Employees’ perceptions of corporate social responsibility and ethical leadership: Are they uniquely related to turnover intention?

© 2020, Emerald Publishing Limited. Purpose: The purpose of this study is to investigate the simultaneous effect of ethical leadership (EL) and corporate social responsibility (CSR) on employees’ turnover intention and examine the mediating mechanism in these relationships. Design/methodology/approach: The authors conducted a field study of 851 employees across a variety of industries. This study applied partial least squares structural equation modelling for hypothesis testing. Findings: The results show that employees’ perceptions of CSR as well as EL are both uniquely and negatively related to turnover intention. The authors also found that employees’ job satisfaction but not commitment, mediates these relationships. Research limitations/implications: This study answers the recent call (Schminke and Sheridan, 2017) for ethics researchers to put competing explanations to the test to determine their relative importance. Research limitations have been discussed in the paper. Social implications: Through providing empirical support for the positive impact of CSR and EL on employee-related outcomes and creating a decent and empowering work environment, this study provides further support for CSR and EL. As CSR and EL require accountability, responsible management and addressing societal well-being of stakeholders, this study can contribute to the United Nations sustainable development goals. Originality/value: Previous research has found that both employees’ perceptions of supervisory EL and CSR are negatively related to employees’ turnover intentions. Yet, the authors know little about their relative importance because these relationships have not been adequately examined simultaneously

Influence of oxidative stress, diaphragm fatigue, and inspiratory muscle training on the plasma cytokine response to maximum sustainable voluntary ventilation

The influence of oxidative stress, diaphragm fatigue, and inspiratory muscle training (IMT) on the cytokine response to maximum sustainable voluntary ventilation (MSVV) is unknown. Twelve healthy males were divided equally into an IMT or placebo (PLA) group, and before and after a 6-wk intervention they undertook, on separate days, 1h of (1) passive rest and (2) MSVV, whereby participants undertook volitional hyperpnea at rest that mimicked the breathing and respiratory muscle recruitment patterns commensurate with heavy cycling exercise. Plasma cytokines remained unchanged during passive rest. There was a main effect of time (P < 0.01) for plasma interleukin-1 (IL-1) and interleukin-6 (IL-6) concentrations and a strong trend (P = 0.067) for plasma interleukin-1 receptor antagonist concentration during MSVV. Plasma IL-6 concentration was reduced after IMT by 27 + 18% (main effect of intervention, P = 0.029), whereas there was no change after PLA (P = 0.753). There was no increase in a systemic marker of oxidative stress [DNA damage in peripheral blood mononuclear cells (PBMC)], and diaphragm fatigue was not related to the increases in plasma IL-1 and IL-6 concentrations. A dose-response relationship was observed between respiratory muscle work and minute ventilation and increases in plasma IL-6 concentration. In conclusion, increases in plasma IL-1 and IL-6 concentrations during MSVV were not due to diaphragm fatigue or DNA damage in PBMC. Increases in plasma IL-6 concentration during MSVV are attenuated following IMT, and the plasma IL-6 response is dependent upon the level of respiratory muscle work and minute ventilation

Sphingosine kinase 1–mediated inhibition of Fas death signaling in rheumatoid arthritis B lymphoblastoid cells

Objective It is becoming increasingly apparent that B cells play an important role in the pathogenesis of rheumatoid arthritis (RA). Due to the scarcity of B cells in RA, it has been technically difficult to functionally characterize B cell apoptosis in this disease. As a necessary first step to identify candidate aberrations, we investigated Fas-mediated signaling events in immortalized peripheral blood B lymphoblastoid cell lines (LCLs) from patients with RA and controls. Methods Cell death was determined by the MTS assay, and apoptosis was detected by the TUNEL assay and DNA laddering. Proteolytic activation of caspase 3 was determined by immunoblotting, and its enzymatic activity was determined by a fluorometric technique. Messenger RNA (mRNA) expression was quantified by real-time polymerase chain reaction (PCR) analysis. The functional role of sphingosine kinase (SPHK) was determined by measuring its enzymatic activity, by quantifying the levels of its product, sphingosine 1-phosphate (S1P), and by investigating the ability of the SPHK inhibitor N , N -dimethylsphingosine and isozyme-specific small interfering RNA (siRNA) oligonucleotides to reverse signaling aberrations. Results LCLs from patients with RA displayed disease-specific Fas-mediated signal transduction impairment with consequent resistance to cell death. RA LCLs displayed high constitutive SPHK activity and increased levels of S1P. Real-time PCR analysis showed higher SPHK-1 mRNA expression levels in RA patients compared with paired controls. Increased SPHK-1 (but not SPHK-2) mRNA levels were observed in synovial tissue from RA patients. Competitive inhibitors of SPHK reversed the resistance of RA LCLs to Fas-induced apoptosis. Additionally, resistance to Fas-mediated signaling was reversed by siRNA oligonucleotides specific for SPHK-1 but not by oligonucleotides specific for SPHK-2. Conclusion These findings demonstrate disease-specific resistance to Fas-mediated death signaling in patients with RA and implicate increased SPHK-1 activity as the cause of this aberration.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/49513/1/21635_ftp.pd

Expanding Australia\u27s defence capabilities for technological asymmetric advantage in information, cyber and space in the context of accelerating regional military modernisation: A systemic design approach

Introduction. The aim of the project was to conduct a systemic design study to evaluate Australia\u27sopportunities and barriers for achieving a technological advantage in light of regional military technological advancement. It focussed on the three domains of (1) cybersecurity technology, (2) information technology, and (3) space technology. Research process. Employing a systemic design approach, the study first leveraged scientometric analysis, utilising informetric mapping software (VOSviewer) to evaluate emerging trends and their implications on defence capabilities. This approach facilitated a broader understanding of the interdisciplinary nature of defence technologies, identifying key areas for further exploration. The subsequent survey study, engaging 828 professionals across STEM, space, aerospace, defence/ law enforcement, and ICT, aimed to assess the impact, deployment likelihood, and developmental timelines of the identified technologies. Finally, five experts were interviewed to help elaborate on the findings in the survey and translate them into implications for the ADF. Findings. Key findings revealed significant overlaps in technology clusters, highlighting ten specific technologies or trends as potential force multipliers for the ADF. Among these, cybersecurity of critical infrastructure and optimisation and other algorithmic technologies were recognised for their immediate potential and urgency, suggesting a prioritisation for development investment. The analysis presented a clear imperative for urgent and prioritised technological investments, specifically in cybersecurity and information technologies, followed by space technologies. The research also suggested partnerships that Australia should develop to keep ahead in terms of regional military modernisation. Implications. To maintain a competitive edge, there is an urgent need for investment in the development and application of these technologies, as nearly all disruptive technologies identified for their potential impact, deployment/utilization likelihood, extensive use, and novelty for defence purposes are needed in the near-term (less than 5 years – cybersecurity and information technologies) or medium-term (less than 10 years – space technologies). In line with this, technology investments should be prioritized as follows: Priority 1 includes Cyber Security of critical infrastructure and optimization algorithms; Priority 2 encompasses Unmanned and autonomous systems and weapons, Deep/Machine Learning, and Space-based command and communications systems; and Priority 3 involves Industry 4.0 technologies, Quantum technology, Electromagnetic and navigation warfare systems, Hypersonic weapons, and Directed energy weapons. At the policy level, underfunding, bureaucratic inertia and outdated procurement models needed to be addressed to enhance agility of innovation. More critically, Australia needed to come up with creative ways to recruit, train and retain human capital to develop, manage and use these sophisticated technologies. Finally, in order to maintain a lead over competitors (China, Russia, Iran, North Korea) in the regional military technology competition, the survey and interviews indicate that Australia should continue its military technology alliances with long-standing partners (US, Europe, Israel), broaden its collaborations with more recent partners (Japan, Singapore, South Korea), and establish partnerships with new ones (India, Malaysia, Vietnam, Pacific Island nations). Conclusion. This study sheds light on the future direction for the ADF and Defence in general, underscoring the importance of strategic investments in up-and-coming technologies. By pinpointing strategic voids, potential partnerships, and sovereign technologies with high potential, this report acts as a roadmap for bolstering Australia’s defence capabilities and safeguarding its strategic interests amidst regional technological changes

Vascular Dysfunction in Patients with Chronic Arsenosis Can Be Reversed by Reduction of Arsenic Exposure

Chronic arsenic exposure causes vascular diseases associated with systematic dysfunction of endogenous nitric oxide. Replacement of heavily arsenic-contaminated drinking water with low-arsenic water is a potential intervention strategy for arsenosis, although the reversibility of arsenic intoxication has not established. In the present study, we examined urinary excretion of cyclic guanosine 3′,5′-monophosphate (cGMP), a second messenger of the vasoactive effects of nitric oxide, and signs and symptoms for peripheral vascular function in 54 arsenosis patients before and after they were supplied with low-arsenic drinking water in an endemic area of chronic arsenic poisoning in Inner Mongolia, China. The arsenosis patients showed a marked decrease in urinary excretion of cGMP (mean ± SEM: male, 37.0 ± 6.1; female, 37.2 ± 5.4 nmol/mmol creatinine), and a 13-month period of consuming low-arsenic drinking water reversed this trend (male, 68.0 ± 5.6; female, 70.6 ± 3.0 nmol/mmol creatinine) and improved peripheral vascular response to cold stress. Our intervention study indicates that peripheral vascular disease in arsenosis patients can be reversed by exposure cessation and has important implications for the public health approach to arsenic exposure

Gate-Controlled Ionization and Screening of Cobalt Adatoms on a Graphene Surface

We describe scanning tunneling spectroscopy (STS) measurements performed on individual cobalt (Co) atoms deposited onto backgated graphene devices. We find that Co adatoms on graphene can be ionized by either the application of a global backgate voltage or by the application of a local electric field from a scanning tunneling microscope (STM) tip. Large screening clouds are observed to form around Co adatoms ionized in this way, and we observe that some intrinsic graphene defects display a similar behavior. Our results provide new insight into charged impurity scattering in graphene, as well as the possibility of using graphene devices as chemical sensors.Comment: 19 pages, 4 figure

Loss of AMP-activated protein kinase alpha 2 subunit in mouse beta-cells impairs glucose-stimulated insulin secretion and inhibits their sensitivity to hypoglycaemia

AMPK (AMP-activated protein kinase) signalling plays a key role in whole-body energy homoeostasis, although its precise role in pancreatic β-cell function remains unclear. In the present stusy, we therefore investigated whether AMPK plays a critical function in β-cell glucose sensing and is required for the maintenance of normal glucose homoeostasis. Mice lacking AMPKα2 in β-cells and a population of hypothalamic neurons (RIPCreα2KO mice) and RIPCreα2KO mice lacking AMPKα1 (α1KORIPCreα2KO) globally were assessed for whole-body glucose homoeostasis and insulin secretion. Isolated pancreatic islets from these mice were assessed for glucose-stimulated insulin secretion and gene expression changes. Cultured β-cells were examined electrophysiologically for their electrical responsiveness to hypoglycaemia. RIPCreα2KO mice exhibited glucose intolerance and impaired GSIS (glucose-stimulated insulin secretion) and this was exacerbated in α1KORIPCreα2KO mice. Reduced glucose concentrations failed to completely suppress insulin secretion in islets from RIPCreα2KO and α1KORIPCreα2KO mice, and conversely GSIS was impaired. β-Cells lacking AMPKα2 or expressing a kinase-dead AMPKα2 failed to hyperpolarize in response to low glucose, although KATP (ATP-sensitive potassium) channel function was intact. We could detect no alteration of GLUT2 (glucose transporter 2), glucose uptake or glucokinase that could explain this glucose insensitivity. UCP2 (uncoupling protein 2) expression was reduced in RIPCreα2KO islets and the UCP2 inhibitor genipin suppressed low-glucose-mediated wild-type mouse β-cell hyperpolarization, mimicking the effect of AMPKα2 loss. These results show that AMPKα2 activity is necessary to maintain normal pancreatic β-cell glucose sensing, possibly by maintaining high β-cell levels of UCP2

Mechanisms underlying the diminished sensitivity to prolactin negative feedback during lactation: Reduced STAT5 signaling and up-regulation of cytokine-inducible SH2 domain-containing protein (CIS) expression in tuberoinfundibular dopaminergic neurons

Hyperprolactinaemia during lactation is a consequence of the sucking stimulus and in part due to reduced prolactin (PRL) negative feedback. To date, the mechanisms involved in this diminished sensitivity to PRL feedback are unknown but may involve changes in PRL signal transduction within tuberoinfundibular dopaminergic (TIDA) neurons. Therefore, we investigated signal transducers and activators of transcription (STAT) 5 signaling in the TIDA neurons of lactating rats. Dual-label confocal immunofluorescence studies were used to determine the intracellular distribution of STAT5 within TIDA neurons in the dorsomedial arcuate nucleus. In lactating rats with pups removed for 16 h, injection of ovine PRL significantly (P < 0.05) increased the STAT5 nuclear/cytoplasmic ratio compared with vehicle-treated mothers. In contrast, ovine PRL injection did not increase the STAT5 nuclear/cytoplasmic ratio in lactating mothers with pups, demonstrating that PRL signal transduction through STAT5 is reduced in TIDA neurons in the presence of pups. To investigate possible mechanisms involved in reduced PRL signaling, we examined the expression of suppressors of cytokine signaling (SOCS) proteins. Northern analysis on whole hypothalamus showed that CIS (cytokine-inducible SH2 domain-containing protein), but not SOCS1 or SOCS3, mRNA expression was significantly (P < 0.01) up-regulated in suckled lactating rats. Semiquantitative RT-PCR on arcuate nucleus micropunches also showed up-regulation of CIS transcripts. Immunofluorescence studies demonstrated that CIS is expressed in all TIDA neurons in the dorsomedial arcuate nucleus, and the intensity of CIS staining in these neurons is significantly (P < 0.05) increased in lactating rats with sucking pups. Together, these results support the hypothesis that loss of sensitivity to PRL-negative feedback during lactation is a result of increased CIS expression in TIDA neurons

Hadoop distributed file system for the Grid

Data distribution, storage and access are essential to CPU-intensive and data-intensive high performance Grid computing. A newly emerged file system, Hadoop distributed file system (HDFS), is deployed and tested within the Open Science Grid (OSG) middleware stack. Efforts have been taken to integrate HDFS with other Grid tools to build a complete service framework for the Storage Element (SE). Scalability tests show that sustained high inter-DataNode data transfer can be achieved for the cluster fully loaded with data-processing jobs. The WAN transfer to HDFS supported by BeStMan and tuned GridFTP servers shows large scalability and robustness of the system. The hadoop client can be deployed at interactive machines to support remote data access. The ability to automatically replicate precious data is especially important for computing sites, which is demonstrated at the Large Hadron Collider (LHC) computing centers. The simplicity of operations of HDFS-based SE significantly reduces the cost of ownership of Petabyte scale data storage over alternative solutions

Inflation at the Electroweak Scale

We present a simple model for slow-rollover inflation where the vacuum energy that drives inflation is of the order of $G_F^{-2}$; unlike most models, the conversion of vacuum energy to radiation (``reheating'') is moderately efficient. The scalar field responsible for inflation is a standard-model singlet, develops a vacuum expectation value of the order of 4\times 10^6\GeV, has a mass of order 1\GeV, and can play a role in electroweak phenomena.Comment: 14 page