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JCI early table of contents for Feb. 1, 2013

A gut feeling about neural stem cells

Proper function of the digestive system requires coordinated contraction of the muscle in the wall of the intestinal tract, regulated by the enteric nervous system. Damage or loss of these neurons can result in intestinal motility disorders, such as Hirschsprung's disease, for which there is a dearth of effective treatments. In principle, disorders of the enteric nervous system could be treated by cell therapy, but it was previously unknown whether transplanted stem cells could migrate to the appropriate location in the gut and then become neurons that could properly innervate the bowel. In this issue of the Journal of Clinical Investigation, Heather Young and colleagues at the University of Melbourne, isolated neural stem cells from mice, cultured them to promote the formation of neural precursor cells, and implanted them into the muscle in the colons of recipient mice. Young and colleagues found that these cells were able to migrate away from the transplantation site and develop into neurons that provided stimulation to the portions of the gut the regulate motility. These findings suggest that the transplantation of neural stem cells is a promising therapeutic avenue for the treatment of gastrointestinal motility disorders.

Transplanted progenitors generate functional enteric neurons in the postnatal colon

Heather Young
University of Melbourne, Parkville, UNK, AUS
Phone: +61383440007; E-mail:

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A cellular adhesion protein protects against inflammation

Cellular inflammation is mediated by a group of proteins known as the inflammasome. In this issue of the Journal of Clinical Investigation, Ziad Mallat and colleagues at Addenbrooke's Hospital in Cambridge, England, identified a protein, MFGE8, that blocks inflammasome activity. Using a mouse model of stroke, Mallat and colleagues determined that expression of MFGE8 inhibited the production of pro-inflammatory products and limited the area of injury after stroke. These results identify MFGE8 as an important regulator of inflammation that could potentially serve as a useful therapeutic target in inflammatory disease.

MFGE8 inhibits inflammasome-induced IL-1β production and limits post-ischemic cerebral injury

Ziad Mallat
University of Cambridge, Cambridge, GBR
Phone: +44 (0)1223 746720; E-mail:

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IQGAP1 suppresses TβRII-mediated myofibroblastic activation and metastatic growth in liver

Ningling Kang
Mayo Clinic in Rochester, Rochester, MN, USA
Phone: 5075387552; E-mail:

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Virus-induced hepatocellular carcinomas cause antigen-specific local tolerance

Thomas Blankenstein
Max Delbrck Center for Molecular Medicine, Berlin, DEU
Phone: 49-30-9406-2816; Fax: 49-30-9406-2453; E-mail:

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Host immunity contributes to the anti-melanoma activity of BRAF inhibitors

Mark J. Smyth
Peter MacCallum Cancer Institute, Victoria, AUS
Phone: 61 3 96563728; Fax: 61 3 92561411; E-mail:

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Adeno-associated virus capsid antigen presentation is dependent on endosomal escape

R. Jude Samulski
The Gene Therapy Center, Chapel Hill, NC, USA
Phone: 919.962.3285; Fax: 919-966-0907; E-mail:

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Two-photon imaging of phagocyte-mediated T cell activation in the CNS

Naoto Kawakami
*Ludwig Maximilians Universitt Mnchen, Institute of Clinical Neuroimmunol, Munich, DEU
Phone: +49 89 7095 8386; Fax: +49 89 7095 8380; E-mail:

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p53 centrosomal localization diagnoses ataxia-telangiectasia homozygotes and heterozygotes

Silvia Soddu
Regina Elena Cancer Institute, Rome, ITA
Phone: +39 065266 2492; Fax: +39 065266 2505;

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Contact: Jillian Hurst
Journal of Clinical Investigation

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