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2007 Annual Meeting
"Lung Injury and Repair"
June 6-9, 2007
David D.H. Riches, Ph.D. , Chair
Gregory P. Cosgrove, M.D., Co-Chair
Stephen K. Frankel, M.D., Co-Chair
Given Institute - www.giveninstitute.org
Aspen, Colorado
Tuesday, June 5, 2007 -- Evening
5:00-7:00 PM
Evening Registration -- Wine and Cheese Reception Given Institute
Wednesday, June 6, 2007 -- Morning
8:00-8:15 AM
Introduction/Welcome
David W.H. Riches, Ph.D., Chair
8:15-8:30 AM
Perspective
Thomas L. Petty, M.D.
Mechanisms of Lung Injury - Moderators:
David Riches, Ph.D. and Thomas Petty, M.D.
8:30-9:15 AM
STATE OF THE ART
"Injury to the Alveolar Epithelium:
The Intersection Between Mechanical and Biologic Mechanisms"
Thomas R. Martin, M.D.
Veterans Affairs Puget Sound Health Care System
9:15-9:30 AM
Discussion
9:30-9:45 AM
INTEGRINS avß3 and avß5 RECIPROCALLY REGULATE PULMONARY ENDOTHELIAL BARRIER FUNCTION THROUGH DIFFERENTIAL EFFECTS ON THE ACTIN CYTOSKELETON.
G. Su1,2*, N. Wu1, A. Atakilit1, J.K. Kim1, D. Sheppard1,2, 1Lung Biology Center, 2Division of Pulmonary and Critical Care Medicine, UCSF, San Francisco, CA.
9:45-10:00 AM
MODULATION OF INTRA-ALVEOLAR FIBRIN DEPOSITION BY THE ALVEOLAR EPITHELIUM IN ACUTE LUNG INJURY: CLINICAL AND EXPERIMENTAL EVIDENCE.
L.B. Ware*, J.A. Bastarache, L. Wang, M.A. Matthay, Pulmonary and Critical Care Medicine, Vanderbilt University and Cardiovascular Research Institute, University of San Francisco, San Francisco, CA.
10:00-10:30 AM
Coffee Break
10:30-11:15 AM
STATE OF THE ART
"Treatment of Acute Lung Injury:
Clinical and Experimental Studies"
Michael A. Matthay, M.D.
University of California, San Francisco
11:15-11:30 AM
Discussion
11:30-11:45 AM
PAR2 INTERRUPTS E-CADERIN ADHESION AND DECREASES THE TRANSEPTHELIAL RESISTANCE OF EPITHELIA BY PHOSPHOR- LATING TYROSINES 489 AND 654 OF BETA-CATENIN.
M.C. Winter, S. Shasby, J. Lilien, J. Balsamo, D.M. Shasby*, University of Iowa College of Medicine, Iowa City, IA.
11:45-12:00
DISSECTING THE LUNG’S TRANSCRIPTIONAL PROGRAM DURING NON-INJURIOUS MECHANICAL VENTILATION.
S.A. Gharib1, W.C. Liles2, W.A. Altemeier1*, 1Department of Medicine, University of Washington School of Medicine, Seattle, WA and 2Department of Medicine, University of Toronto, Toronto, Ontario, CANADA.
12:00-1:30 PM
Lunch
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Wednesday, June 6, 2007 -- Afternoon
Resolution of Lung Injury - Moderators:
Ivor Douglas, M.D. and Robert Winn, M.D.
1:30-2:15 PM
PARKER B. FRANCIS LECTURESHIP
"MECHANISMS OF LUNG REPAIR:
INSIGHTS FROM LUNG DEVELOPMENT"
Brigid L.M. Hogan, Ph.D.
Professor and Chair
Department of Cell Biology
Duke University Medical Center
Durham, North Carolina
2:15-2:30 PM
Discussion
2:30-2:45 PM
CD4+CD25+T-REGULATORY CELLS ARE REQUIRED FOR RESOLUTION OF LPS-INDUCED LUNG INJURY.
F.R. D’Alessio*, K. Tsushima, N.R. Aggarwal, E.E. West, J.F. McDyer, R.M. Tuder, L.S. King, Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.
2:45-3:00 PM
EPITHELIAL PROGENITOR CELLS IN LUNG DEVELOPMENT AND REPAIR.
E.M. Rawlins*, B.L.M. Hogan, Department of Biology, Duke University, Durham, NC.
3:00-3:30 PM
Break
3:30-4:15 PM
STATE OF THE ART
"What Differentiates Normal Lung Repair and Fibrosis? Inflammation, Resolution of Repair and Fibrosis"
Robert M. Strieter, M.D.
University of Virginia Health System
4:15-4:30 PM
Discussion
4:30-4:45 PM
MECHANICAL STRAIN INDUCES CYTOKINE RELEASE VIA RHO/RHO KINASE.
J.C. Lavelle, K.C. Malcolm, A.A. VanLinden, G.S. Worthen, 1University of Colorado Denver, Denver, CO and National Jewish Medical and Research Center, Denver, CO.
4:45-5:00 PM
EVIDENCE AND STRUCTURAL MECHANISM FOR LATE LUNG ALVEOLARIZATION.
J.C. Schittny, S.I. Mund, M. Stampanoni, Institute of Anatomy, University of Bern, Switzerland and Swiss Light Source, Paul-Scherrer-Institut, Villigen, SWITZERLAND.
5:00 PM
POSTER VIEWING --- SOCIAL HOUR
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Thursday, June 7, 2007 -- Morning
Epithelium, Mesenchyme and Matrix - Moderators:
Marc Moss, M.D. and Marvin Schwarz, M.D.
8:00-8:45 AM
THOMAS A. NEFF LECTURE
"MECHANISMS OF MATRIX DEPOSITION
IN PULMONARY FIBROSIS"
Professor Geoffrey J. Laurent, Ph.D.
Director, The Centre for Respiratory Research
University College London
London,
United Kingdom
8:45-9:00 AM
Discussion
9:00-9:15 AM
PATHOGENIC AND PROTECTIVE T CELL POPULATIONS IN THE DEVELOPMENT OF PULMONARY FIBROSIS.
P.L. Simonian*, C.L. Roark†, B.E. Palmer*, W.K. Born†, R.L. O’Brien†, A.P. Fontenot*†, *University of Colorado Denver, Denver, CO and †National Jewish Medical and Research Center, Denver, CO.
9:15-9:30 AM
MMP-13 Protects Against Fibrosis During Recovery After Acute Hyperoxic Lung Injury. Sen, A.1*, Foronjy, R.2, and D’Armiento, J.2 Department of Pediatrics1 and Department of Medicine2, College of Physicians and Surgeons of Columbia University, New York, NY
9:30-10:00 AM
Coffee Break
10:00-10:45 AM
STATE OF THE ART
"Epithelial Cell/Matrix Interactions in the
Mammary Gland and Lung"
Derek C. Radisky, Ph.D.
Mayo Clinic College of Medicine Jacksonville
10:45-11:00 AM
Discussion
11:00-11:15 AM
HISTONE DEACETYLASE 6 REGULATES TGF-ß1-MEDIATED EPITHELIAL-MESENCHYMAL TRANSITION.
B. Shan, T.P. Yao, Y. Zhuo, H.T. Nguyen, R.C. Klingsberg, J.A. Lasky*, Department of Medicine, Tulane University Health Sciences Center, New Orleans, LA.
11:15-11:30 AM
MMP-12 MEDIATES FIBROSIS AFTER LUNG INJURY IN MICE.
G. Matute-Bello (1,3)(*), M.M. Wurfel (1), J.S. Lee (2), C.W. Frevert (1,3), S. Shapiro (2), T.R. Martin (1,3), from the (1) Division of Pulmonary and Critical Care Medicine, University of Washington; (2) Division of Pulmonary, Allergy and Critical Care, University of Pittsburgh; and (3) the VA Puget Sound HealthCare System.
12:30 PM
Picnic at East Maroon Bells Portal
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Friday, June 8, 2007 -- Morning
Stem Cells in Alveolar Repair? - Moderators:
William Janssen, M.D. and Norbert Voelkel, M.D.
8:00-8:45 AM
STATE OF THE ART
"Bone Marrow-Derived Stem Cells
and Alveolar Repair"
Diane S. Krause, M.D., Ph.D.
Yale University School of Medicine
8:45-9:00 AM
Discussion
9:00-9:15 AM
SYNERGISTIC EFFECTS OF MESENCHYMAL STEM CELLS AND ANGIOPOIETIN-1 IN THE PREVENTION OF LPS-INDUCED ACUTE LUNG INJURY.
S.H.J. Mei*, S.D. McCarter, Y. Deng, C.H. Parker, W. C. Liles, D.J. Stewart, St. Michael’s Hospital, Toronto, Ontario, CANADA.
9:15-9:30 AM
INTERLEUKIN 1 RECEPTOR ANTAGONIST MEDIATES THE ANTI-INFLAMMATORY EFFECTS OF BONE MARROW DERIVED MESENCHYMAL STEM CELLS DURING LUNG INJURY.
L.A. Ortiz*, C.L. Fattman, G. Torres, M. Du Treil, D.G. Phinney, Department of Environmental and Occupational Health, University of Pittsburgh Graduate School of Public Health, Pittsburgh, PA, and Center for Gene Therapy, Tulane Health Science Center, New Orleans, LA.
9:30-10:00 AM
Coffee Break
10:00-10:45 AM
STATE OF THE ART
"Region-Specific Stem Cells in Lung Injury and Repair"
Barry R. Stripp, Ph.D.
University of Pittsburgh
10:45-11:00 AM
Discussion
11:00-11:15 AM
CORD BLOOD-DERIVED MESENCHYMAL STEM CELLS CAN PARTICIPATE IN LUNG EPITHELIAL REMODELING IN VIVO.
V. Sueblinvong, P.L. Eisenhauer, I.M. Bernstein, J.L. Spees, D.J. Weiss*, The University of Vermont, Burlington, VT.
11:15-11:30 AM
ENDOGENOUS LUNG STEM CELLS INCREASED AFTER LUNG INJURY.
H. Kubo*, A.E. Hegab, M. He, M. Yamada, K. Ishizawa, Tohoku University, Sendai, JAPAN.
11:30-1:30 PM
Lunch
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Friday, June 8, 2007 -- Afternoon
Mechanisms of Fibrosis - Moderators:
Arnold Brody, Ph.D. and Gregory Cosgrove, M.D.
1:30-2:15 PM
STATE OF THE ART
"Biology of Fibroblasts, Myofibroblasts and Fibrocytes"
Sem H. Phan, Ph.D.,M.D.
University of Michigan Medical School
2:15-2:30 PM
Discussion
2:30-2:45 PM
THE LYSOPHOSPHATIDIC ACID RECEPTOR LPA1 LINKS PULMONARY FIBROSIS TO LUNG INJURY BY MEDIATING FIBROBLAST RECRUITMENT AND VASCULAR LEAK.
A.M. Tager1,2*, P. LaCamera1,2, B.S. Shea1,2, G.K. Campanella1, B.A. Karimi-Shah1,2, N.D. Kim1, Z. Zhao3, V. Polosukhin4, W.K. Hart1, E.C. Poorvu1, S.D. Bercury1, Y. Xu3, T.S. Blackwell4, J. Chun5, A.D. Luster1, 1Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, and 2Pulmonary and Critical Care Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA; 3Department of Obstetrics and Gynecology, Indiana University School of Medicine, Indianapolis, IN; 4Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, TN; and 5Department of Molecular Biology, Helen L. Dorris Institute for Neurological and Psychiatric Diseases, The Scripps Research Institute, La Jolla, CA.
2:45-3:00 PM
EPIGENETIC REGULATION CONTRIBUTES TO THY-1 GENE SILENCING AND TO THE INDUCTION OF MYOFIBROBLAST PHENOTYPE.
Y. Sanders, J. Cisneros, G. Nuovo, M. Selman, J. Hagood*, University of Alabama, Department of Pediatrics, Birmingham, AL; Instituto Nacional de Enfermedades Respiratorias, Mexico City, MEXICO; Ohio State University, Department of Pathology, Columbus, OH.
3:00-3:30 PM
Break
3:30-4:15 PM
ROGER S. MITCHELL LECTURE
"INJURY, FIBROSIS AND NOVEL THERAPIES:
INSIGHTS FROM THE LIVER"
David A. Brenner, M.D.
Vice Chancellor for Health Sciences
Dean, University of California San Diego
School of Medicine
La Jolla, California
4:15-4:30 PM
Discussion
4:30-4:45 PM
FRNK INHIBITS TGF-ß1-INDUCED MYOFIBROBLAST DIFFER-ENTIATION THROUGH BOTH FAK-DEPENDENT AND FAK-INDEPENDENT PATHWAYS.
Q. Ding1*, C.L. Gladson1, H. Wu1, S.K. Hanks2, J.T. Parsons3, M.A. Olman1, 1University of Alabama at Birmingham, Birmingham, AL, 2Vanderbilt University, Nashville, TN and 3University of Virginia, Charlottesville, Virginia.
4:45-5:00 PM
LUNG FIBROBLAST BEHAVIOR IS TUNED BY SUBSTRATE STIFFNESS.
J.D. Mih, D.J. Tschumperlin*, Harvard School of Public Health, Boston, MA.
5:00 PM
POSTER VIEWING --- SOCIAL HOUR
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Saturday, June 9, 2007
Genetics of Lung Injury, Repair and Fibrosis -
Moderators: Mark Geraci, M.D. and Stephen Frankel, M.D.
8:00-8:45 AM
GILES F. FILLEY LECTURE
"GENETIC ANALYSES IN FAMILIAL
PULMONARY FIBROSIS"
David A. Schwartz, M.D.
Director
National Institute of
Environmental Health Sciences
and
National Toxicology Program
Research Triangle Park, North Carolina
8:45-9:00 AM
Discussion
9:00-9:15 AM
TELOMERASE MUTATIONS IN FAMILIES WITH IDIOPATHIC PULMONARY FIBROSIS.
M.Y. Armanios1*, J.J-L. Chen2,3, J.D. Cogan4, J.K. Alder1, R.G. Ingersoll5, C. Markin6, W.E. Lawson6, M. Xie2, I. Vulto7, J.A. Phillips III4, P.M. Lansdorp7,8, C.W. Greider1,9, J.E. Loyd6, Department of Oncology1, Institute of Genetic Medicine5, and Department of Molecular Biology and Genetics9, Johns Hopkins University School of Medicine, Department of Chemistry & Biochemistry2, and School of Life Sciences Arizona State University3, Departments of Pediatrics4 and Medicine6, Vanderbilt University School of Medicine, Terry Fox Laboratory7, BC Cancer Agency and Department of Medicine8, University of British Columbia, CANADA.
9:15-9:30 AM
GENETIC VARIATAION IN THE FAS GENE AND ASSOCIATIONS WITH OUTCOMES IN ACUTE LUNG INJURY.
B.J. Glavan*, T.D. Holden, C.H. Goss, R.A. Black, T.R. Martin, M.M. Wurfel, Section of Pulmonary/Critical Care Medicine, Harborview Medical Center; Division of Pulmonary/Critical Care Medicine, University of Washington; Medical Research Service, VA Puget Sound Medical Center, Seattle, WA.
9:30-10:00 AM
Coffee Break
10:00-10:45 AM
STATE OF THE ART
"Genetics of Acute Lung Injury"
Joe G.N."Skip" Garcia, M.D.
University of Chicago Pritzker School of Medicine
10:45-11:00 AM
Discussion
11:00-11:15 AM
A COMMON TLR1 POLYMORPHISM MARKING A HYPER-RESPONSIVE FORM OF TLR1 IS ASSOCIATED WITH INCREATED MORTALITY AND ORGAN DYSFUNCTION IN SEPSIS.
M.M. Wurfel1, A.C. Gordon2, T.D. Holden1, G.P. Jarvik4, D.A. Nickerson6, K.R. Walley2, J.A. Russell2, T.R. Martin1,3, 1Divisions of Pulmonary and Critical Care Medicine and 4Medical Genetics, and the 5Departments of Immunology and 6Genome Sciences, University of Washington, Seattle, WA. 3Medical Research Service of the VA Puget Sound Medical Center. 2The James Hogg iCAPTURE Center for Cardiovascular and Pulmonary Research, St. Paul’s Hospital and the University of British Columbia, Vancouver, British Columbia, CANADA.
11:15-11:30 AM
THE SURFACTANT PROTEIN B +1580 POLYMORPHISM AND LUNG INJURY IN CHILDREN WITH COMMUNITY-ACQUIRED PNEUMONIA.
P.O’Cain1*, P. Patwari2, M. Smith3, M. Dahmer3, M. Quasney3, Department of Pediatrics, University of Tennessee Health Science Center1, Memphis, TN; Northwestern University2, Evanston, IL, and Children’s Research Institute, Medical College of Wisconsin3, Milwaukee, WI.
11:30-12:30 PM
CONFERENCE SUMMARY
Paul W. Noble, M.D.
Professor of Medicine
Director, Division of Pulmonary, Allergy
and Critical Care Medicine
Duke University School of Medicine
Durham, North Carolina, USA
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POSTER VIEWING -- SOCIAL HOUR
Wednesday, June 6, 2007
5:00 PM -- POSTERS
MECHANISM OF EPITHELIAL INJURY TRIGGERED BY ANTI-IL-8 AUTOANTIBODY:IL-8 IMMUNE COMPLEXES.
D. Stankowska, R. Fudala, A. Kurdowska*, University of Texas Health Center, Tyler, TX.
A ROLE FOR LIVER X RECEPTOR IN PULMONARY INNATE IMMUNITY.
M.B. Fessler1*, S. Jeyaseelan2, B. Williams2, K. Smoak1, K.R. Poch2, J.A. Nick2, G.S. Worthen2, 1Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC; 2Department of Medicine, National Jewish Medical and Research Center, Denver, CO.
PROSTAGLANDIN E2 MEDIATES IL-1ß-RELATED FIBROBLAST MITOGENIC EFFECTS IN ACUTE LUNG INJURY THROUGH DIFFERENTIAL UTILIZATION OF PROSTANOID RECEPTORS.
HK.E. White, HQ. Ding, IB.B. Moore, IM. Peters-Golden, §L.B. Ware, ¶M.A. Matthay, HM.A. Olman*, HUniversity of Alabama, Birmingham, AL, IUniversity of Michigan, Ann Arbor, MI, §Vanderbilt University, Nashville, TN, and ¶University of California at San Francisco, San Francisco, CA.
NRF2-DEPENDENT GLUTATHIONE REGULATED TRANSCRIPTIONAL PROGRAM CONTROLS LUNG TYPE II CELL PROLIERATION AND PROTECTION AGAINST OXIDATIVE STRESS.
N.M. Reddy, S.R. Kleeberger1, M. Yamamoto2, S.P. Reddy*, Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, 1NIEHS Research Triangle Park, NC; 2Tohoku University, Sendai, JAPAN.
SURFACTANT PHOSPHOLIPIDS SUPPRESS THE INFLAMMATION OF BRONCHIAL EPITHELIUM INDUCED BY TLR2 AND TLR3 LIGANDS.
M. Nakamura*, H.W. Chu, E.D. Chan, D.R. Voelker, National Jewish Medical and Research Center, Denver, CO.
siRNA KNOCKDOWN OF NAD(P)H:QUINONE OXIDOREDUCTASE 1 LEADS TO DECREASED PRODUCTION OF REACTIVE OXYGEN SPECIES AFTER IN VITRO EXPOSURE TO HYPEROXIA.
A.J. Reddy1,2*, S.R. Kleeberger1, 1Duke University Center, Durham, NC, 2National Institute of Environmental Health Science, Durham, NC.
MOLECULAR IMAGING OF INTLAMMATION AND GENE EXPRESSION TO STUDY LUNG INJURY AND REPAIR.
D.P. Schuster*, Washington, University School of Medicine, St. Louis, MO.
EFFECTS OF ALCOHOL AND GM-CSF ON ALVEOLAR TIGHT JUNCTIONS.
M. Koval1*, X. Fan2, A.L. Fernandez1,2, L.N. Johnson1, P.C. Joshi1,2, D.M. Guidot1,2, 1Emory University School of Medicine, Pulmonary, Allergy and Critical Care Medicine, Atlanta, GA, and 2VA Medical Center, Atlanta, GA.
ROLE OF MINERALOCORTICOID RECEPTOR IN PARAQUAT-INDUCED RAT LUNG FIBROSIS.
R. Bhagat1*, E.P. Gomez-Sanchez2, M. Warden2, A. de Rodriguez2, J. Spurzem1, T.M. Dwyer1,3, C.E. Gomez-Sanchez2, Divisions of 1Pulmonary, Critical Care & Sleep & 2Endocrinology; 3Department of Physiology & Biophysics; G.V. (Sonny) Montgomery VA & University of Mississippi Medical Center, Jackson, MS.
IMMUNE MODULATION PREVENTS DEVELOPMENT OF AUTOIMMUNE EMPHYSEMA.
L. Taraseviciene-Stewart*, M. Hanaoka, D. Kraskauskas, M.R. Nicolls, N. Burns, N.F. Voelkel, Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado School of Medicine, Denver, CO.
HUMAN PULMONARY MICROVASCULAR ENDOTHELIAL CELLS FORM A LESS PERMEABLE MONOLAYER WHEN GROWN TO CONFLUENCE IN HYPOXIA.
V. Solodushko, J. Parker, B. Fouty*, Center for Lung Biology, University of South Alabama, Mobile, AL.
EXTRACELLULAR SUPEROXIDE INDUCES EGR-1 AND PROMOTES HYPOXIC PULMONARY VASCULAR REMODELING.
E. Nozik-Grayck1*, K. Roush1, J. Albietz1, A. Hopkins1, H. Suliman2, K. Stenmark1, 1Developmental Lung Biology Lab, University of Colorado Denver, Denver, CO and 2Pulmonary Medicine, Duke University, Durham, NC.
ACTIVATION OF NF-?B BY G PROTEIN COUPLED RECEPTORS: IDENTIFICATION OF A Gq-COUPLED PATHWAY IN LUNG EPITHELIAL CELLS.
G.W. Hoyle*, H. Tao, X. Zou, R. Williams, Departments of Medicine and Pediatrics, Tulane University Health Sciences Center, New Orleans, LA.
IMBALANCE OF APOPTOSIS AND CELL PROLIFERATION CONTRIBUTE TO THE DEVELOPMENT AND MAINTENANCE OF EMPHYSEMA.
J.H. Lee1,2, M. Hanaoka2, Y. Kitaguchi2, D. Kraskauskas2, L. Taraseviciene-Stewart2, N.F. Voelkel2*, 1Department of Medicine, Pochon CHA University, Seongnam, KOREA, Department of Medicine; 2Division of Pulmonary and Critical Care Medicine, University of Colorado School of Medicine, Denver, CO.
AGE DEPENDENT EFFECTS OF MECHANICAL VENTILATION ON LUNG GENE EXPRESSION.
L.S. Smith*, S.A. Gharib, C.W. Frevert, T.R. Martin, University of Washington, Children’s Hospital and Regional Medical Center, and Puget Sound VA Health Care System, Seattle, WA.
PULMONARY MICROVASCULAR ENDOTHELIAL CELLS EXPRESSING CD40 EXHIBIT INCREASED PERMEABILITY IN RESPONSE TO SOLUBLE CD40 LIGAND.
T.M. Moore*, University of South Alabama College of Medicine, Center for Lung Biology, Mobile, AL.
DEFORMATION-INDUCED LUNG CELL INJURY IS GLUCOSE-CONCENTRATION AND CELL-TYPE DEPENDENT.
D.S. Ayo, S.A. Ensminger, G. Liu, N.E. Vlahakis*, Thoracic Disease Research Unit, Division of Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, MN.
PULMONARY ANGIOTENSIN-CONVERTING ENYZME MEDIATES VENTILATOR-INDUCED LUNG INJURY IN RATS.
R.M. Wösten-van Asperen1*, R. Lutter2, J.J. Haitsma3,4, M.P. Merkus5, J.B. van Woensel1, S. Florquin6, B. Lachmann3, A.P. Bos1 1Pediatric Intensive Care Department, Emma Children’s Hospital/Academic Medical Center, Amsterdam, The Netherlands; 2Departments of Pulmonology and Experimental Immunology, Academic Medical Center; 3Department of Anesthesiology, Erasmus-MC, Rotterdam; 4Department of Critical Care Medicine, St. Michael’s Hospital, Toronto, Ontario, Canada; 5Center for Pediatric Clinical Epidemiology, Academic Medical Center; 6Department of Pathology, Academic Medical Center.
PROTEOMIC ANALYSIS OF BRONCHOALVEOLAR LAVAGE FLUID FROM PATIENTS WITH ACUTE LUNG INJURY USING TWO-DIMENSIONAL DIFFERENCE GEL ELECTROPHORESIS.
D.W. Chang*, S. Hayashi, S. Gharib, M. Wurfel, D.R. Park, M. Tsuchiya, G. Matute-Bello, T. Vaisar, R.E. Bumgarner, J.W. Heineke, T.R. Martin, VA Puget Sound Healthcare System and the University of Washington, Seattle, WA.
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Friday, June 8, 2007
5:00 PM
POSTER VIEWING -- SOCIAL HOUR
FUNCTIONAL MICROCIRCULATION IS LOST IN AIRWAY FIBROSIS.
A.N. Babu*, T. Murakawa, N.F. Voelkel, M.R. Zamora, P. Henson, M.R. Nicolls, University of Colorado Denver; Denver, CO.
A NOVEL NONSTEROIDAL ANTIFIBROTIC DECOY: PROTEOMIC EVIDENCE THAT THE PROLYL HYDROXYLASE ß SUBUNIT INHIBITS TYPE 1 PROCOLLAGEN SYNTHESIS.
K.R. Cutroneo*, Department of Biochemistry, S.L. White, Department of Anatomy and Neurobiology, College of Medicine, University of Vermont, Burlington, VT; H.P. Ehrlich, Division of Past. Surg., Pennsylvania State College of Medicine, Hershey, PA; C.N. Lok, J.-F. Chiu, Department of Anatomy, Hong Kong University, Hong Kong, CHINA.
INTRA-ALVEOLAR TISSUE FACTOR PATHWAY INHIBITOR IS NOT SUFFICIENT TO BLOCK TISSUE FACTOR PROCOAGULANT ACTIVITY.
J.A. Bastarache*, L. Wang, N.E Wickersham, K.H. Albertine, M.A. Matthay, L.B. Ware, Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University, Department of Pediatrics, University of Utah, and Cardiovascular Research Institute, University of California, San Francisco.
SULFATED EXTRACELLULAR MATRIX MODULATES REGULATION OF ALVEOLAR EPITHELIAL DIFFERENTIATION IN THE ADULT.
K. Apparao, D. Newman, H. Zhang, J. Khosla, P. Sannes*, Department of Molecular Biomedical Sciences, North Carolina State University, Raleigh, NC.
A TH2 RESPONSE TO CHRONIC INTERMITTENT ANTIGEN EXPOSURE INDUCES PULMONARY ARTERIAL REMODELING.
E. Daley1, C. Emson2, L. Taraseviciene-Stewart3, V.P. Kurup4, R. de Waal-Malefyt2, C. Hogaboam5, E. Grunig6*, N.F. Voelkel3, G. Grunig7, 1St. Luke’s Roosevelt Hospital, New York, NY; 2Schering Plough Biopharma, Palo Alto, CA; 3University of Colorado, Denver, CO; 4Medical Center of Wisconsin, VA Medical Center, Milwaukee, WI; 5University of Michigan, Ann Arbor, MI; 6University of Heidelberg, Heidelberg, GERMANY; 7Columbia University, New York, NY.
INTRA-ALVEOLAR 3,3’,5 TRIIODO-L-THRONINE STIMULATES ALVEOLAR FLUID CLEARANCE IN NORMAL RAT LUNGS AND HYPEROXIA INDUCED LUNG INJURY IN RATS.
M. Bhargava*, M. Runyon, C. Mariash, O.D. Wangensteen, D.H. Ingbar, Departments of Medicine and Physiology, University of Minnesota Medical School, MN.
A RAPID SCREENING METHOD FOR COMPOUNDS DISPLAYING SYNERGY FOR THE TREATMENT OF LUNG FIBROSIS.
T.J. Kottom*, A.H. Limper, Thoracic Diseases Research Unit, Mayo Clinic College of Medicine, Rochester, MN.
HIGH TIDAL VOLUME VENTILATION INDUCES A PRO-COAGULANT SHIFT IN EXPERIMENTAL STREPTOCOCCUS PNEUMONIAE PNEUMONIA.
J.J. Haitsma1, M.J. Schultz1,2, H. Zhang1, A.S. Slutsky1, Interdepartmental Division of Critical Care1, University of Toronto, St. Michael’s Hospital, Toronto, Ontario, CANADA; Laboratory for Experimental Intensive Care and Anesthesiology2, AMC, University of Amsterdam, Amsterdam, The Netherlands.
SPHINGOSINE 1-PHOSPHATE AUGMENTS FIBROBLAST MEDIATED COLLAGEN GEL CONTRACTION VIA THE S1P2 RECEPTOR AND THE RHOA PATHWAY.
X.Q. Wang*, X. Liu, L. Mao, S. Togo, K. Kamio, S. Kawasaki, M.L. Toews, S. Rennard, Pulmonary, Critical Care, Sleep and Allergy Medicine, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska.
TGF-ß1 MODULATES FIBROBLAST DIFFERENTIATION FROM MOUSE EMBRYONIC STEM CELLS.
X. Liu*, H. Sugiura, S. Togo, M. Hashimoto, H. Kim, T. Kobayashi, X. Wang, S. Kawasaki, K. Kamio, S. Rennard, Pulmonary, Critical Care, Sleep and Allergy Medicine, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska.
POLYMORPHISMS IN THE IL-1 GENE FAMILY AND LUNG DISEASE SEVERITY IN PATIENTS WITH CYSTIC FIBROSIS, H.
Levy1,2,3*, A. Murphy2.4, F. Zou5, C. Gerard1,2, B. Klanderman2,3, J. Celedón2,3, M. Drumm6, M. Knowles5, M.Dahmer7, M. Quasney7, G. Pier2,3, C. Lange2,4, S. Weiss2,3, 1Division of Pulmonary Medicine, Children’s Hospital, Boston, MA; 2Harvard Medical School, Boston, MA; 3Channing Laboratory, Brigham and Women’s Hospital, Boston, MA; 4Harvard School of Public Health, Boston, MA; 5Division of Pulmonary and Critical Care Medicine, University of North Carolina School of Medicine, Chapel Hill, NC; 6Department of Pediatrics and Genetics, Case Western Reserve University, Cleveland, OH; 7Department of Pediatrics and Critical Care, Children’s Hospital of Wisconsin, Milwaukee, WI.
VASCULAR ENDOTHELIAL GROWTH FACTOR IS ESSENTAIL FOR MAINTAINING PULMONARY SURFACTANT PROTEIN D EXPRESSION IN VIVO.
K. Tang, J. Malloy, E.C. Breen*, Division of Physiology, Department of Medicine, University of California, San Diego, La Jolla, CA.
INTERLEUKIN-1 RECEPTOR ANTAGONIST INTRON 2 POLYMORPHISMS AND LUNG INJURY IN CHILDREN WITH COMMUNITY-ACQUIRED PNEUMONIA.
M. Dahmer1*, P. Patwari2, P. O’Cain3, D. Goodman2, J. Krushkal4, G. Somes4, C. Liu4, M. Smith1, M. Quasney1, 1Children’s Research Institute, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI, 2Department of Pediatrics, Northwestern University, Department of Pediatrics3 and 4Preventive Medicine University of Tennessee Health Science Center.
NEUTROPHIL CHEMOTACTIC COLLAGEN FRAGMENTS ARE GENERATED FROM CYSTIC FIBROSIS SPUTUM.
A. Gaggar1*, P. Jackson1, B. Noerager1, P.J. OReilly1, J.P. Clancy1, J.E. Blalock1, 1University of Alabama-Birmingham, Birmingham, AL.
REMODELING OF RESPIRATORY UNIT IN SILICA-EXPOSED MICE.
C.L. Fattman*, G. Torres, B.L. Brockway, B.R. Stripp, L.A. Ortiz, Department of Environmental and Occupational Health, University of Pittsburgh Graduate School of Public Health, Pittsburgh, PA.
IGF-1 ALONE DOES NOT INDUCE PULMONARY FIBROSIS: HOWEVER, IT DOES CAUSE A DOSE-CORRELATED INFLAMMATORY RESPONSE IN C57BL/6 MOUSE LUNGS.
A. Ni, C. Mowat, D. Muruve, F. Green, B.W. Winston*, University of Calgary, Calgary, Alberta, CANADA.

Objectives of the Thomas L. Petty Aspen Lung Conference
- To provide an international forum for leading
clinicians and researchers to exchange of ideas relating to clinical problems
and research of the lung.
- To fill a recognized need in a field where knowledge is
doubling every five years.
- To focus on a single topic, exhaustively
reviewing it with significant time allowed for discussion.
- To provide the stimulus and impetus to
further research in pulmonary medicine.
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