The Pulpit and the Press in Reformation Italy

The converting sea: Religious change and cross‐cultural interaction in the early modern Mediterranean

“…Consequently, Catholic efforts to combat Protestantism and heresy across the Northern Mediterranean littoral and into the European heartland (Armstrong, ; Luria, , pp. 47–102; Michelson, ) and Catholic missionary work among Eastern Rite Christians (Clines, ; Forrestal & Smith, ; Piccirillo, ; Ruiu, ) should be considered pan‐Mediterranean processes of confessional and political consolidation through evangelization, the very processes that were also applied in missions further afield. In other words, early modern Catholicism became a global faith partly because of the conversionary tactics sharpened in the Mediterranean both before and after the opening up of the Atlantic and Indian Ocean Worlds (Selwyn, ).…”

Genetic Loci Associated with Platelet Traits and Platelet Disorders

“…Platelet function is complex: with vascular injury, normal platelets adhere to exposed collagen and to von Willebrand factor bound to collagen. [1][2][3] This triggers the generation and secretion of thromboxane A 2 (TXA 2 ) and platelet storage granule release. [1][2][3] Platelets then undergo further activation, with intracellular signaling triggered by their released TXA 2 , adenosine diphosphate (ADP), serotonin, and other agonists (such as thrombin) that are generated at the sites of vessel injury.…”

“…[1][2][3] This triggers the generation and secretion of thromboxane A 2 (TXA 2 ) and platelet storage granule release. [1][2][3] Platelets then undergo further activation, with intracellular signaling triggered by their released TXA 2 , adenosine diphosphate (ADP), serotonin, and other agonists (such as thrombin) that are generated at the sites of vessel injury. [1][2][3] Genetic defects can impair platelet hemostatic function in many ways, from modifying platelet-vessel wall interactions, through changes in the number of circulating platelets, and/or their size, adhesive properties, responses to agonists, intracellular signaling, granule release, and the feedback that signaling and secretion have on platelet activation and prohemostatic function.…”

“…[1][2][3] Platelets then undergo further activation, with intracellular signaling triggered by their released TXA 2 , adenosine diphosphate (ADP), serotonin, and other agonists (such as thrombin) that are generated at the sites of vessel injury. [1][2][3] Genetic defects can impair platelet hemostatic function in many ways, from modifying platelet-vessel wall interactions, through changes in the number of circulating platelets, and/or their size, adhesive properties, responses to agonists, intracellular signaling, granule release, and the feedback that signaling and secretion have on platelet activation and prohemostatic function. [1][2][3] The purpose of this review is to summarize the current state of knowledge on the genetic loci that influence platelet functions and traits, including the genes that may contain disease-causing mutations in those characterized forms of inherited platelet disorders and other conditions that modify platelets.…”

“…[1][2][3] Genetic defects can impair platelet hemostatic function in many ways, from modifying platelet-vessel wall interactions, through changes in the number of circulating platelets, and/or their size, adhesive properties, responses to agonists, intracellular signaling, granule release, and the feedback that signaling and secretion have on platelet activation and prohemostatic function. [1][2][3] The purpose of this review is to summarize the current state of knowledge on the genetic loci that influence platelet functions and traits, including the genes that may contain disease-causing mutations in those characterized forms of inherited platelet disorders and other conditions that modify platelets. association studies (GWAS) of different populations have expanded the list of genetic loci that show significant associations to platelet traits (►Table 1 summarizes information on the associations with p values 1 Â 10 À5 ).…”