Ethics And Retail Management Professionals: An Examination Of Age, Education, And Experience Variables

Ethical maturity and behavior are of great concern to all educators, firms, and investors, and even more so in a recession. This research surveyed managers and employees in the retail environment to measure their Personal Business Ethics Scores (PBES) to see if age, education, and management experience makes a difference in making more ethical decisions. The PBES measures personal commitment to integrity, honesty, and observance of the laws regulating current business activities. This research takes into consideration the respondents age, management experience, and education. This study contributes to the theory of moral development as it is tested with retail managers and employees. The results of this research suggest that while age and management experience are significant factors, higher education may also play a role in the moral development of associates and managers. Kohlbergs moral development theory is supported by this research since older workers, more highly educated workers, and those with more years of management experience have a higher level of moral maturity

Attenuated mTOR Signaling and Enhanced Autophagy in Adipocytes from Obese Patients with Type 2 Diabetes

Type 2 diabetes (T2D) is strongly linked to obesity and an adipose tissue unresponsive to insulin. The insulin resistance is due to defective insulin signaling, but details remain largely unknown. We examined insulin signaling in adipocytes from T2D patients, and contrary to findings in animal studies, we observed attenuation of insulin activation of mammalian target of rapamycin (mTOR) in complex with raptor (mTORC1). As a consequence, mTORC1 downstream effects were also affected in T2D: feedback signaling by insulin to signal-mediator insulin receptor substrate-1 (IRS1) was attenuated, mitochondria were impaired and autophagy was strongly upregulated. There was concomitant autophagic destruction of mitochondria and lipofuscin particles, and a dependence on autophagy for ATP production. Conversely, mitochondrial dysfunction attenuated insulin activation of mTORC1, enhanced autophagy and attenuated feedback to IRS1. The overactive autophagy was associated with large numbers of cytosolic lipid droplets, a subset with colocalization of perlipin and the autophagy protein LC3/atg8, which can contribute to excessive fatty acid release. Patients with diagnoses of T2D and overweight were consecutively recruited from elective surgery, whereas controls did not have T2D. Results were validated in a cohort of patients without diabetes who exhibited a wide range of insulin sensitivities. Because mitochondrial dysfunction, inflammation, endoplasmic-reticulum stress and hypoxia all inactivate mTORC1, our results may suggest a unifying mechanism for the pathogenesis of insulin resistance in T2D, although the underlying causes might differ