Digitalisation anxiety: development and validation of a new scale

<jats:title>Abstract</jats:title><jats:p>The increasing spread of digital technologies and respective consequences for the way we live, work, and communicate can evoke feelings of tension and discomfort. This so-called digitalisation anxiety is related to existing and future technologies, includes the process of digitalisation in everyday life, and refers to multiple levels (the individual, organisations, and society). Existing scales measuring technology-related fears due not adequately reflect these features. Therefore, we developed the German version of the Digitalisation Anxiety Scale (DAS). Having generated items based on a qualitative interview study (Study 1, n = 26), we demonstrated the DAS’s factor structure, internal consistency and construct validity in Study 2a (n = 109) and test-retest reliability in Study 2b (n = 30). In Study 3 (n = 223), the scale’s structure was confirmed and correlates of digitalisation anxiety were examined. The final version of the DAS consists of 35 items with a four-factor structure (societal triggers for digitalisation anxiety, triggers related to interaction and leadership, triggers within oneself and triggers resulting from the digitalisation implementation process). Digitalisation Anxiety had negative relationships with well-being and performance. The scale allows practitioners and researchers to measure and benchmark individuals’ levels of digitalisation anxiety, and to track changes over time. The scale can inform interventions aiming at reducing digitalisation anxiety and stress resulting from digitalisation. </jats:p&gt

Clinical and morphological phenotype of the filamin myopathy: a study of 31 German patients

Mutations in the filamin C gene (FLNC) cause a myofibrillar myopathy (MFM), morphologically characterized by focal myofibrillar destruction and abnormal accumulation of several proteins within skeletal muscle fibres. We studied 31 patients from four German families to evaluate the phenotype of filaminopathy. All patients harboured the same p.W2710X mutation in FLNC. Haplotype analysis suggested a founder mutation in these German filaminopathy families. The mean age at onset of clinical symptoms was 44 +/− 6 years (range, 24-57 years). Slowly progressive muscle weakness was mostly pronounced proximally, initially affecting the lower extremities and involving the upper extremities in the course of disease progression, similar to the distribution of weakness seen in limb-girdle muscular dystrophies (LGMD). Patients frequently developed respiratory muscle weakness. About one-third of the patients showed cardiac abnormalities comprising conduction blocks, tachycardia, diastolic dysfunction and left ventricular hypertrophy indicating a cardiac involvement in filaminopathy. Serum creatine kinase levels varied from normal up to 10-fold of the upper limit. Magnetic resonance imaging studies showed a rather homogenous pattern of muscle involvement in the lower extremities differing from that in other types of MFM. Myopathological features included perturbation of myofibrillar alignment, accumulation of granulofilamentous material similar to that seen in primary desminopathies and abnormal intracellular protein deposits typical of MFM. Decreased activities of oxidative enzymes and fibre hypertrophy seem to be early features, whereas dystrophic changes were present in advanced stages of filaminopathy. Rimmed vacuoles were detected in only a few cases. The intracellular aggregates were composed of a variety of proteins including filamin C, desmin, myotilin, Xin, dystrophin and sarcoglycans. Therapy is so far limited to symptomatic treatment. The German filaminopathy cohort, the largest group of patients studied so far, shares phenotypic features with LGMD and presents with characteristic histopathological findings of MF