Foreword Special Issue on "New Simulation Methodologies for Next-Generation TCAD Tools"

Technology computer-aided design (TCAD) is an integral part of the development process of semiconductor technologies and devices, a field which has become increasingly complex and heterogeneous. Processing of integrated circuits requires nowadays over 400 process steps, and the resulting devices often have an intricate 3-D structure and contain various specifically designed materials. The full device behavior can only be understood by considering effects on all length scales from atomistic (material properties, interfaces, defects, and so on), to nanometric (quantum confinement, non-bulk properties, tunneling, ballistic transport, and so on), to full-chip dimensions (strain, heat transport, and so on), and time scales from femtoseconds (scattering, ferroelectric switching time, and so on) to seconds (trapping times, degradation, and so on). Voltages, currents, and charges have been scaled to such low levels that statistical effects and process variations have a strong impact. Devices based on new materials (e.g., 2-D crystals) and physical principles (ferroelectrics, magnetic materials, qubits, and so on) challenge standard TCAD approaches. While the simulation methods developed by the physics community can describe the basic device behavior, they often lack important simulation capabilities like, for example, transient simulations or integration with other TCAD tools, and are often too slow for daily use. Due to the complexity of semiconductor technology, it becomes more and more difficult to assess the impact of a change in processing or device structure on circuit performance by looking at a single aspect of an isolated device under idealized conditions. Instead, a TCAD tool chain is required which can handle realistic device structures embedded in a chip environment. New methodologies are required for all aspects of TCAD to ensure an efficient tool chain covering from atomistic effects to circuit behavior based on flexible simulation models that can handle new materials, device principles, and the ensuing large-scale simulations and that make use of artificial intelligence for well-chosen (sub)routines to decrease the overall simulation time. This Special Issue features six invited and 18 regular papers that address these problems

Household Responses to Price Incentives for Recycling: Some Further Evidence

This paper investigates the role of waste disposal service fees and household characteristics in determining recycling rates and waste generation. Using individual household data from Portland, Oregon, we model a multistage household decision process regarding waste generation and recycling effort under a block pricing system, including the choice of container size and reduced-form demand equations for recyclables, non-recyclables, and recycling rate. The choice of container size is not affected by the price of waste disposal services, but within a given container size, households respond to a price increase by increasing recycling to avoid charges for waste generation above contracted volumes.

Synthesis of UV/blue light-emitting aluminum hydroxide with oxygen vacancy and their application to electrically driven light-emitting diodes

Aluminum hydroxide nanoparticles, one of the essential luminescent materials for display technology, bio-imaging, and sensors due to their non-toxicity, affordable pricing, and rare-earth-free phosphors, are synthesized via a simple method at a reaction time of 10 min at a low temperature of 200 degrees C. By controlling the precursor's ratio of aluminum acetylacetonate to oleic acid, UV or blue light-emitting aluminum hydroxides with oxygen defects and carbonyl radicals can be synthesized. As a result, aluminum hydroxide (Al(OH)(3-x)) nanoparticles overwhelmingly emit UVA light (390 nm) because of the oxygen defects in nanoparticles, and carbon-related radicals on the nanoparticles are responsible for the blue-light emission at 465 nm. Electrically driven light-emitting devices are applied using luminescent aluminum hydroxide as an emissive layer, that consists of a cost-efficient inverted bottom-emission structure as [ITO (cathode)/ZnO/emissive layers/2,2 '-bis(4-(carbazol-9-yl)phenyl)-biphenyl (BCBP)/MoO3/Al (anode)]. The device with aluminum hydroxide as an emissive layer shows a maximum luminance of 215.48 cd m(-2) and external quantum efficiency (EQE) of 0.12%. The new method for synthesizing UV-blue emitting aluminum hydroxides and their application to LEDs will contribute to developing the field of non-toxic optoelectronic material or UV-blue emitting devices.N

Lattice Distortion, Amorphization and Wear Resistance of Carbon-Doped SUS304 by Laser Ablation

Lattice distortion and amorphization of carbon-doped SUS304 by variation of the laser output were investigated in terms of phase formation and the bonding state. The laser output was changed by 10% in the range of 60% to 100% after covering the SUS304 with carbon paste. A graphite peak and expanded austenite (S-phase) peak were observed in the carbon-doped SUS304, and Rietveld refinement was performed to identify the lattice distortion. The lattice constant of SUS304 was initially 3.612 Å, but expansion lattice distortion occurred in the carbon-doped SUS304 as a result of the S phase formation and carbon doping, and the lattice constant increased to 3.964 Å (100% laser output). X-ray photoelectron spectroscopy analysis for the bonding state of the carbon-doped SUS304 showed that the sp2/sp3 ratio decreased from 3.21 (70% laser output) to 2.52 (100% laser output). The residual stress in the lattice was accumulated due to carbon doping by high thermal energy, which resulted in the formation of amorphous carbon. The bonding environment was represented by the ID/IG ratio using Raman analysis, and it increased from 0.55 (70% laser output) to 1.68 (100% laser output). During microstructure analysis of the carbon-doped SUS304, disordered structures by amorphization were observed in the carbon-doped SUS304 by the greater than 90% laser output. The amorphous carbon filled the lattice grains or voids to lubricate the surface, which improved the friction coefficient and wear rate from 0.23 and 7.63 mm3(Nm)−110−6 to 0.09 and 1.43 mm3(Nm)−110−6, respectively

Phase Formation and Wear Resistance of Carbon-Doped TiZrN Nanocomposite Coatings by Laser Carburization

Carbon-doped TiZrN nanocomposite coatings were investigated for phase formation and wear behavior. They were prepared by laser carburization using carbon paste, and the thermal energy of the pulsed laser was limited to the range of 20 to 50%. X-ray photoelectron spectroscopy analysis revealed that the ratio of carbide (TiC, ZrC) increased as the thermal energy of the laser increased. The sp2/sp3 ratio increased by approximately 16% when the laser thermal energy was raised from 30 to 40%, and the formation of amorphous carbon was confirmed in the carbon-doped TiZrN coatings. As a result of microstructural analysis, the carbon-doped TiZrN nanocomposite was formed by an increase of hybrid bonds in expanded localized carbon clusters. Wear resistance was evaluated using a ball-on-disc tester, which showed that the friction coefficient decreased from 0.74 to 0.11 and the wear rate decreased from 7.63 × 10−6 mm3 (Nm)−1 to 1.26 × 10−6 mm3 (Nm)−1. In particular, the friction coefficient and wear rate improved by 71 and 66%, respectively, owing to the formation of carbon-doped TiZrN nanocomposite with amorphous carbon while the thermal energy was increased from 30 to 40%

PGC1α Cooperates with FOXA1 to Regulate Epithelial Mesenchymal Transition through the TCF4-TWIST1

The peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) is a critical transcriptional coactivator that maintains metabolic homeostasis and energy expenditure by cooperating with various transcription factors. Recent studies have shown that PGC1α deficiency promotes lung cancer metastasis to the bone through activation of TCF4 and TWIST1-mediated epithelial–mesenchymal transition (EMT), which is suppressed by the inhibitor of DNA binding 1 (ID1); however, it is not clear which transcription factor participates in PGC1α-mediated EMT and lung cancer metastasis. Here, we identified forkhead box A1 (FOXA1) as a potential transcription factor that coordinates with PGC1α and ID1 for EMT gene expression using transcriptome analysis. Cooperation between FOXA1 and PGC1α inhibits promoter occupancy of TCF4 and TWIST1 on CDH1 and CDH2 proximal promoter regions due to increased ID1, consequently regulating the expression of EMT-related genes such as CDH1, CDH2, VIM, and PTHLH. Transforming growth factor beta 1 (TGFβ1), a major EMT-promoting factor, was found to decrease ID1 due to the suppression of FOXA1 and PGC1α. In addition, ectopic expression of ID1, FOXA1, and PGC1α reversed TGFβ1-induced EMT gene expression. Our findings suggest that FOXA1- and PGC1α-mediated ID1 expression involves EMT by suppressing TCF4 and TWIST1 in response to TGFβ1. Taken together, this transcriptional framework is a promising molecular target for the development of therapeutic strategies for lung cancer metastasis

ER Stress-Activated HSF1 Governs Cancer Cell Resistance to USP7 Inhibitor-Based Chemotherapy through the PERK Pathway

Ubiquitin-specific protease 7 inhibitors (USP7i) are considered a novel class of anticancer drugs. Cancer cells occasionally become insensitive to anticancer drugs, known as chemoresistance, by acquiring multidrug resistance, resulting in poor clinical outcomes in patients with cancer. However, the chemoresistance of cancer cells to USP7i (P22077 and P5091) and mechanisms to overcome it have not yet been investigated. In the present study, we generated human cancer cells with acquired resistance to USP7i-induced cell death. Gene expression profiling showed that heat stress response (HSR)- and unfolded protein response (UPR)-related genes were largely upregulated in USP7i-resistant cancer cells. Biochemical studies showed that USP7i induced the phosphorylation and activation of heat shock transcription factor 1 (HSF1), mediated by the endoplasmic reticulum (ER) stress protein kinase R-like ER kinase (PERK) signaling pathway. Inhibition of HSF1 and PERK significantly sensitized cancer cells to USP7i-induced cytotoxicity. Our study demonstrated that the ER stress–PERK axis is responsible for chemoresistance to USP7i, and inhibiting PERK is a potential strategy for improving the anticancer efficacy of USP7i