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JCI table of contents, January 2, 2004

in association with enhanced antiapoptotic gene expression. Diabetic mice showed significantly more damage, and there was no detectable protection afforded by estrogen replacement therapy. Such impaired wound healing is analogous to that seen in peripheral tissues but has never before been considered as part of the pathophysiology of ischemic stroke in the context of diabetes.

TITLE: Estrogen stimulates microglia and brain recovery from hypoxia-ischemia in normoglycemic but not diabetic female mice

AUTHOR CONTACT:
Susan J. Vannucci
Morgan Stanley Children's Hospital of New York, Columbia University College of Physicians and Surgeons, New York, New York, USA.
Phone: 212-305-8458
Fax: 212-342-2293
E-mail: sv2020@columbia.edu

View the PDF of this article at: https://www.the-jci.org/press/18336.pdf

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Avicins boost the stress response

Chronic disease states develop during the aging process as cellular stress responses and repair systems are worn down. In an effort to address the broad concept of disease mechanisms during stress and aging, Jordan Gutterman and colleagues from the University of Texas examined avicins, triterpenoid electrophiles isolated from the Australian desert tree Acacia victoriae, and their ability to control gene transcription. They found that avicin-treated cells had increased nuclear localization of the redox-regulated transcription factor Nrf-2. This, in turn, activated the transcription of genes containing the antioxidant response element (ARE) and a battery of stress response genes. In vivo experiments with mouse models stressed by UV light exposure resulted in significantly less severe skin damage after avicin treatment. These studies show the potential of a new class of metabolites for the treatment of stress-associat
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Contact: Brooke Grindlinger
science_editor@the-jci.org
212-342-9006
Journal of Clinical Investigation
2-Jan-2004


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