We investigated implicit memory for unfamiliar objects with a task in which subjects decided whether structurally possible and impossible line drawings could exist in three-dimensional space. In Experiment 1, significant priming effects on object decision performance were observed after encoding of global, three-dimensional object structure but not local, two-dimensional object features. Explicit memory did not differ significantly as a function of global vs. local study processing. In Experiments 2 and 3, elaborative encoding had different effects on object decision and recognition performance, thus providing evidence for functional dissociation between implicit and explicit memory. Stochastic independence between object decision and recognition performance was also observed. Results were consistent with the hypothesis that implicit memory, as indexed by priming on the object decision task, depends on encoding of and access to structural descriptions of objects.

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Four experiments examined implicit memory or priming effects on an object decision task in which subjects decided whether structurally possible or impossible novel objects could exist in three-dimensional form. Results revealed equivalent levels of priming for possible objects after 1 vs. 4 5-s exposures to the same structural encoding task (Experiment 1) and when objects were studied with a single structural encoding task or 2 different structural encoding tasks (Experiment 3). Explicit memory, by contrast, was greatly affected by both manipulations. However, priming of possible objects was not observed when Ss were given only a single 1-s exposure to perform a structural encoding task (Experiment 2). No evidence for priming of impossible objects was observed in any of the 4 experiments. The data suggest that object decision priming depends on a presemantic structural description system that is distinct from episodic memory.

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The critical role for ADP in arterial thrombogenesis was established by the clinical success of P2Y12 antagonists, currently used at doses that block 40–50% of the P2Y12 on platelets. This study was designed to determine the role of P2Y12 in platelet thrombosis and how its complete absence affects the thrombotic process. P2Y12-null mice were generated by a gene-targeting strategy. Using an in vivo mesenteric artery injury model and real-time continuous analysis of the thrombotic process, we observed that the time for appearance of first thrombus was delayed and that only small, unstable thrombi formed in P2Y12–/– mice without reaching occlusive size, in the absence of aspirin. Platelet adhesion to vWF was impaired in P2Y12–/– platelets. While adhesion to fibrinogen and collagen appeared normal, the platelets in thrombi from P2Y12–/– mice on collagen were less dense and less activated than their WT counterparts. P2Y12–/– platelet activation was also reduced in response to ADP or a PAR-4–activating peptide. Thus, P2Y12 is involved in several key steps of thrombosis: platelet adhesion/activation, thrombus growth, and stability. The data suggest that more aggressive strategies of P2Y12 antagonism will be antithrombotic without the requirement of aspirin cotherapy and may provide benefits even to the aspirin-nonresponder population