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Sekine, K.

Publications and source records attributed to Sekine, K..

2 recordsLinked to original sources

The time course of co-speech gesture production: An MEG study

People frequently gesture while speaking, even when listeners cannot see them--for instance, during phone calls or behind barriers. Congenitally blind individuals also gesture, indicating that gestures serve functions beyond visual communication. Previous models of gesture production (e.g., Kita & Ozyurek, 2003; Rauscher et al., 1996) suggest that gestures facilitate speech, but they rely heavily on behavioural data and provide limited insight into temporal dynamics. This study used magnetoencephalography (MEG), a neuroimaging technique with high temporal resolution, to investigate when gestures influence speech. Twenty-three native Japanese speakers took part in a storytelling task under two conditions: Gesture-Required (gesture use instructed) and Gesture-Prohibited (hands kept still). Participants described cartoon clips across multiple sessions (30 trials x 3 sessions per condition). Using speech onset as the reference point, we compared root mean square (RMS) values within a -0.25 to 0 second window. RMS values were higher in the Gesture-Prohibited condition, with increased activity in the bilateral anterior temporal lobes (Left ATL: p = .049; Right ATL: p = .027), but not in motor regions (p = .29). These findings suggest that gestures reduce neural load in language-related regions before articulation. Co-speech gestures may support speech planning by facilitating lexical retrieval or semantic structuring. The lack of motor region effects indicates that this influence is linguistic rather than motoric. This study provides direct direct neurophysiological evidence of the timing of gesture-speech interaction, supporting models that view gestures as an integral part of speech production.

neuroscience↗

Investigating EMT-mediated resistance to EGFR tyrosine kinase inhibitors in NSCLC using innovative organoid models

BackgroundEpithelial-mesenchymal transition (EMT) has emerged as a key mechanism underlying resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) in EGFR-mutant non-small cell lung cancer (NSCLC). However, the intricacies of EMT-mediated resistance, driven by tumor microenvironment (TME) interactions, remain enigmatic. This study aimed to probe EMT-induced resistance in NSCLC using innovative in vitro organoid models. MethodsWe generated organoids by co-culturing EGFR-mutant NSCLC cells (HCC827, H1975), mesenchymal stem cells and endothelial cells. Drug susceptibility was compared between organoids and spheroids (cancer cells only) using EGFR TKIs - Gefitinib, Afatinib, Osimertinib. EMT marker (E-cadherin, ZEB1) expression was analyzed via immunofluorescence and western blotting. The effects of Bevacizumab and miR200c on overcoming resistance were also investigated. ResultsThe study identified a significant link between EMT and EGFR-TKI resistance. Notable findings included the decrease of E-cadherin and an increase in ZEB1, both of which influenced EMT and resistance to treatment. Bevacizumab showed promise in improving drug resistance and mitigating EMT, suggesting an involvement of the VEGF cascade. Transfection with miR200c was associated with improved EMT and drug resistance, further highlighting the role of EMT in TKI resistance. ConclusionsThis study offered vital insights into EMT-driven EGFR TKI resistance, highlighting the utility of organoid models in evaluating resistance modulated by TME interactions. Our findings reveal promising directions for overcoming EMT-mediated resistance involving Bevacizumab and miR200c, warranting further in vivo validation.

cancer biology↗