Dysregulated arginine metabolism, hemolysis-associated pulmonary hypertension, and mortality in sickle cell disease.

By C. Morris, Gregory J. Kato, M. Poljakovic, Xunde Wang, W. Blackwelder, V. Sachdev, S. Hazen, E. Vichinsky, S. Morris, M. Gladwin. Journal of the American Medical Association (JAMA), 2005

698 citations recorded by the source corpus.

Subfields: Genetics, Physiology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/58c727b6268b8bbab93eb608d03f9f866a7b7f16

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Genetics

1. Thomas Spencer
2. Gregory J. Kato
3. F. Bazer
4. M. Gladwin

In Physiology

1. Thomas Spencer
2. S. Kim
3. Peng Li
4. M. Satterfield
5. F. Bazer

Citations in the corpus

• Arginine metabolism and nutrition in growth, health and disease (2008, background): “…the injury to other cell types, results in elevated levels of arginase and reduced concentrations of Arg in plasma, impaired NO synthesis by endothelial cells (Morris et al. 2005; Romero et al. 2002), as well as microvascular vaso-occlusion, vasoculopathy, and multiorgan injury (Wood et al. 2008).”
• Arginine metabolism: boundaries of our knowledge. (2007, background): “However, recent studies of patients with sickle cell disease have revealed a new paradigm for pathological effects of the arginases, namely, changes in localization of arginase (80).”
• Lactate dehydrogenase as a biomarker of hemolysis-associated nitric oxide resistance, priapism, leg ulceration, pulmonary hypertension, and death in patients with sickle cell disease. (2005, methodology): “The second involves the release of erythrocyte arginase, which converts plasma L-arginine into ornithine, resulting in depletion of plasma L-arginine, the required substrate for nitric oxide production by nitric oxide synthase, with associated pulmonary hypertension.(19;20;37) LDH also correlates wi”