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JCI early table of contents for March 26, 2012
Date:3/20/2012

normally function in Ca2+-mediated signaling pathways that couple adaptive/neurotrophic responses to metabolic and oxidative stress, and suggest that disruption of these pathways may contribute to PD.

COMMENTARY TITLE:

Parkinson Disease: Don't Mess with Calcium

COMMENTARY AUTHOR CONTACT:

Mark Mattson

National Institute on Aging, Baltimore, MD, USA

Phone: 410 558 8463; E-mail: mattsonm@grc.nia.nih.gov

View this article at: http://www.jci.org/articles/view/62835?key=24384dcabf70f47d05f3

RESEARCH ARTICLE TITLE

Neurotoxin-induced ER stress in mouse dopaminergic neurons involves downregulation of TRPC1 and inhibition of AKT/mTOR signaling

CORRESPONDING AUTHOR CONTACT:

Brij Singh

School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND, USA

Phone: 701-777-0834; Fax: 701-777-2382; E-mail: brij.singh@med.und.edu

View this article at: http://www.jci.org/articles/view/61332?key=256b328425acdd810dd2


HEMATOLOGY
Unintended consequences: how transfusions of aged blood impact recipients

Blood transfusion represents the first and most prescribed cell-based therapy, however, clinical safety and efficacy trials are lacking. Clinical cohort studies have suggested that massive transfusion and/or transfusion of aged stored blood may contribute to multi-organ dysfunction in susceptible patients. In this issue of the JCI, Baek and colleagues report that aged stored blood hemolyzes after massive transfusion in a guinea pig model. Hemolysis led to vascular and kidney injury that was mediated by cell-free plasma hemoglobin and prevented by co-infusion of the
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Contact: Sarah Jackson
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

Page: 1 2 3 4 5 6

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