después de la instilación de estreptoquinasa intrapleural fue significativamente menor que después de la toracotomía (p < 0,001). En el grupo tratado con toracotomía una proporción mayor de pacientes requirió neumonectomía parcial atípica (p = 0,051). Ninguno de los pacientes incluidos en el estudio falleció. Conclusiones: La instilación de estreptoquinasa intrapleural es una alternativa válida para el tratamiento de niños con empiema paraneumónico complicado. : Introduction: Parapneumonic empyema is a frequent cause of admission in the Pediatric Hospital of the Pereira Rossell Hospital Center. In January 2005, we implemented a treatment protocol that included intrapleural streptokinase (STK) for children with complicated parapneumonic empyema as an alternative to surgery. Objectives: To describe the results of intrapleural STK in the treatment of hospitalized children with complicated parapneumonic empyema and to compare these results with those of early thoracotomy. Patients and methods: Children with complicated parapneumonic empyema admitted between January 1st 2004 and October 1st 2005 were included. The children were divided into two groups: a historical group, composed of children hospitalized between January 1st and December 31st 2004, treated with conventional thoracotomy before day 8 of chest drain placement and a prospective group, composed of children hospitalized between January 1st and October 1st 2005, treated with intrapleural STK before day 8 of chest drain placement. The variables used to compare outcome and treatment complications were duration of chest tube drainage after the treatment procedure, complications, re-admission, length of hospital stay, and death. Results: The results in both groups were similar. Length of hospital stay showed no significant differences. Duration of chest tube drainage after intrapleural STK was significantly shorter than after thoracotomy (p < 0.001). In the thoracotomy group a significantly higher proportion of patients required partial atypical pneumonectomy (p = 0.051). There were no deaths. Conclusions: Intrapleural STK is a valid alternative for the treatment of children with complicated parapneumonic empyema.

Published
2007

5. [Intrapleural streptokinase in the treatment of complicated parapneumonic empyema]

Author

A, Fernández Fernández, G, Giachetto Larraz, G, Giannini Fernández, M C, Garat Gómez, M A, Vero Acevedo, J, Pastorini Correa, C, Castillo Casati, M C, Pírez García, L, Servente Luquetti, and A M, Ferrari Castilla

Subjects
Male, Treatment Outcome, Fibrinolytic Agents, Thoracotomy, Child, Preschool, Drainage, Humans, Infant, Female, Streptokinase, Injections, Intralesional, Empyema, Pleural
Abstract

Parapneumonic empyema is a frequent cause of admission in the Pediatric Hospital of the Pereira Rossell Hospital Center. In January 2005, we implemented a treatment protocol that included intrapleural streptokinase (STK) for children with complicated parapneumonic empyema as an alternative to surgery.To describe the results of intrapleural STK in the treatment of hospitalized children with complicated parapneumonic empyema and to compare these results with those of early thoracotomy.Children with complicated parapneumonic empyema admitted between January 1st 2004 and October 1st 2005 were included. The children were divided into two groups: a historical group, composed of children hospitalized between January 1st and December 31st 2004, treated with conventional thoracotomy before day 8 of chest drain placement and a prospective group, composed of children hospitalized between January 1st and October 1st 2005, treated with intrapleural STK before day 8 of chest drain placement. The variables used to compare outcome and treatment complications were duration of chest tube drainage after the treatment procedure, complications, re-admission, length of hospital stay, and death.The results in both groups were similar. Length of hospital stay showed no significant differences. Duration of chest tube drainage after intrapleural STK was significantly shorter than after thoracotomy (p0.001). In the thoracotomy group a significantly higher proportion of patients required partial atypical pneumonectomy (p = 0.051). There were no deaths.Intrapleural STK is a valid alternative for the treatment of children with complicated parapneumonic empyema.

Published
2007

7. The integrin alpha v beta 6 binds and activates latent TGF beta 1: a mechanism for regulating pulmonary inflammation and fibrosis

Author

J S, Munger, X, Huang, H, Kawakatsu, M J, Griffiths, S L, Dalton, J, Wu, J F, Pittet, N, Kaminski, C, Garat, M A, Matthay, D B, Rifkin, and D, Sheppard

Subjects
Keratinocytes, Mice, Knockout, Integrins, Pulmonary Fibrosis, Proteins, Epithelial Cells, 3T3 Cells, CHO Cells, Ligands, Peptide Fragments, Transforming Growth Factor beta1, Bleomycin, Mice, Esophagus, Antigens, Neoplasm, Transforming Growth Factor beta, Cricetinae, Tumor Cells, Cultured, Animals, Humans, Protein Precursors, Protein Binding
Abstract

Transforming growth factor beta (TGF beta) family members are secreted in inactive complexes with a latency-associated peptide (LAP), a protein derived from the N-terminal region of the TGF beta gene product. Extracellular activation of these complexes is a critical but incompletely understood step in regulation of TGF beta function in vivo. We show that TGF beta 1 LAP is a ligand for the integrin alpha v beta 6 and that alpha v beta 6-expressing cells induce spatially restricted activation of TGF beta 1. This finding explains why mice lacking this integrin develop exaggerated inflammation and, as we show, are protected from pulmonary fibrosis. These data identify a novel mechanism for locally regulating TGF beta 1 function in vivo by regulating expression of the alpha v beta 6 integrin.

Published
1999

8. [Speech and music]

Author

M C, Garat

Subjects
Child Psychiatry, Clinical Protocols, Child, Preschool, Psychotherapy, Group, Humans, Organizational Objectives, Language Development Disorders, Child, Music Therapy
Published
1993

9. Measurement of the mass and width of the Z$^0$-particle from multihadronic final states produced in e$^+$e$^-$ annihilation

Author

P. Aarnio, P. Abreu, W. Adam, P. Adrianos, T. Adye, G. Akopdzhanov, G. Alekseev, J. Allaby, P. Allen, P. Allport, S. Almehed, S. Alvsvaag, U. Amaldi, E. Anassontzis, P. Antilogus, W. Apel, E. Aria, B. Asman, F. Astesan, C.Astor Ferreres, C. Aubret, J. Augustin, A. Augustinus, P. Baillon, F. Barao, G. Barbiellini, D. Bardin, S. Barlag, J. Barlow, A. Baroncelli, M. Barranco-Luque, G. Barreira, O. Barring, W. Bartl, M. Bates, M. Baubillier, K. Becks, C. Beeston, W. Bell, I. Belokopytov, P. Beltran, D. Benedic, J. Benlloch, M. Berggren, J. Berst, D. Bertrand, S. Biagi, F. Bianchi, J. Bibby, M. Bilenky, P. Billoir, N. Bingefors, J. Bjarne, D. Bloch, P. Bogolubov, D. Bollini, T. Bolognese, M. Bonapart, P. Booth, M. Boratav, P. Borgeaud, H. Borner, C. Bosio, O. Botner, B. Bouquet, M. Bozzo, S. Braibant, P. Branchini, C. Brand, K. Brand, C. Bricman, R. Brown, N. Brummer, J. Brunet, L. Bugge, T. Buran, H. Burmeister, C. Buttar, J. Buytaert, G. Cabras, M. Caccia, S. Cairanti, M. Calvi, A.Camacho Rozas, J. Campagne, A. Campion, T. Camporesi, V. Canale, F. Cao, L. Carroll, C. Caso, E. Castelli, V. Castillo Gimenez, A. Cattai, F. Caoallo, L. Cerrito, G. Chadwick, P. Charpentier, P. Checchia, G. Chelkov, L. Chevalier, C. Chiccoli, P. Chiliapnikov, V. Chorowicz, E. Christophel, R. Cirio, M. Clara, J. Contreras, R. Contri, F. Couchot, P. Courty, H. Crawley, D. Crennell, M. Cresti, M. Croissiaux, G. Crosetti, N. Crosland, M. Crozon, J. Cuevas Maestro, L. Curwen, S. Czellar, E. Dahl-Jensen, B. Dalmagne, M. Dam, G. Damgaard, G. Darbo, E. Daubie, M. Davenport, A. De Angelis, M. De Beer, C. De Clercq, N. De Groot, M. De Jode, C. De La Vaissiere, D. Delikaris, P. Delpierre, L. Di Ciaccio, A. Diddens, H. Dijkstra, N Dimitriou, F. Djama, J. Dolbeau, K. Doroba, R. Downs, M. Dracos, J. Drees, M. Dris, S. Du, W. Dulinski, R. Dzhelyadin, D. Edwards, L. Eek, P. Eerola, T. Ekelof, G. Ekspong, M. Ellila, J. Engel, V. Falaleev, A. Fenyuk, M. Fernandez Alonso, A. Ferrer, S. Ferroni, T. Filippas, A. Firestone, H. Fischer, B. Fjeld, M. Flinn, H. Foeth, E. Fokitis, P. Folegati, F. Fontanelli, H. Forsbach, D. Fraissard, B. Franek, K. Fransson, P. Frenkiel, D. Fries, J. Froberger, A. Frodesen, R. Fruhwirth, F. Fulda-Quenzer, J. Fuster, J. Gago, M. Gaillard, G. Galeazzi, D. Gamba, C. Garat, C. Gaspar, U. Gasparini, P. Gavillet, S. Gawne, E. Gazis, J. Genat, J. Gerber, K. Glitza, R. Gokieli, V. Golovatyuk, P. Gomes, J. Gomez Y Cadenas, A. Goobar, G. Gopal, M. Gorbics, B. Goret, B. Gorski, G. Goujon, V. Gracco, A. Grant, F. Grard, E. Graziani, J. Grillet, M. Gros, G. Grosdidier, B. Grossetete, B. Grung, L. Guglielmi, S. Gumenyuk, J. Guy, F. Hahn, S. Haider, J. Haissinski, Z. Hajduk, A. Hakansson, A. Hallgren, K. Hamacher, G. Hamel De Monchenault, F. Harris, B. Heck, I. Herbst, J. Hernandez, P. Herquet, H. Herr, E. Higon, H. Hilke, H. Hofmann, T. Hofmokl, S. Holmgren, J. Hooper, R. Horisberger, M. Houlden, A. Hrisoho, J. Hrubec, K. Huitu, P. Hulth, K. Hultqvist, D. Husson, B. Hyams, D. Imbault, M. Innocente, P. Ioannou, P. Iversen, J. Jackson, P. Jalocha, G. Jarlskog, P. Jarry, B. Jean-Marie, J. Joensuu, E. Johansson, H. Johansson, S. Johansson, M. Jonker, P. Juillot, R. Kadyrov, V. Kadyshevsky, G. Kalkanis, G. Kalmus, G. Kantardjian, S. Katsanevas, E. Katsoufis, R. Keranen, J. Kesteman, B. Khomenko, N. Khovanski, B. King, B. Kisielewski, H. Klein, W. Klempt, A. Klovning, P. Kluit, B. Koene, P. Kokkinias, I. Kontaxis, M. Kopf, M. Koratzinos, K. Korcyl, A. Korytov, B. Korzen, P. Kostarakis, C. Kourkoumelis, P. Kremizis, T. Kreuzberger, J. Krolikowski, J. Krstic, W. Kucewicz, G. Kuhn, K. Kurvinen, M. Laakso, C. Lambropoulos, L. Lanceri, D. Langerveld, V. Lapin, J. Laugier, R. Lauhakangas, P. Laurikainen, B. Lavigne, J. Le Grand, H. Lebbolo, E. Lebreton, G. Leder, J. Lemonne, G. Lenzen, V. Lepeltier, J. Lidbury, E. Lieb, E. Lillestol, E. Lillethun, I. Lippi, R. Llosa, B. Loerstad, J. Loken, M. Lopez Aguera, P. Lorenz, D. Loukas, R. 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Quinton, A. Rademakers, D. Radojicic, S. Ragazzi, R. Ragazzon, W. Range, J. Raoul, P. Ratoff, A. Read, N. Redaelli, M. Regler, D. Reid, M. Reis, P. Renton, L. Resvanis, F. Richard, J. Ridky, G. Rinaudo, A. Romaya, A. Romero, I. Roncagliolo, P. Ronchese, R. Rongved, E. Rosenberg, F. Rossel, E. Rosso, P. Roudeau, T. Rovelli, V. Ruhlmann, A. Ruiz, K. Rybicki, H. Saarikko, D. Sacco, Y. Sacquin, A. Sadovsky, C. Salgado, J. Salt, A. Samarin, E. Sanchez, E. Sanchis, M. Sannino, M. Schaeffer, H. Schneider, F. Scuri, R. Sebastia, A. Segar, R. Sekulin, M. Sessa, G. Sette, R. Seufert, R. Shellard, P. Siegrist, S. Simonetti, F. Simonetto, T. Skaali, J. Skeens, G. Skjevling, G. Smadja, G. Smith, R. Sosnowski, K. Spang, T. Spassov, P. Spentzouris, E. Spiriti, S. Squarcia, H. Staeck, C. Stanescu, G. Stavropoulos, F. Stichelbaut, A. Stocchi, J. Strauss, R. Strub, E. Sundell, M. Szczekowski, M. Szeptycka, P. Szymanski, S. Tavernier, G. Theodosiou, A. Tilquin, J. Timmermans, L. Tkachev, D. Toet, S. 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Zumerle, Laboratoire de l'Accélérateur Linéaire (LAL), Centre National de la Recherche Scientifique (CNRS)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Université Paris-Sud - Paris 11 (UP11), Institut de Recherches Subatomiques (IReS), Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Cancéropôle du Grand Est-Université Louis Pasteur - Strasbourg I-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Physique Nucléaire et de Hautes Énergies (LPNHE), Centre National de la Recherche Scientifique (CNRS)-Université Paris Diderot - Paris 7 (UPD7)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Université Pierre et Marie Curie - Paris 6 (UPMC), DELPHI, Université Paris-Sud - Paris 11 (UP11)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), Aarnio, P, Abreu, P, Adam, W, Adrianos, P, Adye, T, Akopdzhanov, G, Alekseev, G, Allaby, J, Allen, P, Allport, P, Almehed, S, Alvsvaag, S, Amaldi, U, Anassontzis, E, Antilogus, P, Apel, W, Aria, E, Asman, B, Astesan, F, Ferreres, C, Aubret, C, Augustin, J, Augustinus, A, Baillon, P, Barao, F, Barbiellini, G, Bardin, D, Barlag, S, Barlow, J, Baroncelli, A, Barranco-Luque, M, Barreira, G, Barring, O, Bartl, W, Bates, M, Baubillier, M, Becks, K, Beeston, C, Bell, W, Belokopytov, I, Beltran, P, Benedic, D, Benlloch, J, Berggren, M, Berst, J, Bertrand, D, Biagi, S, Bianchi, F, Bibby, J, Bilenky, M, Billoir, P, Bingefors, N, Bjarne, J, Bloch, D, Bogolubov, P, Bollini, D, Bolognese, T, Bonapart, M, Booth, P, Boratav, M, Borgeaud, P, Borner, H, Bosio, C, Botner, O, Bouquet, B, Bozzo, M, Braibant, S, 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Zimin, N, Zinchenko, A, Zito, M, Zitoun, R, Zukanovich Funchal, R, Zumerle, G, P., Aarnio, P., Abreu, W., Adam, P., Adriano, T., Adye, G., Akopdzhanov, G., Alekseev, J., Allaby, P., Allen, P., Allport, S., Almehed, S., Alvsvaag, U., Amaldi, E., Anassontzi, P., Antilogu, W., Apel, E., Aria, B., Asman, F., Astesan, C., Astor Ferrere, C., Aubret, J., Augustin, A., Augustinu, P., Baillon, F., Barao, BARBIELLINI AMIDEI, Guido, D., Bardin, S., Barlag, J., Barlow, A., Baroncelli, M., Barranco Luque, G., Barreira, O., Barring, W., Bartl, M., Bate, M., Baubillier, K., Beck, C., Beeston, W., Bell, I., Belokopytov, P., Beltran, D., Benedic, J., Benlloch, M., Berggren, J., Berst, D., Bertrand, S., Biagi, F., Bianchi, J., Bibby, M., Bilenky, P., Billoir, N., Bingefor, J., Bjarne, D., Bloch, P., Bogolubov, D., Bollini, T., Bolognese, M., Bonapart, P., Booth, M., Boratav, P., Borgeaud, H., Borner, C., Bosio, O., Botner, B., Bouquet, M., Bozzo, S., Braibant, P., Branchini, C., Brand, K., Brand, C., Bricman, R., Brown, N., Brummer, J., Brunet, L., Bugge, T., Buran, H., Burmeister, C., Buttar, J., Buytaert, G., Cabra, M., Caccia, S., Cairanti, M., Calvi, A., Camacho Roza, J., Campagne, A., Campion, T., Camporesi, V., Canale, F., Cao, L., Carroll, C., Caso, E., Castelli, V., Castillo Gimenez, A., Cattai, F., Caoallo, L., Cerrito, G., Chadwick, P., Charpentier, P., Checchia, G., Chelkov, L., Chevalier, C., Chiccoli, P., Chiliapnikov, V., Chorowicz, E., Christophel, R., Cirio, M., Clara, J., Contrera, R., Contri, F., Couchot, P., Courty, H., Crawley, D., Crennell, M., Cresti, M., Croissiaux, G., Crosetti, N., Crosland, M., Crozon, J., Cuevas Maestro, L., Curwen, S., Czellar, E., Dahl Jensen, B., Dalmagne, M., Dam, G., Damgaard, G., Darbo, E., Daubie, M., Davenport, A., De Angeli, M., De Beer, C., De Clercq, N., De Groot, M., De Jode, C., De La Vaissiere, D., Delikari, P., Delpierre, L., Di Ciaccio, A., Didden, H., Dijkstra, N., Dimitriou, F., Djama, J., Dolbeau, K., Doroba, R., Down, M., Draco, J., Dree, M., Dri, S., Du, W., Dulinski, R., Dzhelyadin, D., Edward, L., Eek, P., Eerola, T., Ekelof, G., Ekspong, M., Ellila, J., Engel, V., Falaleev, A., Fenyuk, M., Fernandez Alonso, A., Ferrer, S., Ferroni, T., Filippa, A., Firestone, H., Fischer, B., Fjeld, M., Flinn, H., Foeth, E., Fokiti, P., Folegati, F., Fontanelli, H., Forsbach, D., Fraissard, B., Franek, K., Fransson, P., Frenkiel, D., Frie, J., Froberger, A., Frodesen, R., Fruhwirth, F., Fulda Quenzer, J., Fuster, J., Gago, M., Gaillard, G., Galeazzi, D., Gamba, C., Garat, C., Gaspar, U., Gasparini, P., Gavillet, S., Gawne, E., Gazi, J., Genat, J., Gerber, K., Glitza, R., Gokieli, V., Golovatyuk, P., Gome, J. Gomez Y., Cadena, A., Goobar, G., Gopal, M., Gorbic, B., Goret, B., Gorski, G., Goujon, V., Gracco, A., Grant, F., Grard, E., Graziani, J., Grillet, M., Gro, G., Grosdidier, B., Grossetete, B., Grung, L., Guglielmi, S., Gumenyuk, J., Guy, F., Hahn, S., Haider, J., Haissinski, Z., Hajduk, A., Hakansson, A., Hallgren, K., Hamacher, G., Hamel De Monchenault, F., Harri, B., Heck, I., Herbst, J., Hernandez, P., Herquet, H., Herr, E., Higon, H., Hilke, H., Hofmann, T., Hofmokl, S., Holmgren, J., Hooper, R., Horisberger, M., Houlden, A., Hrisoho, J., Hrubec, K., Huitu, P., Hulth, K., Hultqvist, D., Husson, B., Hyam, D., Imbault, M., Innocente, P., Ioannou, P., Iversen, J., Jackson, P., Jalocha, G., Jarlskog, P., Jarry, B., Jean Marie, J., Joensuu, E., Johansson, H., Johansson, S., Johansson, M., Jonker, P., Juillot, R., Kadyrov, V., Kadyshevsky, G., Kalkani, G., Kalmu, G., Kantardjian, S., Katsaneva, E., Katsoufi, R., Keranen, J., Kesteman, B., Khomenko, N., Khovanski, B., King, B., Kisielewski, H., Klein, W., Klempt, A., Klovning, P., Kluit, B., Koene, P., Kokkinia, I., Kontaxi, M., Kopf, M., Koratzino, K., Korcyl, A., Korytov, B., Korzen, P., Kostaraki, C., Kourkoumeli, P., Kremizi, T., Kreuzberger, J., Krolikowski, J., Krstic, W., Kucewicz, G., Kuhn, K., Kurvinen, M., Laakso, C., Lambropoulo, Lanceri, Livio, D., Langerveld, V., Lapin, J., Laugier, R., Lauhakanga, P., Laurikainen, B., Lavigne, J., Le Grand, H., Lebbolo, E., Lebreton, G., Leder, J., Lemonne, G., Lenzen, V., Lepeltier, J., Lidbury, E., Lieb, E., Lillestol, E., Lillethun, I., Lippi, R., Llosa, B., Loerstad, J., Loken, M., Lopez Aguera, P., Lorenz, D., Louka, R., Lucock, B., Lund Jensen, P., Lutz, L., Lyon, G., Maehlum, O., Maeland, J., Maillard, A., Makoussi, A., Maltezo, F., Mandl, J., Marco, J., Marin, A., Markou, L., Mathi, C., Matteuzzi, G., Matthiae, L., Mattsson, N., Mayet, M., Mazzucato, M., Mc Cubbin, R., Mc Kay, E., Menichetti, C., Meroni, W., Meyer, M., Michael, J., Michalowski, W., Mitaroff, G., Mitselmakher, U., Mjoernmark, T., Moa, R., Moeller, K., Moenig, R., Monge, G., Montalbano, P., Morettini, H., Mueller, H., Muller, M., Mur, B., Muryn, G., Myatt, F., Navarria, P., Negri, B., Nielsen, M., Nigro, V., Nikolaenko, J., Noppe, M., Nordberg, S., Nouno, V., Obraztsov, R., Orava, A., Ouraou, J., Pagot, R., Pain, K., Pakonski, H., Palka, S., Palma Lope, T., Papadopoulou, L., Pape, P., Pasini, J., Passeneau, M., Passeneau, A., Passeri, J., Pattison, M., Pegoraro, V., Perevozchikov, J., Perez, M., Pernicka, A., Perrotta, G., Petrucci, T., Pettersen, M., Pimenta, O., Pingot, C., Pinori, A., Pinsent, C., Poiret, M., Pol, B., Poliakov, G., Polok, Poropat, Paolo, P., Privitera, A., Pullia, J., Pyyhtia, P., Queru, S., Quinton, A., Rademaker, D., Radojicic, S., Ragazzi, R., Ragazzon, W., Range, J., Raoul, P., Ratoff, A., Read, N., Redaelli, M., Regler, D., Reid, M., Rei, P., Renton, L., Resvani, F., Richard, J., Ridky, G., Rinaudo, A., Romaya, A., Romero, I., Roncagliolo, P., Ronchese, R., Rongved, E., Rosenberg, F., Rossel, E., Rosso, P., Roudeau, T., Rovelli, V., Ruhlmann, A., Ruiz, K., Rybicki, H., Saarikko, D., Sacco, Y., Sacquin, A., Sadovsky, C., Salgado, J., Salt, A., Samarin, E., Sanchez, E., Sanchi, M., Sannino, M., Schaeffer, H., Schneider, F., Scuri, R., Sebastia, A., Segar, R., Sekulin, M., Sessa, G., Sette, R., Seufert, R., Shellard, P., Siegrist, S., Simonetti, F., Simonetto, T., Skaali, J., Skeen, G., Skjevling, G., Smadja, G., Smith, R., Sosnowski, K., Spang, T., Spassov, P., Spentzouri, E., Spiriti, S., Squarcia, H., Staeck, C., Stanescu, G., Stavropoulo, F., Stichelbaut, A., Stocchi, J., Strau, R., Strub, E., Sundell, M., Szczekowski, M., Szeptycka, P., Szymanski, S., Tavernier, G., Theodosiou, A., Tilquin, J., Timmerman, L., Tkachev, D., Toet, S., Topp Jorgensen, A., Topphol, L., Tortora, D., Treille, U., Trevisan, C., Tristram, C., Troncon, T., Truong, E., Tsyganov, M., Turala, R., Turchetta, J., Turlot, M., Turluer, T., Tuuva, I., Tyapkin, M., Tyndel, N., Tyurin, F., Udo, S., Ueberschaer, O., Ullaland, G., Valenti, G., Van Apeldoorn, P., Van Dam, W., Van Doninck, B., Van Eijk, N., Van Eijndhoven, C., Vander Velde, J., Vanuxem, J., Varela, P., Vaz, G., Vegni, M., Veitch, E., Vela, J., Velasco, L., Ventura, W., Venu, F., Verbeure, P., Vergezac, D., Vilanova, L., Viseu Melo, E., Vlasov, S., Vlassopoulo, A., Vodopianov, M., Vollmer, S., Volponi, G., Voulgari, M., Voutilainen, V., Vrba, H., Wahlen, C., Walck, F., Waldner, M., Wayne, P., Weilhammer, J., Werner, A., Wetherell, J., Wicken, W., William, M., Winter, B., Witecki, G., Wormser, K., Woschnagg, N., Yamdagni, J., Yelton, A., Zaitsev, A., Zalewska, P., Zalewski, E., Zevgolatako, G., Zhang, N., Zimin, A., Zinchenko, M., Zito, R., Zitoun, R., Zukanovich Funchal, G., Zumerle, Delphi, Collaboration, Abreu, P., Adam, W., and Canale, Vincenzo

Subjects
Nuclear and High Energy Physics, Particle physics, Electron–positron annihilation, Hadron, scientific journals, electron positron annihilation, 01 natural sciences, 7. Clean energy, electronic journals, Standard Model, Nuclear physics, Z0 boson mass and width, electron positron annihilations, DELPHI detector at LEP, Particle decay, 0103 physical sciences, authors, [PHYS.HEXP]Physics [physics]/High Energy Physics - Experiment [hep-ex], Invariant mass, 010306 general physics, Nuclear Experiment, GeneralLiterature_REFERENCE(e.g.,dictionaries,encyclopedias,glossaries), infometrics, Physics, Annihilation, 010308 nuclear & particles physics, 3. Good health, papers, citations, Physique des particules élémentaires, High Energy Physics::Experiment, Neutrino, Particle Physics - Experiment, Lepton
Abstract

First measurements of the mass and width of the Z0 performed at the newly commissioned LEP Collider by the DELPHI Collaboration are presented. The measuements are derived from the study of multihadronic final states produced in e+e- annihilations at several energies around the Z0 mass. The values found for the mass and width are M(Z0)=91.06±0.09 (stat) ±0.045 (syst.) GeV and Γ(Z0)=2.42±0.21 (stat.) GeV respectively, froma three-parameter fit to the line shape. A two-parameter fit in the framework of the standard model yields for the number of light neutrino species Nν=2.4±0.4 (stat.) ±0.5 (syst.), 0, SCOPUS: ar.j, info:eu-repo/semantics/published

Published
1989

10. Quantification of the Environmental Impact of Feeding Yeast Probiotic Saccharomyces cerevisiae Actisaf Sc 47 in Dairy Cow: A Life Cycle Assessment Approach.

Author

Salah N, Legendre H, Paiva E, Duclos J, Briche M, Maaoui M, Scholten J, and Garat Boute C

Abstract

Today, one of the major challenges of dairy farmers is to reduce their environmental footprint to establish more effective, efficient, and sustainable production systems. Feed additives such as yeast probiotics could potentially allow them to achieve these objectives through the improvement of milk production, feed efficiency, and ration valorization, hence mitigating the environmental impacts of milk production. In this study, the life cycle assessment (LCA) principle was performed to estimate the environmental impact of the production and supplementation of a commercial yeast probiotic (Actisaf Sc 47) in three trials performed in three different countries that are representative for around 50% of the milk production in Europe: France (French trial), United Kingdom (UK trial), and Germany (German trial). For each trial, two groups of animals were compared: control, without Actisaf Sc 47 supplementation, used as baseline; and experimental, with Actisaf Sc 47 supplementation at 5 or 10 g/cow/day. Different impact categories were analyzed for each group to calculate the impact of producing 1 kg of fat- and protein-corrected milk. An initial analysis was done only during the period of Actisaf Sc 47 supplementation and showed than the supplementation with Actisaf Sc 47 reduced, on average by 5%, the carbon footprint during the three trials. A second analysis was done via the extrapolation of all the data of each trial to an annual farm level, including the lactation period (305 days), dry period (60 days), and the period with and without Actisaf Sc 47 supplementation. Reported at a farm annual scale, the average reduction allowed by Actisaf Sc 47 supplementation was 2.9, 2.05, 2.47, 1.67, 2.28, 2.18, 2.14, and 2.28% of the carbon footprint, land use, water use, resource use, acidification, freshwater eutrophication, marine eutrophication, and terrestrial eutrophication, respectively. On average, the production of 1 kg of fat- and protein-corrected milk by using Actisaf Sc 47 was shown to improve environmental impacts compared to control. Regarding Actisaf Sc 47 production, the LCA showed that the production of 1 kg of Actisaf Sc 47 emitted 2.1 kg CO 2 eq with a negligible contribution to total the carbon footprint of milk ranging from 0.005 to 0.016%. The use of Actisaf Sc 47 in dairy cows could then result in different positive outcomes: improving performance and efficiency while reducing the global carbon footprint.

Published
2024
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11. The pathology of bleomycin-induced fibrosis is associated with loss of resident lung mesenchymal stem cells that regulate effector T-cell proliferation.

Author

Jun D, Garat C, West J, Thorn N, Chow K, Cleaver T, Sullivan T, Torchia EC, Childs C, Shade T, Tadjali M, Lara A, Nozik-Grayck E, Malkoski S, Sorrentino B, Meyrick B, Klemm D, Rojas M, Wagner DH Jr, and Majka SM

Subjects
Animals, Bleomycin pharmacology, Familial Primary Pulmonary Hypertension, Hypertension, Pulmonary pathology, Lung Injury, Mesenchymal Stem Cells cytology, Mice, Mice, Inbred C57BL, Polymerase Chain Reaction, Pulmonary Fibrosis pathology, Bleomycin adverse effects, Cell Proliferation, Mesenchymal Stem Cells drug effects, Pulmonary Fibrosis chemically induced, T-Lymphocytes cytology
Abstract

Tissue-resident mesenchymal stem cells (MSCs) are important regulators of tissue repair or regeneration, fibrosis, inflammation, angiogenesis, and tumor formation. Here, we define a population of resident lung MSCs (luMSCs) that function to regulate the severity of bleomycin injury via modulation of the T-cell response. Bleomycin-induced loss of these endogenous luMSCs and elicited fibrosis (pulmonary fibrosis), inflammation, and pulmonary arterial hypertension (PAH). Replacement of resident stem cells by administration of isolated luMSCs attenuated the bleomycin-associated pathology and mitigated the development of PAH. In addition, luMSC modulated a decrease in numbers of lymphocytes and granulocytes in bronchoalveolar fluid and demonstrated an inhibition of effector T-cell proliferation in vitro. Global gene expression analysis indicated that the luMSCs are a unique stromal population differing from lung fibroblasts in terms of proinflammatory mediators and profibrotic pathways. Our results demonstrate that luMSCs function to protect lung integrity after injury; however, when endogenous MSCs are lost, this function is compromised illustrating the importance of this novel population during lung injury. The definition of this population in vivo in both murine and human pulmonary tissue facilitates the development of a therapeutic strategy directed at the rescue of endogenous cells to facilitate lung repair during injury., (Copyright © 2011 AlphaMed Press.)

Published
2011
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12. Stimulation of MAP kinase pathways after maternal IL-1beta exposure induces fetal lung fluid absorption in guinea pigs.

Author

Bhattacharjee R, Li T, Koshy S, Beard LL, Sharma K, Carter EP, Garat C, and Folkesson HG

Subjects
Absorption drug effects, Animals, Extracellular Signal-Regulated MAP Kinases metabolism, Female, Fetus metabolism, Gestational Age, Guinea Pigs, Injections, Subcutaneous, Interleukin-1beta administration & dosage, Mitogen-Activated Protein Kinase Kinases metabolism, Pregnancy, Rats, Recombinant Proteins administration & dosage, Recombinant Proteins pharmacology, Body Fluids metabolism, Hydrocortisone metabolism, Interleukin-1beta pharmacology, Lung embryology, Mitogen-Activated Protein Kinases metabolism, Pregnancy, Animal metabolism
Abstract

Background: We tested the hypothesis that maternal interleukin-1beta (IL-1beta) pretreatment and induction of fetal cortisol synthesis activates MAP kinases and thereby affects lung fluid absorption in preterm guinea pigs., Methods: IL-1beta was administered subcutaneously daily to timed-pregnant guinea pigs for three days. Fetuses were obtained by abdominal hysterotomy and instilled with isosmolar 5% albumin into the lungs and lung fluid movement was measured over 1 h by mass balance. MAP kinase expression was measured by western blot., Results: Lung fluid absorption was induced at 61 days (D) gestation and stimulated at 68D gestation by IL-1beta. Maternal IL-1beta pretreatment upregulated ERK and upstream MEK expression at both 61 and 68D gestation, albeit being much more pronounced at 61D gestation. U0126 instillation completely blocked IL-1beta-induced lung fluid absorption as well as IL-1beta-induced/stimulated ERK expression. Cortisol synthesis inhibition by metyrapone attenuated ERK expression and lung fluid absorption in IL-1beta-pretreated fetal lungs. JNK expression after maternal IL-1beta pretreatment remained unaffected at either gestation age., Conclusion: These data implicate the ERK MAP kinase pathway as being important for IL-1beta induction/stimulation of lung fluid absorption in fetal guinea pigs.

Published
2007
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14. Platelet-derived growth factor-BB-mediated activation of Akt suppresses smooth muscle-specific gene expression through inhibition of mitogen-activated protein kinase and redistribution of serum response factor.

Author

Kaplan-Albuquerque N, Garat C, Desseva C, Jones PL, and Nemenoff RA

Subjects
Actins genetics, Actins metabolism, Animals, Arginine Vasopressin pharmacology, Becaplermin, Cells, Cultured, DNA genetics, DNA metabolism, Enzyme Activation drug effects, Gene Expression drug effects, JNK Mitogen-Activated Protein Kinases, MAP Kinase Signaling System drug effects, Mitogen-Activated Protein Kinases metabolism, Models, Biological, Muscle, Smooth drug effects, Muscle, Smooth metabolism, Phosphatidylinositol 3-Kinases metabolism, Proto-Oncogene Proteins c-akt, Proto-Oncogene Proteins c-sis, Rats, Serum Response Factor metabolism, p38 Mitogen-Activated Protein Kinases, Mitogen-Activated Protein Kinases antagonists & inhibitors, Platelet-Derived Growth Factor pharmacology, Protein Serine-Threonine Kinases, Proto-Oncogene Proteins metabolism
Abstract

Platelet-derived growth factor (PDGF) inhibits expression of smooth muscle (SM) genes in vascular smooth muscle cells and blocks induction by arginine vasopressin (AVP). We have previously demonstrated that suppression of SM-alpha-actin by PDGF-BB is mediated in part through a Ras-dependent pathway. This study examined the role of phosphatidylinositol 3-kinase (PI3K)y and its downstream effector, Akt, in regulating SM gene expression. PDGF caused a rapid sustained activation of Akt, whereas AVP caused only a small transient increase. PDGF selectively caused a sustained stimulation of p85/p110 alpha PI3K. In contrast, p85/110 beta PI3K activity was not altered by either PDGF or AVP, whereas both agents caused a delayed activation of Class IB p101/110 gamma PI3K. Expression of a gain-of-function PI3K or myristoylated Akt (myr-Akt) mimicked the inhibitory effect of PDGF on SM-alpha-actin and SM22 alpha expression. Pretreatment with LY 294002 reversed the inhibitory effect of PDGF. Expression of myr-Akt selectively inhibited AVP-induced activation of c-Jun N-terminal kinase and p38 mitogen-activated protein kinases, which we have shown are critical for induction of these genes. Nuclear extracts from PDGF-stimulated or myr-Akt expressing cells showed reduced serum response factor binding to SM-specific CArG elements. This was associated with appearance of serum response factor in the cytoplasm. These data indicate that activation of p85/p110 alpha/Akt mediates suppression of SM gene expression by PDGF.

Published
2003
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15. Regulation of SM22 alpha expression by arginine vasopressin and PDGF-BB in vascular smooth muscle cells.

Author

Kaplan-Albuquerque N, Garat C, Van Putten V, and Nemenoff RA

Subjects
Animals, Becaplermin, Cells, Cultured, Electrophoresis, Polyacrylamide Gel, Gene Expression physiology, Gene Expression Regulation physiology, Microfilament Proteins genetics, Mitogen-Activated Protein Kinases metabolism, Muscle Proteins genetics, Muscle, Smooth, Vascular cytology, Muscle, Smooth, Vascular drug effects, Myocytes, Smooth Muscle drug effects, Promoter Regions, Genetic drug effects, Promoter Regions, Genetic physiology, Proto-Oncogene Proteins c-sis, Rats, Signal Transduction physiology, Arginine Vasopressin pharmacology, Microfilament Proteins metabolism, Muscle Proteins metabolism, Muscle, Smooth, Vascular metabolism, Myocytes, Smooth Muscle metabolism, Platelet-Derived Growth Factor pharmacology, Vasoconstrictor Agents pharmacology
Abstract

Vascular smooth muscle (SM) cells (VSMC) undergo phenotypic modulation in vivo and in vitro. This process involves coordinated changes in expression of multiple SM-specific genes. In cultured VSMC, arginine vasopressin (AVP) increases and PDGF decreases expression of SM alpha-actin (SMA), the earliest marker of SM cells (SMC). However, it is unknown whether these agents regulate other SM genes in a similar fashion. SM22 alpha appears secondary to SMA during development and is also a marker for SMC. This study examined the regulation of SM22 alpha expression by AVP and PDGF in cultured VSMC. Levels of SM22 alpha mRNA and protein were increased by AVP and suppressed by PDGF. Consistent with these changes, AVP increased SM22 alpha promoter activity, whereas PDGF inhibited basal promoter activity and blocked AVP-induced increase. Activation of both JNK and p38 MAPK pathways was necessary for AVP-mediated induction of SM22 alpha promoter. Expression of constitutively active Ras produced similar suppressions on SM22 alpha promoter activity as PDGF. Signaling relayed from PDGF/Ras activation involved Raf, or a protein that competes for this site, Ral-GDS, and phosphatidylinositol 3-kinase activation. Truncational analysis showed that the proximal location of three CArG boxes in the promoter was sufficient for AVP stimulation. Mutations in this CArG box reduced basal and AVP-stimulated promoter activity without effecting PDGF suppression. Overexpression of serum response factor enhanced basal and AVP-stimulated promoter activity but had no effect on PDGF-BB-induced suppression. These data indicate that AVP and PDGF initiate specific signaling pathways that control expression of multiple SM genes leading to phenotypic modulation.

Published
2003
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16. Intracellular IL-1Ra type 1 inhibits IL-1-induced IL-6 and IL-8 production in Caco-2 intestinal epithelial cells through inhibition of p38 mitogen-activated protein kinase and NF-kappaB pathways.

Author

Garat C and Arend WP

Subjects
Caco-2 Cells, Humans, Mitogen-Activated Protein Kinases antagonists & inhibitors, Mitogen-Activated Protein Kinases metabolism, NF-kappa B metabolism, Receptors, Interleukin-1 Type I, Time Factors, p38 Mitogen-Activated Protein Kinases, Interleukin-1 metabolism, Interleukin-6 metabolism, Interleukin-8 metabolism, Receptors, Interleukin-1 metabolism
Abstract

Interleukin-1 (IL-1) plays a pivotal role in the pathogenesis of inflammatory bowel disease (IBD). IL-1 action is regulated in part by its naturally occurring inhibitor, the IL-1 receptor antagonist (IL-1Ra). Four splice variants of IL-1Ra gene product have been described, one secreted (sIL-1Ra) and three intracellular (icIL-1Ra1, 2, 3). Although sIL-1Ra and icIL-1Ra1 bind to type I IL-1 receptor with equal affinity, icIL-1Ra1 may carry out unique functions inside cells. The goal of this study was to determine the role of icIL-1Ra1 in regulation of cytokine-induced IL-6 and IL-8 production in Caco-2 intestinal epithelial cells. icIL-1Ra1 inhibited IL-1-induced IL-6 and IL-8 production. IL-1 activated all three mitogen-activated protein (MAP) kinase family members: p38 MAP kinase, extracellular-regulated kinases (ERK), and c-Jun amino-terminal kinases (JNK). Specific inhibitors of each MAP kinase pathway decreased IL-1-induced IL-6 and IL-8 production. Overexpression of icIL-1Ra1 inhibited p38 MAP kinase phosphorylation, but had no effect on ERK and JNK phosphorylation. In addition, icIL-1Ra1 inhibited nuclear translocation of NF-kappaB after IL-1 stimulation. In conclusion, these data indicate that icIL-1Ra1, acting in the cytoplasm of Caco-2 cells, decreased IL-1-induced IL-6 and IL-8 production. This intracellular anti-inflammatory activity of icIL-1Ra1 was mediated through inhibition of p38 MAP kinase and NF-kappaB signal transduction pathways.

Published
2003
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17. Decreased renal heme oxygenase-1 expression contributes to decreased renal function during cirrhosis.

Author

Miyazono M, Garat C, Morris KG Jr, and Carter EP

Subjects
Animals, Body Weight, Carbon Monoxide metabolism, Glomerular Filtration Rate, Heme Oxygenase (Decyclizing) metabolism, Heme Oxygenase-1, Immunohistochemistry, Male, Nitric Oxide metabolism, Nitric Oxide Synthase biosynthesis, Nitric Oxide Synthase metabolism, Nitric Oxide Synthase Type III, Rats, Rats, Sprague-Dawley, Renal Circulation, Heme Oxygenase (Decyclizing) biosynthesis, Kidney enzymology, Liver Cirrhosis metabolism
Abstract

Heme oxygenase (HO) is the rate-limiting enzyme in the degradation of heme, catalyzing the oxidative cleavage of heme molecules to biliverdin, carbon monoxide, and iron. The present study was designed to investigate the role of HO-1 in the pathogenesis of renal dysfunction during cirrhosis. Biliary cirrhosis was induced in rats by common bile duct ligation (CBDL). Animals were studied 2 and 5 wk after surgery. In kidney from CBDL rats, HO-1 protein expression increased slightly at 2 wk but was abolished at 5 wk. In addition, we confirmed histologically that HO-1 expression was suppressed in renal tubules and interlobular arterioles in 5-wk-old CBDL rats. Conversely, HO-1 expression in liver was strongly increased. Consistent with the development of cirrhosis and renal dysfunction mean arterial pressure (MAP), glomerular filtration rate (GFR), and renal blood flow (RBF) were decreased in CBDL rats compared with sham-operated controls. In sham rats, treatment with the selective HO inhibitor zinc protoporphyrin markedly decreased GFR and RBF to values similar to those measured in CBDL rats without decreasing MAP. In conclusion, decreased renal HO-1 expression contributes to deteriorated renal function and hemodynamics during cirrhosis. This finding provides a novel mechanism for the pathophysiology of renal dysfunction during cirrhosis.

Published
2002
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18. Induction of smooth muscle alpha-actin in vascular smooth muscle cells by arginine vasopressin is mediated by c-Jun amino-terminal kinases and p38 mitogen-activated protein kinase.

Author

Garat C, Van Putten V, Refaat ZA, Dessev C, Han SY, and Nemenoff RA

Subjects
Animals, Cells, Cultured, Enzyme Activation, JNK Mitogen-Activated Protein Kinases, Rats, Signal Transduction drug effects, p38 Mitogen-Activated Protein Kinases, Actins biosynthesis, Arginine Vasopressin pharmacology, Mitogen-Activated Protein Kinases metabolism, Muscle, Smooth, Vascular metabolism, Vasoconstrictor Agents pharmacology
Abstract

Exposure of vascular smooth muscle cells to arginine vasopressin (AVP) increases smooth muscle alpha-actin (SM-alpha-actin) expression through activation of the SM- alpha-actin promoter. The goal of this study was to determine the role of the mitogen-activated protein kinase (MAP kinase) family in regulation of SM-alpha-actin expression. AVP activated all three MAP kinase family members: ERKs, JNKs, and p38 MAP kinase. Inhibition of JNKs or p38 decreased AVP-stimulated SM-alpha-actin promoter activity, whereas inhibition of ERKs had no effect. A 150-base pair region of the promoter containing two CArG boxes was sufficient to mediate regulation by vasoconstrictors. Mutations in either CArG box decreased AVP-stimulated promoter activity. Electrophoretic mobility shift assays using oligonucleotides corresponding to either CArG box resulted in a complex of similar mobility whose intensity was increased by AVP. Antibodies against serum response factor (SRF) completely super-shifted this complex, indicating that SRF binds to both CArG boxes. Overexpression of SRF increased basal promoter activity, but activity was still stimulated by AVP. AVP stimulation rapidly increased SRF phosphorylation. These data indicate that both JNKs and p38 participate in regulation of SM- alpha-actin expression. SRF, which binds to two critical CArG boxes in the promoter, represents a potential target of these kinases.

Published
2000
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19. The integrin alpha v beta 6 binds and activates latent TGF beta 1: a mechanism for regulating pulmonary inflammation and fibrosis.

Author

Munger JS, Huang X, Kawakatsu H, Griffiths MJ, Dalton SL, Wu J, Pittet JF, Kaminski N, Garat C, Matthay MA, Rifkin DB, and Sheppard D

Subjects
3T3 Cells, Animals, Bleomycin pharmacology, CHO Cells, Cricetinae, Epithelial Cells physiology, Esophagus pathology, Humans, Integrins biosynthesis, Integrins physiology, Keratinocytes physiology, Ligands, Mice, Mice, Knockout, Protein Binding, Proteins metabolism, Pulmonary Fibrosis chemically induced, Pulmonary Fibrosis pathology, Pulmonary Fibrosis prevention & control, Transforming Growth Factor beta physiology, Transforming Growth Factor beta1, Tumor Cells, Cultured, Antigens, Neoplasm, Integrins metabolism, Peptide Fragments, Protein Precursors, Pulmonary Fibrosis metabolism, Transforming Growth Factor beta metabolism
Abstract

Transforming growth factor beta (TGF beta) family members are secreted in inactive complexes with a latency-associated peptide (LAP), a protein derived from the N-terminal region of the TGF beta gene product. Extracellular activation of these complexes is a critical but incompletely understood step in regulation of TGF beta function in vivo. We show that TGF beta 1 LAP is a ligand for the integrin alpha v beta 6 and that alpha v beta 6-expressing cells induce spatially restricted activation of TGF beta 1. This finding explains why mice lacking this integrin develop exaggerated inflammation and, as we show, are protected from pulmonary fibrosis. These data identify a novel mechanism for locally regulating TGF beta 1 function in vivo by regulating expression of the alpha v beta 6 integrin.

Published
1999
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20. New in situ mouse model to quantify alveolar epithelial fluid clearance.

Author

Garat C, Carter EP, and Matthay MA

Subjects
Adrenergic beta-Agonists pharmacology, Adrenergic beta-Antagonists pharmacology, Amiloride pharmacology, Animals, Atenolol pharmacology, Bronchoalveolar Lavage, Disease Models, Animal, Iodine Radioisotopes metabolism, Isoproterenol pharmacology, Male, Mice, Mice, Inbred Strains, Perfusion methods, Pulmonary Edema physiopathology, Serum Albumin metabolism, Sodium Channel Blockers, Terbutaline pharmacology, Extracellular Space physiology, Pulmonary Alveoli physiology
Abstract

Because the availability of transgenic mice makes it possible to examine the contribution of single genes to in vivo function, we developed a simple in situ mouse model that can be used to quantify isosmolar alveolar epithelial fluid clearance (AFC). Mice were killed, a tracheostomy was done, and then a test solution of a 5% isosmolar albumin solution with 0.1 micro Ci of 125I-labeled albumin was instilled via the trachea into the distal air spaces of both lungs. After instillation, the lungs were inflated to 7 cmH2O with 100% O2 and maintained at 37 degrees C by placing the animals under an infrared lamp. AFC was measured by the progressive increase in concentration of labeled and unlabeled protein over 1 h. The results indicated the following. 1) Basal, unstimulated AFC in mouse lungs was significantly faster than in ex vivo rat lungs (27 +/- 5% in in situ mice vs. 11 +/- 3% in ex vivo rat lungs; P < 0.05). 2) Comparison of equivalent doses (10(-4) M) of beta-adrenergic agonist (isoproterenol) and beta2-adrenergic agonists (terbutaline and salmeterol) indicated that stimulated clearance occurred only in presence of isoproterenol. 3) Because atenolol, a specific beta1-antagonist, abolished the effect of isoproterenol, the beta-adrenergic stimulation appears to be mediated by beta1-receptors. The rate of AFC in nonperfused mouse lungs was significantly faster than in prior studies of nonperfused lungs in rats and sheep. Interestingly, the stimulated clearance rate in mice was similar to the fast rates of AFC that we recently reported in patients recovering from hydrostatic pulmonary edema. This in situ model is a unique experimental preparation that can be readily used to quantify isosmolar epithelial fluid clearance in mice.

Published
1998
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21. Effects of inhaled nitric oxide or inhibition of endogenous nitric oxide formation on hyperoxic lung injury.

Author

Garat C, Jayr C, Eddahibi S, Laffon M, Meignan M, and Adnot S

Subjects
Administration, Inhalation, Animals, Enzyme Inhibitors pharmacology, Guanidines pharmacology, Hyperoxia metabolism, Hyperoxia mortality, Lipid Peroxides metabolism, Lung drug effects, Lung metabolism, Male, NG-Nitroarginine Methyl Ester pharmacology, Nitric Oxide therapeutic use, Oxygen pharmacology, Rats, Rats, Wistar, Survival Analysis, Time Factors, Hyperoxia pathology, Lung pathology, Nitric Oxide administration & dosage, Nitric Oxide antagonists & inhibitors
Abstract

Nitric oxide (NO) may either protect against or contribute to oxidant-induced lung injury. In this study, we sought to determine whether either inhaled NO in concentration of 10 and 100 parts per million (ppm) or inhibition of endogenous NO formation with L-NG nitroarginine methyl ester (L-NAME) or aminoguanidine alters the extent of lung injury in rats breathing 100% O2. Lung thiobarbituric acid reactive substances (TBARS), wet to dry lung weight ratio (Q(W)/Q(D)), vascular and epithelial permeability (assessed by simultaneous intravenous administration of 131I-labeled albumin and intraalveolar instillation of 125I-labeled albumin), alveolar liquid clearance (evaluated based on the increase in alveolar protein concentration), and lung liquid clearance (gravimetric method) were determined after 40 h exposure to either 100% or 21% O2. Exposure to hyperoxia caused increases in lung TBARS from 10.5 +/- 0.7 to 13.7 +/- 1.5 micromol/mg protein (p < 0.05); in blood hemoglobin concentration (Hb) from 14 +/- 1 g/dl to 17 +/- 1 g/dl (p < 0.05); in the Q(W)/Q(D) ratio from 4.02 +/- 0.3 to 5.31 +/- 0.5 (p < 0.05); and in alveolar-arterial oxygen tension difference from 124 +/- 14 mm Hg to 241 +/- 61 mm Hg (p < 0.05); as well as a decrease in blood pressure, from 131 +/- 15 mm Hg to 72 +/- 26 mm Hg (p < 0.05). Hyperoxia also increased vascular albumin leakage and moderately altered epithelial barrier permeability to protein. Inhalation of 10 ppm NO prevented the increases in TBARS and Q(W)/Q(D), had no effect on the alveolar barrier impermeability to protein, and improved alveolar liquid clearance. Inhalation of 100 ppm NO did not alter the increases in TBARS and Q(W)/Q(D) but increased vascular permeability to protein. Survival of rats exposed to hyperoxia was not improved by inhaled NO. Treatment with L-NAME or aminoguanidine reduced survival. L-NAME, but not aminoguanidine, increased lung TBARs. These results suggest that, depending on its concentration, inhaled NO can either reduce or increase the early consequences of hyperoxic lung injury. Treatment with L-NAME, and to a lesser extent aminoguanidine, worsened hyperoxic lung injury, indicating a protective effect of endogenous NO.

Published
1997
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22. Alveolar epithelial fluid clearance mechanisms are intact after moderate hyperoxic lung injury in rats.

Author

Garat C, Meignan M, Matthay MA, Luo DF, and Jayr C

Subjects
Adrenergic beta-Agonists pharmacology, Albumins, Animals, Blood Pressure, Blood-Air Barrier drug effects, Disease Models, Animal, Epithelium drug effects, Epithelium metabolism, Iodine Radioisotopes, Lung metabolism, Male, Organ Size, Oxygen adverse effects, Oxygen blood, Pulmonary Alveoli drug effects, Pulmonary Edema etiology, Pulmonary Edema metabolism, Radiopharmaceuticals, Rats, Rats, Wistar, Respiratory Distress Syndrome drug therapy, Respiratory Distress Syndrome metabolism, Terbutaline pharmacology, Ventilation-Perfusion Ratio, Extravascular Lung Water metabolism, Hyperoxia metabolism, Lung Diseases metabolism, Pulmonary Alveoli metabolism
Abstract

The capacity of the alveolar epithelial barrier to remove excess alveolar fluid from the airspaces of the lung was studied in an experimental model of moderate hyperoxic lung injury. Rats were exposed to 100% oxygen for 40 h in an exposure chamber and compared with control animals exposed to room air. Extravascular lung water was calculated gravimetrically. Alveolar and lung liquid clearance were studied over 1 h by instillation of a 5% albumin solution with 1.5 microCi of 125I-labeled albumin (6 mL/kg into both lungs). The concentration of both the unlabeled and labeled albumin was used to calculate alveolar liquid clearance. Hyperoxic rats developed pulmonary edema, with a 33% increase in extravascular lung water to 5.3 +/- 0.1 g of water per gram of dry lung, compared with 4.0 +/- 0.2 g of water per gram of dry lung in control rats (p < 0.05). This degree of edema was associated with a significant increase in the alveolar-arterial oxygen difference (241 +/- 61 vs 124 +/- 14 mm Hg in control animals exposed to room air, p < 0.05). Despite this moderate degree of lung injury, alveolar fluid clearance was normal (30 +/- 3%) compared with control rats (33 +/- 6%). Furthermore, the hyperoxic injured rats responded normally to an exogenous beta-adrenergic agonist (terbutaline, 10(-4) mol/L) with a 67% increase in the rate of alveolar liquid clearance (50 +/- 5%). Thus, in the setting of moderate hyperoxic lung injury, the alveolar epithelial barrier is still capable of removing fluid at a normal rate and responding to beta-adrenergic agonist treatment. These experimental results have potential clinical implications for patients with acute lung injury.

Published
1997
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23. Protein tyrosine phosphatases mediate cell readhesion in alveolar epithelial cells mechanically separated from in vitro matrix.

Author

Oliver BL, Garat C, Pytela R, and Matthay MA

Subjects
Animals, Arsenicals pharmacology, Calcium-Calmodulin-Dependent Protein Kinases metabolism, Cell Adhesion drug effects, Cell Adhesion Molecules metabolism, Cell Separation methods, Cells, Cultured, Cytoskeletal Proteins metabolism, Enzyme Inhibitors pharmacology, Epithelial Cells, Epithelium enzymology, Extracellular Matrix, Focal Adhesion Kinase 1, Focal Adhesion Protein-Tyrosine Kinases, Genistein, Isoflavones pharmacology, Male, Mitogen-Activated Protein Kinase 1, Paxillin, Phosphoproteins metabolism, Phosphorylation, Protein Tyrosine Phosphatases antagonists & inhibitors, Protein-Tyrosine Kinases antagonists & inhibitors, Protein-Tyrosine Kinases metabolism, Proto-Oncogene Proteins pp60(c-src) metabolism, Rats, Rats, Sprague-Dawley, Cell Adhesion physiology, Protein Tyrosine Phosphatases metabolism, Pulmonary Alveoli cytology, Pulmonary Alveoli enzymology
Abstract

Alveolar epithelial type II cells are the progenitor cells for restoring the alveolar epithelial barrier after acute lung injury. During repair of lung injury, the alveolar epithelial type II cells reepithelialize denuded air spaces, a process that involves breaking and reforming cell adhesions. A novel technique of mechanical separation of cultured alveolar epithelial cells from in vitro matrix was used to examine the intracellular signals that result when alveolar epithelial cell adhesions are broken. The results show that the tyrosine phosphorylation levels of focal adhesion kinase, paxillin, and pp60(src) decreased immediately after mechanical separation of the cells. Levels returned to nearly normal by 24 h after mechanical separation. Paxillin and pp60(scr) coprecipitated with focal adhesion kinase regardless of their phosphorylation state. Interestingly, the tyrosine phosphorylation level of the mitogen-activated protein kinase, p42(erk2), increased 15 min after mechanical separation. Preincubation of cell monolayers with phenylarsine oxide, a protein tyrosine phosphatase inhibitor, blocked the decrease in tyrosine phosphorylation levels of focal adhesion kinase, paxillin and pp60(src). Phenylarsine oxide incubation also prevented readhesion of mechanically separated cells at 24 h, but genistein, a tyrosine kinase inhibitor, had no effect. We conclude that protein tyrosine phosphatases are activated immediately after cultured alveolar epithelial cells are mechanically separated from in vitro matrix, and their activation is required for alveolar epithelial cell readhesion.

Published
1997
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24. Acute bacterial pneumonia in rats increases alveolar epithelial fluid clearance by a tumor necrosis factor-alpha-dependent mechanism.

Author

Rezaiguia S, Garat C, Delclaux C, Meignan M, Fleury J, Legrand P, Matthay MA, and Jayr C

Subjects
Adrenergic beta-Antagonists pharmacology, Amiloride pharmacology, Animals, Antibodies pharmacology, Bronchoalveolar Lavage Fluid cytology, Epithelium metabolism, Extravascular Lung Water drug effects, Male, Metabolic Clearance Rate, Permeability, Pneumonia, Bacterial mortality, Pneumonia, Bacterial pathology, Propranolol pharmacology, Proteins metabolism, Pseudomonas Infections mortality, Pseudomonas Infections pathology, Rats, Rats, Sprague-Dawley, Sodium-Potassium-Exchanging ATPase antagonists & inhibitors, Tumor Necrosis Factor-alpha immunology, Extravascular Lung Water metabolism, Pneumonia, Bacterial metabolism, Pseudomonas Infections metabolism, Pulmonary Alveoli metabolism, Tumor Necrosis Factor-alpha metabolism
Abstract

To study the rate and regulation of alveolar fluid clearance in acute pneumonia, we created a model of Pseudomonas aeruginosa pneumonia in rats. To measure alveolar liquid and protein clearance, we instilled into the airspaces a 5% bovine albumin solution with 1.5 microCi of 125I-human albumin, 24 h after intratracheal instillation of bacteria. The concentration of unlabeled and labeled protein in the distal airspaces over 1 h was used as an index of net alveolar fluid clearance. Since there was histologic evidence of alveolar epithelial injury, several methods were used to measure alveolar fluid clearance, including the use of experiments in rats with blood flow and the use of experiments in rats without blood flow, so that movement across the epithelial barrier would be minimized in the latter group. The results with each method were identical. We found that P. aeruginosa pneumonia increased alveolar liquid clearance over 1 h by 48% in studies with blood flow, and by 43% in rats without blood flow, compared with respective controls (P < 0.05). In both studies, this increase was inhibited with amiloride. However, propranolol had no inhibitory effect, thus ruling out a catecholamine-dependent mechanism to explain the increase in alveolar fluid clearance. An antitumor necrosis factor-alpha neutralizing antibody, instilled into the lung 5 min before bacteria, prevented the increase in alveolar liquid clearance in rats with pneumonia (P < 0.05). Also, TNFalpha (5 microg) instilled in normal rats increased alveolar liquid clearance by 43% over 1 h compared with control rats (P < 0.05). In normal rats instilled with TNFalpha, propranolol had no inhibitory effect. In conclusion, gram-negative pneumonia markedly upregulates net alveolar epithelial fluid clearance, in part by a TNFalpha-dependent mechanism. This finding provides a novel mechanism for the upregulation of alveolar epithelial sodium and fluid transport from the distal airspaces of the lung.

Published
1997
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25. Soluble and insoluble fibronectin increases alveolar epithelial wound healing in vitro.

Author

Garat C, Kheradmand F, Albertine KH, Folkesson HG, and Matthay MA

Subjects
Animals, Cell Division, Cell Movement drug effects, Cells, Cultured, Epithelial Cells, Epithelium drug effects, Epithelium physiology, Extracellular Matrix Proteins pharmacology, Extracellular Matrix Proteins physiology, Fluorescent Antibody Technique, Kinetics, Microscopy, Video, Models, Biological, Pulmonary Alveoli cytology, Pulmonary Alveoli drug effects, Rats, Rats, Sprague-Dawley, Time Factors, Vinculin analysis, Wound Healing drug effects, Fibronectins pharmacology, Pulmonary Alveoli physiology, Wound Healing physiology
Abstract

Adhesive interactions between cells and extracellular matrix proteins are important in cell attachment, migration, and proliferation. The present work defines the role of fibronectin (soluble and insoluble) compared with type I and type IV collagen on in vitro alveolar epithelial wound healing. Repeated video microscopy experiments demonstrated that the half-time of wound closure was decreased in the presence of soluble fibronectin (6.6 +/- 2.1 vs. 17.4 +/- 0.8 h in serum-free medium, P < 0.05). Video microscopy, electron microscopy, and vinculin distribution demonstrated the contribution of two main events during the repair process: the migration of epithelial cell sheets and the spreading of the cells. During the wound healing, the internuclear distance between two adjacent cells at the migrating edge of the wound was significantly increased 10 h after wounding in the presence of soluble fibronectin (67 +/- 3.0 vs. 45 +/- 1.5 microns in serum-free medium, P < 0.05), indicating that cell spreading is involved as part of the mechanism for wound closure. Compared with type I and type IV collagen, insoluble fibronectin was the most potent stimulus for alveolar type II cell motility and wound healing in the absence of other serum factors. These results demonstrate that alveolar epithelial wound healing can be modulated in vitro by the composition of the extracellular matrix, an effect that may be mediated by changes in cell shape.

Published
1996
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26. Alveolar endotoxin increases alveolar liquid clearance in rats.

Author

Garat C, Rezaiguia S, Meignan M, D'Ortho MP, Harf A, Matthay MA, and Jayr C

Subjects
Amiloride pharmacology, Animals, Hemodynamics, Lipopolysaccharides pharmacology, Male, Permeability drug effects, Rats, Rats, Sprague-Dawley, Time Factors, Endotoxins pharmacology, Lung drug effects
Abstract

Under some pathological conditions, ion transport across alveolar epithelial cells is downregulated, whereas under other pathological conditions, it may be upregulated. Because endotoxin is a biologically relevant pathological stimulus, we investigated the effect of endotoxin on alveolar epithelial liquid clearance in vivo. Escherichia coli endotoxin (220 micrograms/kg) was instilled into the lungs via the trachea of rats. Then, 24 or 40 h after endotoxin instillation, alveolar and lung liquid clearances were studied over 1 h by instillation of a 5% albumin solution with 1.5 microCi of 125I-labeled albumin (6 ml/kg into both lungs). Alveolar liquid clearance was significantly greater at 24 h (36 +/- 5%) and 40 h (38 +/- 7%) after endotoxin exposure than in saline-instilled controls (27 +/- 6%). Although there was an influx of neutrophils into the air space, there was no increase in lung epithelial permeability to protein at 24 or 40 h. Amiloride (2 x 10(-3) M), a sodium channel inhibitor, significantly reduced alveolar liquid clearance in the rats exposed to endotoxin. However, the increase in alveolar liquid clearance was not inhibited when propranolol (2 x 10(-5) M) was added to the 5% albumin solution. Thus exposure to alveolar endotoxin upregulates net alveolar fluid clearance in vivo for up to 40 h, a potentially important mechanism for accelerating alveolar fluid clearance under some pathological conditions. The increase in alveolar liquid clearance 24 and 40 h after instillation of endotoxin into the air spaces is mediated by an increased uptake of sodium through amiloride-sensitive sodium channels.

Published
1995
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27. Alveolar liquid and protein clearance in anesthetized ventilated rats.

Author

Jayr C, Garat C, Meignan M, Pittet JF, Zelter M, and Matthay MA

Subjects
Adrenergic beta-Agonists pharmacology, Adrenergic beta-Antagonists pharmacology, Airway Resistance drug effects, Amiloride pharmacology, Animals, Blood Gas Analysis, Extravascular Lung Water drug effects, Hemodynamics drug effects, Iodine Radioisotopes, Male, Ouabain pharmacology, Pulmonary Alveoli drug effects, Rats, Rats, Wistar, Sodium-Potassium-Exchanging ATPase antagonists & inhibitors, Anesthesia, Body Fluids physiology, Proteins metabolism, Pulmonary Alveoli physiology, Respiration, Artificial
Abstract

Alveolar and lung liquid clearances were studied over 1, 4, and 6 h in intact anesthetized ventilated rats by instillation of 5% albumin solution with 1.5 microCi of 125I-labeled albumin (3 ml/kg into 1 lung or 6 ml/kg into both lungs). Alveolar protein clearance as measured by residual 125I-albumin in the lung over 6 h was similar to the slow rates measured in other species. Alveolar liquid clearance was estimated by the concentration of albumin in the air spaces. After 1 h, this concentration was 7.8 +/- 0.7 g/dl, which was significantly greater than the initial protein concentration of 5.3 +/- 0.2 g/dl (P < 0.05). Amiloride (10(-3) M) inhibited 45% of the basal alveolar liquid clearance, and ouabain (10(-3) M), instilled and intravenously infused (0.004 mg), inhibited 30% of the clearance. beta-Adrenergic agonist instillation increased alveolar liquid clearance to the fastest 1-h rate (48 +/- 3% of instilled volume) that we observed in any intact species. The removal of the instilled fluid from the lung (expressed as lung liquid clearance; 0.96 +/- 0.3 ml/h) was twice as fast as the rate of alveolar and lung liquid clearance reported in the isolated or in situ rat lung models. The rate of alveolar and lung liquid clearance in these intact rats was significantly faster than those in prior studies in dogs and sheep and was similar to the rates in rabbits.

Published
1994
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