(Q48612035)

13 February 2018

title

Hypoxaemia in sickle cell disease: biomarker modulation and relevance to pathophysiology (English)

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13 February 2018

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1

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13 February 2018

Carlton Dampier

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13 February 2018

author name string

Marie J Stuart

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13 February 2018

Darcy Brodecki

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13 February 2018

Julian L Allen

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13 February 2018

language of work or name

English

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publication date

1 November 2003

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13 February 2018

published in

The Lancet

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13 February 2018

volume

362

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13 February 2018

issue

9394

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13 February 2018

page(s)

1450-1455

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13 February 2018

Sickle cell vaso-occlusion: multistep and multicellular paradigm

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Microvascular sites and characteristics of sickle cell adhesion to vascular endothelium in shear flow conditions: pathophysiological implications

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Nocturnal hypoxaemia and central-nervous-system events in sickle-cell disease

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Enhanced levels of soluble VCAM-1 in sickle cell patients and their specific increment during vasoocclusive crisis

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Perfusion with sickle erythrocytes up-regulates ICAM-1 and VCAM-1 gene expression in cultured human endothelial cells

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Hypoxia-mediated induction of endothelial cell interleukin-1 alpha. An autocrine mechanism promoting expression of leukocyte adhesion molecules on the vessel surface

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Hypoxia decreases constitutive nitric oxide synthase transcript and protein in cultured endothelial cells

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Neutrophil activation in sickle cell disease

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Platelet and leucocyte activation in childhood sickle cell disease: association with nocturnal hypoxaemia.

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Hypoxia/reoxygenation causes inflammatory response in transgenic sickle mice but not in normal mice

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The acute chest syndrome in sickle cell disease. Possible role of nitric oxide in its pathophysiology and treatment

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Identifiers

DOI

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13 February 2018

1 reference

13 February 2018