Encouraging Environmentally Sustainable Holiday Travel

Holiday travel behavior, individual characteristics of holiday travelers and strategies to change holiday travel behavior are the subjects of this article. From the environmental perspective, the journey to the destinations is the most critical aspect of traveling. Based on a 2003 survey of 1991 German inhabitants, the kilometers traveled and the choice of transportation mode for holiday purposes have been quantified. According to the number of trips and kilometers traveled, four travel groups have been identified. The groups vary according to socio-demographics, psychological factors, number of holiday trips, and travel mode choice. Persons who traveled to more distant destinations also traveled more often and used air travel for more than 60% of their trips. For the other groups, car travel was more important. Correlating the four travel groups with greenhouse gas emissions reveals that the smallest group—the long-haul travelers—was responsible for 80% of the emissions of the whole sample. Income, education, and openness to change were main indicators of individual greenhouse gas emissions. Target group oriented strategies to reduce the environmental impact of holiday mobility are discussed against the background of 84 in-depth interviews conducted with selected representatives of the first survey

Child and parental executive functioning in type 1 diabetes : their unique and interactive role toward treatment adherence and glycemic control

Objective: Managing type 1 diabetes (T1D) requires the ability to make complex and critical decisions regarding treatment, to execute complex tasks accurately, and to make adjustments when problems arise. This requires effective neuropsychological competences of patients and their families, especially in the domain of executive functioning (EF): the ability to self-monitor, plan, solve problems, and set priorities. Previous research focused mainly on child EF, neglecting the impact of parental EF. This study included both mothers and fathers and examined associations between child and parental EF and treatment adherence to T1D in a broad age range of patients. Methods: Parents of 270 patients (6-18years) with T1D (mean age 12.7years; 52.6% female) were included. Mothers (N=232) and fathers (N=168) completed questionnaires on child and parental EF and on treatment adherence. Analyses examined the associations linking child and parental EF to treatment adherence and glycemic control (and potential moderation effects in these associations) using hierarchical linear regression. Results: Child EF problems were negatively associated with treatment adherence. As an indication of moderation, this effect was stronger in older children. Better treatment adherence and glycemic control were reported when both child and parent showed less EF problems. Effects were more pronounced in mothers than in fathers. Conclusions: This study demonstrated a significant interplay between child and parental EF in the association with treatment adherence and glycemic control. Researchers and clinicians should remain attentive toward the role of neuropsychological concepts such as EF. Implementation in clinical practice seems meaningful

A patient-based model of RNA mis-splicing uncovers treatment targets in Parkinson's disease.

Parkinson's disease (PD) is a heterogeneous neurodegenerative disorder with monogenic forms representing prototypes of the underlying molecular pathology and reproducing to variable degrees the sporadic forms of the disease. Using a patient-based in vitro model of PARK7-linked PD, we identified a U1-dependent splicing defect causing a drastic reduction in DJ-1 protein and, consequently, mitochondrial dysfunction. Targeting defective exon skipping with genetically engineered U1-snRNA recovered DJ-1 protein expression in neuronal precursor cells and differentiated neurons. After prioritization of candidate drugs, we identified and validated a combinatorial treatment with the small-molecule compounds rectifier of aberrant splicing (RECTAS) and phenylbutyric acid, which restored DJ-1 protein and mitochondrial dysfunction in patient-derived fibroblasts as well as dopaminergic neuronal cell loss in mutant midbrain organoids. Our analysis of a large number of exomes revealed that U1 splice-site mutations were enriched in sporadic PD patients. Therefore, our study suggests an alternative strategy to restore cellular abnormalities in in vitro models of PD and provides a proof of concept for neuroprotection based on precision medicine strategies in PD