Flexible working and its relations with work-life conflict and well-being among crowdworkers in Germany.

BACKGROUND: New forms of digital work such as crowdwork promise to increase potentials for flexible working. As crowdworkers can work highly autonomous and from anywhere at any time via the internet, they may be able to make work and private demands more compatible and avoid role conflicts between the life spheres, and in turn, experience enhanced well-being. OBJECTIVE: This research asked whether crowdworkers benefit from flexible working potentials. It investigated the association of the use of different dimensions of flexible working (flex-time, flex-place, and task autonomy) in crowdwork with work-life conflict and well-being. Moreover, it explored whether the relationship between flexible working and well-being was mediated by work-life conflict. METHODS: The study drew upon a sample of 470 crowdworkers from a cross-sectional self-assessment survey on four different German crowdwork platforms. Structural equation modeling was conducted to estimate the effects of flexible working on work-life conflict, somatic health symptoms, and life satisfaction. Indirect effects were estimated to test the mediation hypothesis. RESULTS: The findings suggest that if crowdworkers use temporal and task flexibility, they experience fewer work-life conflict, fewer somatic health symptoms, and greater life satisfaction. This does not apply to flex-place. The relationship between flexible working and well-being is partly mediated by work-life conflict experiences. CONCLUSION: This study supports that crowdwork offers a high potential for working highly autonomous and flexibly in time and place. It is associated with lower levels of work-life conflict and enhanced well-being, but the benefits of this flexibility are not universally included in crowdwork.

Flexible, Self-Determined and Unhealthy? An Empirical Study on Somatic Health Among Crowdworkers.

Crowdwork is a new form of digitally enabled work in which organizations assign tasks to an anonymous group of workers via platform intermediaries. For crowdworkers, crowdwork offers both opportunities and risks. On the one side, crowdworkers enjoy high flexibility on when, where, and how much to work. On the other side, risks comparable to other forms of atypical employment arise: no labor regulation, unstable income, and uncertainty about whether enough tasks are available. Regulation of working hours lies within the crowdworkers' own authority. Also, crowdwork in industrialized nations is often conducted during leisure times as a side-job to some other kind of employment. In accordance with Conservation of Resources Theory, we state that when leisure time gets used up with crowdwork, regeneration cannot occur and health declines. On a sample of N=748 German crowdworkers recruited from four different platform types, we analyzed whether participation in crowdwork is linked to increased somatic symptoms compared to regularly employed personnel. We found that crowdworkers show significantly increased somatic symptoms as compared to a German norm sample, that are stable across different kinds of tasks and platforms, gender, and age groups, and that is statistically due to the extent of participation in crowdwork. Specifically, we found that total work hours per week were not associated with an increase in somatic symptoms, but we did find associations with strain-based work-family conflict and the primary motivation to do crowdwork being to earn money. Consequences for research and labor regulations are discussed.

COVID-19 and Work-Family Conflicts in Germany: Risks and Chances Across Gender and Parenthood.

The COVID-19 pandemic has dramatically affected everyone's daily life in one way or another, requiring a re-negotiation of existing strategies for work-life integration, not only for individuals but also within families and partnerships. To contribute to existing knowledge on work-life integration during COVID-19 in Germany, we look at gender and parenthood differences in the experiences of work-to-family (WFC) and family-to-work (FWC) conflicts. By accounting for employees' previous conflict experiences, we were able to reveal the extent to which the current conditions contributed to differences in these conflicts. Moreover, we explored the relevance of demands and resources in the family and work spheres as a way to explain different levels of WFC and FWC across gender and parenthood. Our analyses are based on a sample of 660 employees from a German linked employer-employee panel study and a COVID-19 follow-up survey conducted in late 2020. Results revealed that work-family conflict experiences before the pandemic play an important role in current conflict perceptions. Whereas WFC were more likely to be accentuated during the pandemic, prior FWC experiences may have helped to mitigate conflicts under these new conditions. Work-family conflicts in general have increased during the COVID-19 pandemic, but this finding applied only to conflicts in the family-to-work direction. Although such increases were not limited to parents, they were particularly high in this group. Overall, gender differences in work-family conflicts were absent, but differences were found between mothers and fathers. The need to compensate for a lack of external childcare, as well as having to work from home, increased FWC, especially among fathers. This study suggests that FWC in particular became more important during the pandemic; however, parents were not the only ones who were disadvantaged when it came to work-life integration; childless individuals likewise struggled to balance the demands of work and private life.

The moderating role of overcommitment in the relationship between psychological contract breach and employee mental health.

OBJECTIVES: This study investigated whether the association between perceived psychological contract breach (PCB) and employee mental health is moderated by the cognitive-motivational pattern of overcommitment (OC). Linking the psychological contract approach to the effort-reward imbalance model, this study examines PCB as an imbalance in employment relationships that acts as a psychosocial stressor in the work environment and is associated with stress reactions that in turn negatively affect mental health. METHODS: The analyses were based on a sample of 3,667 employees who participated in a longitudinal linked employer-employee survey representative of large organizations (with at least 500 employees who are subject so social security contributions) in Germany. Fixed-effects regression models, including PCB and OC, were estimated for employee mental health, and interaction effects between PCB and OC were assessed. RESULTS: The multivariate fixed-effects regression analyses showed a significant negative association between PCB and employee mental health. The results also confirmed that OC does indeed significantly increase the negative effect of PCB on mental health and that OC itself has a significant and negative effect on mental health. CONCLUSIONS: The results suggest that employees characterized by the cognitive-motivational pattern of OC are at an increased risk of developing poor mental health if they experience PCB compared with employees who are not overly committed to their work. The results of this study support the assumption that psychosocial work stressors play an important role in employee mental health.

A P19 and P19CL6 cell-based complementary approach to determine paracrine effects in cardiac tissue engineering.

The negligible self-repair potential of the myocardium has led to cell-based tissue engineering approaches to restore heart function. There is more and more consensus that, in addition to cell development, paracrine effects in particular play a pivotal role in the repair of heart tissue. Here, we present two complementary murine P19 and P19CL6 embryonic carcinoma cell-based in vitro test approaches to study the potential of repair cells and the factors secreted by these cells to induce cardiomyogenesis. P19 cells were 3-dimensionally cultured in hanging drops and P19CL6 cells in a monolayer. Both systems, capable of inducible differentiation towards the cardiomyogenic lineage shown by the appearance of beating cells, the expression of connexin 43 and cardiac troponins T and I, were used to test the cardiomyogenesis-inducing potential of human cardiac-derived adherent proliferating (CardAP) cells, which are candidates for heart repair. CardAP cells in coculture as well as CardAP cell-conditioned medium initiated beating in P19 cells, depending on the cell composition and concentration of the medium. CardAP cell-dependent beating was not observed in P19CL6 cultures, but connexin 43 and cardiac troponin formation as well as expression of GATA-binding protein 4 indicated the dose-dependent stimulatory cardiomyogenic effect of human CardAP cells. In summary, in different ways, P19 and P19CL6 cells have shown their capability to detect paracrine effects of human CardAP cells. In a complementary approach, they could be beneficial for determining the stimulatory cardiomyogenic potential of candidate cardiac-repair cells in vitro.

N-truncation and pyroglutaminylation enhances the opsonizing capacity of Aß-peptides and facilitates phagocytosis by macrophages and microglia.

Abnormal accumulations of amyloid-ß (Aß)-peptides are one of the pathological hallmarks of Alzheimer's disease (AD). The precursor of the Aß-peptides, the amyloid precursor protein (APP), is also found in peripheral blood cells, but its function in these cells remains elusive. We previously observed that mononuclear phagocytes release Aß-peptides during activation and phagocytosis, suggesting a physiologic role in inflammatory processes. Here, we show that supplementing the media with soluble N-terminally truncated Aß(2-40) and Aß(2-42) as well as Aß(1-42) induced the phagocytosis of polystyrene particles (PSPs) by primary human monocytes. If the PSPs were pre-incubated with Aß-peptides, phagocytosis was induced by all tested Aß-peptide species. N-terminally truncated Aß(x-42) induced the phagocytosis of PSPs significantly more effectively than did Aß(x-40). Similarly, the phagocytosis of Escherichia coli by GM-CSF- and M-CSF-elicited macrophages as well as microglia was particularly facilitated by pre-incubation with N-terminally truncated Aß(x-42). The proinflammatory polarization of monocytes was indicated by the reduced MSRI expression and IL-10 secretion after phagocytosis of PSPs coated with Aß(1-42), Aß(2-42) and Aß(3p-42). Polarization of the macrophages by GM-CSF reduced the phagocytic activity, but it did not affect the capabilities of Aß-peptides to opsonize prey. Taken together, Aß-peptides support phagocytosis as soluble factors and act as opsonins. Differential effects among the Aß-peptide variants point to distinct mechanisms of interaction among monocytes/macrophages, prey and Aß-peptides. A proinflammatory polarization induced by the phagocytosis of Aß-peptide coated particles may provide a model for the chronic inflammatory reaction and sustained plaque deposition in AD.

Molecular changes in the heart of a severe case of arrhythmogenic right ventricular cardiomyopathy caused by a desmoglein-2 null allele.

INTRODUCTION: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetic disorder caused by mutations in desmosomal genes. It is often associated with life-threatening arrhythmias. Some affected individuals develop progressive heart failure and may require cardiac transplantation. METHODS: The explanted heart of a young adult with end-stage heart failure due to a null allele in desmoglein-2 was studied at macroscopic, microscopic, and molecular level. Myocardial samples were probed for junctional localization of desmosomal components and the gap junction protein connexin43 by immunohistochemical staining. In addition, the protein content of desmosomal and adherens junction markers as well as connexin43 was assessed by Western blotting. RESULTS: Histological analysis confirmed ARVC. Despite the loss of specific immunoreactive signal for desmosomal components at the cardiac intercalated disks (shown for plakoglobin, desmoplakin, and plakophilin-2), these proteins could be detected by Western blotting. Only for desmoglein-2, desmocollin-2, and plakoglobin were reduced protein levels observed. Adherens junction proteins were not affected. Lower phosphorylation levels were observed for connexin43; however, localization of the gap junction protein displayed regional differences. At the molecular level, disease progression was more severe in the right ventricle compared to the left ventricle. CONCLUSION: Our data suggest that, in the ARVC heart, plakoglobin is mainly redistributed from the junctions to other cellular pools and that protein degradation only plays a secondary role. Homogenous changes in the phosphorylation status of connexin43 were observed in multiple ARVC samples, suggesting that this might be a general feature of the disease.