Why employees and managers engage in unethical practices

The scope of this paper is to investigate the reasons as to why employees and managers in the workplace engage willingly in unethical practices. The paper begins by exploring the concept of ethics in the corporate world. It further highlights the different forms of unethical practices in the various companies in the contemporary world. The various theories that explore the issue of unethical practices in the workplace are highlighted and how they relate to the occurrence of unethical demeanor. The social contract theory and the psychological theories are highlighted in the paper. The study further delves in exploring the various types of reasons as depicted in different forms of literature in the world. The reasons include the pressure for performance at work, the effect of groupthink in the workplace, pressure from management, management control, demographic factors, and psychological traps, broken window theory. The paper also recommends the executive techniques that can be used to curb the psychological traps in the corporations. The paper also explores the broken window theory as a cause for unethical practices in the workplace. In conclusion, the paper comes up with recommendations for corporations

IκBβ is an essential co-activator for LPS-induced IL-1β transcription in vivo

IkBβ forms a complex with the NF-κB subunits RelA and c-Rel that inhibits the transcription of IL-1β and other genes. Mice lacking IkBβ are protected against LPS-induced shock

The Warburg Effect Suppresses Oxidative Stress Induced Apoptosis in a Yeast Model for Cancer

BACKGROUND: Otto Warburg observed that cancer cells are often characterized by intense glycolysis in the presence of oxygen and a concomitant decrease in mitochondrial respiration. Research has mainly focused on a possible connection between increased glycolysis and tumor development whereas decreased respiration has largely been left unattended. Therefore, a causal relation between decreased respiration and tumorigenesis has not been demonstrated. METHODOLOGY/PRINCIPAL FINDINGS: For this purpose, colonies of Saccharomyces cerevisiae, which is suitable for manipulation of mitochondrial respiration and shows mitochondria-mediated cell death, were used as a model. Repression of respiration as well as ROS-scavenging via glutathione inhibited apoptosis and conferred a survival advantage during seeding and early development of this fast proliferating solid cell population. In contrast, enhancement of respiration triggered cell death. CONCLUSION/SIGNIFICANCE: Thus, the Warburg effect might directly contribute to the initiation of cancer formation--not only by enhanced glycolysis--but also via decreased respiration in the presence of oxygen, which suppresses apoptosis

Phosphorylation bar-coding of Free Fatty Acid receptor 2 is generated in a tissue-specific manner

All the source data files associated with the paper "Phosphorylation bar-coding of Free Fatty Acid receptor 2 is generated in a tissue-specific manner

Defective granulation tissue formation in mice with specific ablation of integrin-linked kinase in fibroblasts - role of TGF beta 1 levels and RhoA activity

Wound healing crucially relies on the mechanical activity of fibroblasts responding to TGF beta 1 and to forces transmitted across focal adhesions. Integrin-linked kinase (ILK) is a central adapter recruited to integrin beta 1 tails in focal adhesions mediating the communication between cells and extracellular matrix. Here, we show that fibroblast-restricted inactivation of ILK in mice leads to impaired healing due to a severe reduction in the number of myofibroblasts, whereas inflammatory infiltrate and vascularization of the granulation tissue are unaffected. Primary ILK-deficient fibroblasts exhibit severely reduced levels of extracellular TGF beta 1, alpha-smooth muscle actin (alpha SMA) production and myofibroblast conversion, which are rescued by exogenous TGF beta 1. They are further characterized by elevated RhoA and low Rac1 activities, resulting in abnormal shape and reduced directional migration. Interference with RhoA-ROCK signaling largely restores morphology, migration and TGF beta 1 levels. We conclude that, in fibroblasts, ILK is crucial for limiting RhoA activity, thus promoting TGF beta 1 production, which is essential for dermal repair following injury

Phosphorylation bar-coding of Free Fatty Acid receptor 2 is generated in a tissue-specific manner

Free Fatty Acid receptor 2 (FFA2) is activated by short-chain fatty acids and expressed widely, including in white adipocytes and various immune and enteroendocrine cells. Using both wild type human FFA2 and a Designer Receptor Exclusively Activated by Designer Drugs (DREADD) variant we explored the activation and phosphorylation profile of the receptor, both in heterologous cell lines and in tissues from transgenic knock-in mouse lines expressing either human FFA2 or the FFA2-DREADD. FFA2 phospho-site specific antisera targeting either pSer296/pSer297 or pThr306/pThr310 provided sensitive biomarkers of both constitutive and agonist-mediated phosphorylation as well as an effective means to visualise agonist-activated receptors in situ. In white adipose tissue phosphorylation of residues Ser296/Ser297 was enhanced upon agonist activation whilst Thr306/Thr310 did not become phosphorylated. By contrast, in immune cells from Peyer’s patches Thr306/Thr310 become phosphorylated in a strictly agonist-dependent fashion whilst in enteroendocrine cells of the colon both Ser296/Ser297 and Thr306/Thr310 were poorly phosphorylated. The concept of phosphorylation bar-coding has centred to date on the potential for different agonists to promote distinct receptor phosphorylation patterns. Here we demonstrate that this occurs for the same agonist-receptor pairing in different patho-physiologically relevant target tissues. This may underpin why a single G protein-coupled receptor can generate different functional outcomes in a tissue-specific manner

Intergenerational transmission: Theoretical and methodological issues and an introduction to four Dutch cohorts

Behaviors, traits and characteristics are transmitted from parents to offspring because of complex genetic and non-genetic processes. We review genetic and non-genetic mechanisms of intergenerational transmission of psychopathology and parenting and focus on recent methodological advances in disentangling genetic and non-genetic factors. In light of this review, we propose that future studies on intergenerational transmission should aim to disentangle genetic and non-genetic transmission, take a long-term longitudinal perspective, and focus on paternal and maternal intergenerational transmission. We present four large longitudinal cohort studies within the Consortium on Individual Development, which together address many of these methodological challenges. These four cohort studies aim to examine the extent to which genetic and non-genetic transmission from the parental generation shapes parenting behavior and psychopathology in the next generation, as well as the extent to which self-regulation and social competence mediate this transmission. Conjointly, these four cohorts provide a comprehensive approach to the study of intergenerational transmission