A longitudinal analysis of motivation profiles at work

This paper examines the multidimensional nature of workplace motivation and the importance of a continuum structure in self-determination theory through application of complementary variable- and person-centered approaches. This approach is taken to simultaneously model the complexity of motivation and highlight interactions between motivational factors. Additionally, this study represents an initial test of the temporal stability of work motivation profiles. A sample of 510 full-time employees were recruited from a range of occupations. Results support the central importance of a general factor representing self-determination as the most influential factor in an employee’s motivation profile. However, smaller effects associated with the motivation subscales, especially identified regulation, were also noticed. Importantly, motivation profiles were found to be highly stable over the 4-month duration of this study. Results lend support to the theoretical position that while general self-determination is an essential component of motivation, it alone does not fully describe an employee’s motivation

Toxic response caused by a misfolding variant of the mitochondrial protein short-chain acyl-CoA dehydrogenase

Variations in the gene ACADS, encoding the mitochondrial protein short-chain acyl CoA-dehydrogenase (SCAD), have been observed in individuals with clinical symptoms. The phenotype of SCAD deficiency (SCADD) is very heterogeneous, ranging from asymptomatic to severe, without a clear genotype-phenotype correlation, which suggests a multifactorial disorder. The pathophysiological relevance of the genetic variations in the SCAD gene is therefore disputed, and has not yet been elucidated, which is an important step in the investigation of SCADD etiology. To determine whether the disease-associated misfolding variant of SCAD protein, p.Arg107Cys, disturbs mitochondrial function. We have developed a cell model system, stably expressing either the SCAD wild-type protein or the misfolding SCAD variant protein, p.Arg107Cys (c.319 C > T). The model system was used for investigation of SCAD with respect to expression, degree of misfolding, and enzymatic SCAD activity. Furthermore, cell proliferation and expression of selected stress response genes were investigated as well as proteomic analysis of mitochondria-enriched extracts in order to study the consequences of p.Arg107Cys protein expression using a global approach. We found that expression of the p.Arg107Cys variant SCAD protein gives rise to inactive misfolded protein species, eliciting a mild toxic response manifested though a decreased proliferation rate and oxidative stress, as shown by an increased demand for the mitochondrial antioxidant SOD2. In addition, we found markers of apoptotic activity in the p.Arg107Cys expressing cells, which points to a possible pathophysiological role of this variant protei