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Inflammation and Stroke
Benefits Without Harm?
Giora Z. Feuerstein, MD;
Xinkang Wang, PhD
From the Department of Cardiovascular Sciences, Dupont Pharmaceuticals
Co, Wilmington, Del.
Reprints: Giora Z. Feuerstein, MD, Senior Director, Department of
Cardiovascular Sciences, DuPont Pharmaceuticals Co, Experimental Station,
E400/3257A, Wilmington, DE 19880-0400 (e-mail: giora.z.feuerstein@dupontpharma.com).
Arch Neurol. 2001;58:672-674.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings. |
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AT THE onset of the 21st century, stroke is the third-leading cause
of death in most developed countries and the primary cardiovascular cause
of death in Japan and China.1 The health burden
of the disease is staggering as loss of a productive life inflicts a heavy
toll on patients, families, and society. Yet this disease has no effective
therapy beyond a limited group of patients (5%) who are treated with thrombolytics,
which have significant adverse effects. This situation prevails despite intense
research efforts and numerous clinical trials that have attempted to develop
drugs to reduce morbidity and mortality from stroke. So far, drug development
efforts have targeted modulators of ion channels (Ca2+and Na+), scavengers of oxygen radicals, and antagonists of excitotoxic neurotransmitters
(primarily glutamate and glycine receptors). However, clinical trials with
modulators of these targets have failed so far because of . . . [Full Text of this Article]
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