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PUBLIC RELEASE DATE:
16-Jan-2013

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Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
@jclinicalinvest

JCI early table of contents for Jan. 16, 2013

Could probiotics help HIV patients?

Antiretroviral (ARV) drugs are the first line therapy for patients with HIV; however, ARV-treated, HIV-infected individuals still have a higher mortality rate than uninfected individuals. During the course of infection, HIV patients develop inflammation that damages the walls of the intestines, known as the gut mucosa, allowing intestinal microbes to escape and enter the blood stream to cause a life-threatening systemic infection. The health of the gut mucosa is significantly influenced by the complement of bacteria in the gut and there is mounting evidence that probiotic supplements benefit patients intestinal disorders, such as irritable bowel syndrome, C. difficile infection, and inflammatory bowel disease.

In this issue of the Journal of Clinical Investigation, researchers led by Jason Brenchley at the National Institute of Allergy and Infectious Disease, demonstrated that probiotic supplementation may also be beneficial for ARV-treated HIV patients. Brenchley and colleagues treated SIV-infected macaques (a model of human HIV-infection) with either ARV alone or ARV in combination with a mixture of probiotics. Macaques treated with probiotics had enhanced gastrointestinal immune function and decreased inflammation compared to macaques treated with ARV alone. In a companion article, Judith Aberg and colleagues at New York University School of Medicine discuss how these findings could benefit HIV patients.

TITLE:
Probiotic/prebiotic supplementation of antiretrovirals improves gastrointestinal immunity in SIV-infected macaques

AUTHOR CONTACT:
Jason M. Brenchley
NIAID NIH, Bethesda, MD, USA
Phone: 301-496-1498; E-mail: jbrenchl@mail.nih.gov

View this article at: http://www.jci.org/articles/view/66227?key=1cff041937d9040dfed7

ACCOMPANYING ARTICLE:

TITLE:
Clash of the microbes: let's bring back the good guys

AUTHOR CONTACT:
Judith Aberg
New York University School of Medicine, New York, NY, USA
Phone: 2122637300; E-mail: judith.aberg@nyumc.org

View this article at: http://www.jci.org/articles/view/66736?key=64b158b04e2a168811a3


Hepatitis B virus promotes oncogenesis through microRNA modulation

Viruses prompt oncogenic transformation by genetically altering infected cells. Several recent studies have demonstrated that viruses alter the expression of microRNAs, non-coding RNA molecules that can block the expression of target genes. In this issue of the Journal of Clinical Investigation, Xiaoje Xu and colleagues at the Beijing Institute of Biotechnology report that miR-148a is repressed by hepatitis B virus (HBV) X protein (HBx) to promote growth and metastasis of liver cancer. In normal liver cells, miR-148a represses the expression of the oncogenic protein HPIP, but the hepatitis B virus prevents expression of miR-148a, leading to increased levels of HPIP and subsequent oncogenic transformation. This study demonstrates that a cancer-associated virus promotes carcinogenesis through direct manipulation of a microRNA.

TITLE:
Hepatitis B virus X protein represses miRNA-148a to enhance tumorigenesis

AUTHOR CONTACT:
Qinong Ye
Beijing Institute of Biotechnology, Beijing, CHN
Phone: (8610)68180809; Fax: (8610)68248045; E-mail: yeqn66@yahoo.com

View this article at: http://www.jci.org/articles/view/64265?key=267b145ad442aacf5c02


ALSO IN THIS ISSUE

Osteoclast-specific cathepsin K deletion stimulates S1P-dependent bone formation

Dynamic visualization of RANKL and Th17-mediated osteoclast function

KDM2B promotes pancreatic cancer via Polycomb-dependent and -independent transcriptional programs

MiR-374a activates Wnt/ β-catenin signaling to promote breast cancer metastasis

mTORC1 inhibition restricts inflammation-associated gastrointestinal tumorigenesis in mice

Loss of SPARC in bladder cancer enhances carcinogenesis and progression | Back to top BONE BIOLOGY

TITLE:
Osteoclast-specific cathepsin K deletion stimulates S1P-dependent bone formation

AUTHOR CONTACT:
Roland Baron
Harvard School of Medicine and of Dental Medicine, Boston, MA, USA
Phone: 617.432.7320 or 7325; Fax: 617.432.1897; E-mail: roland_baron@hsdm.harvard.edu

View this article at: http://www.jci.org/articles/view/64840?key=c8170fcece15001cf8c0

TITLE:
Dynamic visualization of RANKL and Th17-mediated osteoclast function

AUTHOR CONTACT:
Masaru Ishii
WPI-Immunology Frontier Research Center, Osaka University, Osaka, JPN
Phone: 81668794268; Fax: 81668798296; E-mail: mishii@ifrec.osaka-u.ac.jp

View this article at: http://www.jci.org/articles/view/65054?key=63bed6989736b83be7fd

ONCOLOGY

TITLE:
KDM2B promotes pancreatic cancer via Polycomb-dependent and -independent transcriptional programs

AUTHOR CONTACT:
Nabeel Bardeesy
Massachusetts General Hospital, Boston, MA, USA
Phone: 617-643-2579; E-mail: bardeesy.Nabeel@mgh.harvard.edu

View this article at: http://www.jci.org/articles/view/64535?key=aecb23f1f9fae807216b

TITLE:
MicroRNA-374a activates Wnt/β-catenin signaling to promote breast cancer metastasis

AUTHOR CONTACT:
Mengfeng Li
Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, UNK, CHN
Phone: +86(20)87332748; Fax: +86(20)87331209; E-mail: limf@mail.sysu.edu.cn

View this article at: http://www.jci.org/articles/view/65871?key=3d080eabb1106f73d520

TITLE:
mTORC1 inhibition restricts inflammation-associated gastrointestinal tumorigenesis in mice

AUTHOR CONTACT:
Matthias Ernst
Ludwig Institute for Cancer Research Cancer Research, Melbourne, AUS
Phone: +61-3-9341-3155; Fax: +61-3-9341-3104; E-mail: matthias.ernst@ludwig.edu.au

View this article at: http://www.jci.org/articles/view/65086?key=30a0deb622897138b7bf

TITLE:
Loss of SPARC in bladder cancer enhances carcinogenesis and progression

AUTHOR CONTACT:
Dan Theodorescu
University of Colorado Denver, Aurora, CO, USA
Phone: 303-724-7135; E-mail: dan.theodorescu@ucdenver.edu

View this article at: http://www.jci.org/articles/view/64782?key=4dcefabf20a4259617c5

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