Publications by authors named "Yu-hui Tang"

We exploit bias polarity dependent low-frequency noise (LFN) spectroscopy to investigate charge transport dynamics in ultra-thin AlO-based magnetic tunnel junctions (MTJs) with bipolar resistive switching (RS). By measuring the noise characteristics across the entire bias voltage range of bipolar RS, we find that the voltage noise level exhibits an bias polarity dependence. This distinct feature is intimately correlated with reconfiguring of the inherently existing oxygen vacancies ( ) in as-grown MTJ devices during the SET and RESET switching processes.

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Formaldehyde (FA) has neurotoxic characteristics and causes neurodegenerative disease. Our previous study demonstrated the neuroprotective effects of hydrogen sulfide (HS) on FA-induced neurotoxicity in HT22 cells. Emerging evidence have supported that ferroptosis is involved in FA-induced neurotoxicity.

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Diabetes mellitus (DM) is a common chronic metabolic disease, and the C57BLKsJ-db/db mice are good animal models for type 2 diabetes mellitus (T2DM). In this study, Western blotting and immunohistochemistry (IHC) were employed to examine the protein expression of adiponectin in the liver tissues of T2DM mice with different disease courses (4, 16, and 32 weeks). Adiponectin expression reduced in the liver tissues of T2DM mice in different disease courses.

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We employ the first-principles calculation with non-equilibrium Green's function method to comprehensively investigate the crucial role of interfacial geometry in spin transport properties of Co/1,4-benzenediamine (BDA)/Co single-molecule magnetic junctions (SMMJs). Two bonding mechanisms are proposed for the hard-hard Co-N coupling: (1) the covalent bonding between the H-dissociated amine linker and spin-polarized Co apex atoms and (2) the dative interaction between the H-non-dissociated (denoted by +H) amine linker and Co apex atoms. The former covalent contact dominates the π-resonance interfacial spin selection that can be well preserved in H-dissociated cases regardless of the choice of top, bridge, and hollow contact sites.

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Background: Sodium valproate inhibits proliferation in neuroblastoma and glioma cells, and inhibits proliferation and induces apoptosis in hepatoblastoma cells. Information describing the molecular pathways of the antitumor effects of sodium valproate is limited; therefore, we explored the mechanisms of action of sodium valproate in the human hepatoblastoma cell line, HepG2.

Methods: The effects of sodium valproate on the proliferation of HepG2 cells were evaluated by the Walsh-schema transform and colony formation assays.

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