News & Views in 2003

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    • Charlotte Schubert
    • Pierrette Lo
    News & Views
  • Epilepsy remains a hard-to-treat disorder for millions of patients. Gene therapy to target brain regions with seizure-reducing compounds is one approach that has met with limited experimental success. An innovative form of genetic manipulation now reduces seizure susceptibility and seizure-induced brain injury in rats (pages 1076–1080).

    • Gregory L Holmes
    • Yezekiel Ben-Ari
    News & Views
  • Anthrax toxin is known to impair key signaling pathways, but exactly how does this damage the body or benefit the bacterium? Impairment of host immunity is now linked to an enzymatic activity of the toxin.

    • Michael N Starnbach
    • R John Collier
    News & Views
  • When do cancer cells acquire metastatic identity? Recent reports have indicated that the propensity to metastasize might be hardwired early during tumor development. Now it seems that breast cancer cells might acquire a gene signature early in tumorigenesis that predicts the site of metastasis.

    • Laura J Van't Veer
    • Britta Weigelt
    News & Views
  • Two new therapeutic strategies show promise in mouse models of hemophilia. One uses an RNA repair approach relying on trans-splicing to patch a genetic defect in a mouse model. Another aims at microparticles, cell fragments that seem to promote coagulation (pages 1015–1019 and 1020–1025).

    • Katherine A High
    News & Views
  • Stabilization of the cardiac ryanodine receptor may represent a new concept in treating sudden cardiac death in several heart disorders.

    • Patrick Most
    • Walter J Koch
    News & Views
  • New antibodies specific for the misfolded, and presumably pathogenic, form of the PrP protein have now made their long-awaited debut. These antibodies could provide tools for diagnostics, research and therapy (pages 893–899).

    • Byron Caughey
    News & Views
  • Autoantibodies to group A streptococcocal sugar moieties are now implicated in Sydenham chorea, a neuropsychiatric complication of rheumatic fever. These antibodies appear to disturb neuronal cell function by binding to glycolipids (pages 914–920).

    • Robert S Fujinami
    • Thayne L Sweeten
    News & Views
  • Expanded glutamine repeats cause brain degeneration associated with protein misfolding and aggregation. Two studies now look beyond the repeat, implicating the phosphatidylinositol-3-kinase (PI-3K)/Akt signaling pathway and 14-3-3 proteins in polyglutamine toxicity.

    • Henry Paulson
    News & Views
  • Improper ion balance resulting from defects in the ion channel CFTR underlies cystic fibrosis. Separate control mechanisms are now shown to regulate the flux of chloride and bicarbonate through this channel.

    • Jeffrey J Wine
    News & Views
  • Angiogenesis inhibitors have shown promise in hindering blood supply and holding tumors in check. But it now seems that such inhibitors, by depriving tumors of oxygen, could have an unintended effect: promotion of metastasis.

    • Patricia S Steeg
    News & Views
    • Charlotte Schubert
    • Stacie Grossman
    News & Views
  • Astrocyte projections extend to the blood-brain barrier (BBB) and promote its maturation. These astrocytes are now shown to secrete a factor that appears to integrate signaling networks necessary for BBB development and maintenance (pages 900–906).

    • Peter Rieckmann
    • Britta Engelhardt
    News & Views
  • Interleukin (IL)-2 can shrink tumors in patients with refractory melanoma and renal cancer, two of the deadliest types of solid tumors, but the use of IL-2 is limited by its high toxicity. A new drug reduces the side effects in mouse models and boosts the tumor-busting capacity of IL-2 (pages 750–755).

    • Jeffrey A Sosman
    • James W Mier
    News & Views
  • Vaccines using DNA for priming and recombinant modified vaccinia Ankara virus (MVA) for boosting have shown great promise in preclinical models. Now, this novel protocol appears effective in humans (pages 729–735).

    • Harriet L Robinson
    News & Views
  • Mutations in the gene that encodes nuclear lamins A and C cause a host of diseases, ranging from dilated cardiomyopathy to lipid disorders. The aging syndrome, Hutchinson-Gilford progeria, is now added to the list.

    • Robert A Hegele
    News & Views