Epitaxy of (11-22) AlN Films on a Sputtered Buffer Layer with Different Annealing Temperatures via Hydride Vapour Phase Epitaxy.

AlN epilayers were grown on magnetron-sputtered (MS) (11-22) AlN buffers on m-plane sapphire substrates at 1450 °C via hydride vapour phase epitaxy (HVPE). The MS buffers were annealed at high temperatures of 1400-1600 °C. All the samples were characterised using X-ray diffraction, atomic force microscopy, scanning electron microscope and Raman spectrometry. The crystal quality of epilayers regrown by HVPE was improved significantly compared to that of the MS counterpart. With an increasing annealing temperature, the crystal quality of both MS buffers and AlN epilayers measured along [11-23] and [1-100] improved first and then decreased, maybe due to the decomposition of MS buffers, while the corresponding anisotropy along the two directions decreased first and then increased. The optimum quality of the AlN epilayer was obtained at the annealing temperature of around 1500 °C. In addition, it was found that the anisotropy for the epilayers decreased significantly compared to that of annealed MS buffers when the annealing temperature was below 1500 °C.

TMEM16A deficiency in alveolar type 2 epithelial cells protected against endoplasmic reticulum stress-induced ferroptosis during acute lung injury.

Transmembrane protein 16A (TMEM16A) is one of the members of the ten-member family of "transmembrane protein 16", playing critical roles in infection and solid organ injury. Acute lung injury (ALI) is a devastating disease which could be triggered by sepsis, trauma, and ischemia reperfusion. However, molecular mechanisms contributing to ALI are poorly understood at presently. In this study, we investigated the role of TMEM16A in sepsis-induced ALI using TMEM16A-deficient mice. Sepsis-induced ALI model was established by intratracheal injection of lipopolysaccharide (LPS). Our results showed that LPS stimulation significantly upregulated the expression levels of TMEM16A in lung tissues and in alveolar epithelial type II (AT2) cells. Knockout of TMEM16A in AT2 cells significantly improved pulmonary function and alleviated lung pathological injury in LPS-treated mice. Meanwhile, TMEM16A deficiency also inhibited endoplasmic reticulum (ER) stress and ferroptosis in AT2 cells from LPS-treated mice. In vitro experiments further demonstrated that ER stress and ferroptosis were inhibited after TMEM16A was knocked out. Furthermore, we used ER stress inducer thapsigargin to induce ER stress in TMEM16A-null AT2 cells and found that the induction of ER stress abolished the inhibition of ferroptosis by TMEM16A deficiency in LPS-treated AT2 cells. Finally, we disclosed that pharmacological inhibition of TMEM16A by shikonin also showed similar therapeutic effect on LPS-induced ALI in vivo. In conclusion, TMEM16A deficiency in AT2 cells could alleviate sepsis-induced ALI by decreasing ER stress-induced ferroptosis during ALI.

Improvement of Crystal Quality of AlN Films with Different Polarities by Annealing at High Temperature.

High-quality AlN film is a key factor affecting the performance of deep-ultraviolet optoelectronic devices. In this work, high-temperature annealing technology in a nitrogen atmosphere was used to improve the quality of AlN films with different polarities grown by magnetron sputtering. After annealing at 1400-1650 °C, the crystal quality of the AlN films was improved. However, there was a gap between the quality of non-polar and polar films. In addition, compared with the semi-polar film, the quality of the non-polar film was more easily improved by annealing. The anisotropy of both the semi-polar and non-polar films decreased with increasing annealing temperature. The results of Raman spectroscopy, scanning electron microscopy and X-ray photoelectron spectroscopy revealed that the annihilation of impurities and grain boundaries during the annealing process were responsible for the improvement of crystal quality and the differences between the films with different polarities.