Nogo‐B expression,in arterial intima,is impeded in the early stages of atherosclerosis in humans

Nogo‐B (Reticulon 4B) is considered to be a novel vascular marker, which may have a protective role in injury‐induced neointima formation and atherosclerosis. Nogo A/B is found to be crucial for monocyte/macrophage recruitment in acute inflammation and it is expressed in CD68 + macrophages. We hypothesize that macrophage infiltration in atherosclerosis is not dependent on Nogo‐B expression in arterial wall. We have assessed Nogo‐B expression and macrophage accumulation in the iliac arteries of healthy organ donors and organ donors with cardiovascular risk factors. Paraffin sections of 66 iliac arteries, from 44 deceased organ donors (17 women and 27 men), were studied. The healthy and cardiovascular risk (CVR) subgroups were created. With regard to staging of the atherosclerotic process, the thickness of arterial intima was measured in digitalized images of H+E stained tissue sections. Immunohistochemical reactions (Nogo‐B and CD68) were carried out in all arteries (66 samples). Western blotting (WB‐19 samples) and real‐time PCR (27 samples) were performed on selected arteries. Significantly higher Nogo‐B expression was demonstrated in the intima of the healthy subjects' subgroup, using immunohistochemistry. WB and real‐time PCR revealed a trend toward lower Nogo‐B expression in the adventitia of the CVR subgroup. Furthermore, the thickness of the intima was found to negatively correlate with the expression of Nogo‐B in the intima and media (r = ?0.32; p < 0.05; r = ?0.32; p < 0.05). Macrophage infiltrates were more prominent in intima of CVR subjects (0.65 vs 3.52 a.u.; p < 0.01). Macrophage density in intima increased with atherosclerosis progression (r = 0.37; p < 0.01). CD68 macrophages density in adventitia was lower in CVR arteries than in healthy arteries. The expression of Nogo‐B, in arterial intima, is impeded in the early stages of atherosclerosis. Accumulation of arterial intimal CD68 macrophages has been shown to progress; however, the overall macrophage density in the adventitia is reduced in arteries shown to have intimal thickening. Macrophage infiltration is not accompanied by Nogo‐B expression in atherosclerotic arteries.     

High and Low Stimulus-Driven Conflict Engage Segregated Brain Networks,Not Quantitatively Different Resources

Task-irrelevant information is constantly present in our environment and may interfere with the processing of the information necessary to achieve goal-directed behavior. While task goals determine which information must be suppressed, the demand for inhibitory control depends on the strength of the interference induced by incoming, task-irrelevant information. Whether the same or distinct inhibitory processes are engaged to suppress various degrees of interference from task-irrelevant information remains largely unresolved. We investigated this question by manipulating the strength of the conflict induced by automatic word reading in a classical color Stroop task. High conflict was induced by presenting words in participant’s native language and low conflict by presenting words in a less familiar language. Behavioral performance and electrical neuroimaging analyses of event-related potentials to the words were analyzed following a two-by-two within-subject design with factors conflict strength (high; low) and color word/word ink congruency (congruent; incongruent). Behaviorally, we observed a significant conflict strength × congruency driven by a smaller Stroop effect in the low- than high conflict condition. Electrophysiologically, we observed a significant conflict strength × congruency interaction at the topographic level during the period of the N450 components, indicative of the engagement of distinct configurations of brain networks. No such interaction was found at the level of response strength. Electrical sources analyses localized the topographic effect within the anterior cingulate cortex and basal ganglia, left middle frontal and occipital areas. We interpret our results in terms of qualitatively distinct executive mechanisms for reactive inhibitory control in conditions of high versus low stimulus-driven conflict.