Strong public support is a prerequisite for ambitious and thus costly climate change mitigation policy, and strong public concern over climate change is a prerequisite for policy support. Why, then, do most public opinion surveys indicate rather high levels of concern and rather strong policy support, while de facto mitigation efforts in most countries remain far from ambitious? One possibility is that survey measures for public concern fail to fully reveal the true attitudes of citizens due to social desirability bias. In this paper, we implemented list-experiments in representative surveys in Germany and the United States (N = 3620 and 3640 respectively) to assess such potential bias. We find evidence that people systematically misreport, that is, understate their disbelief in human caused climate change. This misreporting is particularly strong amongst politically relevant subgroups. Individuals in the top 20% of the income distribution in the United States and supporters of conservative parties in Germany exhibit significantly higher climate change skepticism according to the list experiment, relative to conventional measures. While this does not definitively mean that climate skepticism is a widespread phenomenon in these countries, it does suggest that future research should reconsider how climate change concern is measured, and what subgroups of the population are more susceptible to misreporting and why. Our findings imply that public support for ambitious climate policy may be weaker than existing survey research suggests.Urban greenspace is a valuable component of the urban form that has the potential to improve the health and well-being of residents. click here Most quantitative studies of relationships between health and greenspace to date have investigated associations only with what greenspace exists in the local environment (i.e. provision of greenspace), rather than to what extent it is used. This is due to the difficulty of obtaining usage data in large amounts. In recent years, GPS functionality integrated into mobile phones has provided a potential solution to this problem by making it possible to track which parts of the environment people experience in their day-to-day lives. In this paper, we demonstrate a method to derive cleaned, trip-level information from raw GPS data collected by a mobile phone app, then use this data to investigate the characteristics of trips to urban greenspace by residents of the city of Sheffield, UK. We find that local users of the app spend an average of an hour per week visiting greenspaces, including around seven trips per week and covering a total distance of just over 2.5 km. This may be enough to provide health benefits, but is insufficient to provide maximal benefits. Trip characteristics vary with user demographics ethnic minority users and users from more socioeconomically deprived areas tend to make shorter trips than White users and those from less deprived areas, while users aged 34 years and over make longer trips than younger users. Women, on average, make more frequent trips than men, as do those who spent more time outside as a child. Our results suggest that most day-to-day greenspace visits are incidental, i.e. travelling through rather than to greenspace, and highlight the importance of including social and cultural factors when investigating who uses and who benefits from urban greenspace.ARHGAP42 encodes Rho GTPase activating protein 42 that belongs to a member of the GTPase Regulator Associated with Focal Adhesion Kinase (GRAF) family. ARHGAP42 is involved in blood pressure control by regulating vascular tone. Despite these findings, disorders of human variants in the coding part of ARHGAP42 have not been reported. Here, we describe an 8-year-old girl with childhood interstitial lung disease (chILD), systemic hypertension, and immunological findings who carries a homozygous stop-gain variant (c.469G>T, p.(Glu157Ter)) in the ARHGAP42 gene. The family history is notable for both parents with hypertension. Histopathological examination of the proband lung biopsy showed increased mural smooth muscle in small airways and alveolar septa, and concentric medial hypertrophy in pulmonary arteries. ARHGAP42 stop-gain variant in the proband leads to exon 5 skipping, and reduced ARHGAP42 levels, which was associated with enhanced RhoA and Cdc42 expression. This is the first report linking a homozygous stop-gain variant in ARHGAP42 with a chILD disorder, systemic hypertension, and immunological findings in human patient. Evidence of smooth muscle hypertrophy on lung biopsy and an increase in RhoA/ROCK signaling in patient cells suggests the potential mechanistic link between ARHGAP42 deficiency and the development of chILD disorder.During development, signal-regulated transcription factors (TFs) act as basal repressors and upon signalling through morphogens or cell-to-cell signalling shift to activators, mediating precise and transient responses. Conversely, at the final steps of neuron specification, terminal selector TFs directly initiate and maintain neuron-type specific gene expression through enduring functions as activators. C. elegans contains 3 types of serotonin synthesising neurons that share the expression of the serotonin biosynthesis pathway genes but not of other effector genes. Here, we find an unconventional role for LAG-1, the signal-regulated TF mediator of the Notch pathway, as terminal selector for the ADF serotonergic chemosensory neuron, but not for other serotonergic neuron types. Regulatory regions of ADF effector genes contain functional LAG-1 binding sites that mediate activation but not basal repression. lag-1 mutants show broad defects in ADF effector genes activation, and LAG-1 is required to maintain ADF cell fate and functions throughout life. Unexpectedly, contrary to reported basal repression state for LAG-1 prior to Notch receptor activation, gene expression activation in the ADF neuron by LAG-1 does not require Notch signalling, demonstrating a default activator state for LAG-1 independent of Notch. We hypothesise that the enduring activity of terminal selectors on target genes required uncoupling LAG-1 activating role from receiving the transient Notch signalling.