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* From the Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, Denver, CO.
Correspondence to: David Riches, PhD, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, 4200 East 9th Ave, Box C272, Denver, CO 80262
(CHEST 2001; 120:1S)
Although Arthur C. Clarke considered 2001 to be the first year of the new millenium, the Pope disagreed and declared the year 2000 to be the first year of the new millenium. It was therefore fitting that the first meeting of the 43rd Annual Thomas L. Petty Aspen Lung Conference in the new millenium should focus on the mechanisms of pulmonary fibrosis, an appropriate return to the theme that was last visited in this forum a decade ago. In reviewing the program from the 1990 meeting, it was striking to note the remarkable progress that has been made in understanding the processes that lead from alveolar inflammation to dysregulation of the repair process and the ensuing interstitial and alveolar fibrosis. The results of studies completed in the last decade have revealed much about the nature of the initial inflammatory response in the lung and the mechanisms of epithelial injury. We have also learned a great deal about the cytokines, chemokines, and growth factors that promote excessive collagen matrix accumulation. However, while much progress has been made, many of the underlying concepts of the pathogenesis of pulmonary fibrosis have remained unchanged. Thus, the goal of the conference this year was to develop a program that would review, question, and hopefully challenge current paradigms of the pathogenesis of these disorders.
To address this goal, a thematic program was developed around six fundamental areas: (1) mechanisms of the initiation and resolution of injury, with an emphasis on the emerging role of death receptors in the apoptosis of inflammatory and epithelial cells; (2) the regulation of inflammation by chemokine and cytokines; (3) mechanisms and consequences of epithelial, fibroblast, and myofibroblast interactions; (4) the critical role of metalloproteinases and (5) growth factors in matrix remodelling; and (6) novel approaches to diagnosis, staging, and treatment of idiopathic pulmonary fibrosis. The program was anchored by an outstanding number of state-of-the-art speakers whose interests were highly relevant to the meeting focus, and was complemented by short presentations and posters that were selected from the submitted abstracts. For many of the participants, the conference this year will also be remembered as the year of the "confession," not to the seven deadly sins, but to the unexpected findings from knockout mice that turned out to be the exact opposite of what have been predicted. As is often the case in science and medicine, it is the unexpected that frequently provides the greatest clues and insights into the pathogenesis of a particular disorder or problem. The meeting concluded with a masterful and revealing conference summary by Robert Strieter, to whom we are indebted for his contributions to the success of this conference.
Last, but not least, we wish to express our gratitude to a number of people without whom this meeting would not be possible. Firstly, we are indebted to all the speakers and participants who so actively contributed to the success of this meeting, both in the formal sessions as well as during the social hours. Secondly, we wish to thank the Francis Family Foundation for their continuing and generous support of the Parker B. Francis Lectureship. Lastly, we wish to thank Jeanne Cleary, who kept us on track with regard to the planning and organization of the meeting and who took care of the arrangements for the state-of-the-art speakers and the catering for the social events. We hope you will enjoy reading the proceedings of the conference.
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