A 2.8 kV Breakdown Voltage α-Ga2O3 MOSFET with Hybrid Schottky Drain Contact.

Among various polymorphic phases of gallium oxide (Ga2O3), α-phase Ga2O3 has clear advantages such as its heteroepitaxial growth as well as wide bandgap, which is promising for use in power devices. In this work, we demonstrate α-Ga2O3 MOSFETs with hybrid Schottky drain (HSD) contact, comprising both Ohmic and Schottky electrode regions. In comparison with conventional Ohmic drain (OD) contact, a lower on-resistance (Ron) of 2.1 kΩ mm is achieved for variable channel lengths. Physics-based TCAD simulation is performed to validate the turn-on characteristics of the Schottky electrode region and the improved Ron. Electric-field analysis in the off-state is conducted for both the OD and HSD devices. Furthermore, a record breakdown voltage (BV) of 2.8 kV is achieved, which is superior to the 1.7 kV of the compared OD device. Our results show that the proposed HSD contact with a further optimized design can be a promising drain electrode scheme for α-Ga2O3 power MOSFETs.

Reconfigurable Physical Reservoir in GaN/α-In2Se3 HEMTs Enabled by Out-of-Plane Local Polarization of Ferroelectric 2D Layer.

Significant effort for demonstrating a gallium nitride (GaN)-based ferroelectric metal-oxide-semiconductor (MOS)-high-electron-mobility transistor (HEMT) for reconfigurable operation via simple pulse operation has been hindered by the lack of suitable materials, gate structures, and intrinsic depolarization effects. In this study, we have demonstrated artificial synapses using a GaN-based MOS-HEMT integrated with an α-In2Se3 ferroelectric semiconductor. The van der Waals heterostructure of GaN/α-In2Se3 provides a potential to achieve high-frequency operation driven by a ferroelectrically coupled two-dimensional electron gas (2DEG). Moreover, the semiconducting α-In2Se3 features a steep subthreshold slope with a high ON/OFF ratio (∼1010). The self-aligned α-In2Se3 layer with the gate electrode suppresses the in-plane polarization while promoting the out-of-plane (OOP) polarization of α-In2Se3, resulting in a steep subthreshold slope (10 mV/dec) and creating a large hysteresis (2 V). Furthermore, based on the short-term plasticity (STP) characteristics of the fabricated ferroelectric HEMT, we demonstrated reservoir computing (RC) for image classification. We believe that the ferroelectric GaN/α-In2Se3 HEMT can provide a viable pathway toward ultrafast neuromorphic computing.

Transgenic Anopheles mosquitoes expressing human PAI-1 impair malaria transmission.

In mammals, the serine protease plasmin degrades extracellular proteins during blood clot removal, tissue remodeling, and cell migration. The zymogen plasminogen is activated into plasmin by two serine proteases: tissue-type plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA), a process regulated by plasminogen activator inhibitor 1 (PAI-1), a serine protease inhibitor that specifically inhibits tPA and uPA. Plasmodium gametes and sporozoites use tPA and uPA to activate plasminogen and parasite-bound plasmin degrades extracellular matrices, facilitating parasite motility in the mosquito and the mammalian host. Furthermore, inhibition of plasminogen activation by PAI-1 strongly blocks infection in both hosts. To block parasite utilization of plasmin, we engineered Anopheles stephensi transgenic mosquitoes constitutively secreting human PAI-1 (huPAI-1) in the midgut lumen, in the saliva, or both. Mosquitoes expressing huPAI-1 strongly reduced rodent and human Plasmodium parasite transmission to mosquitoes, showing that co-opting plasmin for mosquito infection is a conserved mechanism among Plasmodium species. huPAI-1 expression in saliva induced salivary gland deformation which affects sporozoite invasion and P. berghei transmission to mice, resulting in significant levels of protection from malaria. Targeting the interaction of malaria parasites with the fibrinolytic system using genetically engineered mosquitoes could be developed as an intervention to control malaria transmission.

Beyond cuts and scrapes: plasmin in malaria and other vector-borne diseases.

Plasmodium and other vector-borne pathogens have evolved mechanisms to hijack the mammalian fibrinolytic system to facilitate infection of the human host and the invertebrate vector. Plasmin, the effector protease of fibrinolysis, maintains homeostasis in the blood vasculature by degrading the fibrin that forms blood clots. Plasmin also degrades proteins from extracellular matrices, the complement system, and immunoglobulins. Here, we review some of the mechanisms by which vector-borne pathogens interact with components of the fibrinolytic system and co-opt its functions to facilitate transmission and infection in the host and the vector. Further, we discuss innovative strategies beyond conventional therapeutics that could be developed to target the interaction of vector-borne pathogens with the fibrinolytic proteins and prevent their transmission.

The fibrinolytic system enables the onset of Plasmodium infection in the mosquito vector and the mammalian host.

Plasmodium parasites must migrate across proteinaceous matrices to infect the mosquito and vertebrate hosts. Plasmin, a mammalian serine protease, degrades extracellular matrix proteins allowing cell migration through tissues. We report that Plasmodium gametes recruit human plasminogen to their surface where it is processed into plasmin by corecruited plasminogen activators. Inhibition of plasminogen activation arrests parasite development early during sexual reproduction, before ookinete formation. We show that increased fibrinogen and fibrin in the blood bolus, which are natural substrates of plasmin, inversely correlate with parasite infectivity of the mosquito. Furthermore, we show that sporozoites, the parasite form transmitted by the mosquito to humans, also bind plasminogen and plasminogen activators on their surface, where plasminogen is activated into plasmin. Surface-bound plasmin promotes sporozoite transmission by facilitating parasite migration across the extracellular matrices of the dermis and of the liver. The fibrinolytic system is a potential target to hamper Plasmodium transmission.