Over the past decade, the field of two-dimensional (2D) layered materials has surged, promising a new platform for studying diverse physical phenomena that are scientifically intriguing and technologically relevant. Contacts are the communication links between these 2D materials and the three-dimensional world for probing and harnessing their exquisite electronic properties. However, fundamental challenges related to contacts often limit the ultimate performance and potential of 2D materials and devices. This article provides a comprehensive overview of the basic understanding and importance of contacts to 2D materials and various strategies for engineering and improving them. In particular, we elucidate the phenomenon of Fermi level pinning at the metal/2D contact interface, the Schottky versus Ohmic nature of the contacts and various contact engineering approaches including interlayer contacts, phase engineered contacts, and basal versus edge plane contacts, among others. Finally, we also discuss some of the relatively under-addressed and unresolved issues, such as contact scaling, and conclude with a future outlook.

Neurotransmitter release in chemical synapses is fundamental to diverse brain functions such as motor action, learning, cognition, emotion, perception, and consciousness. Moreover, improper functioning or abnormal release of neurotransmitter is associated with numerous neurological disorders such as epilepsy, sclerosis, schizophrenia, Alzheimer's disease, and Parkinson's disease. We have utilized hysteresis engineering in a back-gated MoS field effect transistor (FET) in order to mimic such neurotransmitter release dynamics in chemical synapses. All three essential features, i.e., quantal, stochastic, and excitatory or inhibitory nature of neurotransmitter release, were accurately captured in our experimental demonstration. We also mimicked an important phenomenon called long-term potentiation (LTP), which forms the basis of human memory. Finally, we demonstrated how to engineer the LTP time by operating the MoS FET in different regimes. Our findings could provide a critical component toward the design of next-generation smart and intelligent human-like machines and human-machine interfaces.

Patients with mutations in FOXC2 and GJC2 have reduced venous valve number and leaflet length. Experiments in mice by Lyons et al. show that Foxc2-Calcineurin-Nfatc1, and Gja4, Gjc2, Gja1 regulate valve-forming cell organization. Foxc2, Calcineurin-Nfatc1, and blood flow regulate leaflet growth/maturation.