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AlN Schottky barrier diodes with low ideality factor (<1.2), low differential ON-resistance (<0.6 mΩ cm²), high current density (>5 kA cm⁻²), and high breakdown voltage (680 V) are reported. The device structure consisted of a two-layer, quasi-vertical design with a lightly doped AlN drift layer and a highly doped Al_0.75Ga_0.25N ohmic contact layer grown on AlN substrates. A combination of simulation, current–voltage measurements, and impedance spectroscopy analysis revealed that the AlN/AlGaN interface introduces a parasitic electron barrier due to the conduction band offset between the two materials. This barrier was found to limit the forward current in fabricated diodes. Further, we show that introducing a compositionally-graded layer between the AlN and the AlGaN reduces the interfacial barrier and increases the forward current density of fabricated diodes by a factor of 10⁴. 

Near-ideal behavior in Schottky contacts to Si-doped AlN was observed as evidenced by a low ideality factor of 1.5 at room temperature. A temperature-independent Schottky barrier height of 1.9 eV was extracted from temperature-dependent I–V measurements. An activation energy of ∼300 meV was observed in the series resistance, which corresponded to the ionization energy of the deep Si donor state. Both Ohmic and Schottky contacts were stable up to 650 °C, with around four orders of magnitude rectification at this elevated temperature. These results demonstrate the potential of AlN as a platform for power devices capable of operating in extreme environments. 

Abstract Aging, often considered a result of random cellular damage, can be accurately estimated using DNA methylation profiles, the foundation of pan-tissue epigenetic clocks. Here, we demonstrate the development of universal pan-mammalian clocks, using 11,754 methylation arrays from our Mammalian Methylation Consortium, which encompass 59 tissue types across 185 mammalian species. These predictive models estimate mammalian tissue age with high accuracy (r > 0.96). Age deviations correlate with human mortality risk, mouse somatotropic axis mutations and caloric restriction. We identified specific cytosines with methylation levels that change with age across numerous species. These sites, highly enriched in polycomb repressive complex 2-binding locations, are near genes implicated in mammalian development, cancer, obesity and longevity. Our findings offer new evidence suggesting that aging is evolutionarily conserved and intertwined with developmental processes across all mammals.