The influence of geomorphological features on the distribution of Cystoseira populations along the coasts of four pristine islands in the Tyrrhenian Sea (Italy, central Mediterranean) was studied by means of a model-based statistical analysis. The most relevant trait that determined the presence of these populations was found to be the coastline slope at the level of the infralittoral fringe. Our findings indicate that slopes above 60 • reduce the likelihood of Cystoseira communities. The effects of the coastline slope on the CARLIT index are considered and discussed in view of these findings. Pending further studies on the implementation of the CARLIT index in the Mediterranean basin, we suggest that any changes to the procedure or the hasty multiplication of reference sites be avoided, and instead propose a simple empirical adjustment of the EQ values to be able to more accurately monitor coasts with steep slopes using this index.

Periodic fever syndromes include autoinflammatory disorders (AID) that involve innate immunity. These disorders are characterized by recurrent fevers and aberrant multi-organ inflammation, without any involvement of T or B cells or the presence of autoantibodies. A complex genetic architecture has been recognized for many AID. However, this complexity has only been partially uncovered for familial Mediterranean fever and other conditions that have a classical monogenic origin and Mendelian transmission. Several gene panels are currently available for molecular diagnosis in patients suspected of having AID. However, even when an extensive number of genes (up to 50–100) are tested in a cohort of clinically selected patients, the diagnostic yield of AID ranges between 15% and 25%, depending on the clinical criteria used for patient selection. In the remaining 75–85% of cases, it is conceivable that the causative gene or genes responsible for a specific condition are still elusive. In these cases, the disease could be explained by variants, either recessive or dominant, that have a major effect on unknown genes, or by the cumulative impact of different variants in more than one gene, each with minor additive effects. In this study, we focused our attention on five familial cases of AID presenting with classical autosomal dominant transmission. To identify the probable monogenic cause, we performed exome sequencing. Through prioritization, filtering, and segregation analysis, we identified a few variants for each family. Subsequent bioinformatics evaluation and pathway analysis helped to narrow down the best candidate genes for each family to FCRL6, PKN1, STAB1, PTDGR, and VCAM1. Future studies on larger cohorts of familial cases will help confirm the pathogenic role of these genes in the pathogenesis of these complex disorders.