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Objective The mechanism of neutrophil adhesion to the endothelium during the earliest stages of acute inflammation, especially before the induction of adhesion molecules on endothelial cells, remains unknown.Westudied the possible involvement of platelets in this process.MethodsNeutrophils were added to humanumbilical vein-derived endothelial cells (HUVEC)with or without adherent platelets in the presence or absence of adhesionblocking monoclonal antibodies (mAbs). Adhesion of neutrophils to HUVEC at dynamic flow conditions was assessed using a flow chamber. Conclusions Immobilized platelets on the vessel wall with induced P-selectin on the surface biochemically and functionally promote the adhesion of neutrophils to endothelial cells.

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EUS was very useful for evaluation of submucosal injury in patients with GERD. EUS showed that a 6-wk course of lansoprazole therapy reduced thickening of esophageal wall, which was resistant to histamine H2-receptor antagonist therapy. Our results also suggest that inflammatory damage to the submucosal and muscle layers of the lower esophagus is the underlying mechanism of heartburn and associated symptoms in patients with endoscopically negative reflux disease.

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