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Stroke. 2004;35:2613-2614
Published online before print September 30, 2004, doi: 10.1161/01.STR.0000144053.28166.a4
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(Stroke. 2004;35:2613.)
© 2004 American Heart Association, Inc.


Articles

Princeton Conference Supplement

Preface

Richard J. Traystman, PhD

From the Oregon Health and Science University, Portland, Ore.

Correspondence to Dr Richard J. Traystman, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Mail Code L335, Portland, OR. 97239-3098. Email traystma{at}ohsu.edu


*    Introduction
up arrowTop
*Introduction
down arrowMajor Sponsors
down arrowSponsors
down arrowContributors
 
The Princeton Conference has a one-half century history as a unique, highly focused forum for the presentation and discussion of current scientific information and future directions in stroke research. The 24th Princeton Conference on Cerebrovascular Disease was held in Baltimore, Maryland, April 2 to 4, 2004, at the Baltimore Marriott Waterfront Hotel. This conference focused on the current status and future directions of stroke pathophysiology, diagnosis and treatment, with emphasis on cellular and molecular mechanisms of ischemic cell death and cell repair, and clinical aspects of imaging, risk factors, and therapeutic strategies in stroke. There were 10 major areas of presentation and discussion. The meeting began with a discussion of vascular dementia and included discussion of amyloid and epidemiology of Alzheimer disease and vascular dementias. The next discussion concerned multimodal imaging and its future in stroke. The role of sex steroids in stroke was the next area of discussion. Estrogen and progesterone were discussed as potential neuroprotection agents, and their differences as neuroprotectants in animal models was discussed in light of the recent major negative clinical trials. The ischemic penumbra, what it is, how to image it and its molecular identification was then discussed, and this was followed by an in-depth discussion of ischemic preconditioning. Cerebral ischemic preconditioning was considered from its genomic aspects and its occurrence in humans and the similarities between cerebral ischemic preconditioning and myocardial ischemic preconditioning. The conference continued forward to discuss recovery and rehabilitation in stroke, including progenitor cells, functional imaging and forced use-constraint therapy trials. Attention was then focused on statins and stroke, how they work in vessels and neurons, how they work in endothelium and on signaling mechanisms, and finally their role in inflammation in stroke. Clot lysis and thrombolysis were the next areas of discussion, and attention was focused on imaging clots, extracting clots, ultrasound identification of clots, and the potential injurious effect of lytic agents. Genomics and proteomics in stroke took the next discussion session, and topics such as multiple genes in stroke, clinical translated stroke genomics and phosphodiesterase 4D were discussed. The final session of the conference was devoted to emerging stroke therapies, new therapeutic targets for neuroprotection, and fast track therapy for drugs for stroke.

These sessions were unique in that each session was comprised of four speakers, two of whom were clinically oriented individuals, and two were basic scientists. Each speaker was instructed to orient their comments along "translational"$lines and to try to make their comments relevant to the patient. This translational theme was assisted by the fact that the co-chairs of each session (one a clinician, one a researcher) were instructed to lead the discussion along translational lines and bring the discussion back to the patient. Thus, this Princeton Conference provided a unique forum for promoting collaborative interaction in stroke research between the clinician and the basic scientist. There were vigorous interactive discussions among the participants, and the speakers presenting state-of-the-art information made for a very successful and memorable conference. The attendees were also treated to a fantastic lecture given by Peter Agre, the Nobel Prize winner in chemistry in 2003, concerning Aquaporin Water Channels, from Atomic Structure to Clinical Medicine. This lecture, too, kept in mind the overall theme of the conference of translational science.

There was much enthusiasm and excitement in the presentations and in the discussions that ensued, and I believe this reflected the success of the conference. I hope the excitement and enthusiasm of this conference carries over into the next Princeton Conference, and I hope that much new work will result from the discussions of the 24th Princeton Conference and thus advance our knowledge of the basic and clinical aspects of stroke in patients.


*    Major Sponsors
up arrowTop
up arrowIntroduction
*Major Sponsors
down arrowSponsors
down arrowContributors
 
Astra Zeneca Pharmaceuticals

Centocor, Inc

Janssen-Ortho McNeil-Johnson & Johnson

Mitsubishi Pharma

National Institutes of Health - National Institute of Neurological Disorders and Stroke

Bristol-Myers Squibb/Sanofi-Synthelabo


*    Sponsors
up arrowTop
up arrowIntroduction
up arrowMajor Sponsors
*Sponsors
down arrowContributors
 
American Heart Association, American Stroke Association, Stroke Council

Boehringer-Ingelheim

Eisai Medical Research, Inc

Galileo Pharmaceuticals

Merck Research Laboratories

Millennium Pharmaceuticals

Pfizer Global Research & Development

Suntory Pharma Co., Ltd

Taisho Pharmaceutical Research & Development, Inc


*    Contributors
up arrowTop
up arrowIntroduction
up arrowMajor Sponsors
up arrowSponsors
*Contributors
 
Alsius Corporation

ESP Pharma

Fibrogen, Inc

Guilford Pharmaceuticals

Indevus Pharmaceuticals

La Jolla Pharma

Eli Lilly & Company

ThromboGenics, Ltd


*    Acknowledgments
 
The success of the 24th Princeton Conference on Cerebrovascular Disease was highly dependent on the contributions and cooperation of many individuals, including those who gave generously of their time as part of the Scientific Program Committee (Richard J. Traystman, PhD; Marc Fisher, MD; Philip B. Gorelick, MD, MPH; James C. Grotta, MD; Costantino Iadecola, MD; Kennedy R. Lees, MD; Michael A. Moskowitz, MD; Roger P. Simon, MD; Peter C.M. van Zijl, PhD). Ms Alysa Kowalski is greatly appreciated for her outstanding contribution in coordinating the events of the conference. This conference could not have been coordinated and executed so effectively without the able assistance and support of my long-term administrative assistant, Ms Candace J. Berryman. Her role to keep the organization of this conference on straight tracks cannot be overemphasized, and her role in keeping me well organized for the past 25 years is enormously appreciated. The Princeton Conference received very generous support from the National Institute of Neurological Disorders and Stroke (NINDS) and from many colleagues in the pharmaceutical industry and the American Stroke Association. A list of these contributors can be found here. Special thanks to our colleagues at NINDS who provided encouragement and support, in particular Tom P. Jacobs, PhD, and Katherine Woodbury-Harris, PhD. Their consistent, positive attitudes toward the Princeton Conference were helpful. We are also extremely grateful to Vladimir Hachinski, MD, who agreed to publish the Princeton Conference Proceedings as a supplement to the journal Stroke, and to Rebecca Nott whose consistent hard work managed to allow most of our manuscripts to be published in this supplement.

Received August 24, 2004; accepted August 24, 2004.





This Article
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01.STR.0000144053.28166.a4v1
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Right arrow Acute coronary syndromes