Emails From the Boss—Curse or Blessing? Relations Between Communication Channels, Leader Evaluation, and Employees’ Attitudes

The present research investigates if and how a more digitally centered communication between supervisors and employees satisfies employees’ needs regarding the communication with their supervisors and influences employees’ attitudes toward the supervisor and the job. In a cross-sectional online study, 261 employees rated their supervisors’ actual and ideal use of different communication channels (i.e., telephone, face-to-face, email) regarding quality and quantity. Employees’ job satisfaction and their perceptions of their supervisors’ effectiveness and team identification were measured as dependent variables. Employees perceived face-to-face communication to be of higher quality than telephone and email communication, and they indicated a preference for more face-to-face communication with their supervisors than they actually had. Moreover, the perceived quality of communication, especially via face-to-face, was strongly and positively related to the dependent variables. These results provide insights into potential problems of increasing e-leadership in organizations. We conclude with recommendations to reduce these problems

Exogenous Administration of a Recombinant Variant of TWEAK Impairs Healing after Myocardial Infarction by Aggravation of Inflammation

Background: Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factorinducible 14 (Fn14) are upregulated after myocardial infarction (MI) in both humans and mice. They modulate inflammation and the extracellular matrix, and could therefore be important for healing and remodeling after MI. However, the function of TWEAK after MI remains poorly defined. Methods and results: Following ligation of the left coronary artery, mice were injected twice per week with a recombinant human serum albumin conjugated variant of TWEAK (HSA-Flag-TWEAK), mimicking the activity of soluble TWEAK. Treatment with HSA-Flag-TWEAK resulted in significantly increased mortality in comparison to the placebo group due to myocardial rupture. Infarct size, extracellular matrix remodeling, and apoptosis rates were not different after MI. However, HSA-Flag-TWEAK treatment increased infiltration of proinflammatory cells into the myocardium. Accordingly, depletion of neutrophils prevented cardiac ruptures without modulating all-cause mortality. Conclusion: Treatment of mice with HSA-Flag-TWEAK induces myocardial healing defects after experimental MI. This is mediated by an exaggerated neutrophil infiltration into the myocardium