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Platelets triggered by thrombin had decreased levels of vWF binding sites on the GPIb-IX complex but increased levels of GPIV critical to thrombospondin, shown in Figure 5 (146)

The review in antioxidant science concluded that while promising, more randomized studies are needed before such therapies can be considered proven

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Conclusions The present review summarizes the molecular mechanisms underlying the vascular cell toxicity effects of BaP in CVDs as follows: (1) numerous studies have demonstrated that BaP can accelerate the pathological progress of AS, and many lines of evidence show that excessive daily BaP intake is a potent risk factor which accompanied by AAA, HTN, and MI