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Volume 8 Issue 12, December 2002

Sickle-cell anemia is a painful disease in which red blood cells (RBC) become crescent shaped due to inheritance of an abnormal type of hemoglobin. Sickled RBCs break down, releasing hemoglobin into the circulation. On page 1383, Reiter et al. show that the excess circulating hemoglobin reacts with nitric oxide (NO) more rapidly than hemoglobin in normal RBCs. NO plays an important role in regulating blood flow and when NO is unavailable (due to elimination by circulating hemoglobin) vessels constrict unnecessarily, resulting in severe pain. The cover image shows a sickled RBC among normal erythrocytes. Magnificaiton x 7400; photo by Photo Researchers.

Volume 8 Issue 12

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Editorial

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Letters to the Editor

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News

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Commentary

  • Breast cancer is the most common malignancy in females in most western countries, with about 1 in 10 women at risk of developing the disease in the course of their lifetimes. Since its introduction over 30 years ago, tamoxifen has been the mainstay of the endocrine treatment of breast cancer. It has become the most widely used anticancer drug, and may be thought of as among the first targeted therapies. Yet the results of a major new trial of endocrine therapy after surgery for breast cancer using aromatase inhibitors cast into question tamoxifen's future role.

    • Mitch Dowsett
    • Anthony Howell
    Commentary
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Book Review

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News & Views

  • Responses to group A streptococcal infection vary from slight discomfort to death. Now it seems that human susceptibility can depend on polymorphisms in genes encoding human leukocyte antigen class II (pages 1398–1404).

    • Birgitta Henriques Normark
    • Staffan Normark
    News & Views

  • Studies on patients with sickle-cell disease now shed light on the physiological battle between hemoglobin and the vasoregulator nitric oxide. It appears that hemoglobin scavenges NO in these patients, likely contributing to vascular complications (pages 1383–1389).

    • James C. Liao
    News & Views

  • In Duchenne muscular dystrophy, functional muscle fibers enlarge to compensate for damaged fibers. A new treatment in a mouse model makes muscles even larger and ameliorates symptoms of the disease.

    • Peter S. Zammit
    • Terence A. Partridge
    News & Views

  • Dysregulation of T cells and B cells occurs in lupus and other autoimmune diseases. A monoclonal antibody therapy that seems to activate T cells restores some balance in a mouse model of lupus (pages 1405–1413).

    • Gary M. Kammer
    News & Views

  • Epithelial peptides called defensins can kill microbes directly. New data reveal another function for some of these host antibiotics—enhancement of the innate immune response.

    • Elizabeth Kopp
    • Ruslan Medzhitov
    News & Views

  • Cancer can ensue when cells do not know who they are or where they are. In the intestine, a single regulator seems to take care of both of these issues of identity.

    • Catherine Booth
    • Gerard Brady
    • Christopher S. Potten
    News & Views

    • Charlotte Schubert
    • Ushma Savla
    News & Views
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Review Article

  • The cytokine, TNF, participates in virtually every aspect of stroke. Its effects, however, often appear contradictory. Analysis of the current model for TNF receptor signaling and TNF interactions with other stroke mediators helps to resolve some of these apparent discrepancies.

    • John M. Hallenbeck
    Review Article
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