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Preview of articles to be published Jan. 3, 2012
Date:1/3/2012

conditions such as ICD. The researchers found that Zn-deficient individuals also lacked epidermal LCs. Kawamura and colleagues suggest that ATP released from injured keratinocytes, which accumulates because there are insufficient epidermal LCs to hydrolyze it, causes the skin inflammation observed in Zn-deficiency.

TITLE: Severe dermatitis with loss of epidermal Langerhans cells in human and mouse zinc deficiency

AUTHOR CONTACT:
Tatsuyoshi Kawamura
Departments of Dermatology, Faculty of Medicine, University of Yamanashi, Yamanashi, JPN
Phone: +81-55-273-6766; E-mail: tkawa@yamanashi.ac.jp
View this article at: http://www.jci.org/articles/view/58618?key=eee11997df6e91290768


NEUROLOGICAL DISEASE

New insight into genetic movement disorder

Paroxysmal non-kinesigenic dyskinesia (PNKD) is aa genetic movement disorder, with episodes precipitated by alcohol, coffee, and stress. It is caused by mutations in the PNKD gene, but the normal function of that gene had been a mystery. In new research, Louis J. Ptček and colleagues at the University of California, San Francisco, investigated the expression pattern and function of Pknd in mice. The group generated mice that expressed known human disease mutations in Pnkd, and found that mouse had a movement disorder similar to the human disease. In these mice, attacks of dyskinesia were characterized by activation of neurons in the basal ganglia and alteration of dopamine signaling in the striatum. This research helps uncover the function of PKND, and in part explains what goes wrong in PKND patients.

TITLE: Dopamine dysregulation in a mouse model of paroxysmal nonkinesigenic dyskinesia

AUTHOR CONTACT:
Louis J. Ptacek
University of California San Francisco, San Francisco, CA, USA
Phone: (415
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Contact: Karen Honey
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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