Interplay between local moment and itinerant magnetism in the layered metallic antiferromagnet TaFe1.14_{1.14}Te3_3

Two-dimensional (2D) antiferromagnets have garnered considerable interest for the next generation of functional spintronics. However, many available bulk materials from which 2D antiferromagnets are isolated are limited by their sensitivity to air, low ordering temperatures, and insulating transport properties. TaFe$_{1+y}$Te$_3$ offers unique opportunities to address these challenges with increased air stability, metallic transport properties, and robust antiferromagnetic order. Here, we synthesize TaFe$_{1+y}$Te$_3$ ($y$ = 0.14), identify its structural, magnetic, and electronic properties, and elucidate the relationships between them. Axial-dependent high-field magnetization measurements on TaFe$_{1.14}$Te$_3$ reveal saturation magnetic fields ranging between 27-30 T with a saturation magnetic moment of 2.05-2.12 $\mu_B$. Magnetotransport measurements confirm TaFe$_{1.14}$Te$_3$ is metallic with strong coupling between magnetic order and electronic transport. Angle-resolved photoemission spectroscopy measurements across the magnetic transition uncover a complex interplay between itinerant electrons and local magnetic moments that drives the magnetic transition. We further demonstrate the ability to isolate few-layer sheets of TaFe$_{1.14}$Te$_3$ through mechanical exfoliation, establishing TaFe$_{1.14}$Te$_3$ as a potential platform for 2D spintronics based on metallic layered antiferromagnets.Comment: 30 pages, 5 main figures, 23 supporting figures, and 3 supporting table

0.6V threshold voltage thin film transistors with solution processable indium oxide (In₂O₃) Channel and Anodized High-κ Al₂O₃ Dielectric

Low-voltage operation and low processing temperature of metal oxide transistors remain a challenge. Commonly metal oxide transistors are fabricated at very high processing temperatures (above 500°C) and their operating voltage is quite high (30-50 V). Here, thin-film transistors (TFT) are reported based upon solution processable indium oxide (In2O3) and room temperature processed anodized high- κ aluminum oxide (Al2O3) for gate dielectrics. The In2O3 TFTs operate well below the drain bias (Vds) of 3.0 V, with on/off ratio 105, subthreshold swing (SS) 160 mV/dec, hysteresis 0.19 V, and low threshold voltage (Vth)~0.6 V. The electron mobility (μ) is as high as 3.53 cm2/V.s in the saturation regime and normalized transconductance (gm) is 75μS/mm. In addition, the detailed capacitance-voltage (C-V) analysis to determine interface trap states density was also investigated. The interface trap density (Dit) in the oxide/semiconductor interface was quite low, i.e., 0.99 × 1011 - 2.98 × 1011 eV-1· cm2, signifying acceptable compatibility of In2O3 with anodic Al2O3.acceptedVersionPeer reviewe

Fusobacterium nucleatum secretes amyloid‐like FadA to enhance pathogenicity

Fusobacterium nucleatum (Fn) is a Gram-negative oral commensal, prevalent in various human diseases. It is unknown how this common commensal converts to a rampant pathogen. We report that Fn secretes an adhesin (FadA) with amyloid properties via a Fap2-like autotransporter to enhance its virulence. The extracellular FadA binds Congo Red, Thioflavin-T, and antibodies raised against human amyloid β42. Fn produces amyloid-like FadA under stress and disease conditions, but not in healthy sites or tissues. It functions as a scaffold for biofilm formation, confers acid tolerance, and mediates Fn binding to host cells. Furthermore, amyloid-like FadA induces periodontal bone loss and promotes CRC progression in mice, with virulence attenuated by amyloid-binding compounds. The uncleaved signal peptide of FadA is required for the formation and stability of mature amyloid FadA fibrils. We propose a model in which hydrophobic signal peptides serve as "hooks" to crosslink neighboring FadA filaments to form a stable amyloid-like structure. Our study provides a potential mechanistic link between periodontal disease and CRC and suggests anti-amyloid therapies as possible interventions for Fn-mediated disease processes