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Ken W Grant

Publications and source records attributed to Ken W Grant.

4 recordsLinked to original sources
PubMed2006

Temporal window of integration in auditory-visual speech perception.

Forty-three normal hearing participants were tested in two experiments, which focused on temporal coincidence in auditory visual (AV) speech perception. In these experiments, audio recordings of/pa/and/ba/were dubbed onto video recordings of /ba/or/ga/, respectively (ApVk, AbVg), to produce the illusory "fusion" percepts /ta/, or /da/ [McGurk, H., & McDonald, J. (1976). Hearing lips and seeing voices. Nature, 264, 746-747]. In Experiment 1, an identification task using McGurk pairs with asynchronies ranging from -467 ms (auditory lead) to +467 ms was conducted. Fusion responses were prevalent over temporal asynchronies from -30 ms to +170 ms and more robust for audio lags. In Experiment 2, simultaneity judgments for incongruent and congruent audiovisual tokens (AdVd, AtVt) were collected. McGurk pairs were more readily judged as asynchronous than congruent pairs. Characteristics of the temporal window over which simultaneity and fusion responses were maximal were quite similar, suggesting the existence of a 200 ms duration asymmetric bimodal temporal integration window.

Acoustic Stimulation↗
PubMed2005

Visual speech speeds up the neural processing of auditory speech.

Synchronous presentation of stimuli to the auditory and visual systems can modify the formation of a percept in either modality. For example, perception of auditory speech is improved when the speaker's facial articulatory movements are visible. Neural convergence onto multisensory sites exhibiting supra-additivity has been proposed as the principal mechanism for integration. Recent findings, however, have suggested that putative sensory-specific cortices are responsive to inputs presented through a different modality. Consequently, when and where audiovisual representations emerge remain unsettled. In combined psychophysical and electroencephalography experiments we show that visual speech speeds up the cortical processing of auditory signals early (within 100 ms of signal onset). The auditory-visual interaction is reflected as an articulator-specific temporal facilitation (as well as a nonspecific amplitude reduction). The latency facilitation systematically depends on the degree to which the visual signal predicts possible auditory targets. The observed auditory-visual data support the view that there exist abstract internal representations that constrain the analysis of subsequent speech inputs. This is evidence for the existence of an "analysis-by-synthesis" mechanism in auditory-visual speech perception.

Adult↗
PubMed2005

Selective inactivation of a Fas-associated death domain protein (FADD)-dependent apoptosis and autophagy pathway in immortal epithelial cells.

Although evasion of apoptosis is thought to be required for the development of cancer, it is unclear which cell death pathways are evaded. We previously identified a novel epithelial cell death pathway that works in normal cells but is inactivated in tumor cells, implying that it may be targeted during tumor development. The pathway can be activated by the Fas-associated death domain (FADD) of the adaptor protein but is distinct from the known mechanism of FADD-induced apoptosis through caspase-8. Here, we show that a physiological signal (tumor necrosis factor-related apoptosis-inducing ligand) can kill normal epithelial cells through the endogenous FADD protein by using the novel FADD death domain pathway, which activates both apoptosis and autophagy. We also show that selective resistance to this pathway occurs when primary epithelial cells are immortalized and that this occurs through a mechanism that is independent of known events (telomerase activity, and loss of function of p53, Rb, INK4a, and ARF) that are associated with immortalization. These data identify a novel cell death pathway that combines apoptosis and autophagy and that is selectively inactivated at the earliest stages of epithelial cancer development.

ADP-Ribosylation Factors↗