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(Stroke. 2006;37:286.)
© 2006 American Heart Association, Inc.

Advances in Stroke 2005

Introduction

Vladimir Hachinski, MD, DSc, Editor-in-Chief

From the London Health Sciences Center, University of Western Ontario, London, Ontario, Canada

Correspondence to Dr Vladimir Hachinski, University of Western Ontario, London Health Sciences Center, 339 Windermere Rd, London, Ontario N6A 5A5 Canada. E-mail vladimir.hachinski@lhsc.on.ca

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Knowledge about stroke continues to advance at a slow but unrelenting pace. In this issue of Stroke clinical and basic scientists highlight the progress made in 2005 in all areas of stroke.

The association of specific genes with a heterogeneous condition such as stroke can both delight and despair. Delight in identifying potential new causal factors and despair in the contradictory results of confirmatory studies. The identification of the phosphodiesterase 4D (PDE4D) and 5-Lipoxygenase activating protein (ALOX5AP) genes provide examples of associations with stroke risk, but subsequent studies both confirm and deny a relationship, despairing certainty seekers.

The recent completion of a halplotype map of the entire human genome (the Hap Map Project) may help narrow down the most relevant possibilities and accelerate the discovery and confirmation of disease-related genes. The alternative approach of monogenic disease continues to yield results. For example, a sickle cell disease model identified the 12 genes that interact with fetal hemoglobin to modulate risk of stroke, and allowed prediction of the occurrence of stroke with 95.2% accuracy.

Atherosclerosis may be the most common chronic inflammatory condition. Inflammation plays a role of both cause and effect in atherosclerosis. Inflamed vessels and inflamed blood interact, both affecting coagulation and blood flow.

Preconditioning affords the unique opportunity to study the repertoire of endogenous responses that confer neuroprotection after cerebral ischemia. One of the most encouraging recent developments has been the demonstration that preconditioning with lipopolysacharide, a TLR4 ligand, interleukin-1 and tissue necrotic factor confer . . . [Full Text of this Article]

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