Leader workaholism and subordinates' psychological distress: The moderating role of justice climate.

Leader workaholism, characterized by an excessive drive to work long hours, is prevalent among organizational leaders. Its impact on subordinates' mental health warrants examination. This study investigated the direct relationship between leader workaholism and subordinates' psychological distress. Drawing on substitutes for leadership theory, it also assessed the buffering effects of procedural, interactional, and distributive justice climates in this relationship. Data from an online survey of 40 leaders and 200 subordinate employees revealed a positive correlation between leader workaholism and subordinates' psychological distress. However, the procedural and interactional justice climates negatively moderated this relationship, whereas the distributive justice climate did not. This disparity may result from the strong link between distributive justice climate and specific, objective outcomes. The study enhances understanding of the adverse effects of leader workaholism on employee psychological health and suggests organizational strategies, such as fostering procedural and interactional justice climates, to mitigate these effects.

The influence of leader-follower cognitive style congruence on organizational citizenship behaviors and the mediating role of trust.

This study examined the impact of cognitive style congruence between leaders and followers on followers' organizational citizenship behaviors (OCBs) by integrating the similarity-attraction and signaling theories. We collected dyadic data from 80 leaders and 223 followers in ten manufacturing companies in China. Using polynomial regression analysis and response surface modeling, the study supported the positive influence of cognitive style congruence on followers' OCBs. Specifically, we found that dyads with more intuitive than analytical leader-follower cognitive styles had higher levels of OCBs. However, there were no significant differences in followers' OCBs between dyads consisting of an intuitive leader and an analytic follower versus those consisting of an analytic leader and an intuitive follower under conditions of cognitive style incongruence. Additionally, the study found that interpersonal trust mediated the relationship between leader-follower cognitive style congruence and followers' OCBs, offering valuable insights for promoting OCBs in the workplace.

The effect of mindfulness training on executive function in youth with depression.

Youth depression is often associated with impairments in cognitive function, especially in executive function. This study examines the effect of an 8-session-long mindfulness training that can improve executive function in youth with depression. Sixty youths (age range 15-27 years) with depression were selected as participants and were randomized into a mindfulness training group (MTG) and a waitlist-control group (WCG). The MTG received an 8-week mindfulness training while the WCG received no intervention. Both groups performed the Stroop, N-back, and More-odd shifting tasks at baseline and after eight weeks to examine inhibitory control, working memory, and cognitive flexibility of executive function, respectively. The results showed that mindfulness training significantly reduced the Stroop effect size for MTG (p < 0.001), but the effect on the switching cost was not statistically significant (p = 0.975). There was an age effect of mindfulness training on working memory. For young adults, mindfulness training improved accuracy on the N-back task (p < 0.01) and shortened reaction time, although this effect slightly exceeded the significance level (p = 0.075). However, mindfulness training failed to improve the working memory of adolescents with depression. In conclusion, mindfulness training improved inhibitory control in youth with depression. It also improved working memory in young adults with depression, but future studies with large samples are needed to validate the improvement in working memory.

Does similarity trigger cooperation? Dyadic effect of similarity in social value orientation and cognitive resources on cooperation.

Although a considerable amount of research has demonstrated a robust relationship between social value orientation and cooperation, these studies may be limited by focusing solely on the individual. Building on the growing literature documenting the effect of group formation on cooperation and personality similarity on negotiation, the present study explored whether similarity in social value orientation (both being pro-social or pro-self) leads to more cooperation in social dilemmas among dyad members. Drawing from expectancy theory and the concept of cognitive resources, we further predicted that the relationship between similarity in social value orientation and cooperation uniquely depends on whether the individual is cognitively busy. To test our hypothesis, we grouped our participants according to their social value orientation into three different dyads (similar-pro-self, similar-pro-social, and pro-self-pro-social) to complete a repeated prisoner's dilemma task, and controlled their cognitive resources using a simultaneous digit memory task. The results suggested that (1) heterogeneous dyads' (pro-self-pro-social) cooperation possibility experience a steeper decay as the number of rounds increases compared with the two homogeneous dyads (similar-pro-self, similar-pro-social). In addition, (2) similarity in social value orientation, interacting with participants' cognitive resources, significantly influenced individual-level cooperation. Specifically, both pro-selfs and pro-socials, paired with unlike-minded counterparts, were more cooperative when they had abundant cognitive resources. However, cognitive resources had no significant influence on dyads with similar social value orientation. Overall, these findings demonstrate the importance of considering personality configuration when attempting to understand cooperation in social dilemmas among dyads. Supplementary Information: The online version contains supplementary material available at 10.1007/s12144-022-03276-8.

The Effect of Work Connectivity Behavior After-Hours on Employee Psychological Distress: The Role of Leader Workaholism and Work-to-Family Conflict.

Background: The work connectivity behavior after-hours (WCBA) has become increasingly intense among Chinese employees in recent years, especially in the rapidly developed internet industry. This has made the after-hours work connectivity behavior, a popular topic in the organizational psychology field. Based on boundary theory, we explored the mechanism of after-hour work connectivity behavior on employees' psychological distress and identified the work-to-family conflict (WFC) as mediator. Besides, leader characteristics are essential environmental variables and always play as moderators, among which leader workaholism is prevalent in the internet industry. However, the impact of leader workaholism on employees' behavior is still inconsistent and even contradictory. Thus, this study further examines the moderating effect of leader workaholism between the after-hour work connectivity behavior and employees' psychological distress. Methods: We conducted a multitime, multisource questionnaire survey in Internet companies in China. Before collecting the data, all participants were assured that their responses would be confidential and used only for academic research. At time 1, the team leader rated his or her workaholism, and team members rated WCBA. At time 2 (3 weeks later), team members were asked to complete the questionnaire containing scales of WFC, psychological distress. The two rounds of data collection resulted in 211 matched team leader-team member responses. We performed a path analysis using Mplus 7.4. Results: Both the duration and frequency of WCBA can positively predict employees' psychological distress through WFC (the mediating effect = 0.628, 95% CI = [0.593, 0.663]). Specifically, WCBA can increase the level of WFC, which leads to the employees' psychological distress further. Leader workaholism can negatively moderate the relationship between WCBA and WFC, further moderating the mediating effect of WFC. Conclusions: Work-to-family conflict played as a mediator in the relationship between WCBA and employees' psychological distress. These results may be helpful to recognize the negative effect of WCBA and the role of leader workaholism in the relationship.

Pharmacological inhibition of P2RX7 ameliorates liver injury by reducing inflammation and fibrosis.

Extracellular adenosine triphosphate (eATP) released by damaged cells, and its purinergic receptors, comprise a crucial signaling network after injury. Purinergic receptor P2X7 (P2RX7), a major driver of NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation and IL-1ß processing, has been shown to play a role in liver injury in murine diet- and chemically-induced liver injury models. It is unclear, however, whether P2RX7 plays a role in non-alcoholic steatohepatitis (NASH) and which cell type is the main target of P2RX7 pharmacological inhibition. Here, we report that P2RX7 is expressed by infiltrating monocytes and resident Kupffer cells in livers from NASH-affected individuals. Using primary isolated human cells, we demonstrate that P2RX7 expression in CD14+ monocytes and Kupffer cells primarily mediates IL-1ß release. In addition, we show that pharmacological inhibition of P2RX7 in monocytes and Kupffer cells, blocks IL-1ß release, reducing hepatocyte caspase 3/7 activity, IL-1ß-mediated CCL2 and CCL5 chemokine gene expression and secretion, and hepatic stellate cell (HSC) procollagen secretion. Consequently, in a chemically-induced nonhuman primate model of liver fibrosis, treatment with a P2RX7 inhibitor improved histological characteristics of NASH, protecting from liver inflammation and fibrosis. Taken together, these findings underscore the critical role of P2RX7 in the pathogenesis of NASH and implicate P2RX7 as a promising therapeutic target for the management of this disease.

Structures of AMP-activated protein kinase bound to novel pharmacological activators in phosphorylated, non-phosphorylated, and nucleotide-free states.

AMP-activated protein kinase (AMPK) is an attractive therapeutic target for managing metabolic diseases. A class of pharmacological activators, including Merck 991, binds the AMPK ADaM site, which forms the interaction surface between the kinase domain (KD) of the α-subunit and the carbohydrate-binding module (CBM) of the ß-subunit. Here, we report the development of two new 991-derivative compounds, R734 and R739, which potently activate AMPK in a variety of cell types, including ß2-specific skeletal muscle cells. Surprisingly, we found that they have only minor effects on direct kinase activity of the recombinant α1ß2γ1 isoform yet robustly enhance protection against activation loop dephosphorylation. This mode of activation is reminiscent of that of ADP, which activates AMPK by binding to the nucleotide-binding sites in the γ-subunit, more than 60 Å away from the ADaM site. To understand the mechanisms of full and partial AMPK activation, we determined the crystal structures of fully active phosphorylated AMPK α1ß1γ1 bound to AMP and R734/R739 as well as partially active nonphosphorylated AMPK bound to R734 and AMP and phosphorylated AMPK bound to R734 in the absence of added nucleotides at <3-Å resolution. These structures and associated analyses identified a novel conformational state of the AMPK autoinhibitory domain associated with partial kinase activity and provide new insights into phosphorylation-dependent activation loop stabilization in AMPK.

A Fiber Bragg Grating Interrogation System with Self-Adaption Threshold Peak Detection Algorithm.

A Fiber Bragg Grating (FBG) interrogation system with a self-adaption threshold peak detection algorithm is proposed and experimentally demonstrated in this study. This system is composed of a field programmable gate array (FPGA) and advanced RISC machine (ARM) platform, tunable Fabry-Perot (F-P) filter and optical switch. To improve system resolution, the F-P filter was employed. As this filter is non-linear, this causes the shifting of central wavelengths with the deviation compensated by the parts of the circuit. Time-division multiplexing (TDM) of FBG sensors is achieved by an optical switch, with the system able to realize the combination of 256 FBG sensors. The wavelength scanning speed of 800 Hz can be achieved by a FPGA+ARM platform. In addition, a peak detection algorithm based on a self-adaption threshold is designed and the peak recognition rate is 100%. Experiments with different temperatures were conducted to demonstrate the effectiveness of the system. Four FBG sensors were examined in the thermal chamber without stress. When the temperature changed from 0 °C to 100 °C, the degree of linearity between central wavelengths and temperature was about 0.999 with the temperature sensitivity being 10 pm/°C. The static interrogation precision was able to reach 0.5 pm. Through the comparison of different peak detection algorithms and interrogation approaches, the system was verified to have an optimum comprehensive performance in terms of precision, capacity and speed.

Global metabolite profiling of mice with high-fat diet-induced obesity chronically treated with AMPK activators R118 or metformin reveals tissue-selective alterations in metabolic pathways.

BACKGROUND: The novel small molecule R118 and the biguanide metformin, a first-line therapy for type 2 diabetes (T2D), both activate the critical cellular energy sensor 5'-AMP-activated protein kinase (AMPK) via modulation of mitochondrial complex I activity. Activation of AMPK results in both acute responses and chronic adaptations, which serve to restore energy homeostasis. Metformin is thought to elicit its beneficial effects on maintenance of glucose homeostasis primarily though impacting glucose and fat metabolism in the liver. Given the commonalities in their mechanisms of action and that R118 also improves glucose homeostasis in a murine model of T2D, the effects of both R118 and metformin on metabolic pathways in vivo were compared in order to determine whether R118 elicits its beneficial effects through similar mechanisms. RESULTS: Global metabolite profiling of tissues and plasma from mice with diet-induced obesity chronically treated with either R118 or metformin revealed tissue-selective effects of each compound. Whereas metformin treatment resulted in stronger reductions in glucose and lipid metabolites in the liver compared to R118, upregulation of skeletal muscle glycolysis and lipolysis was apparent only in skeletal muscle from R118-treated animals. Both compounds increased ß-hydroxybutyrate levels, but this effect was lost after compound washout. Metformin, but not R118, increased plasma levels of metabolites involved in purine metabolism. CONCLUSIONS: R118 treatment but not metformin resulted in increased glycolysis and lipolysis in skeletal muscle. In contrast, metformin had a greater impact than R118 on glucose and fat metabolism in liver tissue.

Exercise performance and peripheral vascular insufficiency improve with AMPK activation in high-fat diet-fed mice.

Intermittent claudication is a form of exercise intolerance characterized by muscle pain during walking in patients with peripheral artery disease (PAD). Endothelial cell and muscle dysfunction are thought to be important contributors to the etiology of this disease, but a lack of preclinical models that incorporate these elements and measure exercise performance as a primary end point has slowed progress in finding new treatment options for these patients. We sought to develop an animal model of peripheral vascular insufficiency in which microvascular dysfunction and exercise intolerance were defining features. We further set out to determine if pharmacological activation of 5'-AMP-activated protein kinase (AMPK) might counteract any of these functional deficits. Mice aged on a high-fat diet demonstrate many functional and molecular characteristics of PAD, including the sequential development of peripheral vascular insufficiency, increased muscle fatigability, and progressive exercise intolerance. These changes occur gradually and are associated with alterations in nitric oxide bioavailability. Treatment of animals with an AMPK activator, R118, increased voluntary wheel running activity, decreased muscle fatigability, and prevented the progressive decrease in treadmill exercise capacity. These functional performance benefits were accompanied by improved mitochondrial function, the normalization of perfusion in exercising muscle, increased nitric oxide bioavailability, and decreased circulating levels of the endogenous endothelial nitric oxide synthase inhibitor asymmetric dimethylarginine. These data suggest that aged, obese mice represent a novel model for studying exercise intolerance associated with peripheral vascular insufficiency, and pharmacological activation of AMPK may be a suitable treatment for intermittent claudication associated with PAD.

AMPK activation through mitochondrial regulation results in increased substrate oxidation and improved metabolic parameters in models of diabetes.

Modulation of mitochondrial function through inhibiting respiratory complex I activates a key sensor of cellular energy status, the 5'-AMP-activated protein kinase (AMPK). Activation of AMPK results in the mobilization of nutrient uptake and catabolism for mitochondrial ATP generation to restore energy homeostasis. How these nutrient pathways are affected in the presence of a potent modulator of mitochondrial function and the role of AMPK activation in these effects remain unclear. We have identified a molecule, named R419, that activates AMPK in vitro via complex I inhibition at much lower concentrations than metformin (IC50 100 nM vs 27 mM, respectively). R419 potently increased myocyte glucose uptake that was dependent on AMPK activation, while its ability to suppress hepatic glucose production in vitro was not. In addition, R419 treatment of mouse primary hepatocytes increased fatty acid oxidation and inhibited lipogenesis in an AMPK-dependent fashion. We have performed an extensive metabolic characterization of its effects in the db/db mouse diabetes model. In vivo metabolite profiling of R419-treated db/db mice showed a clear upregulation of fatty acid oxidation and catabolism of branched chain amino acids. Additionally, analyses performed using both (13)C-palmitate and (13)C-glucose tracers revealed that R419 induces complete oxidation of both glucose and palmitate to CO2 in skeletal muscle, liver, and adipose tissue, confirming that the compound increases mitochondrial function in vivo. Taken together, our results show that R419 is a potent inhibitor of complex I and modulates mitochondrial function in vitro and in diabetic animals in vivo. R419 may serve as a valuable molecular tool for investigating the impact of modulating mitochondrial function on nutrient metabolism in multiple tissues and on glucose and lipid homeostasis in diabetic animal models.