A growing body of literature suggests that cognitive impairment in people with schizophrenia (PSZ) results from disrupted cortical excitatory/inhibitory (E-I) balance, which may be linked to gamma entrainment and can be measured noninvasively using electroencephalography (EEG). However, it is not yet known the degree to which these entrainment abnormalities covary within subjects across sensory modalities. Furthermore, the degree to which cross-modal gamma entrainment reflects variation in biological processes associated with cognitive performance remains unclear. We used EEG to measure entrainment to repetitive auditory and visual stimulation at beta (20 Hz) and gamma (30 and 40 Hz) frequencies in PSZ (n = 78) and healthy control subjects (HCS; n = 80). Three indices were measured for each frequency and modality: event-related spectral perturbation (ERSP), intertrial coherence (ITC), and phase-lag angle (PLA). Cognition and symptom severity were also assessed. We found little evidence that gamma entrainment covaried across sensory modalities. PSZ exhibited a modest correlation between modalities at 40 Hz for ERSP and ITC measures (r = 0.23-0.24); however, no other significant correlations between modalities emerged for either HCS or PSZ. Both univariate and multivariate analyses revealed that (a) the pattern of entrainment abnormalities in PSZ differed across modalities, and (b) modality rather than frequency band was the main source of variance. Finally, we observed a significant association between cognition and gamma entrainment in the auditory domain only in HCS. Gamma-band EEG entrainment does not reflect a unitary transcortical mechanism but is instead modality specific. To the extent that entrainment reflects the integrity of cortical E-I balance, the deficits observed in PSZ appear to be modality specific and not consistently associated with cognitive impairment. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Genome-wide DNA sequencing was used to decrypt the phylogeny of multiple samples from distinct areas of cancer and morphologically normal tissue taken from the prostates of three men. Mutations were present at high levels in morphologically normal tissue distant from the cancer, reflecting clonal expansions, and the underlying mutational processes at work in morphologically normal tissue were also at work in cancer. Our observations demonstrate the existence of ongoing abnormal mutational processes, consistent with field effects, underlying carcinogenesis. This mechanism gives rise to extensive branching evolution and cancer clone mixing, as exemplified by the coexistence of multiple cancer lineages harboring distinct ERG fusions within a single cancer nodule. Subsets of mutations were shared either by morphologically normal and malignant tissues or between different ERG lineages, indicating earlier or separate clonal cell expansions. Our observations inform on the origin of multifocal disease and have implications for prostate cancer therapy in individual cases.