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Contact: Corinne Williams
Journal of Clinical Investigation

JCI early table of contents for Dec. 16, 2013

A mouse model to evaluate potential age-promoting compounds

While there are well-established mouse models to identify cancer-causing agents, similar models are not available to readily test and identify age-promoting agents. Recently, a mouse strain (p16LUC mice) was developed that can be used to evaluate the transcription of p16INK4, which is increasingly expressed during aging and in age-associated diseases. In this issue of the Journal of Clinical Investigation, Norman Sharpless and colleagues at the University of North Carolina evaluated potential age-promoting compounds, including arsenic, a high-fat diet, UV light, and cigarette smoke in p16LUC mice. The authors found that a high fat diet did not accelerate p16INK4 expression, but both UV light exposure and cigarette smoke exposure dramatically increased p16INK4 expression compared to controls that had not been exposed to these age-promoting compounds. This study demonstrates that p16LUC mice are an appropriate model system for evaluating potetnail age-promoting compounds.

TITLE: p16INK4A- reporter mice reveal age-promoting effects of environmental toxicants

AUTHOR CONTACT: Norman E. Sharpless
UNC-Chapel Hill, Chapel Hill, NC, USA
Phone: 919.966.8212; E-mail: nes@med.unc.edu

View this article at: http://www.jci.org/articles/view/70960?key=d3965dabfff1a9a955b1

Hybrid protein deregulates complement in dense deposit disease

Dense deposit disease is a rare congenital disorder that is associated with complement dysfunction and often results in end stage renal disease within 10 years of the initial diagnosis. A small percentage of dense deposit disease is associated with mutations in the genes encoding factor H or C3 and autoantibody production. In this issue of the Journal of Clinical Investigation, Peter Zipfel and colleagues at the Leibniz Institute for Natural Products Research and Infection Biology, evaluated an index family that had 2 reported cases of dense deposit disease. The authors identified a chromosomal deletion in the complement factor H–related (CFHR) gene cluster that resulted in production of a hybrid CFHR2/CFRH5, which stabilized C3 convertase. Treatment with soluble C1 restored C3 convertase decay and may be a promising treatment for patients with a similar refractory form of dense despite disease.

TITLE: Complement factor H–related hybrid protein deregulates complement in dense deposit disease

Leibniz Institute for Natural Product Research and Infection Biology, Jena, , DEU
Phone: 49 3641 5321300; Fax: 49 3641 5320807; E-mail: peter.zipfel@hki-jena.de

View this article at: http://www.jci.org/articles/view/71866?key=83adcf2d94cecbc2b962


TITLE: Therapeutic antagonists of microRNAs deplete leukemia-initiating cell activity

AUTHOR CONTACT: H. Leighton Grimes
Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA
Phone: 513-636-6089; Fax: 513-636-5355; E-mail: lee.grimes@cchmc.org

View this article at http://www.jci.org/articles/view/66005?key=461f9c110fddfb96da31

TITLE: Alveolar rhabdomyosarcoma–associated PAX3-FOXO1 promotes tumorigenesis via Hippo pathway suppression

AUTHOR CONTACT: Corinne Linardic
Duke University, Durham, NC, USA
Phone: (919) 681-3709; Fax: (919) 681-6906; E-mail:linar001@mc.duke.edu

View this article at: http://www.jci.org/articles/view/67087?key=a5432f0a3329d724875c

TITLE: Nervous glucose sensing regulates postnatal β cell proliferation and glucose homeostasis

AUTHOR CONTACT: Bernard Thorens
University of Lausanne, Lausanne, , CHE
Phone: +41 21 692 3981; Fax: +41 21 692 3985; E-mail: bernard.thorens@unil.ch

View this article at: http://www.jci.org/articles/view/69154?key=6b2f4b5a245d96b3aa7f

TITLE: Carbon monoxide-based therapy ameliorates acute pancreatitis via TLR4 inhibition

AUTHOR CONTACT: Aida Habtezion
Stanford University, Stanford, CA, USA
Phone: 650-725-3362; E-mail: aidah@stanford.edu

View this article at: http://www.jci.org/articles/view/71362?key=db62bacdf4a18d58900f

TITLE: Pancreatic cancer-associated retinoblastoma 1 dysfunction enables TGF-β to promote proliferation

Indiana University Medical School, Indianapolis, IN, USA
Phone: 3172786410; Fax: 317-274-8046; E-mail: mkorc@iu.edu

View this article at: http://www.jci.org/articles/view/71526?key=1116c32e0f4e94abbd75

TITLE: Lysosomal β-glucuronidase regulates Lyme and rheumatoid arthritis severity

University of Utah School of Medicine, Salt Lake City, UT, USA
Phone: 801 581-8386; Fax: 801-585-2417; E-mail: janis.weis@path.utah.edu

View this article at: http://www.jci.org/articles/view/72339?key=075142ed8f86221102fc


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