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Photosensitive micellar solutions of mixed surfactants and photosensitive additives have gained much interest. However, there are no reports on photosensitive micellar solutions containing trimeric cationic surfactant. In the study, novel photosensitive viscoelastic micellar solutions consisting of trimeric cationic surfactant (TEC) and trans‐ortho‐methoxycinnamic acid (trans‐OMCA) were investigated. This study utilized rheology, UV–vis spectroscopy, and cryo‐TEM to investigate the photo‐responsive behavior and mechanism of the TEC/trans‐OMCA micellar solutions. Rheological studies revealed that the concentration of TEC and trans‐OMCA, as well as temperature, significantly affected the viscoelastic properties of the micellar solutions. Furthermore, the Carreau and Maxwell models might be used to characterize the flow curves and viscoelasticity of the micellar solutions, respectively. Notably, TEC/trans‐OMCA micellar solutions exhibited excellent light‐induced thinning characteristic, with the optimal performance at a mass ratio of φ = 0.5. After UV irradiation, the zero‐shear viscosity of TEC/trans‐OMCA (0.6/0.3 wt%) micellar solution was reduced by 352 times, while the viscoelasticity and the area of hysteresis loops were significantly reduced. This drastic change in the rheological characteristics of the micellar solutions could be attributed to the photoisomerization of trans‐OMCA and the resulting changes in the internal microstructure of the solutions. Moreover, the viscosity of the micellar solutions diminished as the temperature increased, with the remaining viscosity of the TEC/trans‐OMCA (1.0/0.5 wt%) micellar solution at 36.4 mPa s at 95°C. This study expands on the potential utilization of oligomeric surfactants in the construction of photorheological viscoelastic fluids. [ABSTRACT FROM AUTHOR]

Strain engineering has been reported to improve the optical and electrical properties of two-dimensional materials, and the adjustable bandgap of MoS2 has great application value in strain engineering. In this work, to explore the influence of the Si3N4 stress liner on the MoS2 photodetector, plasma enhanced chemical vapor deposition was used to deposit a 5 nm Si3N4 film on the surface of the device to introduce strain. The simulation results show that there is tensile strain in the MoS2 area under a Si3N4 layer, which can decrease the bandgap and electron effective mass of MoS2. The measurement results of the device show that the Si3N4 stress liner devices exhibit a higher light response than the Al2O3/MoS2/sapphire photodetector (control devices) under 365 and 460 nm laser illuminations. The maximum photocurrent (I p h ) and responsivity (R) of the stress liner device under 365 nm illumination are 4.1 mA and 739.9 A/W, respectively, which are more than 30 times the corresponding value of the control device. Also, the maximum specific detectivity (D*) reached 2.5 × 1011 Jones, and the lowest noise equivalent power is 8.7 × 10−16 W/Hz1/2. Our work proved the feasibility of the Si3N4 stress liner to improve the performance of MoS2 photodetectors. [ABSTRACT FROM AUTHOR]

Sorafenib provides survival benefits in patients with advanced renal cell carcinoma (RCC), but its use is hampered by acquired drug resistance. It is important to fully clarify the molecular mechanisms of sorafenib resistance, which can help to avoid, delay or reverse drug resistance. Extracellular vesicles (EVs) can mediate intercellular communication by delivering effector molecules between cells. Here, we studied whether EVs are involved in sorafenib resistance of RCC and its possible molecular mechanisms. Using differential centrifugation, EVs were isolated from established sorafenib‐resistant RCC cells (786‐0 and ACHN), and EVs derived from sorafenib‐resistant cells were uptaken by sensitive parental RCC cells and thus promoted drug resistance. Elevated exogenous miR‐31‐5p within EVs effectively downregulated MutL homolog 1 (MLH1) expression and thus promoted sorafenib resistance in vitro. Mice experiments also confirmed that miR‐31‐5p could mediate drug sensitivity in vivo. In addition, low expression of MLH1 was observed in sorafenib‐resistant RCC cells and upregulation of MLH1 expression restored the sensitivity of resistant cell lines to sorafenib. Finally, miR‐31‐5p level in circulating EVs of RCC patients with progressive disease (PD) during sorafenib therapy was higher when compared to that in the pretherapy status. In conclusion, EVs shuttled miR‐31‐5p can transfer resistance information from sorafenib‐resistant cells to sensitive cells by directly targeting MLH1, and thus magnify the drug resistance information to the whole tumor. Furthermore, miR‐31‐5p and MLH1 could be promising predictive biomarkers and therapeutic targets to prevent sorafenib resistance. What's new? Sorafenib resistance is a major reason for treatment failure in patients with advanced renal cell carcinoma (RCC). The molecular mechanisms leading to sorafenib resistance remain elusive, however. This study showed that extracellular vesicles (EVs) from sorafenib‐resistant RCC cell lines could transfer resistance information to sensitive cells via shuttling of miR‐31‐5p. MiR‐31‐5p promoted sorafenib resistance in vitro and in vivo by targeting MLH1. miR‐31‐5p level was elevated in circulating EVs of RCC patients with progressive disease during sorafenib therapy. Both miR‐31‐5p and its target gene have the potential to be predictive biomarkers for sorafenib resistance as well as novel therapeutic targets. [ABSTRACT FROM AUTHOR]