|Experimental Biology Meeting Archive
Experimental Biology 2004
Sunday, April 18, 2004 – 10:30 a.m. - 12:30 p.m.
Room 146A – Washington Convention Center
Chair: C. Michael Hart, M.D., Emory University, Atlanta, Georgia
Co-Chair: David M. Guidot, M.D., Emory University, Atlanta, Georgia
In addition to Drs. Hart and Guidot, the panel will include the following speakers:
Ali Banan, M.D., Rush University Medical Center, Chicago, Illinois
Lou Ann Brown, Ph.D., Emory University, Atlanta, Georgia
Joseph H. Sisson, M.D., University of Nebraska Medical Center, Omaha, Nebraska
Although chronic alcohol ingestion injures specific target tissues including the liver, recent evidence demonstrates that chronic alcohol ingestion also predisposes non-traditional tissue targets such as the lung and intestinal epithelium to injury. Chronic alcohol ingestion predisposes to lung injury through alterations in pulmonary epithelial and endothelial function. Chronic alcohol ingestion perturbs gut epithelial function by similar mechanisms. The presenters in this symposium will highlight recent advances in the understanding of mechanisms by which chronic alcohol ingestion mediates epithelial and endothelial cell dysfunction in vitro and in vivo. The roles of alcohol-induced depletion of cellular glutathione, stimulation of reactive species, and activation of angiotensin II and transforming growth factor beta signaling will be discussed. Finally, clinically relevant strategies that prevent tissue and organ dysfunction will be reviewed, and the potential for these interventions as future strategies in the prevention or treatment of alcohol-related disease will be discussed.
Sunday, April 18, 2004 – 3:15 p.m. - 5:15 p.m.
Room 146 C – Washington Convention Center
Chair: Jerry M. Radziuk, M.D., Ottawa Hospital Department of Medicine, Ottawa, Ontario, Canada
Co-Chair: Robert Rizza, M.D., Mayo Clinic, Rochester, Minnesota
In addition to Dr. Radziuk and Rizza, the panel will include the following speakers:
Guenther Boden, M.D., Temple University Health Sciences, Philadelphia, Pennsylvania
Joseph Proietto, M.D., Ph.D., University of Melbourne, Royal Melbourne Hospital, Parkville, Australia
This symposium includes the possible role of increased glucose production in the pathogenesis of type 2 diabetes as well as in its evolution. Topics to be presented include “Is glucose production increased in type 2 diabetes?” “Contributions to glucose production in type 2 diabetes,” “Regulation of glucose production,” and “Molecular basis of glucose production.” Both the utility of glucose production as a primary target and potential molecular targets will be discussed in light of the above. The analysis of the efficacy of drugs that target the liver will be reviewed, as well as the potential for gene therapy.
Monday, April 19, 2004 – 10:30 a.m. - 12:30 p.m.
Room 145A – Washington Convention Center
Chair: Nir Barzilai, M.D., Albert Einstein College of Medicine, Bronx, New York
In addition to Dr. Barzilai, speakers on the panel will include:
Luciano Rossetti, M.D., Albert Einstein College of Medicine, Bronx, New York
Michael Brownlee, M.D., Albert Einstein College of Medicine, Bronx, New York
Meredith Hawkins, M.D., Albert Einstein College of Medicine, Bronx, New York
The ‘metabolic syndrome of aging’ in this program refers to a constellation of metabolic defects including insulin resistance, abdominal obesity, dyslipidemia, hypertension and increased circulating levels of pro-thrombotic and pro-inflammatory peptides. This syndrome is an important risk factor for cardiovascular disease and other age-related diseases, with significant impact on all-cause mortality. We hypothesize that aging is characterized by a decline in hypothalamic function leading to a relative or absolute increase in energy intake, increased fat mass and impaired regulation of fat distribution. We propose that the resulting increases in nutrient availability, total adiposity and abdominal fat distribution contribute both independently and cooperatively to the metabolic syndrome of aging. The hexosamine biosynthetic pathway (HBP) may provide a unifying role as a ‘nutrient-sensing’ pathway, since its activation by nutrient excess results in functional alterations of key intracellular proteins by glycosylation. Activation of the HBP in fat and endothelial cells induces the expression of pro-thrombotic and pro-inflammatory peptides, which may contribute to insulin resistance and endothelial dysfunction. Increased fat mass, and selective increases in the metabolically dangerous abdominal fat, would therefore potentiate the above process. The goals of this symposium are: To demonstrate that excess nutrients can initiate the key components of the metabolic syndrome of aging.; To implicate specific nutrient-sensing pathways in the pathophysiolgy of this syndrome; and to discuss new therapeutic approaches for the protection from age-related diseases. These lectures will be given by a team of investigators at the Albert Einstein College of Medicine. This symposium will spans the full spectrum from cell biology to in vivo animal physiology to ‘translational’ studies in humans.
Wednesday, April 21, 2004 – 8:00 a.m. - 10:00 a.m.
Room 146C – Washington Convention Center
Chair: Meredith Hawkins, M.D., Albert Einstein College of Medicine, Bronx, New York
Co-Chair: Errol D. Crook, M.D., Wayne State University School of Medicine, Detroit, Michigan
In addition to Drs. Hawkins and Crook, speakers on the panel will include:
Richard Burt, M.D., Northwestern University, Chicago, Illinois
Sanjeev Gupta, M.D., Albert Einstein College of Medicine, Bronx, New York
David A. Prentice, Ph.D., Indiana State University, Terre Haute, Indiana
Nigel M. de S. Cameron, Ph.D., Strategic Futures Group, LLC, Deerfield, Illinois
The pluripotent nature of ‘stem cells’ offers tremendous promise for cell therapy approaches to many debilitating diseases. Notwithstanding, this area of science is in its infancy. Embryonic, fetal and adult stem cells all carry unique possibilities alongside sizeable risks and limitations. Furthermore, the potential use of human fetal and embryonic cells opens vast bioethical minefields which must be treaded cautiously. This symposium will combine overviews of the scientific and bioethical issues with up-to-the-minute scientific presentations demonstrating significant advances in using both fetal/embryonic and adult stem cells to treat important clinical conditions. Drs. Prentice and Cameron, in reviewing the relevant science and bioethics, will draw upon considerable experience in presenting these challenging topics to high-profile audiences, including Congress and many Parliaments, as well as diverse scientific audiences. Drs. Gupta and Burt will present specific applications of fetal/embryonic and adult stem cell research in the treatment of such debilitating diseases as liver failure, diabetes mellitus, multiple sclerosis and systemic lupus erythematosis.
Wednesday, April 21, 2004 – 10:30 a.m. - 12:30 p.m.
Chair: Abdulla K. Salahudeen, M.D., University of Mississippi Medical Center, Jackson, Mississippi
In addition to Dr. Salahudeen, speakers on the panel will include:
Hamid Rabb, M.D., Johns Hopkins University School of Medicine, Baltimore, Maryland
Dr. Ursula Rauen, Ph.D., University of Essen, Germany
Kenneth B. Storey, Ph.D., F.R.S.C., Carleton University Dept. of Biology or Dept. of Chemistry, Ottawa, Ontario, K1S 5B6 Canada
Cadaver organs are routinely cold stored while awaiting transplantation. The average cold ischemia time (CIT) for kidney in US is still 18-24 hrs according to the latest United Network of Organs Sharing (UNOS) data. Such extended CIT is detrimental to the allografts and recipients in the short term. Recent UNOS data analysis from our group shows that extended CIT is also detrimental to the long-term survival of renal allograft. So, if cold storage is bad, can we do away with cold storage? The short answer is, not for now. For one, cold storage allows better tissue matching, which confers some survival advantage. Whether such advantage off sets the negative effect of cold ischemia is however, debatable. Now that cold storage is here to stay for now, more needs to be done to protect the organs against cold ischemic injury. Cold storage injury is potentially “intervenable” as most organ retrievals are carried out as an elective procedure, thus, providing opportunity to precondition or pretreat the organs prior to cold ischemia. As it stands, the “art” of cold storage is pretty much stuck in the 80s when Belzar and Southard introduced the University of Wisconsin (UW) solution. The good news is that a number of groups have been working on understanding the molecular and cellular mechanisms of cold ischemic injury. The objective of this symposium will be to recognize cold ischemic injury as an important mediator of short and probably long term allograft damage and attrition so as the clinicians and scientists can discuss possible ways to limit this form of injury in the light of newer cellular and molecular mechanisms.
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