Deep-UV (DUV) laser was used to directly write indium-gallium-zinc-oxide (IGZO) precursor solution and form micro and nanoscale patterns. The directional DUV laser beam avoids the substrate heating and suppresses the diffraction effect. A IGZO precursor solution was also developed to fulfill the requirements for direct photopatterning and for achieving semi-conducting properties with thermal annealing at moderate temperature. The DUV-induced crosslinking of the starting material allows direct write of semi-conducting channels in thin-film transistors but also it improves the field-effect mobility and surface roughness. Material analysis has been carried out by XPS, FTIR, spectroscopic ellipsometry and AFM and the effect of DUV on the final material structure is discussed. The DUV irradiation step results in photolysis and a partial condensation of the inorganic network that freezes the sol-gel layer in a homogeneous distribution, lowering possibilities of thermally induced reorganization at the atomic scale. Laser irradiation allows high-resolution photopatterning and high-enough field-effect mobility, which enables the easy fabrication of oxide nanowires for applications in solar cell, display, flexible electronics, and biomedical sensors.

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Paclitaxel‐based chemotherapy is a common strategy to treat patients with triple‐negative breast cancer (TNBC). As paclitaxel resistance is still a clinical issue in treating TNBCs, identifying molecular markers for predicting pathologic responses to paclitaxel treatment is thus urgently needed. Here, we report that an AT‐rich interaction domain 1A (ARID1A) transcript is up‐regulated in paclitaxel‐sensitive TNBC cells but down‐regulated in paclitaxel‐resistant cells upon paclitaxel treatment. Moreover, ARID1A expression was negatively correlated with the IC 50 concentration of paclitaxel in the tested TNBC cell lines. Kaplan‐Meier analyses revealed that ARID1A down‐regulation was related to a poorer response to paclitaxel‐based chemotherapy in patients with TNBCs as measured by the recurrence‐free survival probability. The pharmaceutical inhibition with p38MAPK‐specific inhibitor SCIO‐469 revealed that p38MAPK‐related signalling axis regulates ARID1A expression and thereby modulates paclitaxel sensitivity in TNBC cells. These findings suggest that ARID1A could be used as a prognostic factor to estimate the pathological complete response for TNBC patients who decide to receive paclitaxel‐based chemotherapy.