Volume 11 Issue 9, 1 September 2005

Technical Report



Brief Communication



Book Review

News & Views

  • News & Views |

    Neurons in the brain of individuals with focal epilepsy exhibit sustained discharges, called paroxysmal depolarization shifts. Unexpected new evidence indicates that glutamate release from glia can generate these events, and may serve to synchronize the activity of neurons ( pages 973–981 ).

    • Michael A Rogawski
  • News & Views |

    Normal cells can respond to expression of activated oncogenes by initiating cellular senescence, a permanent state of proliferative arrest. But whether this process reflects a relevant anticancer mechanism has been debated. Several studies now show that oncogene-induced senescence can occur in vivo and provides a bona fide barrier to tumorigenesis.

    • Masashi Narita
    •  & Scott W Lowe
  • News & Views |

    Loss of the transcription factor Gax is at the center of blood vessel dysregulation in the brain and contributes to Alzheimer disease pathology ( pages 959–965 ).

    • Costantino Iadecola
  • News & Views |

    Small molecules that specifically inhibit PI3Kγ block disease in mouse models of arthritis and lupus ( pages 936–943 ).

    • Pamela S Ohashi
    •  & James R Woodgett
  • News & Views |

    Fresh approaches are needed for antiangiogenesis therapies that target blood vessel growth in tumors. Knocking down multiple regulators of angiogenesis might provide a way forward ( pages 992–997 ).

    • Robert M Strieter
  • News & Views |

    Plague bacteria are renowned for causing some of the most devastating epidemics in human history. We are now closer to understanding why: the pathogen selectively disarms key cells of the innate immune system, weakening the front-line defenses of the body.

    • Frank R DeLeo
    •  & B Joseph Hinnebusch
  • News & Views |

    Molecules that recognize pathogens and activate the immune response are being discovered at a rapid rate. RIG-I, a new protein in this category, recognizes viral RNA. Recent studies show that RIG-I operates independently of Toll-like receptors and that it is targeted for inactivation by the hepatitis C virus.

    • Chris A Benedict
    •  & Carl F Ware