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Transcranial direct current stimulation (tDCS) over the dorsolateral prefrontal cortex (DLPFC) has been shown to enhance divergent and convergent creative thinking. Yet, how stimulation impacts creative performance over time, and what cognitive mechanisms underlie any such enhancement, remain largely unanswered questions. In the present research, we aimed to (1) verify the impact of DLPFC tDCS on both convergent and divergent thinking, and further investigated (2) the temporal dynamics of divergent thinking, focusing on the serial order effect (i.e., the tendency for ideas to become more original and less frequent over time), and (3) any role that cognitive inhibition may play in mediating any effect of stimulation on creative thinking (considering the DLPFC’s involvement in driving inhibitory processes that are also relevant for creative thinking). In a within-subjects design, twenty-six participants received three types of cross-hemispheric tDCS stimulation over the DLPFC (left cathodal and right anodal, L-R+; left anodal and right cathodal, L+R-; and sham). Before stimulation, they completed a pre-flanker task measuring cognitive inhibition; during stimulation, they completed the Alternate Uses Task (AUT), Remote Associates Test (RAT), and post-flanker task. Results showed that, compared with the sham stimulation, originality of responses in the AUT was significantly enhanced in the L+R- condition, while no tDCS effect was observed for the RAT. Additionally, compared with the other stimulation conditions, we found a diminished serial order effect in the L+R- condition characterized by an accelerated production of more original ideas. Critically, the L+R- condition was accompanied by better performance on the flanker task. Our findings thus verify that L+R- tDCS over the DLPFC accelerates idea originality also providing tentative clues that inhibition may act as a cognitive mechanism underlying enhancements in divergent thinking resulting from frontal lobe neuromodulation. 

Metastasis is the leading cause of breast cancer‐related deaths and is often driven by invasion and cancer‐stem like cells (CSCs). Both the CSC phenotype and invasion are associated with increased hyaluronic acid (HA) production. How these independent observations are connected, and which role metabolism plays in this process, remains unclear due to the lack of convergent approaches integrating engineered model systems, computational tools, and cancer biology. Using microfluidic invasion models, metabolomics, computational flux balance analysis, and bioinformatic analysis of patient data, the functional links between the stem‐like, invasive, and metabolic phenotype of breast cancer cells as a function of HA biosynthesis are investigated. These results suggest that CSCs are more invasive than non‐CSCs and that broad metabolic changes caused by overproduction of HA play a role in this process. Accordingly, overexpression of hyaluronic acid synthases (HAS) 2 or 3 induces a metabolic phenotype that promotes cancer cell stemness and invasion in vitro and upregulates a transcriptomic signature predictive of increased invasion and worse patient survival. This study suggests that HA overproduction leads to metabolic adaptations to satisfy the energy demands for 3D invasion of breast CSCs highlighting the importance of engineered model systems and multidisciplinary approaches in cancer research.