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Highlights • Local visual processing in ASD were investigated with EEG during a crowding task. • Target discrimination in presence of interfering flankers predicted ASD symptoms. • ASD group did not show beta desynchronization for resolving visual crowding scenes. • Altered beta response reflected atypical occipital–inferotemporal connectivity. • Altered beta connectivity in ASD may reflect abnormal long-range interactions., Sensory and perceptual anomalies may have a major impact on basic cognitive and social skills in humans. Autism Spectrum Disorder (ASD) represents a special perspective to explore this relationship, being characterized by both these features. The present study employed electroencephalography (EEG) to test whether detail-oriented visual perception, a recognized hallmark of ASD, is associated with altered neural oscillations and functional connectivity in the beta frequency band, considering its role in feedback and top-down reentrant signalling in the typical population. Using a visual crowding task, where participants had to discriminate a peripheral target letter surrounded by flankers at different distances, we found that detail-oriented processing in children with ASD, as compared to typically developing peers, could be attributed to anomalous oscillatory activity in the beta band (15–30 Hz), while no differences emerged in the alpha band (8–12 Hz). Altered beta oscillatory response reflected in turn atypical functional connectivity between occipital areas, where the initial stimulus analysis is accomplished, and infero-temporal regions, where objects identity is extracted. Such atypical beta connectivity predicted both ASD symptomatology and their detail-oriented processing. Overall, these results might be explained by an altered feedback connectivity within the visual system, with potential cascade effects in visual scene parsing and higher order functions.

Autism spectrum disorder (ASD) has long been associated with an inability to experience wholes without full attention to the constituent parts. A zoom-out attentional dysfunction might be partially responsible for this perceptual integration deficit in ASD. In the present study, the efficiency of attentional focusing mechanisms was investigated in children affected by ASD. We measured response latencies to a visual target onset displayed at three eccentricities from the fixation. Attentional resources were focused (zoom-in) or distributed (zoom-out) in the visual field presenting a small (containing only the nearest target eccentricity) or large (containing also the farthest target eccentricity) cue, 100 or 800 msec, before the target onset. Typically developing children, at the short cue-target interval, showed a gradient effect (i.e., latencies are slower at the farthest eccentricity) in the small focusing cue, but not in the large focusing cue condition. These results indicate an efficient zoom-in and zoom-out attentional mechanism. In contrast, children with ASD showed a gradient effect also in the large focusing cue condition, suggesting a specific zoom-out attentional impairment. In addition, the ASD group showed an atypical gradient effect at the long cue-target interval only in the small cue condition, suggesting a prolonged zoom-in and sluggish zoom-out attentional mechanism. This abnormal attentional focusing - probably linked to a dysfunctional top-down feedback from fronto-parietal network to the early visual areas - could contribute to the atypical visual perception associated to individuals with ASD which, in turn, could have consequences in their social-communicative development.

Dialkyltin(IV) and trialkyltin(IV) complexes of the deacetoxycephalo-sporin-antibiotic cephalexin [7-( d -2-amino-2-phenylacetamido)-3-methyl-3-cephem-4-carboxylic acid] (Hceph) have been synthesized and investigated both in solid and solution phase. Analytical and thermogravimetric data supported the general formula Alk 2 SnOHceph · H 2 O and Alk 3 Snceph · H 2 O (Alk=Me, n -Bu), while structural information has been gained by FT-IR, 119 Sn Mossbauer and 1 H, 13 C, 119 Sn NMR data. In particular, IR results suggested polymeric structures both for Alk 2 SnOHceph · H 2 O and Alk 3 Snceph · H 2 O. Moreover, cephalexin appears to behave as monoanionic tridentate ligand coordinating the tin(IV) atom through ester-type carboxylate, as well as through β-lactam carbonyl oxygen atoms and the amino nitrogen donor atoms in Alk 2 SnOHceph · H 2 O complexes. On the basis of 119 Sn Mossbauer spectroscopy it could be inferred that tin(IV) was hexacoordinated in such complexes in the solid state, showing skew trapezoidal configuration. As far as Alk 3 Sn(IV)ceph · H 2 O derivatives are concerned, cephalexin coordinated the Alk 3 Sn moiety through the carboxylate acting as a bridging bidentate monoanionic group. Again, 119 Sn Mossbauer spectroscopy led us to propose a trigonal configuration around the tin(IV) atom, with R 3 Sn equatorial disposition and bridging carboxylate oxygen atoms in the axial positions. The nature of the complexes in solution state was investigated by using 1 H, 13 C and 119 Sn NMR spectroscopy. Finally, the cytotoxic activity of organotin(IV) cephalexinate derivatives has been tested using two different chromosome-staining techniques Giemsa and CMA 3 , towards spermatocyte chromosomes of the mussel Brachidontes pharaonis (Mollusca: Bivalvia). Colchicinized-like mitoses (c-mitoses) on slides obtained from animals exposed to organotin(IV) cephalexinate compounds, demonstrated the high mitotic spindle-inhibiting potentiality of these chemicals. Moreover, structural damages such as ‘chromosome achromatic lesions’, ‘chromosome breakages’ and ‘chromosome fragments’ have been identified through a comparative analysis of spermatocyte chromosomes from untreated specimens (negative controls) and specimens treated with the organotin(IV) complexes.