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Numerous clinical and in vitro studies have demonstrated that endothelial dysfunction induced by cigarette smoke is mediated by a lack of NO bioavailability, production of superoxide anions, and increased production and release of endothelin 18) ( Fig.1 )

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The move follows an intervention last year by a parliamentarian who wanted to know how to regulate the unequal treatment of smokers, who are more frequently absent from their desks, and non-smokers at the workplace