Post-annealing effect of low temperature atomic layer deposited Al2O3on the top gate IGZO TFT.

Electronical properties of top gate amorphous InGaZnO4thin film transistors (TFTs) could be controlled by post-annealing treatment, which has a great impact on the Al2O3insulator. To investigate the effect of post-annealing on Al2O3, Al/Al2O3/p-Si MOS capacitoras with Al2O3films treated under various post-deposition annealing (PDA) temperature were employed to analysis the change of electrical properties, surface morphology, and chemical components by electrical voltage scanning, atomic force microscope (AFM), and x-ray photoelectron spectroscopy (XPS) technologies. After PDA treatment, the top gate TFTs had a mobility about 7 cm2V-1s-1and the minimum subthreshold swing (SS) about 0.11 V/dec, and the threshold voltage (Vth) shifted from positive direction to negative direction as the post-annealing temperature increased. Electrical properties of MOS capacitors revealed the existence of positive fixed charges and the variation of trap state density with increasing PDA temperature, and further explained the change of negative bias stress (NBS) stability in TFT. AFM results clarified the increased leakage current, degraded SS, and NBS stability in MOS capacitors and TFTs, respectively. XPS results not only illuminated the origin of fixed charges and the trap density variation with PDA temperatures of Al2O3films, but also showed the O and H diffusion from Al2O3into IGZO during post-annealing process, which led to the deviation ofVth, the change of current density, and the negativeVthshift after positive bias stress in TFTs.

LncRNA MEG3 suppresses PI3K/AKT/mTOR signalling pathway to enhance autophagy and inhibit inflammation in TNF-α-treated keratinocytes and psoriatic mice.

BACKGROUND: Psoriasis is a common chronic inflammatory skin disorder that causes patches of thick red skin and silvery scales and affects 1-3% of the population, which reduces patient's quality of life. Understanding the pathogenesis of psoriasis is crucial for developing novel therapeutic strategies. METHODS: HaCaT and NHEK cells were treated with TNF-α in vitro. A mouse model of psoriasis was established by topical imiquimod application on back skin. LncRNA MEG3 was cloned into the pcDNA3.1 vector and transfected in TNF-α-treated HaCaT and NHEK cells to overexpress its expression. Liposome-encapsulated pcDNA3.1-MEG3 was injected into imiquimod-treated mice via tail vein. RT-qPCR and western blot assays were used to examine the expression of lncRNA MEG3, IL-6, IL-8, IFN-γ, IL-1ß, LC3, Beclin 1, p62, p-p65, p65, NLRP3, p-PI3K, PI3K, p-AKT, AKT, p-mTOR, mTOR respectively. The secretion of IL-6, IL-8, IFN-γ and IL-1ß was determined using ELISA assay. Immunofluorescence and immunohistochemistry methods were performed for analyzing the expression of LC3 and NLRP3 in cells and skin tissues respectively. LY294002 was used to block the PI3K/AKT/mTOR signalling. MTT assay was applied to test the toxicity of LY294002 to HaCaT and NHEK cells. RESULTS: LncRNA MEG3 expression levels were downregulated in TNF-α-treated HaCaT and NHEK cells and skin tissues of psoriatic mice model. TNF-α treatment enhanced inflammation and suppressed autophagy in HaCaT and NHEK cells, which were largely reversed by overexpression of lncRNA MEG3. Autophagy puncta and NLRP3 inflammasome assembly showed the same patterns with the expression of inflammation and autophagy markers in TNF-α-treated HaCaT and NHEK cells with or without lncRNA MEG3 overexpression. TNF-α-induced activation of the PI3K/AKT/mTOR signalling was abolished by lncRNA MEG3 overexpression in HaCaT and NHEK cells. Blocking the PI3K/AKT/mTOR signalling inhibited TNF-α-induced inflammation and restored autophagy level in TNF-α-treated HaCaT and NHEK cells. Overexpression of lncRNA MEG3 suppressed inflammation, promoted autophagy and inhibited the activation of the PI3K/AKT/mTOR signalling in a mouse model of psoriasis. CONCLUSION: LncRNA MEG3 facilitates autophagy and suppresses inflammation in TNF-α-treated keratinocytes and psoriatic mice, which is dependent on the PI3K/AKT/mTOR signalling pathway. Our study enhances the understanding of psoriasis and provides potential therapeutic targets for psoriasis.