13 February 2013
Vol 5, Issue 172
  • Contents

    • Focus

      • Ovarian Aging: Breaking Up Is Hard to Fix

        Double-stranded breaks (DSBs) in DNA—which are essential for normal development—accumulate with age and contribute to reproductive aging. Age-related inhibition of DSB repair diminishes ovarian reserve in mice and women.

    • Research Articles

    • Editors' Choice

      • TRIPpin’ on a Fat Cell

        A newly discovered role for the transcription coregulator TRIP-Br2 may provide a target for preventing and treating obesity.

      • The Early Bird Gets the Virus

        HIV-positive persons treated soon after infection have a greater chance of retaining functional immune cells.

      • Running Interference on Tumor Growth

        A new clinical trial using siRNA to treat patients with liver tumors demonstrates safety and early signs of efficacy.

      • You Want To Give Me WHAT?

        Administration of feces proves superior to antibiotics for treatment of a common and frequently fatal bowel infection.

      • Revisiting Metformin

        Biguanides suppress hepatic glucagon signaling by decreasing production of cyclic AMP.

About The Cover

Cover image expansion

ONLINE COVER Breeding Infertility. On a depiction of the ovarian surface epithelium (brown), an oocyte (pink circle)—cradling its genome (in the nucleus, dark pink circle)—sits in the center of a stylized ovarian follicle, protected by surrounding support cells. But the mammalian ovary is not a protective environment. Unlike many somatic tissues, the female germ line ages early, with reproductive capacity beginning to diminish after young adulthood. In this week’s issue, Titus et al. show that double-strand breaks (DSBs) collect in oocytes genomes because of age-related missteps in DNA repair, which can stimulate apoptosis and diminish ovarian reserve. See accompanying Focus by Johnson and Keefe. [CREDIT: Y. HAMMOND AND C. BICKEL/SCIENCE TRANSLATIONAL MEDICINE]