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This paper reports the use of stacked resistive switches as logic gates for implementing the “AND” and “OR” operations. These stacked resistive switches consist of two resistive switches that share a middle electrode, and they operate based on the difference in resistance between the low and high resistance states indicating the logical states of “0” and “1”, respectively. The stacked resistive switches can perform either AND or OR operation, using two read schemes in one device. To perform the AND (or OR) operation, two resistive switches are arranged in a serial (or parallel) connection. AND and OR operations have been successfully demonstrated using the stacked resistive switches. The use of stacked resistive switches as logic gates that utilize the advantages of memristive devices shows the possibility of stateful logic circuits. [ABSTRACT FROM AUTHOR]

Reactive oxygen species (ROS)-mediated DNA adducts as well as DNA strand breaks are highly mutagenic leading to genomic instability and tumorigenesis. DNA damage repair pathways and oxidative stress response signaling have been proposed to be highly associated, but the underlying interaction remains unknown. In this study, we employed mutant strains lacking Rad51, the homolog of E. coli RecA recombinase, and Yap1 or Skn7, two major transcription factors responsive to ROS, to examine genetic interactions between double-strand break (DSB) repair proteins and cellular redox regulators in budding yeast Saccharomyces cerevisiae . Abnormal expression of YAP1 or SKN7 aggravated the mutation rate of rad51 mutants and their sensitivity to DSB- or ROS-generating reagents. Rad51 deficiency exacerbated genome instability in the presence of increased levels of ROS, and the accumulation of DSB lesions resulted in elevated intracellular ROS levels. Our findings suggest that evident crosstalk between DSB repair pathways and ROS signaling proteins contributes to cell survival and maintenance of genome integrity in response to genotoxic stress. [ABSTRACT FROM AUTHOR]

Abstract: In this study, the mobility enhancement in an Amorphous Oxide Semiconductor Thin Film Transistor (AOS TFT), particularly the effect of enhanced-mobility current path was investigated. In the TFT structure, the a-IGZO single active channel layer was replaced by double layers. Indium Tin Oxide (ITO) was employed as an enhanced-mobility current path material and was embedded in an amorphous Indium Gallium Zinc Oxide (a-IGZO) channel layer of a conventional bottom gate structure TFT. To analyze the effect of the length of an additional current path, the a-IGZO channel length was fixed at 80μm, and the length of the ITO enhanced-mobility current path was increased to 20, 40, and 60μm. As a result, the mobility increased monotonically with the length of the enhanced-mobility current path and was predictable from the rule of mixture. The maximum saturation mobility of 28.3cm2/Vs resulted when the length of the enhanced-mobility current path was 60μm. This value is more than double that of a single path TFT. Such enhancement in mobility is attributed to the high conductivity of ITO and a good conduction band match between a-IGZO and ITO. [Copyright &y& Elsevier]

Abstract A genetic analysis of synthetic lethal interactions in yeast revealed that the mutation of SOD1 , encoding an antioxidant enzyme that scavenges superoxide anion radical, impaired the growth of a set of mutants defective in homologous recombination (HR) pathway. Hence, SOD1 inhibition has been proposed as a promising approach for the selective killing of HR-deficient cancer cells. However, we show that the deletion of RAD51 and SOD1 is not synthetic lethal but displays considerably slow growth and synergistic sensitivity to both reactive oxygen species (ROS)- and DNA double-strand break (DSB)-generating drugs in the budding yeast Saccharomyces cerevisiae. The function of Sod1 in regard to Rad51 is dependent on Ccs1, a copper chaperone for Sod1. Sod1 deficiency aggravates genomic instability in conjunction with the absence of Rad51 by inducing DSBs and an elevated mutation frequency. Inversely, lack of Rad51 causes a Sod1 deficiency-derived increase of intracellular ROS levels. Taken together, our results indicate that there is a significant and specific crosstalk between two major cellular damage response pathways, ROS signaling and DSB repair, for cell survival. Graphical abstract fx1 Highlights • SOD1 inhibition can be used for selective killing of cancer cells deficient in homologous recombination pathway. • Deletion of RAD51 and SOD1 does not show synthetic lethality in budding yeast. • Sod1 deficiency aggravates genomic instability in conjunction with the absence of Rad51. • Accumulation of Rad51 deficiency-mediated DSB lesions increases intracellular ROS levels in the absence of Sod1. • DSB repair pathways and ROS response signaling have significant mutual genetic crosstalk. [ABSTRACT FROM AUTHOR]