Experimental Validation of High Precision Web Handling for a Two-Actuator-Based Roll-to-Roll System

In this paper, experimental validation of high precision web handling for a two-actuator-based roll-to-roll (R2R) system is presented. To achieve this, the tension control loop is utilized to regulate the tension in the unwinder module, and the velocity loop is utilized to regulate the web speed in the rewinder module owing to the limitation of the number of actuators. Moreover, the radius estimation algorithm is applied to achieve an accurate web speed and the control sequence of the web handling in the longitudinal axis is developed to manipulate the web handling for convenience. Having these, the tension control performances are validated within ±0.79, ±1.32 and ±1.58 percent tension tracking error and 1.6, 1.53 and 1.33 percent web speed error at the speeds of 0.1 m/s, 0.2 m/s, and 0.3 m/s, respectively. The tension control performance is verified within ±0.3 N tracking error in the changes of the reference tension profile at 0.1 m/s web speed. Lastly, the air floating roller is used to minimize the friction terms and the inertia of the idle roller in the tension zone so that tension control performance can be better achieved during web transportation

Experimental Validation of High Precision Web Handling for a Two-Actuator-Based Roll-to-Roll System

In this paper, experimental validation of high precision web handling for a two-actuator-based roll-to-roll (R2R) system is presented. To achieve this, the tension control loop is utilized to regulate the tension in the unwinder module, and the velocity loop is utilized to regulate the web speed in the rewinder module owing to the limitation of the number of actuators. Moreover, the radius estimation algorithm is applied to achieve an accurate web speed and the control sequence of the web handling in the longitudinal axis is developed to manipulate the web handling for convenience. Having these, the tension control performances are validated within ±0.79, ±1.32 and ±1.58 percent tension tracking error and 1.6, 1.53 and 1.33 percent web speed error at the speeds of 0.1 m/s, 0.2 m/s, and 0.3 m/s, respectively. The tension control performance is verified within ±0.3 N tracking error in the changes of the reference tension profile at 0.1 m/s web speed. Lastly, the air floating roller is used to minimize the friction terms and the inertia of the idle roller in the tension zone so that tension control performance can be better achieved during web transportation

Lifshitz Transition and Non-Fermi Liquid Behavior in Highly Doped Semimetals

The classical Fermi liquid theory and Drude model have provided fundamental ways to understand the resistivity of most metals. The violation of the classical theory, known as non-Fermi liquid (NFL) transport, appears in certain metals, including topological semimetals, but quantitative understanding of the NFL behavior has not yet been established. In particular, the determination of the non-quadratic temperature exponent in the resistivity, a sign of NFL behavior, remains a puzzling issue. Here, a physical model to quantitatively explain the Lifshitz transition and NFL behavior in highly doped (a carrier density of ≈1022 cm−3) monoclinic Nb2Se3 is reported. Hall and magnetoresistance measurements, the two-band Drude model, and first-principles calculations demonstrate an apparent chemical potential shift by temperature in monoclinic Nb2Se3, which induces a Lifshitz transition and NFL behavior in the material. Accordingly, the non-quadratic temperature exponent in the resistivity can be quantitatively determined by the chemical potential shift under the framework of Fermi liquid theory. This model provides a new experimental insight for nontrivial transport with NFL behavior or sign inversion of Seebeck coefficients in emerging materials.11Nsciescopu

Auranofin prevents liver fibrosis by system Xc-mediated inhibition of NLRP3 inflammasome

Using mouse models of liver fibrosis, Kim et al examined the mechanisms underlying the antifibrotic inhibition of the NLRP3 inflammasome by auranofin. They demonstrated that auranofin-induced inhibition of the NLRP3 inflammasome in bone marrow-derived macrophages and kupffer cells was mediated via inhibition of the cystine-glutamate antiporter, system Xc, which advances our understanding of the mechanism by which auranofin exerts its therapeutic effects. Demand for a cure of liver fibrosis is rising with its increasing morbidity and mortality. Therefore, it is an urgent issue to investigate its therapeutic candidates. Liver fibrosis progresses following 'multi-hit' processes involving hepatic stellate cells, macrophages, and hepatocytes. The NOD-like receptor protein 3 (NLRP3) inflammasome is emerging as a therapeutic target in liver fibrosis. Previous studies showed that the anti-rheumatic agent auranofin inhibits the NLRP3 inflammasome; thus, this study evaluates the antifibrotic effect of auranofin in vivo and explores the underlying molecular mechanism. The antifibrotic effect of auranofin is assessed in thioacetamide- and carbon tetrachloride-induced liver fibrosis models. Moreover, hepatic stellate cell (HSC), bone marrow-derived macrophage (BMDM), kupffer cell, and hepatocyte are used to examine the underlying mechanism of auranofin. Auranofin potently inhibits activation of the NLRP3 inflammasome in BMDM and kupffer cell. It also reduces the migration of HSC. The underlying molecular mechanism was inhibition of cystine-glutamate antiporter, system Xc. Auranofin inhibits system Xc activity and instantly induced oxidative burst, which mediated inhibition of the NLRP3 inflammasome in macrophages and HSCs. Therefore, to the best of our knowledge, we propose the use of auranofin as an anti-liver fibrotic agent.Y

Synthesis, bioevaluation and docking study of 5-substitutedphenyl-1,3,4-thiadiazole-based hydroxamic acids as histone deacetylase inhibitors and antitumor agents

Since the first histone deacetylase (HDAC) inhibitor (Zolinza (R), widely known as suberoylanilide hydroxamic acid; SAHA) was approved by the Food and Drug Administration for the treatment of T-cell lymphoma in 2006, the search for newer HDAC inhibitors has attracted a great deal of interest of medicinal chemists worldwide. As a continuity of our ongoing research in this area, we designed and synthesized a series of 5-substitutedphenyl-1,3,4-thiadiazole-based hydroxamic acids as analogues of SAHA and evaluated their biological activities. A number of compounds in this series, for example, N-1-hydroxy-N (8)-(5-(2-chlorophenyl)-1,3,4-thiadiazol-2-yl)octandiamide (5b), N-1-hydroxy-N-8-(5-(3-chlorophenyl-1,3,4-thiadiazol-2-yl)octandiamide (5c) and N-1-hydroxy-N-8-(5-(4-chlorophenyl)-1,3,4-thiadiazol-2-yl)octandiamide (5d), were found to possess potent anticancer cytotoxicity and HDAC inhibition effects. Compounds 5b-d were generally two-to five-fold more potent in terms of cytotoxicity compared to SAHA against five cancer cell lines tested. Docking studies revealed that these hydroxamic acid displayed higher affinities than SAHA toward HDAC8.Y