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23rd Annual Conference on Shock
Snowbird, Utah
June 3-6, 2000
SATURDAY, JUNE 3, 2000  
   
   
9:00 - 2:00 PM COUNCIL MEETING
White Pine  
 
1:00 - 6:00 PM Registration
Ballroom Foyer  
   
2:00 - 3:00 PM PENARY SESSION I, Papers 1-5
Ballroom 1 & 2 Moderators: Edwin A. Deitch, MD , UMDNJ-New Jersey Medical School, Newark
  and Gregory Bagby, MD, Louisiana State University Medical Center, New Orleans
   
2:00 PM Post-Hemorrhagic Shock Mesenteric Lymph (PHSML) Lipids Prime Neutrophil Superoxide Production Via Phospholipase A2, Paper 1
  Ricardo J. Gonzalez, MD
  Denver Health Medical Center, Denver, Colorado
2:12 PM Non-Compartmentalization of Granulocyte-Colony Stimulating Factor (G-CSF) Following an Intrapulmonary Bacterial Challenge, Paper 2
  Gregory J. Bagby, MD
  Louisiana State University Medical Center, New Orleans
2:24 PM Glucose-6-P Dehydrogenase (G6PD) Deficiency Predisposes to Sepsis, Worsens Anemia and Results in a
  Pronounced Activation of Circulating Monocytes After Severe Trauma, Paper 3
  Zoltan Spolarics, MD, PhD
  UMDNJ- New Jersey Medical School, Newark
2:36 PM Burn Injury Induces Expression of Two Novel Forms of the TIS11D Gene in
  Mice, Paper 4
  Kristina G. Hobson, MD
  Shriners Hospitals for Children, Sacramento, California
2:48 PM The Role of INF-? and IL-12 on Propioni-Bacterium (PA) Acnes-Primed LPS Hepatic Injury, Paper 5
  Yoshiaki Shimizu, MD
  Washington University, St. Louis, Missouri
   
   
3:00-5:00PM WORKSHOP I: Understanding SIRS and MOF: Time to Change Perspective
Ballroom 1 & 2 Moderator: Gill Cryer, MD, PhD, University of California, Los Angeles
   
  Multiple Organ Failure remains one of the most common causes of death after injury or sepsis.
  Despite incredible advances in critical care technology over the last 30-40 years the mortality rate
  for this syndrome remains very high. There have been tremendous gains in our knowledge from basic
  research, yet this knowledge has not resulted in significant improvements in outcome in the clinical setting.
  Perhaps we need to look at the problem differently. In this symposium we will attempt to look at the problem
  of Multiple Organ Failure from different perspectives. Hopefully we will generate new ideas, which may
  eventually lead to improved outcomes for patients suffering from this disease.
3:00 PM Introduction
  Gill Cryer, MD, PhD
3:10 PM Recent Advances from Basic Research Tells Us It’s Time to Change
  the Definitions of SIRS and MOF
  Edward Abraham, MD, University of Colorado Health Sciences Center, Denver
3:35 PM The Difference Between MOF and SIRS is Really a Failure of Recovery
  Timothy Buchman, MD, PhD, Washington University School of Medicine,
  St. Louis, Missouri
4:00 PM The SIRS-MOF Continuum is a Failed Dynamic Balancing Act Across Time
  John Mannick, MD, Harvard Medical School, Boston, Massachusetts
4:25 PM The Solution to SIRS and MOF: A Challenge for the New Millennium
  Eugen Faist, MD, Ludwig-Maximilians-Universität, München Germany
   
7:30-8:30PM KEYNOTE ADDRESS: Oh, the Places You’ll Go: Will You Succeed? You Will
Ballroom 1 & 2 Indeed! 99 and 3/4 Percent Guaranteed
  Jureta W. Horton, PhD, President-Elect, University of Texas Southwestern
  Medical School, Dallas
   
8:30 - 9:30 PM OPENING RECEPTION
Conference Center  
Terrace  
   
SUNDAY, JUNE 4, 2000  
   
7:00 - 8:00 AM EDITORIAL BOARD BREAKFAST
Maybird  
   
7:00 - 8:00 AM Continental Breakfast
Ballroom 3, Magpie &  
Golden Cliff  
   
7:00 - 9:00 AM POSTER SESSION I, Papers 6-76
Ballroom 3, Magpie &  
Golden Cliff  
  Adhesion Molecules, Paper 6
  Animal Models, Papers 7-10
  Burn/Trauma, Papers 11-18
  Cellular/Molecular, Papers 19-21
  Cytokines, Papers 22-30
  Eicosanoids/PAF, Paper 31
  Endotoxin/Sepsis, Papers 32-48
  Gene Regulation, Paper 49
  Immunologic Dysfunction, Paper 50
  Immunomodulation, Papers 51-55
  Inflammation, Papers 56-58
  Metabolism, Papers 59-60
  Microcirculation, Papers 61-66
  Monocytes/Macrophages, Paper 67
  Multiple Organ Failure, Papers 68-69
  Myocardial Function, Papers 70-72
  Neonatology, Paper 73
  Pulmonary, Paper 74
  Renal, Papers 75-76
   
9:00 - 10:00 AM PLENARY SESSION II, Papers 77-81
Ballroom 1 & 2 Moderator: William Cheadle, PhD, Veterans Administration Medical Center,
  Louisville, Kentucky and Mark Carlson, PhD, Veterans Administration
  Medical Center, Omaha, Nebraska
   
9:00 AM LPS-Induced, Imbalanced Expression of Hepatic Vascular Stress Genes
  in Cirrhosis: Mechanism of Increased Susceptibility to Endotoxemia,
  Paper 77
  Rajiv Baveja
  University of North Carolina, Charlotte
9:12 AM Role of Nitric Oxide in Hemorrhagic Shock-Induced Hepatic Heme
  Oxygenase-1 Expression in the Rat, Paper 78
  Alexander Hoetzel, MD
  University of Freiburg, Germany
9:24 AM Interleukin (IL)-6 Knockout Attenuates Early Sepsis-Associated Hepatic Gene
  Downregulation but Increases Hepatic Necrosis and Death, Paper 79
  Patrick K. Kim, MD
  University of Pennsylvania, Philadelphia
9:36 AM A Dominant Role of P55 TNF-a Receptor in Endotoxemic Myocardial
  Dysfunction, Paper 80
  Xianzhong Meng
  University of Colorado Health Sciences Center, Denver
9:48 AM Evidence for a Role of NF-?B in Acute Hypovolemic Hemorrhagic Shock
  in Rats, Paper 81
  Francesco Squadrito, MD
  University of Messina, Italy
   
   
   
10:00 AM - 12:00 PM SYMPOSIUM I: Signal Transduction and Genetic Regulation of Inflammation
Ballroom 1 & 2 Moderator: Timothy Buchman, MD, PhD, Washington University School
  of Medicine, St. Louis, Missouri
   
   
  In this session, the speakers will explore the regulatory responses to inflammation with a focus on balance
  among intracellular pathways. Dr. DeMaio will speak on the diversity of responses and address
  genotype-phenotype relationships. He will describe approaches to the identification of genes which modulate
  the inflammatory response. Dr. Giroir will focus on TNF-a and the consequences of having too much, or too
  little of this signalling molecule at the surface of a cell. Dr. Callery will describe how binding of specific ligands
  changes the state of second messenger intermediates a systematic and reciprocally regulated mechanism.
  Dr. Moldawer will discuss disruption of regulatory responses using gene therapy as an investigative tool.
  Dr. Cobb will compare and contrast the reductionist analysis of single gene responses with the connectionist
  analysis afforded by gene arrays ("chips") in the study of inflammatory responses. This session will emphasize
  networks over pathways and focus on the idea that the state of biological networks is regulated by competing
  stimuli and not by isolated signals.
   
10:00 AM Genetic Diversity in the Response to Canonical Inflammatory Stimuli
  Antonio DeMaio, PhD, Johns Hopkins University School of Medicine,
  Baltimore, Maryland
10:24 AM TNF-a: Inflammation in Moderation
  Brett Giroir, MD, University of Texas Southwestern Medical School, Dallas
10:48 AM Balanced Responses of the Second Messenger Pathways to Inflammation
  Mark P. Callery, MD, University of Massachusetts Medical School, Worcester
11:12 AM Gene Therapy as a Strategy for Modulating the Response to Inflammation
  Lyle L. Moldawer, PhD, University of Florida College of Medicine, Gainesville
11:36 AM Top-Down (Arrays) Versus Bottom-Up (Specific Gene) Approaches to the
  study of Responses to Inflammation
  J. Perren Cobb, MD, PhD, Washington University, St. Louis, Missouri
   
   
10:45 - 11:00 AM Coffee Available
Ballroom Foyer  
   
12:00 - 1:30 PM Lunch
Cottonwood 1-4  
   
1:45 - 3:15 PM YOUNG INVESTIGATOR AWARD SESSION, Papers 82-85
Ballroom 1 & 2 Presiding: Mohammed M. Sayeed, PhD, Loyola University, Maywood, Illinois
   
1:45 PM Cytokine-Induced Enterocyte-Derived Nitric Oxide Induces Intestinal
  Monolayer Injury in an Autocrine Fashion, Paper 82
  Raquel M. Forsythe, MD
  UMDNJ-New Jersey Medical School, Newark
2:00 PM Progesterone Improves Cardiovascular Function Following Trauma-
  Hemorrhage and Resuscitation, Paper 83
  Joachim Friedrich Kuebler, MD
  Rhode Island Hospital, Providence
2:15 PM Do Peripheral Blood Mononuclear Cells Mimic the Sexually Dimorphic
  Immune Response of Tissue Immune Cells Following Trauma-Hemorrhage?,
  Paper 84
  Christian P. Schneider, MD
  Rhode Island Hospital, Providence
2:30 PM Glutamine Induces Heat Shock Protein and Prevents Mortality from
  Endotoxemia in the Rat, Paper 85
  Paul E. Wischmeyer, MD
  University of Chicago, Illinois
   
   
3:00 - 3:30 pm Coffee Break
Ballroom Foyer  
   
   
   
3:30 - 5:30 PM MINISYMPOSIUM I, Papers 86-95
Ballroom 1 & 2 Moderator: Alfred Ayala, PhD, Rhode Island Hospital, Providence and
  Inge Bauer, PhD, University of Saarland, Homburg, Germany
   
3:30 PM Intraluminal Nutrients Enhance Gut Ischemia/Reperfusion Injury,
  Paper 86
  Rosemary Kozar, MD, PhD
  University of Texas Medical School, Houston
3:42 PM Effects of the Secretion of Metabolic Regulating Hormones (Leptin) and
  Posttraumatic Complications in Blunt Polytrauma Patients, Paper 87
  Martijn van Griensven, PhD
  Hannover Medical School, Germany
3:54 PM Delayed Blockage of FasL Restores Lymphoid Immune Function, Suppresses Apoptosis and Improves Survival in Sepsis, Paper 88
  Chun-Shiang Chung, PhD
  Rhode Island Hospital, Providence
4:06 PM Role of Kupffer Cells and Neutrophils for the Regulation of Heme Oxygenase-
  1 Gene Expression in the Liver Under Stress Conditions, Paper 89
  Markus Paxian, MD
  University of Saarland, Homburg, Germany
4:18 PM Expression Pattern and Regulation of Heme Oxygenase-1/Heat Shock Protein
  32 in Human Liver Cells, Paper 90
  Inge Bauer, PhD
  University of Saarland, Homburg, Germany
4:30 PM Endotoxin Mediated Blockade of Pregnane X Receptor Translocation: Effects
  on Hepatic Cytochrome P-450, Paper 91
  Clinton Chichester
  University of Rhode Island College of Pharmacy, Kingston
4:42 PM Flagellin, A Novel Mediator of Gram Negative Bacteria-Induced Shock
  Paper 92
  Andrew L. Salzman, MD
  Inotek Corporation, Beverly, Massachusetts
4:54 PM CD16 Blockade in Polymicrobial Sepsis Increases Hepatic but Not Pulmonary
  Neutrophil Sequestration, Paper 93
  Stephen A. Rowe, MD
  Veterans Administration Medical Center, Louisville, Kentucky
5:06 PM Adenosine-Mediated Alterations in Testicular Cytokine and Testosterone
  Production, Paper 94
  Andrew M. Clark, BA
  University of Illinois at Chicago, Illinois
5:18 PM Posttraumatic Disturbances of Humoral Bone Factors in Trauma Patients,
  Paper 95
  Otmar A. Trentz, MD
  University Hospital, Zurich, Switzerland
   
   
   
3:30 - 5:30 PM MINISYMPOSIUM II, Papers 96-105
Superior A & B Moderators: Jureta W. Horton, PhD, University of Texas Southwestern Medical
  Center, Dallas and J. Perren Cobb, MD, Washington University, St. Louis,
  Missouri
   
3:30 PM Effects of Lactated Ringers on Cardiomyocyte TNF-a Synthesis,
  Paper 96
  Jureta W. Horton, PhD
  University of Texas Southwestern Medical Center, Dallas
3:42 PM Microvascular Effects of Oral IL-6, Paper 97
  F.M. Rollwagen, PhD
  Uniformed Services of the Health Sciences, Bethesda, Maryland
3:54 PM Removal of Fatty Acids Improves Coupling of Ex-Vivo Myocardial Glycolytic
  Flux to Glucose Oxidation After Hemorrhage, Paper 98
  Lisa T. Thornton
  Carolinas Medical Center, Charlotte, North Carolina
4:06 PM Sepsis Gene Expression Profiling: Murine Splenic Compared to Hepatic
  Responses Determined Using cDNA Microarrays, Paper 99
  J. Perren Cobb, MD
  Washington University, St. Louis, Missouri
4:18 PM Genetic Disruption of Poly (ADP-Ribose) Synthethase Reduces Gut\
  Dysfunction and Distant Organ Damage in Mesenteric Ischemia-Reperfusion
  Injury, Paper 100
  Lucas Liaudet
  Inotek Corporation, Beverly, Massachusetts
4:30 PM Post Hemorrhagic Shock Mesenteric Lymph Upregulates E-Selectin
  Expression in Human Umbilical Vein Endothelial Cells (HUVEC),
  Paper 101
  Justin T. Sambol, MD
  UMDNJ-New Jersey Medical School, Newark
4:42 PM A Time Course Study of the Protective Effect of Mesenteric Lymph Duct
  Ligation on Hemorrhagic Shock-Induced Pulmonary Injury and the Toxic
  Effects of Shock Lymph on HUVEC Cell Monolayer Permeability, Paper 102
  Edwin A. Deitch, MD
  UMDNJ- New Jersey Medical School, Newark
4:54 PM LBP Promotes Bacterial Killing of Silver Sulfadiazine Resistant P. Aeruginosa
  in Infected Burn Wounds, Paper 103
  Richard D. Klein
  University of Michigan, Ann Arbor
5:06 PM Distribution of Monohydroxy Fatty Acids (MHA) in Murine Skin Following
  Thermal Injury, Paper 104
  Kenneth Langen
  Loyola University Medical Center, Maywood, Illinois
5:18 PM Which Receptor Mediates Prostaglandin E2 (PGE2)/Thromboxane A2
  Synergy?, Paper 105
  F. Mahzari, BS
  University of Texas Southwestern Medical School, Dallas
   
6:30 - 7:30 PM RECEPTION
Ballroom Lobby  
   
7:30 - 9:30 PM DINNER/SPEAKER
Ballroom 1 & 2  
   
   
   
MONDAY, JUNE 5, 2000  
   
   
6:30 AM Eighteenth Annual Presidential Run
Meet in Lobby  
8:00 - 9:00 AM Continental Breakfast
Ballroom 3, Magpie &  
Golden Cliff  
   
   
9:00 - 10:00 AM PLENARY SESSION III, Papers 106-110
Ballroom 1 & 2 Moderators: Ronald V. Maier, MD, Harborview Medical Center, Seattle,
  Washington and Lyle Moldawer, PhD, University of Florida College of Medicine,
  Gainesville
   
9:00 AM Mitogen-Activated Protein Kinases (MAPK) in the ICU: Potential Prognostic
  Factors, Paper 106
  Matthew R. Rosengart, MD
  Harborview Medical Center, Seattle, Washington
9:12 AM Protegrin-1 Enhances Bacterial Killing in Thermally Injured Murine Epidermis,
  Paper 107
  Lars Steinstresser
  University of Michigan, Ann Arbor
9:24 AM Burn-Induced T Cell Suppression is Prevented After Neutrophil Depletion in
  Burn-Injured Rats, Paper 108
  Thyyar M. Ravindranath
  Loyola University Medical Center, Maywood, Illinois
9:36 AM STAT 5/6 Protein and Cytokine Expression, Paper 109
  Vicky Chappell, MD
  University of Texas Medical Branch, Galveston
9:48 AM The Inflammatory Response in Severely Injured Patients Following Small
  Volume Resuscitation, Paper 110
  U.C. Liener, MD
  University of Ulm, Germany
   
   
10:00AM-12:00PM SYMPOSIUM II: Neuro Endocrine Interaction: Regulation of Responses
Ballroom 1 & 2 to Shock and Trauma
  Moderator: Naji N. Abumrad, MD, North Shore University Hospital, Manhasset,
  New York
   
   
  Understanding the control mechanisms involved in modulation of the hemodynamic, pro-inflammatory, metabolic and immune
  responses which occur during the ebb and flow phases following injury is crucial in order to establish optimal intervention paradigms
  for the critically ill individual. Studies using various models of physical stress, including hemorrhagic and endotoxic shock, trauma
  and hypoclycemia, have provided significant evidence of a critical role for neuro-endocrine control of these responses. The pathways
  involved in modulation of the magnitude and time course of these post-traumatic stress responses are not limited to
  hypothalamo-pituitary-axis activation, but include central and peripheral release of opioids, excitatory amino acids, serotonin and nitric
  oxide. These neuro-endocrine mediators play redundant, adjuvant or opposing roles affecting the wide array of immune, metabolic
  and hemodynamic responses, which comprise the post-injury phase. The aim of this symposium is to highlight some of the recent
  advances in the understanding of neuro-endocrine control of select responses to shock, trauma and sepsis.
   
10:00 AM Introduction
  Naji N. Abumrad, MD
10:12 AM Modulation of Trauma/Shock-Induced Responses; Interaction of Monoamine
  and Opiate Pathways
  Patricia E. Molina, MD, PhD, Louisiana State University Health Science
  Center, New Orleans
10:39 AM The Stress/Septic Response: The Role of IGF and Growth Hormone
  Charles Lang, PhD, Penn State College of Medicine, Hershey
11:06 AM The Role of Central Parasympathica Systems in the Stress/Septic Response
  Kevin Tracy, MD, Cornell University Medical College, Manhasset, New York
11:33 AM The Role of Adrenomedullin in the Septic Response
  Ping Wang, MD, Brown University and Rhode Island Hospital, Providence
   
10:30 - 11:00 AM Coffee Available
Ballroom Foyer  
   
12:00-1:00 PM BUSINESS MEETING
Ballroom 1 & 2  
   
FREE AFTERNOON  
   
   
TUESDAY, JUNE 6, 2000  
   
7:00 - 8:00 AM Continental Breakfast
Ballroom 3, Magpie &  
Golden Cliff  
   
8:00 - 9:00 AM POSTER SESSION II, Papers 111- 179
Ballroom 3, Magpie &  
Golden Cliff  
   
  Cell Signaling, Papers 111-121
  Hemorrhagic Shock, Papers 122-152
  Neutrophils, Papers 153-161
  Nitric Oxide, Papers 162-167
  Oxygen Metabolites, Papers 168-169
  Pharmacology, Papers 170-174
  Ischemia/Reperfusion, Papers, 175-178
  Liver, Paper 179
   
9:00 - 10:00 AM PLENARY SESSION IV, Papers 180-184
Ballroom 1 & 2 Moderators: Carol Miller-Graziano, PhD, University of Massachusetts
  Medical Center, Worcester and James A. Thomas, MD, University of Texas
  Southwestern Medical Center, Dallas
   
9:00 AM Inducible Nitric Oxide Synthase Is Required for Enterocyte Apoptosis
  After Hemorrhagic Shock, Paper 180
  Evan P. Nadler, MD
  Children’s Hospital of Pittsburgh, Pennsylvania
9:12 AM IRAK Mediates Postburn Myocardial Contractile Dysfunction,
  Paper 181
  James A. Thomas, MD
  University of Texas Southwestern Medical Center, Dallas
  Tuesday Continued
   
9:24 AM Depressed Trauma Patient MØ IL-18 Levels Lead to Decreased T Cell IL-13
  Levels, Paper 182
  Carol Miller-Graziano, PhD
  University of Massachusetts Medical School, Worcester
9:36 AM Inhibition of LPS-Induced ERK ½ Activation and I?Ba Degradation by
  15-Deoxy-?12,14-PGJ2 , Paper 193
  Kelly Guyton, BS
  Medical University of South Carolina, Charleston
9:48 AM Cerebral Perfusion Pressure (CPP) Directed Therapy After Traumatic Brain
  Injury (TBI), Paper 194
  Ajai K. Malhotra, MD
  University of Tennessee Health Science Center, Memphis
   
10:00 AM - 12:00 PM SYMPOSIUM III: Understanding of Myocardial Dysfunction in Hyper
Ballroom 1 & 2 Inflammatory States
  Moderator: Kathleen McDonough, PhD, Louisiana State University, New Orleans
   
  The myocardium is responsible for pumping a cardiac output to match the tissue’s requirements for blood flow. Alterations in
  myocardial function are normally elicited by changes in preload, afterload, contractility and heart rate. However, during inflammatory
  states, sepsis and compromised myocardial blood flow, changes in myocardial contractile function can occur through other
  influences such as acidemia, cytokines and chemokines, oxygen radicals and a number of other mediators that my be produced in
  an inflammatory state. The aim of this symposium is to present an update of t he intracellular mechanisms by which myocardial
  contractile function is depressed and the role of cytokines in this myocardial depression. In response to injury, the myocardium can
  upregulate protective functions that serve to blunt the negative consequences of a second insult to the heart. Mechanisms involved in
  inducing cardioprotection, including the potential role of cytokines, will be discussed. Methods to assess and treat myocardial
  dysfunction in the clinical setting will be presented. Finally, the issues of potential mechanisms of injury versus mechanisms that
  have actually been shown to contribute to dysfunction in a pathophysiological state will be discussed.
   
10:00 AM Alterations in Myocardial Cell Signaling and Calcium Homeostasis as a
  Mechanism of Myocardial Depression
  Leona Rubin, PhD, University of Missouri, Columbia
10:24 AM Cytokine Induced Myocardial Depression and Protection
  Alden Harken, MD, University of Colorado, Denver
10:48 AM Myocardial Preconditioning by Ischemia and Sepsis
  James Downey, MD, University of South Alabama, Mobile
11:12 AM Similarities and Difference Between Cell and Whole Heart Models of
  Myocardial Responses to Sepsis
  Kathleen McDonough, PhD, Louisiana State University, New Orleans
11:36 AM Advances in Quantifying and Treating Myocardial Dysfunction During Critical
  Illness: From Bench to Bedside
  Michael Chang, MD, Wake Forest University School of Medicine, Winston-Salem, North Carolina
   
   
10:30 - 11:00 AM Coffee Available
Ballroom Foyer  
   
   
12:00 - 1:30 PM Lunch
Cottonwood 1-4  
1:30 - 3:30 PM WORKSHOP II: Recent Adjuncts to Resuscitation Strategies to
Ballroom 1 & 2 Prevent the SIRS to MOF Progression: Bench to Bedside
  Moderator: Kenneth Proctor, PhD, University of Tennessee, Memphis
   
  After severe trauma and blood loss, aggressive fluid resuscitation may be the only hope for saving the patient. At the same time,
  reperfusion promotes reactive oxygen metabolite generation and activates PMNs in splanchnic and other tissues that are already
  expressing multiple cytokines and endothelial cell surface adhesion molecules. The resultant hyper-inflammatory state can produce
  secondary injury locally in otherwise undamaged cells, can spill over into remote organs (e.g. lung), or can propagate into a
  malignant unregulated systemic response leading to SIRS or MOF. One speaker will describe clinically-relevant models of battlefield
  injuries designed to mimic these conditions. The second speaker will describe the benefits of a novel blood substitute in urban
  trauma patients, compared to other resuscitation fluids and compared to a potential transfusion-induced cytotoxicity caused by stored,
  packed RBCs. The third speaker will consider novel strategies in the critically ill trauma patient that combine adequate cellular
  resuscitation and avoidance of splanchnic vasopressors. Such strategies prevent or ameliorate the ravages of unfettered oxidative
  stress using agents that attenuate or block unregulated cytotoxin formation and "unprime" PMNs and are initiated in the trauma
  resuscitation area, ER, or surgical OR. The final speaker will provide an updated review on a number of the clinical trials of new
  therapeutic agents for the adjuvant treatment of shock, sepsis, and/or SIRS which have just closed to enrollment, are in progress, or
  are in the final planning stages.
   
1:30 PM Resuscitation Strategies to Minimize End Organ Damage in Large Animal
  Models of Shock Related MOF
  Kenneth Proctor, PhD
2:00 PM Blood Resuscitation: Part of the Solution or Part of the Problem?
  Ernest E. Moore, MD, University of Colorado Health Sciences Center, Denver
2:30 PM Resuscitation Strategies to Minimize SIRS & Multiple Organ Failure
  by Preventing Ischemia-Reperfusion in Trauma Patients
  Orlando Kirton, MD, Hartford Hospital, Hartford, Connecticut
3:00 PM Update on Current Clinical Trials of Adjuncts to Resuscitation to Prevent
  and/or Treat SIRS and MOF
  Mitchell Fink, MD, University of Pennsylvania Medical Center, Pittsburgh
   
3:00 - 3:30 pm Coffee Available
Ballroom Foyer  
   
3:30 - 6:00 PM MINISYMPOSIUM III, Papers 185-196
Ballroom 1 & 2 Moderators: H. Hank Simms, MD, Rhode Island Hospital, Providence and
  Richard Hotchkiss, MD, Washington University, St. Louis, Missouri
   
3:30 PM Effects of Fluid Resuscitation in Cerebral Intracellular Calcium in Traumatic
  Brain Injury Associated with Hemorrhagic Shock, Paper 185
  Marcos Balbino, MD
  University of São Paulo Medical School, Brazil
3:42 PM Paracrine Regulation of Apoptosis by IL-1ß and IL-8-Stimulated PMN:
  Differential Suppression of FasL and TNF-a Induced Apoptosis
  Paper 186
  Patricia S. Grutkoski, PhD
  Rhode Island Hospital, Providence
3:54 PM TNFR-I is Required for Heat Stress Induction of Cytoprotective HSP70 in MØ,
  Paper 187
  Julie K. Heimbach
  University of Colorado Health Sciences Center, Denver
  Tuesday Continued
   
4:06 PM Cerebral Viability After Grade IV Hemorrhage: Is Immediate Fluid
  Resuscitation Necessary?, Paper 188
  Reza Miraliakbari
  East Carolina University Brody School of Medicine, Greenville, North Carolina
4:18 PM COX-1 Induction and IL1ß Expression in Alveolar Macrophages After
  Unilateral Chest Trauma, Paper 189
  Wesley J. Desselle, MD
  University of Tennessee Health Science Center, Memphis
4:30 PM Alveolar Macrophage TNF-a Release is Enhanced Following Trauma-
  Hemorrhage and Sepsis, Paper 190
  Doraid Jarrar, MD
  Rhode Island Hospital, Providence
4:42 PM Lethal Septic Shock Increases Myocardial UCP-2 Expression Coincident with
  Myocardial Dysfunction, Paper 191
  Michael J. Roshon
  Carolinas Medical Center, Charlotte, North Carolina
4:54 PM Mechanisms of PMN Persistence During Inflammation: Suppression of
  Apoptosis by IL-8 and GRO-a Via Diverse Signaling Mechanisms
  Paper 192
  Annmarie L. Dunican, MD
  Rhode Island Hospital, Providence
5:06 PM The Dissociation Between Upregulated Endothelins and Hemodynamic
  Responses During Polymicrobial Sepsis, Paper 193
  David A. Ornan, Sc.B
  Rhode Island Hospital, Providence
5:18 PM Immediate Early Genes (IEG) and Transcription Factors in Liver of Rats
  Preconditioned with Curcumin and Picroliv During Hemorrhagic Shock and
  Resuscitation, Paper 194
  Gurmel S. Sidhu
  Uniformed Services University of Health Sciences, Bethesda, Maryland
5:30 PM Genetic and Gender Components in the Expression of Tumor Necrosis
  Factor-a in Mice During Endotoxemia, Paper 195
  F. Dylan Stewart, MD
  Johns Hopkins School of Medicine, Baltimore, Maryland
5:42 PM Two Stage Response to Endotoxin Infusion into Normal Human Subjects,
  Paper 196
  Fletcher B. Taylor, Jr., MD
  Oklahoma Medical Research Foundation, Oklahoma City
5:54 PM Closing Remarks
   
   
   
3:30 - 6:00 PM MINISYMPOSIUM IV, Papers 197-208
Ballroom 3 Moderators: Allan M. Lefer, PhD, Thomas Jefferson University, Philadelphia,
  Pennsylvania and Lee-Wei Chen, MD, Veterans General Hospital, Kaohsiung,
  Taiwan
   
3:30 PM Characterization of Local and Systemic Cytokine Responses During Acute
  Inflammation in Humans, Paper 197
  Fernando A. Rivera-Chavez
  University of Texas Southwestern Medical Center, Dallas
3:42 PM Safety and Efficacy of Hypertonic Saline Dextran in Pediatric Patients
  Submitted to Cardiac Surgery with Cardiopulmonary Bypass, Paper 198
  Roberto Rocha e Silva
  University of São Paulo, Brazil
3:54 PM Prevention of Multiple Organ Failure (MOF) Secondary to Severe Acute
  Pancreatitis (SAP) with Continuous Hemodiafiltration (CHDF) and Selective
  Digestive Decontamination (SDD), Paper 199
  Hiroyuki Hirasawa, MD, PhD
  Chiba University School of Medicine, Japan
4:06 PM Female Gender is a Risk Factor for Early Postinjury Multiple Organ Failure,
  Paper 200
  Patrick J. Offner, MD
  Denver Health Medical Center, Colorado
4:18 PM Hypoxia Inhibits iNOS Expression in Endothelial Cells, Paper 201
  Haim Bitterman, MD
  Carmel Medical Center, Haifa, Israel
4:30 PM Nitric Oxide Pre-Treatment Protects Against Peroxynitrite-Induced Enterocyte
  Apoptosis, Paper 202
  Douglas A. Potoka, MD
  Children’s Hospital of Pittsburgh, Pennsylvania
4:42 PM The Absence of eNOS Increases Mortality After Hemorrhagic Shock
  Paper 203
  Vaishali D. Schuchert
  University of Pittsburgh, Pennsylvania
4:54 PM Effects of n-Acetylcysteine on Ischemic Brain Injury, Paper 204
  Salvatore Cuzzocrea, PhD
  University of Messina, Italy
5:06 PM Nitric Oxide Synthase Inhibitor Ameliorates Oral Total Parenteral Nutrition-
  Induced Barrier Dysfunction, Paper 205
  Lee-Wei Chen, MD
  Veterans General Hospital, Kaohsiung, Taiwan
5:18 PM Actin Cytoskeleton and Endothelial Cell Response to Osmotic Stress,
  Paper 206
  Saman Arbabi, MD
  Harborview Medical Center, Seattle, Washington
5:30 PM Vascular Endothelial Growth Factor (VEGF) Exerts Beneficial Effects in
  Traumatic Shock Via Preservation of Vascular Endothelial Function
  Paper 207
  Allan M. Lefer, PhD
  Thomas Jefferson University, Philadelphia, Pennsylvania
5:42 PM Shock Induces Bone Marrow Injury and a Migration of Hematopoietic
  Precursors to Remote Organs Which is Partially Mediated Through
  Mesenteric Lymph, Paper 208
  Devashish Anjaria, MD
  New Jersey Medical School, Newark
5:54 PM Closing Remarks
   
   
6:30 - 7:30 PM RECEPTION
Ballroom Foyer  
   
7:30 - 9:30 PM DINNER
Ballroom 1 & 2  
maintained and sponsored by Trauma Care Consult
created by Matthias Redl