Furthermore, all bacterial and archaeal CcSDHlike enzymes lack the cytochrome domain present in some of the fungal enzymes. This observation raises the question as to how eukaryotes such as fungi acquired genes encoding PQQ-dependent enzymes. It is worth noting that this discovery would not have been possible using the usual approach of searching for PQQdependent enzymes. Our results indicate the existence of a previously unknown enzyme family. That PQQ is a beneficial vitamin for humans has been reported. In view of our findings, novel PQQ-dependent enzyme may exist in humans. Platelets and monocytes play a crucial role in the initiation and progression of atherosclerosis. Platelets tether and roll over inflamed endothelial cells through transient interactions between platelet Glycoprotein Iba and endothelial P-selectin. The role of platelet binding to inflamed endothelial cells during the development of atherosclerosis was evidenced by a significant reduction in monocyte accumulation and atherosclerotic plaque progression after treatment with GPIba blocking antibodies. The interaction of platelets with inflamed endothelial cells also facilitates the capturing of monocytes to the vessel wall through interaction between Gp1ba and the constitutively expressed monocyte receptor P-Selectin Glycoprotein Ligand-1. This interaction, together with the interaction between GPIba and the integrin macrophage-1 antigen, results in firm cellular arrest of monocytes and their subsequent Etidronate infiltration into the vascular wall. Besides the capturing of monocytes to the vessel wall by interaction of monocytes with platelets that are bound to inflamed endothelial cells, platelets also bind circulating monocytes. Previous work has shown that formation of these circulating platelet-monocyte complexes results in increased infiltration of monocytes into atherosclerotic plaques in mice and elevated levels of circulating PMCs were observed in patients with coronary artery disease. Infiltration of monocytes into atherosclerotic plaques worsens atherosclerosis. Monocytes migrate into atherosclerotic plaques, where they differentiate into macrophages. These macrophages secrete proteases and inflammatory proteins that weaken the fibrous cap, which increases the risk of plaque rupture. Rupture-prone plaques are characterized by a thin fibrous cap covering a large lipid core that is enriched with macrophages. Stable plaques contain less macrophages and are enriched with smooth muscle cells and high amounts of collagen. After plaque rupture, platelets are activated and the formation of an occlusive thrombus can occur. The role of platelet activation in atherosclerotic disease progression has been demonstrated by a reduction of cardiovascular events after platelet inhibition therapies. Moreover, Pselectin knockout mice showed Cefetamet pivoxil HCl decreased monocyte adherence to the vessel wall and hence decreased atherosclerotic plaque formation. Platelet activation is triggered through stimulation of various receptors that stimulate integrin aIIbb3 activation, which is crucial for platelet aggregation. Several assays that measure platelet aggregation are currently available, e.g.; light transmission aggregometry, VerifyNow and platelet function analysis system. We have optimized a whole blood flow cytometry assay that measures platelet activation instead of platelet aggregation. Our assay is based on the platelet response to increasing concentrations of adenosine diphosphate, which was quantified by the measurement of P-selectin upregulation after stimulation.