Contrast integration across space

AbstractContrast integration across space was studied in respect to stimulus extent and the spatial layout, using high-contrast stimuli. Contrast discrimination thresholds were measured (2AFC) by either increasing the size of a peripheral (2.4°) Gabor signal (GS: λ=0.08°) or by increasing the number of GS elements in a circular arrangement. The supra-threshold mask (pedestal) was either increased with the target or fixed at maximal size and had 30% contrast. For stimuli with an increasing size of both the pedestal and the increment target, we find approximately constant discrimination thresholds. Contrast discrimination improved linearly on a log–log scale with slopes average of −1/4 (fourth-root summation) when the size of the Gabor target was increased but the mask was kept at maximal size, indicating contrast integration across space. Taken together, these results indicate balanced spatial integration of both contrast increment and pedestal, resulting object-size invariant contrast discrimination. Contrast discrimination was found to improve as well when the number of aligned Gabor elements was increased (both pedestal and increment), pointing to independent contrast normalization for disconnected (sparsely positioned) stimuli. The results indicate a complex pattern of spatial integration involved in contrast discrimination, possibly depending on image segmentation

Cross-modal extinction in a boy with severely autistic behaviour and high verbal intelligence

Anecdotal reports from individuals with autism suggest a loss of awareness to stimuli from one modality in the presence of stimuli from another. Here we document such a case in a detailed study of T.M., a 13-year-old boy with autism in whom significant autistic behaviors are combined with an uneven IQ profile of superior verbal and low performance abilities. Although T.M.'s speech is often unintelligible and his behavior is dominated by motor stereotypies and impulsivity, he can communicate by typing or pointing independently within a letter board. A series of experiments using simple and highly salient visual, auditory, and tactile stimuli demonstrated a hierarchy of cross-modal extinction, in which auditory information extinguished other modalities at various levels of processing. T.M. also showed deficits in shifting and sustaining attention. These results provide evidence for mono-channel perception in autism and suggest a general pattern of winner-takes-all processing in which a stronger stimulus-d riven representation dominates behavior, extinguishing weaker representations

Abnormal Speech Spectrum and Increased Pitch Variability in Young Autistic Children

Children with autism spectrum disorder (ASD) who can speak often exhibit abnormal voice quality and speech prosody, but the exact nature and underlying mechanisms of these abnormalities, as well as their diagnostic power are currently unknown. Here we quantified speech abnormalities in terms of the properties of the long-term average spectrum (LTAS) and pitch variability in speech samples of 83 children (41 with ASD, 42 controls) ages 4–6.5 years, recorded while they named a sequence of daily life pictures for 60 s. We found a significant difference in the group's average spectra, with ASD spectra being shallower and exhibiting less harmonic structure. Contrary to the common impression of monotonic speech in autism, the ASD children had a significantly larger pitch range and variability across time. A measure of this variability, optimally tuned for the sample, yielded 86% success (90% specificity, 80% sensitivity) in classifying ASD in the sample. These results indicate that speech abnormalities in ASD are reflected in its spectral content and pitch variability. This variability could imply abnormal processing of auditory feedback or elevated noise and instability in the mechanisms that control pitch. The current results are a first step toward developing speech spectrum-based bio-markers for early diagnosis of ASD

In vivo CHI3L1 (YKL-40) expression in astrocytes in acute and chronic neurological diseases

<p>Abstract</p> <p>Background</p> <p>CHI3L1 (YKL-40) is up-regulated in a variety of inflammatory conditions and cancers. We have previously reported elevated CHI3L1 concentration in the cerebrospinal fluid (CSF) of human and non-human primates with lentiviral encephalitis and using immunohistochemistry showed that CHI3L1 was associated with astrocytes.</p> <p>Methods</p> <p>In the current study CHI3L1 transcription and expression were evaluated in a variety of acute and chronic human neurological diseases.</p> <p>Results</p> <p>ELISA revealed significant elevation of CHI3L1 in the CSF of multiple sclerosis (MS) patients as well as mild elevation with aging. <it>In situ </it>hybridization (ISH) showed CHI3L1 transcription mostly associated with reactive astrocytes, that was more pronounced in inflammatory conditions like lentiviral encephalitis and MS. Comparison of CHI3L1 expression in different stages of brain infarction showed that YKL40 was abundantly expressed in astrocytes during acute phases and diminished to low levels in chronic infarcts.</p> <p>Conclusions</p> <p>Taken together, these findings demonstrate that CHI3L1 is induced in astrocytes in a variety of neurological diseases but that it is most abundantly associated with astrocytes in regions of inflammatory cells.</p

Face matching in a long task: Enforced rest breaks and desk-switching cannot maintain identification accuracy

In face matching, observers have to decide whether two photographs depict the same person or different people. This task is not only remarkably difficult but accuracy declines further during prolonged testing. The current study investigated whether this decline in long tasks can be eliminated with regular rest-breaks (Experiment 1) or room-switching (Experiment 2). Both experiments replicated the accuracy decline for long face-matching tasks and showed that this could not be eliminated with rest or room-switching. These findings suggest that person identification in applied settings, such as passport control, might be particularly error-prone due to the long and repetitive nature of the task. The experiments also show that it is difficult to counteract these problems

Arid1b haploinsufficient mice reveal neuropsychiatric phenotypes and reversible causes of growth impairment.

Sequencing studies have implicated haploinsufficiency of ARID1B, a SWI/SNF chromatin-remodeling subunit, in short stature (Yu et al., 2015), autism spectrum disorder (O'Roak et al., 2012), intellectual disability (Deciphering Developmental Disorders Study, 2015), and corpus callosum agenesis (Halgren et al., 2012). In addition, ARID1B is the most common cause of Coffin-Siris syndrome, a developmental delay syndrome characterized by some of the above abnormalities (Santen et al., 2012; Tsurusaki et al., 2012; Wieczorek et al., 2013). We generated Arid1b heterozygous mice, which showed social behavior impairment, altered vocalization, anxiety-like behavior, neuroanatomical abnormalities, and growth impairment. In the brain, Arid1b haploinsufficiency resulted in changes in the expression of SWI/SNF-regulated genes implicated in neuropsychiatric disorders. A focus on reversible mechanisms identified Insulin-like growth factor (IGF1) deficiency with inadequate compensation by Growth hormone-releasing hormone (GHRH) and Growth hormone (GH), underappreciated findings in ARID1B patients. Therapeutically, GH supplementation was able to correct growth retardation and muscle weakness. This model functionally validates the involvement of ARID1B in human disorders, and allows mechanistic dissection of neurodevelopmental diseases linked to chromatin-remodeling