Emerging Memtransistors for Neuromorphic System Applications: A Review.

The von Neumann architecture with separate memory and processing presents a serious challenge in terms of device integration, power consumption, and real-time information processing. Inspired by the human brain that has highly parallel computing and adaptive learning capabilities, memtransistors are proposed to be developed in order to meet the requirement of artificial intelligence, which can continuously sense the objects, store and process the complex signal, and demonstrate an "all-in-one" low power array. The channel materials of memtransistors include a range of materials, such as two-dimensional (2D) materials, graphene, black phosphorus (BP), carbon nanotubes (CNT), and indium gallium zinc oxide (IGZO). Ferroelectric materials such as P(VDF-TrFE), chalcogenide (PZT), HfxZr1-xO2(HZO), In2Se3, and the electrolyte ion are used as the gate dielectric to mediate artificial synapses. In this review, emergent technology using memtransistors with different materials, diverse device fabrications to improve the integrated storage, and the calculation performance are demonstrated. The different neuromorphic behaviors and the corresponding mechanisms in various materials including organic materials and semiconductor materials are analyzed. Finally, the current challenges and future perspectives for the development of memtransistors in neuromorphic system applications are presented.

TWEAK promotes endothelial progenitor cell vasculogenesis to alleviate acute myocardial infarction via the Fn14-NF-κB signaling pathway.

Acute myocardial infarction (AMI) remains one of the leading causes of mortality worldwide; however, endothelial progenitor cell (EPC) transplantation has been proposed as a promising treatment strategy for EPC. High levels of tumor necrosis factor-related weak inducer of apoptosis (TWEAK) have been reported in AMI, although its effect on EPCs has not been reported. In the present study, immunofluorescence and flow cytometry were performed to assess the effect of TWEAK in isolated mouse EPCs. Echocardiography was used to evaluate the cardiac function of murine hearts following EPC treatment in the AMI model, while collagen synthesis within the heart tissue was assessed using Masson's trichrome staining. A tube formation assay and Transwell migration assay were performed to investigate the effects of TWEAK on vessel formation and EPC migration in vitro. Angiogenesis and arteriogenesis were assessed in vivo using immunohistochemistry and western blotting was performed to determine the effect of TWEAK-mediated nuclear factor (NF)-κB pathway activation in EPCs. The results revealed that TWEAK promotes EPC migration, tube formation and viability in vitro. Furthermore, TWEAK treatment resulted in improved cardiac function, decreased heart collagen and vasculogenesis in mice with AMI, which was mediated by the TWEAK- fibroblast growth factor-inducible 14 (Fn14)-NF-κB signaling pathway, as determined using Fn14 small interfering (si)RNA and Bay 11-7082 (an NF-κB inhibitor). In summary, the results of the present study suggest that activation of the TWEAK-Fn14-NF-κB signaling pathway exerts a beneficial effect on EPCs for the treatment of AMI.