Understanding Financial Risk Tolerance. Institutional, Behavioral and Normative Dimensions

This book focuses on the contribution of financial risk tolerance in shaping the workings of financial markets. It combines very different views to understand how this concept, lying at the crossroads of different domains of study and practice, including financial regulation, scholarly studies, and financial advisory practice, has been formalized over the last 30 years. The book looks at the feedback loop among the different domains in which risk tolerance is assessed and operationalized to reorganize the current stream of research on financial risk tolerance and suggests further relevant domains in which a new risk tolerance definition will need to be defined. Using key landmark moments in the normative evolution of financial services in the European Union (MiFID and MiFID 2), this book highlights the relationship between scholarly definitions of risk tolerance, key measurement tools, and the formal requirements imposed by regulatory institutions to key market players. This book provides a snapshot of the most important dimensions in which financial risk tolerance has been analyzed and highlights the relationship between policy-making and scientific endeavor. We touch upon precursors of financial risk tolerance, reviewing key socio-demographic variables, and move on toward more dynamic versions of financial risk tolerance that include the role of life events. The different chapters focus on the debate on financial risk tolerance in specific time frames marked by regulatory events and provide an in-depth overview of two important changes in European financial markets—sustainable investment and fintech and robo advisory. A practitioner’s view section authored by the CEO of a UK-based investment firm is included as a commentary and includes relevant insights from the world of financial advisory tied to the academic debate discussed in the text

river morphology monitoring using multitemporal sar data preliminary results

AbstractIn this paper, we test the capability of satellite synthetic aperture radar (SAR) images to enhance the monitoring of river geomorphological processes. The proposed approach exploits the recently introduced Level-α products. These products are bi-temporal RGB composites in which the association color-object, being physical-based, is stable whatever the scene is considered. This favors the detection of temporary rivers' characteristics for classification purposes in a change-detection environment. The case study was implemented on the Orco river (northwest Italy), where a set of 39 COSMO-SkyMed SAR stripmap images acquired from October 2008 to November 2014 was used to monitor channel planform changes. This preliminary study is devoted to assess the suitability of Level-α images for geomorphologist, with particular reference to the detection of phenomena of interest in river monitoring. This is prior for semi-automatic or automatic classification activities

Hydrological modeling in ungauged basins using SAR data

In this paper we propose a methodology devoted to exploit high resolution radars for monitoring water bodies in semi-arid countries. The proposed approach is based on appropriate registration, calibration and processing of SAR data, producing information ready to use by end-users. The obtained results were used to (i) estimate a relationship between surface and volume of water stored in reservoirs and (ii) validate a hydrological model that simulates the time evolution of water availability

An explainable model of host genetic interactions linked to COVID-19 severity

We employed a multifaceted computational strategy to identify the genetic factors contributing to increased risk of severe COVID-19 infection from a Whole Exome Sequencing (WES) dataset of a cohort of 2000 Italian patients. We coupled a stratified k-fold screening, to rank variants more associated with severity, with the training of multiple supervised classifiers, to predict severity based on screened features. Feature importance analysis from tree-based models allowed us to identify 16 variants with the highest support which, together with age and gender covariates, were found to be most predictive of COVID-19 severity. When tested on a follow-up cohort, our ensemble of models predicted severity with high accuracy (ACC = 81.88%; AUCROC = 96%; MCC = 61.55%). Our model recapitulated a vast literature of emerging molecular mechanisms and genetic factors linked to COVID-19 response and extends previous landmark Genome-Wide Association Studies (GWAS). It revealed a network of interplaying genetic signatures converging on established immune system and inflammatory processes linked to viral infection response. It also identified additional processes cross-talking with immune pathways, such as GPCR signaling, which might offer additional opportunities for therapeutic intervention and patient stratification. Publicly available PheWAS datasets revealed that several variants were significantly associated with phenotypic traits such as "Respiratory or thoracic disease", supporting their link with COVID-19 severity outcome.A multifaceted computational strategy identifies 16 genetic variants contributing to increased risk of severe COVID-19 infection from a Whole Exome Sequencing dataset of a cohort of Italian patients

The polymorphism L412F in TLR3 inhibits autophagy and is a marker of severe COVID-19 in males

The polymorphism L412F in TLR3 has been associated with several infectious diseases. However, the mechanism underlying this association is still unexplored. Here, we show that the L412F polymorphism in TLR3 is a marker of severity in COVID-19. This association increases in the sub-cohort of males. Impaired macroautophagy/autophagy and reduced TNF/TNFα production was demonstrated in HEK293 cells transfected with TLR3L412F-encoding plasmid and stimulated with specific agonist poly(I:C). A statistically significant reduced survival at 28 days was shown in L412F COVID-19 patients treated with the autophagy-inhibitor hydroxychloroquine (p = 0.038). An increased frequency of autoimmune disorders such as co-morbidity was found in L412F COVID-19 males with specific class II HLA haplotypes prone to autoantigen presentation. Our analyses indicate that L412F polymorphism makes males at risk of severe COVID-19 and provides a rationale for reinterpreting clinical trials considering autophagy pathways. Abbreviations: AP: autophagosome; AUC: area under the curve; BafA1: bafilomycin A1; COVID-19: coronavirus disease-2019; HCQ: hydroxychloroquine; RAP: rapamycin; ROC: receiver operating characteristic; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2; TLR: toll like receptor; TNF/TNF-α: tumor necrosis factor

SARS-CoV-2 susceptibility and COVID-19 disease severity are associated with genetic variants affecting gene expression in a variety of tissues

Variability in SARS-CoV-2 susceptibility and COVID-19 disease severity between individuals is partly due to genetic factors. Here, we identify 4 genomic loci with suggestive associations for SARS-CoV-2 susceptibility and 19 for COVID-19 disease severity. Four of these 23 loci likely have an ethnicity-specific component. Genome-wide association study (GWAS) signals in 11 loci colocalize with expression quantitative trait loci (eQTLs) associated with the expression of 20 genes in 62 tissues/cell types (range: 1:43 tissues/gene), including lung, brain, heart, muscle, and skin as well as the digestive system and immune system. We perform genetic fine mapping to compute 99% credible SNP sets, which identify 10 GWAS loci that have eight or fewer SNPs in the credible set, including three loci with one single likely causal SNP. Our study suggests that the diverse symptoms and disease severity of COVID-19 observed between individuals is associated with variants across the genome, affecting gene expression levels in a wide variety of tissue types

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

A first update on mapping the human genetic architecture of COVID-19

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