Can senior executive characteristics improve carbon emission performance? Evidence from China

In recent years, the backbone of China's market economy has involved controlling corporate carbon emissions and reducing environmental pollution. This study aimed to investigate the relationship between the characteristics of senior managers and the carbon emission performance of enterprises. The empirical study used panel data on high-emission industries operating in the China A-shares market from 2014 to 2017. The results showed that the natural age, education level, and professional background of senior managers in high-emission enterprises were negatively correlated with the carbon emission performance of enterprises. However, in the case of large enterprises, there is no strong relationship between the natural age of executives and carbon emission performance, while professional background and education level are negatively correlated with carbon emission performance. However, natural age is significantly related to carbon emission performance in small and medium-sized enterprises. In the regional classification of enterprises, the natural age and professional background of the core executives of high-emitting enterprises in the eastern region are negatively correlated with carbon emission performance, while the professional background of the core executives of high-emitting enterprises in the central and western regions is positively correlated with carbon emission performance. Moreover, the natural age and educational level of executives are negatively correlated with carbon emission performance. To measure the carbon emission performance of an enterprise, the study used the balanced scorecard evaluation system (CEP). Meanwhile, it innovatively classifies and sorts the sample companies based on their overall size and distribution area, and analyzes the carbon performance and executive characteristics from two perspectives. The study provides suggestions and countermeasures for companies in China, especially those in high-emission industries, to help reduce pollution

Protein phosphatase 1 suppresses androgen receptor ubiquitylation and degradation

The phosphoprotein phosphatases are emerging as important androgen receptor (AR) regulators in prostate cancer (PCa). We reported previously that the protein phosphatase 1 catalytic subunit (PP1α) can enhance AR activity by dephosphorylating a site in the AR hinge region (Ser650) and thereby decrease AR nuclear export. In this study we show that PP1α increases the expression of wildtype as well as an S650A mutant AR, indicating that it is acting through one or more additional mechanisms. We next show that PP1α binds primarily to the AR ligand binding domain and decreases its ubiquitylation and degradation. Moreover, we find that the PP1α inhibitor tautomycin increases phosphorylation of AR ubiquitin ligases including SKP2 and MDM2 at sites that enhance their activity, providing a mechanism by which PP1α may suppress AR degradation. Significantly, the tautomycin mediated decrease in AR expression was most pronounced at low androgen levels or in the presence of the AR antagonist enzalutamide. Consistent with this finding, the sensitivity of LNCaP and C4–2 PCa cells to tautomycin, as assessed by PSA synthesis and proliferation, was enhanced at low androgen levels or by treatment with enzalutamide. Together these results indicate that PP1α may contribute to stabilizing AR protein after androgen deprivation therapies, and that targeting PP1α or the AR-PP1α interaction may be effective in castration-resistant prostate cancer (CRPC)

An algorithm to evaluate implementation cost for liveness-enforcing supervisors designed by deadlock prevention policy

Deadlock prevention policy is widely used to design the liveness-enforcing supervisors because of its advantage that deadlocks are considered and solved in design and planning stages for flexible manufacturing systems modeled with Petri nets. However, how to evaluate the implementation cost of these liveness-enforcing supervisors is not done in the existing literature. This article proposes an algorithm to evaluate the implementation cost performance of different liveness-enforcing supervisors designed by deadlock prevention policy. By designing a multiple objective linear programming problem associated with two parameters (denoted as f 1 and f 2 ) to characterize the corresponding implementation costs for the added control places and the related input and out transitions and control arcs, the proposed algorithm first obtains the variable regions of f 1 and f 2 And then a satisfactory level coefficient (denoted as λ ) concentrating on the optimal compromise solutions of f 1 and f 2 (denoted as f 1 * and f 2 * ) is solved by a linear programming problem. As a result, the implementation cost performance of the corresponding liveness-enforcing supervisor can be indicated conveniently on the basis of the values of λ , f 1 * , and f 2 * . The practical potential of the proposed algorithm is demonstrated via a theoretical analysis and several widely used examples from the existing literature

VO₂(B)/Graphene Composite-Based Symmetrical Supercapacitor Electrode via Screen Printing for Intelligent Packaging

More multipurpose and convenient demand driven by Radio Frequency Identification (RFID) and intelligent packaging require flexible power sources. A VO2(B)/graphene (VO2(B)/GN) core-shell composite was successfully synthesized by the hydrothermal treatment with V2O5 and graphite. The as-obtained sample was characterized by XRD, FT-IR, SEM, TEM, and XPS measurements. In addition, the electrochemical properties of VO2(B)/GN were tested. Due to its great electrochemical performance and mechanical properties, graphene could increase the electrochemical performance and strengthen the structural stability of the material at the same time. With increasing loading amount of GN, the specific capacitance of VO2(B)/GN increased correspondingly. With 20% GN loading, the initial discharge specific capacity could reach 197 F g−1 at 0.5 A g−1, and 160 F g−1 at 1 A g−1 in 0.5 M Na2SO4 electrolyte, which is better than that of pure rod-like VO2(B). The capacitance of the VO2(B)/GN (20%) composite electrode retains 95.49% after 1000 cycles, which is higher than that of a pure VO2(B) electrode (85.43%), indicating that the VO2(B)/GN composite possesses better cycling stability. Moreover, a symmetrical solid-state supercapacitor (SCs) using VO2(B)/GN(20%) as the anode was assembled. Four printed SCs were connected in series to light up a 1.5 V red LED. This demonstrates its potential application in intelligent packaging to trace food safety

The RSL3 Induction of KLK Lung Adenocarcinoma Cell Ferroptosis by Inhibition of USP11 Activity and the NRF2-GSH Axis

Antioxidant transcription factor NRF2 plays a pivotal role in cell ferroptosis. KLK lung adenocarcinoma (LUAD) is a specific molecular subtype of Kras-mutant LUAD. The activation of mutant Kras in combination with the inactivation of Lkb1 and Keap1 abnormally increases NRF2 expression, while high NRF2 confers KLK LUAD cell resistance to ferroptosis. This study assessed the inhibition of NRF2-GSH axis to sensitize a small molecule RSL3 to induce KLK LUAD cell ferroptosis and then explored the underlying molecular mechanisms. The data showed that the NRF2-GSH inhibition sensitized RSL3 induction of KLK LUAD cell ferroptosis in vitro, while RSL3 treatment reduced level of NRF2 protein in KLK LUAD during ferroptosis. Moreover, RSL3 treatment inhibited activity of the NRF2-GSH signaling during in KLK LUAD cell ferroptosis in vitro and in vivo. Mechanistically, the RSL3 reduction of NRF2 expression was through the promotion of NRF2 ubiquitination in KLK LUAD cells. In addition, RSL3 was able to directly bind to USP11, a recently identified de-ubiquitinase of NRF2, and inactivate USP11 protein to induce NRF2 protein ubiquitination and degradation in KLK LUAD cells. These data revealed a novel mechanism of RSL3 induction in KLK LUAD cell ferroptosis by suppression of the USP11-NRF2-GSH signaling. Future study will confirm RSL3 as a novel therapeutic approach in control of KLK lung adenocarcinoma

Melatonin promotes gut anti-oxidative status in perinatal rat by remodeling the gut microbiome

Gut health is important for nutrition absorption, reproduction, and lactation in perinatal and early weaned mammals. Although melatonin functions in maintaining circadian rhythms and preventing obesity, neurodegenerative diseases, and viral infections, its impact on the gut microbiome and its function in mediating gut health through gut microbiota remain largely unexplored. In the present study, the microbiome of rats was monitoring after fecal microbiota transplantation (FMT) and foster care (FC). The results showed that FMT and FC increased intestinal villus height/crypt depth in perinatal rats. Mechanistically, the melatonin-mediated remodeling of gut microbiota inhibited oxidative stress, which led to attenuation of autophagy and inflammation. In addition, FMT and FC encouraged the growth of more beneficial intestinal bacteria, such as Allobaculum, Bifidobacterium, and Faecalibaculum, which produce more short-chain fatty acids to strengthen intestinal anti-oxidation. These findings suggest that melatonin-treated gut microbiota increase the production of SCFAs, which improve gut health by reducing oxidative stress, autophagy and inflammation. The transfer of melatonin-treated gut microbiota may be a new and effective method by which to ameliorate gut health in perinatal and weaned mammals