当社グループは 3,000 以上の世界的なカンファレンスシリーズ 米国、ヨーロッパ、世界中で毎年イベントが開催されます。 1,000 のより科学的な学会からの支援を受けたアジア および 700 以上の オープン アクセスを発行ジャーナルには 50,000 人以上の著名人が掲載されており、科学者が編集委員として名高い
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700 ジャーナル と 15,000,000 人の読者 各ジャーナルは 25,000 人以上の読者を獲得
Yancy Ferrer-Acosta, Marieli González, Mónica Fernández and Valance Washington A*
Platelets and their interaction with cells of the immune system contribute through a variety of molecular mechanisms to support hemostasis and inflammation. These simple yet essential cells exert their effects in lymphocytes, monocytes, and neutrophils, both recruiting and modulating their function after activation. Emerging evidence is starting to define the mechanisms that allow platelets to also play pivotal roles in host defense. For example, platelet cell-surface expression of toll-like receptors allows platelets to direct neutrophil activation toward extracellular trap formation and facilitate the elimination of blood pathogens. In addition to these well-known receptors, two of the most recently discovered platelet receptors, C-type lectin receptor 2 (CLEC-2), and TREM-like transcript-1 (TLT-1), have been shown to modulate hemostatic and inflammation-related roles in platelets. This review will discuss the evolution of our understanding of platelet functions from hemostasis to inflammation, and highlight novel mechanisms that platelets use to mediate hemostasis under inflammatory pressure.