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pubmed-article:11200069pubmed:abstractTextMany inflammatory mediators activate neutrophils (PMN) partly by increasing cytosolic calcium concentration ([Ca2+]i). Modulation of PMN [Ca2+]i might therefore be useful in regulating inflammation after shock or sepsis. The hemodynamic effects of traditional Ca2+ channel blockade, however, could endanger unstable patients. Store-operated calcium influx (SOCI) is known now to contribute to Ca2+ flux in "nonexcitable" cells. Therefore, we studied the role of SOCI in human PMN responses to the proinflammatory ligand PAF. PMN [Ca2+]i was studied by spectrofluorometry with and without external calcium. We studied the effects olld:pubmed
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pubmed-article:11200069pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:11200069pubmed:articleTitlePAF-mediated Ca2+ influx in human neutrophils occurs via store-operated mechanisms.lld:pubmed
pubmed-article:11200069pubmed:affiliationDepartment of Surgery, University of Medicine and Dentistry of New Jersey/New Jersey Medical School, Newark 07103, USA. hausercj@UMDNJ.edulld:pubmed
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