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Showing 1–8 of 8 results
Advanced filters: Author: "Mark T Gladwin" Clear advanced filters

  • Blood transfusion saves many lives but carries the risk of injury, such as severe damage to the lungs. In 'Bedside to Bench', Janet S. Lee and Mark T. Gladwin examine the implications of clinical studies assessing such damage. The risk of injury seems to increase with the number of units transfused and may be greater with blood that has been stored longer. Researchers have yet to understand why, but several mechanisms are under scrutiny. In 'Bench to Bedside', Paul S. Frenette and Narla Mohandas discuss recent studies pinpointing a trigger—a specific antigen on neutrophils for a severe form of transfusion-related acute lung injury (TRALI). The findings could lead to new ways to diagnose TRALI and identify people at risk.

    • Janet S Lee
    • Mark T Gladwin
    Comments & Opinion
    Nature Medicine
    Volume: 16, P: 381-382

  • Adenosine therapy for sickle cell disease has been proposed to improve blood flow, mediate cytoprotection and inhibit natural killer cell activity. Complicating this approach, adenosine signaling also induces hemoglobin S polymerization, promoting 'sickling', vasoocclusion, hemolysis and organ damage (pages 79–86).

    • Mark T Gladwin
    News & Views
    Nature Medicine
    Volume: 17, P: 38-40

  • Cellular production of nitric oxide (NO) by nitric oxide synthase (NOS) in the face of limiting pools of arginine requires the intracellular citrulline-to-NO pathway, catalyzed by the enzyme argininosuccinate lyase (ASL). People with the urea cycle disorder argininosuccinic aciduria, caused by a deficiency of ASL, have systemic NO deficiency, which can be rescued by the use of an alternative, NOS-independent, nitrite-to-NO pathway.

    • Mark T Gladwin
    • Jesús Tejero
    News & Views
    Nature Medicine
    Volume: 17, P: 1556-1557

  • Nitric oxide is a vital signalling molecule that controls blood flow and pressure. Unexpectedly, a redox switch in the protein haemoglobin α within endothelial cells regulates this molecule's diffusion in blood vessels. See Letter p.473

    • Mark T. Gladwin
    • Daniel B. Kim-Shapiro
    News & Views
    Nature
    Volume: 491, P: 344-345

  • Inorganic nitrate and nitrite from endogenous or dietary sources are metabolized in vivo to nitric oxide (NO) and other bioactive nitrogen oxides. The nitrate-nitrite-NO pathway is emerging as an important mediator of blood flow regulation, cell signaling, energetics and tissue responses to hypoxia. The latest advances in our understanding of the biochemistry, physiology and therapeutics of nitrate, nitrite and NO were discussed during a recent 2-day meeting at the Nobel Forum, Karolinska Institutet in Stockholm.

    • Jon O Lundberg
    • Mark T Gladwin
    • Eddie Weitzberg
    News & Views
    Nature Chemical Biology
    Volume: 5, P: 865-869

  • The supposedly inert end products of endogenous nitric oxide (NO) metabolism — nitrate and nitrite — have recently been shown to be an important alternative source of NO, complementing the classical NO-synthase pathway. Lundberg and colleagues discuss the emerging role of the nitrate–nitrite–NO pathway, highlighting the therapeutic potential of nitrate and nitrite in various disorders, including myocardial infarction, stroke, systemic and pulmonary hypertension, and gastric ulceration.

    • Jon O. Lundberg
    • Eddie Weitzberg
    • Mark T. Gladwin
    Reviews
    Nature Reviews Drug Discovery
    Volume: 7, P: 156-167

  • Nitric oxide (NO) is now established as a pivotal signalling molecule in the regulation of the cardiovascular system, and it has an important role in protection against cardiovascular disease. Here, Lundberget al. discuss the limitations of existing NO-targeting agents and assess emerging novel approaches to therapeutically modulate NO bioavailability.

    • Jon O. Lundberg
    • Mark T. Gladwin
    • Eddie Weitzberg
    Reviews
    Nature Reviews Drug Discovery
    Volume: 14, P: 623-641