Interpersonal Mistreatment in the Workplace: The Experience of Envy and Incivility Related to Turnover Intention

Masteroppgave(MSc) in Master of Science in Leadership and Organizational Psychology - Handelshøyskolen BI, 2019Workplace incivility violates the norms of mutual respect between employees. Milder forms of aggression are common in business, despite their negative interpersonal effects and impact on organizations as a whole. Even so, research on the construct of experienced workplace incivility is sparse. We suggest the perception of being envied to be an antecedent of experienced workplace incivility and provide an exploration of turnover intention as a conceivable outcome via organizational commitment. The purpose of the following research study is to enhance the understanding of workplace incivility, given its existing presence as an organizational construct. Through an increased awareness of the antecedents and outcomes of incivility, unfavorable implications may be avoided and thereby improve future organizational well-being. Through the use of a cross-sectional research design with 187 participants from the Norwegian health care sector, findings revealed that employees who experienced envy from others were also more prone to experience workplace incivility. Furthermore, the experience of workplace incivility was directly and significantly related to turnover intention, although including organizational commitment as a mediator of the relationship provided a better model fit. A novel contribution to the research field was the concentration on the perceived experience of incivility, rather than on the actual behaviors. Related limitations and implications of the findings are thoroughly discussed before concluding with an outline for possible future research. Keywords: envy, workplace incivility, organizational commitment, turnover intentio

Optimality Clue for Graph Coloring Problem

In this paper, we present a new approach which qualifies or not a solution found by a heuristic as a potential optimal solution. Our approach is based on the following observation: for a minimization problem, the number of admissible solutions decreases with the value of the objective function. For the Graph Coloring Problem (GCP), we confirm this observation and present a new way to prove optimality. This proof is based on the counting of the number of different k-colorings and the number of independent sets of a given graph G. Exact solutions counting problems are difficult problems (\#P-complete). However, we show that, using only randomized heuristics, it is possible to define an estimation of the upper bound of the number of k-colorings. This estimate has been calibrated on a large benchmark of graph instances for which the exact number of optimal k-colorings is known. Our approach, called optimality clue, build a sample of k-colorings of a given graph by running many times one randomized heuristic on the same graph instance. We use the evolutionary algorithm HEAD [Moalic et Gondran, 2018], which is one of the most efficient heuristic for GCP. Optimality clue matches with the standard definition of optimality on a wide number of instances of DIMACS and RBCII benchmarks where the optimality is known. Then, we show the clue of optimality for another set of graph instances. Optimality Metaheuristics Near-optimal

Estimating genomic heritabilities at the level of family-pool samples of perennial ryegrass using genotyping-by-sequencing

KEYMESSAGE: By using the genotyping-by-sequencing method, it is feasible to characterize genomic relationships directly at the level of family pools and to estimate genomic heritabilities from phenotypes scored on family-pools in outbreeding species. ABSTRACT: Genotyping-by-sequencing (GBS) has recently become a promising approach for characterizing plant genetic diversity on a genome-wide scale. We use GBS to extend the concept of heritability beyond individuals by genotyping family-pool samples by GBS and computing genomic relationship matrices (GRMs) and genomic heritabilities directly at the level of family-pools from pool-frequencies obtained by sequencing. The concept is of interest for species where breeding and phenotyping is not done at the individual level but operates uniquely at the level of (multi-parent) families. As an example we demonstrate the approach using a set of 990 two-parent F2 families of perennial ryegrass (Lolium Perenne). The families were phenotyped as a family-unit in field plots for heading date and crown rust resistance. A total of 728 K single nucleotide polymorphism (SNP) variants were available and were divided in groups of different sequencing depths. GRMs based on GBS data showed diagonal values biased upwards at low sequencing depth, while off-diagonals were little affected by the sequencing depth. Using variants with high sequencing depth, genomic heritability for crown rust resistance was 0.33, and for heading date 0.22, and these genomic heritabilities were biased downwards when using variants with lower sequencing depth. Broad sense heritabilities were 0.61 and 0.66, respectively. Underestimation of genomic heritability at lower sequencing depth was confirmed with simulated data. We conclude that it is feasible to use GBS to describe relationships between family-pools and to estimate genomic heritability directly at the level of F2 family-pool samples, but estimates are biased at low sequencing depth. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00122-015-2607-9) contains supplementary material, which is available to authorized users

Genetic variation and exercise-induced muscle damage: implications for athletic performance, injury and ageing.

Prolonged unaccustomed exercise involving muscle lengthening (eccentric) actions can result in ultrastructural muscle disruption, impaired excitation-contraction coupling, inflammation and muscle protein degradation. This process is associated with delayed onset muscle soreness and is referred to as exercise-induced muscle damage. Although a certain amount of muscle damage may be necessary for adaptation to occur, excessive damage or inadequate recovery from exercise-induced muscle damage can increase injury risk, particularly in older individuals, who experience more damage and require longer to recover from muscle damaging exercise than younger adults. Furthermore, it is apparent that inter-individual variation exists in the response to exercise-induced muscle damage, and there is evidence that genetic variability may play a key role. Although this area of research is in its infancy, certain gene variations, or polymorphisms have been associated with exercise-induced muscle damage (i.e. individuals with certain genotypes experience greater muscle damage, and require longer recovery, following strenuous exercise). These polymorphisms include ACTN3 (R577X, rs1815739), TNF (-308 G>A, rs1800629), IL6 (-174 G>C, rs1800795), and IGF2 (ApaI, 17200 G>A, rs680). Knowing how someone is likely to respond to a particular type of exercise could help coaches/practitioners individualise the exercise training of their athletes/patients, thus maximising recovery and adaptation, while reducing overload-associated injury risk. The purpose of this review is to provide a critical analysis of the literature concerning gene polymorphisms associated with exercise-induced muscle damage, both in young and older individuals, and to highlight the potential mechanisms underpinning these associations, thus providing a better understanding of exercise-induced muscle damage

The interplay between birth weight and obesity in determining childhood and adolescent cardiometabolic risk

BACKGROUND: Birth weight (BW) is associated with risk of cardiometabolic disease (CMD) in adulthood, which may depend on the state of obesity, in particular if developed at a young age. We hypothesised that BW and a polygenic score (PGS) for BW were associated with cardiometabolic risk and related plasma protein levels in children and adolescents. We aimed to determine the modifying effect of childhood obesity on these associations.METHODS: We used data from The cross-sectional HOLBAEK Study with 4263 participants (median [IQR] age, 11.7 [9.2, 14.3] years; 57.1% girls and 42.9% boys; 48.6% from an obesity clinic and 51.4% from a population-based group). We gathered information on BW and gestational age, anthropometrics, cardiometabolic risk factors, calculated a PGS for BW, and measured plasma proteins using Olink Inflammation and Cardiovascular II panels. We employed multiple linear regression to examine the associations with BW as a continuous variable and performed interaction analyses to assess the effect of childhood obesity on cardiometabolic risk and plasma protein levels.FINDINGS: BW and a PGS for BW associated with cardiometabolic risk and plasma protein levels in childhood and adolescence. Childhood obesity modified the associations between BW and measures of insulin resistance, including HOMA-IR (βadj [95% CI per SD] for obesity: -0.12 [-0.15, -0.08]; normal weight: -0.04 [-0.08, 0.00]; Pinteraction = 0.004), c-peptide (obesity: -0.11 [-0.14, -0.08]; normal weight: -0.02 [-0.06, 0.02]; Pinteraction = 5.05E-04), and SBP SDS (obesity: -0.12 [-0.16, -0.08]; normal weight: -0.06 [-0.11, -0.01]; Pinteraction = 0.0479). Childhood obesity also modified the associations between BW and plasma levels of 14 proteins (e.g., IL15RA, MCP1, and XCL1; Pinteraction &lt; 0.05).INTERPRETATION: We identified associations between lower BW and adverse metabolic phenotypes, particularly insulin resistance, blood pressure, and altered plasma protein levels, which were more pronounced in children with obesity. Developing effective prevention and treatment strategies for this group is needed to reduce the risk of future CMD.FUNDING: Novo Nordisk Foundation (NNF15OC0016544, NNF0064142 to T.H., NNF15OC0016692 to T.H. and A.K., NNF18CC0033668 to S.E.S, NNF18SA0034956 to C.E.F., NNF20SA0067242 to DCA, NNF18CC0034900 to NNF CBMR), The Innovation Fund Denmark (0603-00484B to T.H.), The Danish Cardiovascular Academy (DCA) and the Danish Heart Foundation (HF) (PhD2021007-DCA to P.K.R, 18-R125-A8447-22088 (HF) and 21-R149-A10071-22193 (HF) to M.A.V.L., PhD2023009-HF to L.A.H), EU Horizon (668031, 847989, 825694, 964590 to A.K.), Innovative Health Initiative (101132901 for A.K.), A.P. Møller Foundation (19-L-0366 to T.H.), The Danish National Research Foundation, Steno Diabetes Center Sjælland, and The Region Zealand and Southern Denmark Health Scientific Research Foundation.</p

Superior effects of eccentric to concentric knee extensor resistance training on physical fitness, insulin sensitivity and lipid profiles of elderly men

It has been reported that eccentric training of knee extensors is effective for improving blood insulin sensitivity and lipid profiles to a greater extent than concentric training in young women. However, it is not known whether this is also the case for elderly individuals. Thus, the present study tested the hypothesis that eccentric training of the knee extensors would improve physical function and health parameters (e.g., blood lipid profiles) of older adults better than concentric training. Healthy elderly men (60–76 years) were assigned to either eccentric training or concentric training group (n=13/group), and performed 30–60 eccentric or concentric contractions of knee extensors once a week. The intensity was progressively increased over 12 weeks from 10 to 100% of maximal concentric strength for eccentric training and from 50 to 100% for concentric training. Outcome measures were taken before and 4 days after the training period. The results showed that no sings of muscle damage were observed after any sessions. Functional physical fitness (e.g., 30-s chair stand) and maximal concentric contraction strength of the knee extensors increased greater (P ≤ 0.05) after eccentric training than concentric training. Homeostasis model assessment, oral glucose tolerance test and whole blood glycosylated hemoglobin

The effect of exercise on IL-6-induced cachexia in the ApcMin/+ mouse

Background Cachexia involves unintentional body weight loss including diminished muscle and adipose tissue mass and is associated with an underlying disease. Systemic overexpression of IL-6 accelerates cachexia in the ApcMin/+ mouse, but does not induce wasting in control C57BL/6 mice. With many chronic diseases, chronic inflammation and metabolic dysfunction can be improved with moderate exercise. A direct effect of regular moderate exercise on the prevention of IL-6-induced cachexia in the ApcMin/+ mouse has not been investigated. The purpose of this study was to assess the effects of exercise on the development of cachexia in the ApcMin/+ mouse. Methods Mice were randomly assigned to moderate treadmill exercise (18 m/min, 1 h, 6 days/week, 5% grade) or cage control (CC) groups from 6 to 14 weeks of age. At 12 weeks of age, mice were electroporated with either IL-6- containing or control plasmid into the quadriceps muscle. Mice were killed after 2 weeks of systemic IL-6 overexpression or control treatment. Results IL-6 overexpression induced an 8% loss in body weight in CC mice, which was significantly attenuated by exercise. IL-6 overexpression in CC mice increased fasting insulin and triglyceride levels, which were normalized by exercise, and associated with increased oxidative capacity, an induction of AKT signaling, and a repression of AMPK signaling in muscle. These exercise-induced changes occurred despite elevated inflammatory signaling in skeletal muscle. Conclusion We conclude that moderate-intensity exercise can attenuate IL-6-dependent cachexia in ApcMin/+ mice, independent of changes in IL-6 concentration and muscle inflammatory signaling. The exercise effect was associated with improved insulin sensitivity and improved energy status in the muscle. © The Author(s) 2012

Correlation of gene expression and protein production rate - a system wide study

<p>Abstract</p> <p>Background</p> <p>Growth rate is a major determinant of intracellular function. However its effects can only be properly dissected with technically demanding chemostat cultivations in which it can be controlled. Recent work on <it>Saccharomyces cerevisiae </it>chemostat cultivations provided the first analysis on genome wide effects of growth rate. In this work we study the filamentous fungus <it>Trichoderma reesei </it>(<it>Hypocrea jecorina</it>) that is an industrial protein production host known for its exceptional protein secretion capability. Interestingly, it exhibits a low growth rate protein production phenotype.</p> <p>Results</p> <p>We have used transcriptomics and proteomics to study the effect of growth rate and cell density on protein production in chemostat cultivations of <it>T. reesei</it>. Use of chemostat allowed control of growth rate and exact estimation of the extracellular specific protein production rate (SPPR). We find that major biosynthetic activities are all negatively correlated with SPPR. We also find that expression of many genes of secreted proteins and secondary metabolism, as well as various lineage specific, mostly unknown genes are positively correlated with SPPR. Finally, we enumerate possible regulators and regulatory mechanisms, arising from the data, for this response.</p> <p>Conclusions</p> <p>Based on these results it appears that in low growth rate protein production energy is very efficiently used primarly for protein production. Also, we propose that flux through early glycolysis or the TCA cycle is a more fundamental determining factor than growth rate for low growth rate protein production and we propose a novel eukaryotic response to this i.e. the lineage specific response (LSR).</p