MicroRNAs (miRNAs) are small non-coding RNA molecules able to post-transcriptionally regulate gene expression via base-pairing with partially complementary sequences of target transcripts. Prion diseases comprise a singular group of neurodegenerative conditions caused by endogenous, misfolded pathogenic (prion) proteins, associated with molecular aggregates. In humans, classical prion diseases include Creutzfeldt–Jakob disease, fatal familial insomnia, Gerstmann–Sträussler–Scheinker syndrome, and kuru. The aim of this review is to present the connections between miRNAs and prions, exploring how the interaction of both molecular actors may help understand the susceptibility, onset, progression, and pathological findings typical of such disorders, as well as the interface with some prion-like disorders, such as Alzheimer’s. Additionally, due to the inter-regulation of prions and miRNAs in health and disease, potential biomarkers for non-invasive miRNA-based diagnostics, as well as possible miRNA-based therapies to restore the levels of deregulated miRNAs on prion diseases, are also discussed. Since a cure or effective treatment for prion disorders still pose challenges, miRNA-based therapies emerge as an interesting alternative strategy to tackle such defying medical conditions.

No abstract

No abstract

Panagrolaimus superbus nematodes are able to tolerate desiccation by entering into a peculiar state of suspended animation known as anhydrobiosis. When desiccated, anhydrobiotic organisms are also able to tolerate other physical stresses, as high and low levels of temperature and pressure. Here, we decided to investigate the tolerance of desiccated P. superbus to an unprecedented double stress-hypoxia within 99.99% Gallium (Ga) metal cage. The authors observed that regardless of the external relative humidity, desiccated P. superbus tolerated 7 d confined within the metal cage, displaying no negative effects on its survival and population growth rates over 40 d. The results evidence that anhydrobiosis also renders nematodes tolerant to otherwise lethal concentrations of Ga, in an oxygen-poor environment; thus, expanding its polyextremotolerance profile.

The overweight population is growing in the world, and the search for obesityassociated mechanisms is important for a better understanding of this disease. Few studies with the FTO gene and miRs show how they associate to obesity and how they can impact this disease. The aim of this study was to verify the relationship between the FTO gene and the hsa-miR-150-5p expression with overweight/obesity, lipid profi le, and fast blood glucose. Men and women (18 years older or above), with body mass index ≥ 18.5 kg/m 2 , were enrolled in the present study and the FTO gene and hsa-miR-150-5p expression, biochemical parameters of blood and anthropometric measurements were analyzed. The results highlight that the FTO gene expression is associated to obesity (p 0.029), LDL-C (p 0.02) and fasting blood glucose (p 0.02), but not with triglycerides (p 0.69), total cholesterol (p 0.21), and HDL-C (p 0.24). The hsa-miR-150-5p is not associated to obesity (p 0.84), triglycerides (p 0.57), total cholesterol (p 0.51), HDL-C (p 0.75), LDL-C (p 0.32), and fasting blood glucose (p 0.42). The FTO gene expression is related to obesity, LDL-C and blood fasting glucose, representing a good molecular marker for obesity.