Herein, we successfully fabricated an Al-doped α-Ga₂O₃ nanorod array on FTO using the hydrothermal and post-annealing processes. To the best of our knowledge, it is the first time that an Al-doped α-Ga₂O₃ nanorod array on FTO has been realized via a much simpler and cheaper way than that based on metal–organic chemical vapor deposition, magnetron sputtering, molecular beam epitaxy, and pulsed laser deposition. And, a self-powered Al-doped α-Ga₂O₃ nanorod array/FTO photodetector was also realized as a photoanode at 0 V (vs. Ag/AgCl) in a photoelectrochemical (PEC) cell, showing a peak responsivity of 1.46 mA/W at 260 nm. The response speed of the Al-doped device was 0.421 s for rise time, and 0.139 s for decay time under solar-blind UV (260 nm) illumination. Compared with the undoped device, the responsivity of the Al-doped device was ~5.84 times larger, and the response speed was relatively faster. When increasing the biases from 0 V to 1 V, the responsivity, quantum efficiency, and detectivity of the Al-doped device were enhanced from 1.46 mA/W to 2.02 mA/W, from ~0.7% to ~0.96%, and from ~6 × 10⁹ Jones to ~1 × 10¹⁰ Jones, respectively, due to the enlarged depletion region. Therefore, Al doping may provide a route to enhance the self-powered photodetection performance of α-Ga₂O₃ nanorod arrays.

Wet-chemistry synthesis of two-dimensional Pt- and Pd-based intermetallic electrocatalysts for a wide range of applications in fuel cells.

Aims: Type 2 diabetes mellitus (T2DM) can lead to brain dysfunction and a series of neurological complications. Previous research demonstrated that a novel palmitic acid (5‐PAHSA) exerts effect on glucose tolerance and chronic inflammation. Autophagy was important in diabetic‐related neurodegeneration. The aim of the present study was to investigate whether 5‐PAHSA has specific therapeutic effects on neurological dysfunction in diabetics, particularly with regard to autophagy.Methods: 5‐PAHSA was successfully synthesized according to a previously described protocol. We then carried out a series of in vitro and in vivo experiments using PC12 cells under diabetic conditions, and DB/DB mice, respectively. PC12 cells were treated with 5‐PAHSA for 24 h, while mice were administered with 5‐PAHSA for 30 days. At the end of each experiment, we analyzed glucolipid metabolism, autophagy, apoptosis, oxidative stress, cognition, and a range of inflammatory factors.Results: Although there was no significant improvement in glucose metabolism in mice administered with 5‐PAHSA, ox‐LDL decreased significantly following the administration of 5‐PAHSA in serum of DB/DB mice (p < 0.0001). We also found that the phosphorylation of m‐TOR and ULK‐1 was suppressed in both PC12 cells and DB/DB mice following the administration of 5‐PAHSA (p < 0.05 and p < 0.01), although increased levels of autophagy were only observed in vitro (p < 0.05). Following the administration of 5‐PAHSA, the concentration of ROS decreased in PC12 cells and the levels of CRP increased in high‐dose group of 5‐PAHSA (p < 0.01). There were no significant changes in terms of apoptosis, other inflammatory factors, or cognition in DB/DB mice following the administration of 5‐PAHSA.Conclusion: We found that 5‐PAHSA can enhance autophagy in PC12 cells under diabetic conditions. Our data demonstrated that 5‐PAHSA inhibits phosphorylation of the m‐TOR‐ULK1 pathway and suppressed oxidative stress in PC12 cells, and exerted influence on lipid metabolism in DB/DB mice.