vascular ring/nikotini

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3 matokeo

Is arginase a potential drug target in tobacco-induced pulmonary endothelial dysfunction?

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

BACKGROUND Tobacco-induced pulmonary vascular disease is partly driven by endothelial dysfunction. The bioavailability of the potent vasodilator nitric oxide (NO) depends on competition between NO synthase-3 (NOS3) and arginases for their common substrate (L-arginine). We tested the hypothesis

Tobacco-associated pulmonary vascular dysfunction in smokers: role of the ET-1 pathway.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

Pulmonary vascular remodeling and dysfunction associated to tobacco smoking might pave the way for the subsequent development of pulmonary hypertension. Its prognosis is dreadful and its underlying mechanisms are so far largely unknown in humans. To assess the potential role of endothelin-1 and its

Rerouting the plant phenylpropanoid pathway by expression of a novel bacterial enoyl-CoA hydratase/lyase enzyme function.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

The gene for a bacterial enoyl-CoA hydratase (crotonase) homolog (HCHL) previously shown to convert 4-coumaroyl-CoA, caffeoyl-CoA, and feruloyl-CoA to the corresponding hydroxybenzaldehydes in vitro provided an opportunity to subvert the plant phenylpropanoid pathway and channel carbon flux through

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Herbal & Natural Medicine

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