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Contact engineering on monolayer layer (ML) semiconducting transition metal dichalcogenides (TMDs) is considered the most challenging problem towards using these materials as a transistor channel in future advanced technology nodes. The typically observed strong Femi level pinning induced in part by the reaction of the source/drain contact metal and the ML TMD frequently results in a large Schottky barrier height, which limits the electrical performance of ML TMD field-effect transistors (FETs). However, at a microscopic level, little is known about how interface defects or reaction sites impact the electrical performance of ML TMD FETs. In this work, we have performed statistically meaningful electrical measurements on at least 120 FETs combined with careful surface analysis to unveil contact resistance dependencies on the interface chemistry. In particular, we achieved a low contact resistance for ML MoS2 FETs with ultra-high vacuum (UHV, 3×10-11 mbar) deposited Ni contacts, ~500 ohm·μm, which is 5 times lower than the contact resistance achieved when deposited at high vacuum (HV, 3×10-6 mbar) conditions. These electrical results strongly correlate with our surface analysis observations. X-ray photoelectron spectroscopy (XPS) revealed significant bonding species between Ni and MoS2 under UHV conditions compared to HV. We also studied the Bi/MoS2 interface under UHV and HV deposition conditions. Different from the case of Ni, we do not observe a difference in contact resistance or interface chemistry between contacts deposited under UHV and HV. Finally, this article also explores the thermal stability and reliability of the two contact metals employed here. 

Autism Spectrum Disorder (ASD) is a neurodevelopmental disease originating from combined genetic and environmental factors. Post-mortem human studies and some animal ASD models have shown brain neuroinflammation, oxidative stress, and changes in blood–brain barrier (BBB) integrity. However, the signaling pathways leading to these inflammatory findings and vascular alterations are currently unclear. The BBB plays a critical role in controlling brain homeostasis and immune response. Its dysfunction can result from developmental genetic abnormalities or neuroinflammatory processes. In this review, we explore the role of the Sonic Hedgehog/Wingless-related integration site (Shh/Wnt) pathways in neurodevelopment, neuroinflammation, and BBB development. The balance between Wnt-β-catenin and Shh pathways controls angiogenesis, barriergenesis, neurodevelopment, central nervous system (CNS) morphogenesis, and neuronal guidance. These interactions are critical to maintain BBB function in the mature CNS to prevent the influx of pathogens and inflammatory cells. Genetic mutations of key components of these pathways have been identified in ASD patients and animal models, which correlate with the severity of ASD symptoms. Disruption of the Shh/Wnt crosstalk may therefore compromise BBB development and function. In turn, impaired Shh signaling and glial activation may cause neuroinflammation that could disrupt the BBB. Elucidating how ASD-related mutations of Shh/Wnt signaling could cause BBB leaks and neuroinflammation will contribute to our understanding of the role of their interactions in ASD pathophysiology. These observations may provide novel targeted therapeutic strategies to prevent or alleviate ASD symptoms while preserving normal developmental processes.