A global classification of coastal flood hazard climates associated with large-scale oceanographic forcing

Coastal communities throughout the world are exposed to numerous and increasing threats, such as coastal flooding and erosion, saltwater intrusion and wetland degradation. Here, we present the first global-scale analysis of the main drivers of coastal flooding due to large-scale oceanographic factors. Given the large dimensionality of the problem (e.g. spatiotemporal variability in flood magnitude and the relative influence of waves, tides and surge levels), we have performed a computer-based classification to identify geographical areas with homogeneous climates. Results show that 75% of coastal regions around the globe have the potential for very large flooding events with low probabilities (unbounded tails), 82% are tide-dominated, and almost 49% are highly susceptible to increases in flooding frequency due to sea-level rise.A.R., F.J.M. and P.C. acknowledge the support of the Spanish ‘Ministerio de Economia y Competitividad’ under Grants BIA2014-59643-R and BIA2015-70644-R. This work was critically supported by the US Geological Survey under Grant/Cooperative Agreement G15AC00426 and from the US DOD Strategic Environmental Research and Development Program (SERDP Project RC-2644) through the NOAA National Centers for Environmental Information (NCEI). Dynamic atmospheric corrections (storm surge) are produced by CLS Space Oceanography Division using the Mog2D model from Legos and distributed by Aviso, with support from CNES (http://www.aviso.altimetry.fr/). Marine data from global reanalysis are provided by IHCantabria and are available for research purposes upon request at [email protected]

Projections of global-scale extreme sea levels and resulting episodic coastal flooding over the 21st Century

Global models of tide, storm surge, and wave setup are used to obtain projections of episodic coastal flooding over the coming century. The models are extensively validated against tide gauge data and the impact of uncertainties and assumptions on projections estimated in detail. Global “hotspots” where there is projected to be a significant change in episodic flooding by the end of the century are identified and found to be mostly concentrated in north western Europe and Asia. Results show that for the case of, no coastal protection or adaptation, and a mean RCP8.5 scenario, there will be an increase of 48% of the world’s land area, 52% of the global population and 46% of global assets at risk of flooding by 2100. A total of 68% of the global coastal area flooded will be caused by tide and storm events with 32% due to projected regional sea level rise

What explains the North–South divide in Italian tax compliance? An experimental analysis

This is the author accepted manuscript. The final version is available from Palgrave Macmillan via the DOI in this recordI undertake a comparative study assessing the North–South divide in Italian tax compliance, employing the largest behavioral tax compliance experiment to date. Contrary to a large body of literature, I argue that willingness to pay taxes is constructed within a specific institutional environment and reflects the country’s quality of institutions. To test this hypothesis, I use controlled tax compliance experiments from four laboratories in Capua, Rome, Bologna, and Milan. By employing the experimental method, I am able to hold institutions constant allowing me to isolate cultural variation. Contrary to cultural explanations for tax compliance, when controlling the institutional environment, there is no difference in tax compliance. Furthermore, using social value orientation to compare prosociality, I also find no differences between the two regions. I therefore conclude that individuals’ relationship to their states shapes these behavioral differences in tax compliance.Funds for this research were provided by the European Research Council (Grant Agreement No. 295675 )

Role of Myeloid-Derived Suppressor Cells in Amelioration of Experimental Autoimmune Hepatitis Following Activation of TRPV1 Receptors by Cannabidiol

Myeloid-derived suppressor cells (MDSCs) are getting increased attention as one of the main regulatory cells of the immune system. They are induced at sites of inflammation and can potently suppress T cell functions. In the current study, we demonstrate how activation of TRPV1 vanilloid receptors can trigger MDSCs, which in turn, can inhibit inflammation and hepatitis.Polyclonal activation of T cells, following injection of concanavalin A (ConA), in C57BL/6 mice caused acute hepatitis, characterized by significant increase in aspartate transaminase (AST), induction of inflammatory cytokines, and infiltration of mononuclear cells in the liver, leading to severe liver injury. Administration of cannabidiol (CBD), a natural non-psychoactive cannabinoid, after ConA challenge, inhibited hepatitis in a dose-dependent manner, along with all of the associated inflammation markers. Phenotypic analysis of liver infiltrating cells showed that CBD-mediated suppression of hepatitis was associated with increased induction of arginase-expressing CD11b(+)Gr-1(+) MDSCs. Purified CBD-induced MDSCs could effectively suppress T cell proliferation in vitro in arginase-dependent manner. Furthermore, adoptive transfer of purified MDSCs into naïve mice conferred significant protection from ConA-induced hepatitis. CBD failed to induce MDSCs and suppress hepatitis in the livers of vanilloid receptor-deficient mice (TRPV1(-/-)) thereby suggesting that CBD primarily acted via this receptor to induce MDSCs and suppress hepatitis. While MDSCs induced by CBD in liver consisted of granulocytic and monocytic subsets at a ratio of ∼2∶1, the monocytic MDSCs were more immunosuppressive compared to granulocytic MDSCs. The ability of CBD to induce MDSCs and suppress hepatitis was also demonstrable in Staphylococcal enterotoxin B-induced liver injury.This study demonstrates for the first time that MDSCs play a critical role in attenuating acute inflammation in the liver, and that agents such as CBD, which trigger MDSCs through activation of TRPV1 vanilloid receptors may constitute a novel therapeutic modality to treat inflammatory diseases

Modified Cav1.4 Expression in the Cacna1fnob2 Mouse Due to Alternative Splicing of an ETn Inserted in Exon 2

The Cacna1fnob2 mouse is reported to be a naturally occurring null mutation for the Cav1.4 calcium channel gene and the phenotype of this mouse is not identical to that of the targeted gene knockout model. We found two mRNA species in the Cacna1fnob2 mouse: approximately 90% of the mRNA represents a transcript with an in-frame stop codon within exon 2 of CACNA1F, while approximately 10% of the mRNA represents a transcript in which alternative splicing within the ETn element has removed the stop codon. This latter mRNA codes for full length Cav1.4 protein, detectable by Western blot analysis that is predicted to differ from wild type Cav1.4 protein in a region of approximately 22 amino acids in the N-terminal portion of the protein. Electrophysiological analysis with either mouse Cav1.4wt or Cav1.4nob2 cDNA revealed that the alternatively spliced protein does not differ from wild type with respect to activation and inactivation characteristics; however, while the wild type N-terminus interacted with filamin proteins in a biochemical pull-down experiment, the alternatively spliced N-terminus did not. The Cacna1fnob2 mouse electroretinogram displayed reduced b-wave and oscillatory potential amplitudes, and the retina was morphologically disorganized, with substantial reduction in thickness of the outer plexiform layer and sprouting of bipolar cell dendrites ectopically into the outer nuclear layer. Nevertheless, the spatial contrast sensitivity (optokinetic response) of Cacna1fnob2 mice was generally similar to that of wild type mice. These results suggest the Cacna1fnob2 mouse is not a CACNA1F knockout model. Rather, alternative splicing within the ETn element can lead to full-length Cav1.4 protein, albeit at reduced levels, and the functional Cav1.4 mutant may be incapable of interacting with cytoskeletal filamin proteins. These changes, do not alter the ability of the Cacna1fnob2 mouse to detect and follow moving sine-wave gratings compared to their wild type counterparts