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Background: Picking up statistical regularities of patterns from the environment is essential for predictive and adaptive behavior. One of the most important challenges is to understand how statistical learning occurs and how the acquired information consolidates and stabilizes in the brain. Evidence suggests that the prefrontal cortex (PFC) has a critical role in these processes; the division of labor between hemispheres, however, is less characterized., Objective/hypothesis: The aim of the present study was to directly investigate the causal role of the right and left PFC in statistical learning and its consolidation., Methods: Healthy, young adults were trained on a probabilistic sequence learning task. Anodal transcranial direct current stimulation (tDCS) over the right or left dorsolateral PFC (DLPFC) was applied during the training in order to modify learning-related cortical plasticity in the targeted brain regions by increasing neural excitability. Performance was tested during and immediately after the stimulation, 2-h and 24-h later., Results: We found that the anodal tDCS over the right DLPFC led to enhanced learning performance both after the 2-h and 24-h retention periods, suggesting the causal role of this area in statistical learning. In contrast, we did not find any effect of left DLPFC stimulation on learning., Conclusions: These results highlight the role of the right fronto-striatal network in statistical learning and its consolidation., (Copyright © 2015 Elsevier Inc. All rights reserved.)

The Mannose-binding lectin-associated serine proteases (MASPs) have been the subject of intensive research particularly over the past 10 years. First one, then two, and currently 3 MASPs have been characterized. Initially it was thought likely that the MBL + MASPs system would resemble very closely the C1 complex of the complement classical pathway, and that MASP1 and MASP2 would have similar activities to their classical pathway homologues C1r and C1s. MASP2 does certainly have similar activities to C1s, but MASP1 does not have the activities of either C1r or C1s. MASP1 has been thought to act on the complement system by cleaving C3 directly, but work with recombinant and purified native MASP1 shows that direct C3 cleavage by this protease is very slow, and may not be biologically significant. MASP1 and MASP2 appear not to have such a narrow specificity as C1r and C1s, and may have significant substrates other than complement proteins. As an example, MASP1 does cleave fibrinogen, releasing fibrinopeptide B (a chemotactic factor) and also cleaves and activates plasma transglutaminase (Factor XIII). These reactions are also relevant to defence against microorganisms, and may represent a biologically significant action of MASP1.