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An individual's desire to hedge risks, as implied by risk aversion, is accepted as a normative paradigm and documented as valid descriptively. Insurance markets satisfy this desire, wherein the individual's aversion to bear risk allows firms to demand a markup on the expected value of the insured loss. Insurance firms incrementally introduce digital monitoring technology into their policies, making policyholder's behavior transparent. We analyze the implications of such transparency insurance contracts for willingness to pay in a framed behavioral experiment and find that the loss of privacy in such contracts marginalizes the potential profits that insurers could earn on their policies. In particular, our results suggest that the reduction in willingness to pay from introducing digital monitoring is in the range of 25–50% of the expected loss. While an absolute as opposed to a relative monetary valuation concept of privacy appears more likely to explain our data, we cannot clearly confirm this conjecture empirically. Heterogeneous treatment effects for risk preferences are suggestive for increasing utility losses from transparency policies with increasing risk aversion but we also observe indications of nonlinearities in this relationship. Probability misperception is a salient characteristic of our experimental population, suggesting that profitability is less threatened under low-frequency risks as opposed to high-frequency risks.

Knocking out the activity of a pyridoxal 5 '-phosphate phosphatase suppresses the dwarf phenotype of mutants lacking an ATP/ADP transporter and provides insight into vitamin B6 homeostasis.The endoplasmic reticulum (ER)-located ATP/ADP-antiporter (ER-ANT1) occurs specifically in vascular plants. Structurally different transporters mediate energy provision to the ER, but the cellular function of ER-ANT1 is still unknown. Arabidopsis (Arabidopsis thaliana) mutants lacking ER-ANT1 (er-ant1 plants) exhibit a photorespiratory phenotype accompanied by high glycine levels and stunted growth, pointing to an inhibition of glycine decarboxylase (GDC). To reveal whether it is possible to suppress this marked phenotype, we exploited the power of a forward genetic screen. Absence of a so far uncharacterized member of the HaloAcid Dehalogenase (HAD)-like hydrolase family strongly suppressed the dwarf phenotype of er-ant1 plants. Localization studies suggested that the corresponding protein locates to chloroplasts, and activity assays showed that the enzyme dephosphorylates, with high substrate affinity, the B-6 vitamer pyridoxal 5 '-phosphate (PLP). Additional physiological experiments identified imbalances in vitamin B-6 homeostasis in er-ant1 mutants. Our data suggest that impaired chloroplast metabolism, but not decreased GDC activity, causes the er-ant1 mutant dwarf phenotype. We present a hypothesis, setting transport of PLP by ER-ANT1 and chloroplastic PLP dephosphorylation in the cellular context. With the identification of this HAD-type PLP phosphatase, we also provide insight into B-6 vitamer homeostasis.

Greenhouse gases emissions resulting from the combustion of fossil fuels are worsening air quality and affecting the climate system. While climate change impacts on meteorological variables affects air quality by altering the concentration and distribution of pollutants, air pollution significantly influences the climate, leading to negative impacts on human health. Due to the combination of high temperatures, air pollution, and high population density, cities are particularly vulnerable to climate change impacts. The planning and design of public spaces aimed at climate change mitigation and adaptation can result in multiple co-benefits for human health, while reducing social inequalities. To address the major research gaps in the communication between health and planning experts, and the lack of capacity among public sectors and policy makers, it is necessary to promote capacity building and knowledge sharing between the planning and health sectors. The purpose of this article is to develop preliminary recommendations for a process that allows a comprehensive assessment of the interlinkages between climate and health, social, environmental, and economic vulnerabilities, and the quality of the urban spaces, to support local governments, policymakers, and education institutions in making informed decisions for public spaces. The methods applied were a literature review and interviews with experts.

Background: High blood pressure is the primary risk factor for cardiovascular death worldwide. Autosomal dominant hypertension with brachydactyly clinically resembles salt-resistant essential hypertension and causes death by stroke before 50 years of age. We recently implicated the gene encoding phosphodiesterase 3A ( PDE3A ); however, in vivo modeling of the genetic defect and thus showing an involvement of mutant PDE3A is lacking. Methods: We used genetic mapping, sequencing, transgenic technology, CRISPR-Cas9 gene editing, immunoblotting, and fluorescence resonance energy transfer. We identified new patients, performed extensive animal phenotyping, and explored new signaling pathways. Results: We describe a novel mutation within a 15 base pair (bp) region of the PDE3A gene and define this segment as a mutational hotspot in hypertension with brachydactyly. The mutations cause an increase in enzyme activity. A CRISPR/Cas9-generated rat model, with a 9-bp deletion within the hotspot analogous to a human deletion, recapitulates hypertension with brachydactyly. In mice, mutant transgenic PDE3A overexpression in smooth muscle cells confirmed that mutant PDE3A causes hypertension. The mutant PDE3A enzymes display consistent changes in their phosphorylation and an increased interaction with the 14-3-3θ adaptor protein. This aberrant signaling is associated with an increase in vascular smooth muscle cell proliferation and changes in vessel morphology and function. Conclusions: The mutated PDE3A gene drives mechanisms that increase peripheral vascular resistance causing hypertension. We present 2 new animal models that will serve to elucidate the underlying mechanisms further. Our findings could facilitate the search for new antihypertensive treatments.

This paper presents the results of extensive investigations on the lamination strength grading, the production and the mechanical properties of European beech (Fagus sylvatica L.) glued laminated timber (GLT). Based on the analysis of potential influencing parameters on strength and stiffness as well as subsequent tension tests parallel to the grain on single boards, a combined visual/machine approach for grading the raw material into tensile strength classes T50, T42, T33 and T22 was developed. Boards strength graded with the developed procedure were then finger-jointed by a Swiss GLT producer and the strength of the finger joints was investigated by means of tension and bending tests. The strength and durability of the bonding was investigated and verified by means of tensile-shear and delamination tests. It could be shown that the required finger-joint and bondline strengths for GLT of strength classes GL40 and GL48 can be achieved, but that the process parameters for finger jointing (in particular the geometrical properties of the finger joint profile) have to be optimized in order to be able to produce GLT of strength class GL55. Finally, an extensive experimental testing campaign was performed to investigate the mechanical properties of European beech GLT produced based on the strength grading rules and production techniques developed before. Bending, tensile and compressive parallel to the grain, as well as shear tests were carried out on GLT specimens of strength classes GL40, GL48 and GL55 in different sizes in terms of cross-section and length. Based on these investigations and complementing numerical simulations, characteristic strength and stiffness values and formulae for consideration of size effects in bending, tension and shear were determined.

Introduction This study evaluated the reproducibility of electronic color determination system evaluations of the marginal gingiva, which could be important for adhesive cervical fillings or prosthetic restorations that imitate the gingiva. Material and methods In 50 subjects, the L*, a*, and b* color coordinates were evaluated five times at a point in the marginal area of a central incisor using different electronic color determination systems: (SP) Shadepilot, (ES) Easyshade, (CE) Crystaleye, and (SV) X-Rite. The mean color difference (ΔE) and its standard deviation between the five measurements from each participant were calculated separately for each device. Further ICC for interdevice reliability was determined. Results The L*, a*, and b* color coordinates and ΔE values differed significantly among the systems (p < 0.001). Within each patient and measurement system, ΔE ranged from 1.4 to 3.2 (SD 1.1–2.5), L* from 2.6 to 5.7 (SD 2.6–5.7), a* from 11.9 to 21.3 (SD 3.6–3.9), and b* from 15.1 to 28.9 (SD 1.7–4.3). Interdevice reliability ranged between 0.675 and 0.807. Conclusions Color determination of the marginal gingiva using the electronic tooth color determination systems tested herein showed limited reproducibility. The results obtained with the different measurement systems differed enormously. Clinical relevance These results show that the electronic color measurement devices tested allow no high reproducible determination of color coordinates of the marginal gingiva.

Singlet oxygen ( 1 O 2 ), the major reactive oxygen species (ROS) produced in chloroplasts, has been demonstrated recently to be a highly versatile signal that induces various stress responses. In the fluorescent ( flu ) mutant, its release causes seedling lethality and inhibits mature plant growth. However, these drastic phenotypes are suppressed when EXECUTER1 (EX1) is absent in the flu ex1 double mutant. We identified SAFEGUARD1 (SAFE1) in a screen of ethyl methanesulfonate (EMS) mutagenized flu ex1 plants for suppressor mutants with a flu -like phenotype. In flu ex1 safe1 , all 1 O 2 -induced responses, including transcriptional rewiring of nuclear gene expression, return to levels, such as, or even higher than, those in flu . Without SAFE1, grana margins (GMs) of chloroplast thylakoids (Thys) are specifically damaged upon 1 O 2 generation and associate with plastoglobules (PGs). SAFE1 is localized in the chloroplast stroma, and release of 1 O 2 induces SAFE1 degradation via chloroplast-originated vesicles. Our paper demonstrates that flu -produced 1 O 2 triggers an EX1-independent signaling pathway and proves that SAFE1 suppresses this signaling pathway by protecting GMs.

Arabidopsis thaliana contains 13 fibrillins (FBNs), which are all localized to chloroplasts. FBN1 and FBN2 are involved in photoprotection of photosystem II, and FBN4 and FBN5 are thought to be involved in plastoquinone transport and biosynthesis, respectively. The functions of the other FBNs remain largely unknown. To gain insight into the function of FBN6, we performed coexpression and Western analyses, conducted fluorescence and transmission electron microscopy, stained reactive oxygen species (ROS), measured photosynthetic parameters and glutathione levels, and applied transcriptomics and metabolomics. Using coexpression analyses, FBN6 was identified as a photosynthesis‐associated gene. FBN6 is localized to thylakoid and envelope membranes, and its knockout results in stunted plants. The delayed‐growth phenotype cannot be attributed to altered basic photosynthesis parameters or a reduced CO2 assimilation rate. Under moderate light stress, primary leaves of fbn6 plants begin to bleach and contain enlarged plastoglobules. RNA sequencing and metabolomics analyses point to an alteration in sulfate reduction in fbn6. Indeed, glutathione content is higher in fbn6, which in turn confers cadmium tolerance of fbn6 seedlings. We conclude that loss of FBN6 leads to perturbation of ROS homeostasis. FBN6 enables plants to cope with moderate light stress and affects cadmium tolerance.

This special issue is devoted to establishing a benchmark database and framework for the analysis and development of climate change adaptation in coastal communities with less than 100,000 people. These coastal towns and small cities often have limited information about local climate change impacts and typically lack both the financial resources and the engineering and planning bases to develop appropriate adaptation measures. As a result, much more needs to be done to assist small coastal cities and towns to plan and implement adaptation measures. The special issue includes six articles in addition to this Introduction: a typology for collecting and analysing information; an assessment of small island cases; three articles on coastal towns and cities of progressively larger populations, and finally a summary of the work and suggestions for the way forward in research and application.

This article summarizes and reflects upon the work presented in ‘The Unusual Suspects in Climate Change Adaptation – Small Coastal Cities and Towns’ special issue. Across the special issue the challenge of adapting coastal towns and small cities to the impacts of climate change was clearly evident. In order to address some of the challenges, an initial way forward is outlined here to act as a pathway for future research. The areas requiring particular focus include: building a network of coastal towns and small cities; estimates of numbers of coastal towns and small cities worldwide; cost estimates and funding sources; linking adaptation to higher-level agencies through Sustainable Development Goals and other reporting requirements; further research on the influence of tourism on coastal adaptation; and, a focus on more case studies from the Global South. It is hoped that with the momentum provided by the Sustainable Development Goals, the way forward provided by this special issue, and other research, coastal adaptation in smaller coastal settlements will greatly advance in the next decade.

The impacts of climate change will manifest differently in urban areas depending upon the individual characteristics and contexts of each settlement. The study of climate adaptation planning for towns and small cities is a relatively under-researched field, there has thus far not been a standard typology for characterising towns and cities located at the coast. A typology can inform stakeholders about the physical hazards a coastal town or small city may be exposed currently and in the future; identify the impact that may have to the local population and the economic, cultural, and environmental assets in the settlement; and identify any barriers or opportunities to plan, develop, and implement adaptation strategies. A typology is presented here that includes 34 parameters that cover physical, economic, environmental and social characteristics. This typology has been used within this Special Issue to obtain information about all 22 case studies of the Special Issue. Future work will concentrate on developing the typology further and analysing the data collected to provide a systematic understanding of some of the data gaps that still exist within the field of adaptation in coastal towns and small cities and allow future research to focus on the aspects that are most needed.