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Spheres of influence remain one of the most pervasive phenomena in the practice and history of international relations, yet only rarely have they been taken up analytically. To bring conceptual and discursive clarity, this article advances two arguments. First, it argues that spheres of influence are not a distinct form of hierarchy in international relations, but rather practices of control and exclusion that can be found within any ideal-type hierarchy. Second, these hierarchical practices are generally underspecified by those invoking the term. Different theoretical perspectives on international relations offer highly divergent ways of understanding control and exclusion, and all do so with plausible empirical mooring. Spheres of influence do not themselves denote a form of governance even if it does a form of order construction and maintenance. Any given empire, hegemonic order, or alliance may also be a sphere of influence depending on the practices that occur; the key is not to identify whether particular hierarchical traits are dispositive of one of these relational structures, but rather whether, and the extent to which, assertions of control and exclusion define the hierarchy.

Propyl gallate (PG) is a platelet agonist characterized by inducing platelet aggregation, protein tyrosine phosphorylation, and platelet factor 3 activity. The mechanisms of platelet activation following PG stimulation were examined by pre-incubating platelets with well-defined platelet inhibitors using platelet aggregation, protein tyrosine phosphorylation, activated plasma clotting time, and annexin V binding by flow cytometry. PG-induced platelet aggregation and tyrosine phosphorylation of multiple proteins were substantially abolished by aspirin, apyrase, and abciximab (c7E3), suggesting that PG is associated with activation of platelet cyclooxygenase 1, adenosine phosphate receptors, and glycoprotein IIb/IIIa, respectively. The phosphorylation of the cytoskeletal enzyme pp60(c-src) increased following PG stimulation, but was blunted by pre-incubation of platelets with aspirin, apyrase, and c7E3, suggesting that tyrosine kinase is important for the signal transduction of platelet aggregation. Propyl gallate also activates platelet factor 3 by decreasing the platelet coagulation time and increasing platelet annexin V binding. Platelet incubation with aspirin, apyrase, and c7E3 did not alter PG-induced platelet coagulation and annexin V binding. The results suggest that platelet factor 3 activation and membrane phosphotidylserine expression were not involved with activation of platelet cyclooxygenase, adenosine phosphate receptors, and glycoprotein IIb/IIIa. PG is unique in its ability to stimulate platelet aggregation and coagulation simultaneously, and platelet inhibitors in this study affect only platelet aggregation but not platelet coagulation.

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