Nonfinancial Considerations in Eco‐Innovation Decisions: The Role of Family Ownership and Reputation Concerns

Societal pressures for greater sustainability can encourage firms to target part of their innovation activities at ecological initiatives (i.e., eco-innovation). Yet, depending on their value function, firms can respond differently to such pressures and exhibit variance in their eco-innovation activities. In this paper, we investigate the idea that a firm's ownership structure may play a significant role in determining its engagement in eco-innovation. Specifically, we propose that ownership by family blockholders increases the value attached to the company's reputation and that this, in turn, stimulates higher levels of eco-innovation. In other words, we model the company reputation motive as a key mediator in the relationship between family ownership and firm-level eco-innovation. To account for family firm heterogeneity, we also model the moderating role of owners' intention to pass the business on to the next family generation (transgenerational intentions) and of the extent to which these owners reside in the firm's local community (local embeddedness). As theoretical backdrop, our study builds on institutional theory and the mixed gamble logic. To test our hypotheses, we use a large sample of German firms and nonlinear moderated mediation regression analysis. Results reveal that family ownership is positively related to the introduction of eco-innovations by firms, in part because of the stronger emphasis being placed on the company's reputation. We find that this effect is strongest when the owning-family has transgenerational intentions. As such, this study advances our understanding of firm-level drivers of eco-innovation. In view of the prevalence of family-owned firms and the mounting importance of ecological sustainability, it is valuable to extend knowledge on the contingent and indirect effect of family ownership on eco-innovation

The influence of colour scale in lesion detection and patient-based sensitivity in [68Ga]Ga-PSMA-PET/CT.

OBJECTIVE To investigate the influence of colour scales on the interpretation of [68Ga]Ga-PSMA-11 PET/CT for the diagnosis of recurrent prostate cancer. METHODS 50 consecutive patients who underwent [68Ga]Ga-PSMA-11 PET/CT for recurrent prostate cancer were selected for this retrospective study. The scans were randomised, anonymised and read by five different readers first in the visually nonlinear colour scale 'PET-rainbow'. Scans were then rerandomised and read in the visually linear colour scale 'hot-metal new'. For each scan in each colour scale the numbers of pathological, equivocal and benign lesions were noted. Scans where the majority of readers (≥3) reported at least one PET-positive lesion were recorded as 'pathological'. Patient-level sensitivity was obtained by composite standard with 14.8 ± 1.2 months of follow-up. RESULTS Increased numbers of lesions per patient were reported for all readers in PET-rainbow compared to hot-metal new (37.4 ± 15.2 vs. 33.9 ± 16.4, respectively, P = 0.0005). On a per-patient basis, 43 scans were rated pathological in PET-rainbow, compared to 39 in hot-metal new. Follow-up was available for 30 patients confirming 26 pathological scans with positive follow-up in PET-rainbow, and 23 in hot-metal new. Three pathological scans were missed in hot-metal new. Patient-level sensitivity was higher for PET-rainbow (0.96) compared to hot-metal new (0.85). Inter-reader reliability was higher for hot-metal new (Fleiss κ = 0.76) compared to PET-rainbow (Fleiss κ = 0.60). CONCLUSION Use of PET-rainbow was associated with improved lesion detection and sensitivity compared to hot-metal new, although at cost of reduced inter-rater agreement. Consequently, the use of PET-rainbow for clinical routine and future studies involving [68Ga]Ga-PSMA-11 is recommended

Natural Experiments: Missed Opportunities for Causal Inference in Psychology

Knowledge about causal effects is essential for building useful theories and designing effective interventions. The preferred design for learning about causal effects are randomized experiments (i.e., studies in which the researchers randomly assign units to treatment and control conditions). However, randomized experiments are often unethical or unfeasible. On the other hand, observational studies are usually feasible but lack the random assignment that renders randomized experiments causally informative. Natural experiments can sometimes offer unique opportunities for dealing with this dilemma, allowing causal inference on the basis of events that are not controlled by the researcher but that nevertheless establish random or as-if random assignment to treatment and control conditions. Yet, psychological researchers have rarely exploited natural experiments so far. To remedy this shortage, we describe three main types of studies exploiting natural experiments (standard natural experiments, instrumental variable designs, and regression discontinuity designs) and provide examples from psychology and economics to illustrate how natural experiments can be harnessed. Natural experiments are challenging to find, provide information about only specific causal effects, and involve assumptions that are difficult to validate empirically. Nevertheless, we argue that natural experiments provide valuable causal inference opportunities that have not yet been sufficiently exploited by psychologists

Autosomal dominant striatal degeneration (ADSD): clinical description and mapping to 5q13-5q14.

OBJECTIVE: To describe the clinical and neuroradiologic features and chromosomal mapping of a novel autosomal dominant disease affecting the basal ganglia. METHODS: The authors characterized a large family with autosomal dominant basal ganglia disease (ADSD) clinically and by MRI, MR spectroscopy (MRS), and SPECT. The authors performed a whole genome genetic linkage scan to map the underlying genetic defect. RESULTS: The main clinical features of the disease are dysarthria and gait disturbance without any apparent reduction in life expectancy. MRI demonstrated a distinctive lesion pattern restricted mainly to the putamen and caudate nucleus. Genetic linkage analysis localized the causative genetic defect to a 3.25 megabase candidate region on chromosome 5q13.3-q14.1. CONCLUSIONS: ADSD is an autosomal dominant basal ganglia disease mapping to chromosome 5q13.3-q14.1

Clinical and pathophysiological concepts of neuralgic amyotrophy

Item does not contain fulltextNeuralgic amyotrophy--also known as Parsonage-Turner syndrome or brachial plexus neuritis--is a distinct and painful peripheral neuropathy that causes episodes of multifocal paresis and sensory loss in a brachial plexus distribution with concomitant involvement of other PNS structures (such as the lumbosacral plexus or phrenic nerve) in a large number of patients. The phenotype can be limited or extensive and the amount of disability experienced also varies between patients, but many are left with residual disabilities that affect their ability to work and their everyday life. Both idiopathic and hereditary forms exist. The latter form is genetically heterogeneous, but in 55% of affected families, neuralgic amyotrophy is associated with a point mutation or duplication in the SEPT9 gene on chromosome 17q25. The disease is thought to result from an underlying genetic predisposition, a susceptibility to mechanical injury of the brachial plexus (possibly representing disturbance of the epineurial blood-nerve barrier), and an immune or autoimmune trigger for the attacks. The precise pathophysiological mechanisms are still unclear; treatment is empirical, and preventive measures are not yet available. This Review provides an overview of the current clinical and pathophysiological concepts and research topics in neuralgic amyotrophy