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Carboni, A.

Publications and source records attributed to Carboni, A..

2 recordsLinked to original sources

Differential neural encoding of sound under visual attention is shaped by audiovisual precision and unimodal uncertainty priors

Selective attentional biases arising from one sensory modality may manifest in another. The effects of visuospatial attention, often considered a foundation for visual object perception, are unclear in the auditory domain during audiovisual (AV) scene processing. This study investigates temporal and spatial factors that facilitate such cross-modal bias transfer at the neural level. Auditory encoding of random tone pips in AV scenes was investigated via a temporal response function model (TRF) of the participants electroencephalogram (N=30). The spatially uninformative pips were associated with spatially distributed visual contrast reversals ( flips) through asynchronous, probabilistic AV temporal onset distributions. Participants deployed visuospatial selection on these AV stimuli to perform a task. A late (~300 ms) cross-modal transfer of the unimodal attentional bias was found on the neural representation of pips. Transfer depended on the selected visual input being (i) presented during or shortly after a related sound in a relatively limited temporal window (<165 ms); and (ii) positioned across limited (1:4) visual foreground to background ratios. In addition, the magnitude of attentional enhancement was proportional to the proximity of flips to the foreground area. The results indicate that ongoing neural representations of sounds can incorporate relevant visuospatial attributes for auditory stream segregation.

neuroscience

Increasing heart vascularisation after myocardial infarction using brain natriuretic peptide stimulation of endothelial and WT1+ epicardium-derived cells.

Brain natriuretic peptide (BNP) treatment increases heart function and decreases heart dilation after myocardial infarction. Here, we investigated whether part of the cardioprotective effect of BNP in infarcted hearts related to improved neovascularisation. Infarcted mice were treated with saline or BNP for 10 days. BNP treatment increased vascularisation and the number of endothelial cells in the infarct border and remote zones of infarcted hearts. Endothelial cell lineage tracing showed that BNP directly stimulated the proliferation of resident mature endothelial cells in both areas of the infarcted hearts, via NPR-A binding and p38 MAP kinase activation. BNP also stimulated the proliferation of WT1+ epicardium-derived cells but only in the hypoxic area of infarcted hearts. Our results demonstrated that these immature cells have a natural capacity to differentiate into endothelial cells in infarcted hearts. BNP treatment increased their proliferation but not their differentiation capacity. We identified new roles for BNP and new therapeutic strategies to improve heart recovery in infarcted hearts.

cell biology