Estimating the time since death (post mortem interval, PMI) represents one of the most important tasks in daily forensic casework. For decades, forensic scientists have investigated changes in post mortem body composition, focusing on different physical, chemical, or biological aspects, to discover a reliable method for estimating PMI; nevertheless, all of these attempts remain unsuccessful considering the currently available methodical spectrum characterized by great inaccuracies and limitations. However, recent promising approaches focus on the post mortem decomposition of biomolecules. In particular, significant advances have been made in research on the post mortem degradation of proteins. In the present study, we investigated early post mortem changes (during the first 24 h) in the proteome profile of the pig skeletal muscle looking for new PMI specific biomarkers. By mass spectrometry (MS)-based proteomics, we were able to identify a total of nine potential PMI biomarkers, whose quantity changed constantly and progressively over time, directly or inversely proportional to the advancement of post mortem hours. Our preliminary study underlines the importance of the proteomic approach in the search for a reliable method for PMI determination and highlights the need to characterize a large number of reliable marker proteins useful in forensic practice for PMI estimation.

This work aims to clarify the effect of dietary supplementation with Bisphenol A (BPA), a chemical widely present in beverage and food containers, on placental glucose transfer and pregnancy outcome. The study was performed on female Sprague Dawley rats fed with a diet containing BPA (2.5, 25 or 250 μg/Kg/day) for a period of a month (virgin state) plus 20 days during pregnancy. Western blot analysis and immunohistochemistry were performed in placental tissues for glucose type 1 transporter (GLUT1). Furthermore, human trophoblast, HTR8-SV/neo cells, were used to evaluate the effect of BPA on glucose transport and uptake. Studies in rats showed that food supplementation with BPA, produces a higher fetal weight (FW) to placenta weight (PW) ratio at the lowest BPA concentration. Such low concentrations also reduced maternal weight gain in late pregnancy and up-regulated placental expression of GLUT1. Treatment of HTR8-SV/neo with the non-toxic dose of 1 nM BPA confirmed up-regulation of GLUT1 expression and revealed higher activity of the transporter with an increase in glucose uptake and GLUT1 membrane translocation. Overall, these results indicate that prenatal exposure to BPA affects pregnancy and fetal growth producing changes in the placental nutrients-glucose transfer.

In recent years, microplastic pollution has become one of the major global concerns and represents a complex, multidimensional, and multisectoral reality. The considerable existing data relating to microplastic pollution in matrices such as water and soil suggests that microplastics are widespread globally, but there are several knowledge gaps regarding their actual distribution mostly in remote locations far from sources. In this review we examine current knowledge on microplastic pollution in the Antarctic continent. Antarctica, the unique continent not permanently anthropized, is the southernmost part of the planet but its geographic isolation does not protect against the harmful impact of human activities. This continent is characterized by limited internal pollution sources but high-burden external routes of contaminants and represents a unique natural laboratory to analyze how pollution can reach every part of the biosphere. This review reports the presence of microplastics in organic and inorganic matrices not only at marine level (water, sediments, benthic organisms, krill, and fish) but also in freshwater (lakes, rivers, snow, and glaciers) highlighting that microplastic contamination is endemic in the Antarctic environment. Microplastic pollution is of great environmental concern everywhere, but the characteristics of remote ecosystems suggest that they could be more sensitive to harm from this pollution.

Caloric restriction is an effective intervention to protract healthspan and lifespan in several animal models from yeast to primates, including humans. Caloric restriction has been found to induce cardiometabolic adaptations associated with improved health and to delay the onset and progression of kidney disease in different species, particularly in rodent models. In both aging and obesity, fibrosis is a hallmark of kidney disease, and epithelial–mesenchymal transition is a key process that leads to fibrosis and renal dysfunction during aging. In this study, we used an aged and obese rat model to evaluate the effect of long-term (6 months) caloric restriction (−40%) on renal damage both from a structural and functional point of view. Renal interstitial fibrosis was analyzed by histological techniques, whereas effects on mesenchymal (N-cadherin, Vimentin, Desmin and α-SMA), antioxidant (SOD1, SOD2, Catalase and GSTP1) inflammatory (YM1 and iNOS) markers and apoptotic/cell cycle (BAX, BCL2, pJNK, Caspase 3 and p27) pathways were investigated using Western blot analysis. Our results clearly showed that caloric restriction promotes cell cycle division and reduces apoptotic injury and fibrosis phenotype through inflammation attenuation and leukocyte infiltration. In conclusion, we highlight the beneficial effects of caloric restriction to preserve elderly kidney function.

Although the clinical differences between hemodialysis (HD) and peritoneal dialysis (PD) are well established, the specific biological mechanisms underlying these differences remain incompletely understood. We performed untargeted proteomic and transcriptomic analyses of peripheral blood mononuclear cells (PBMCs) from healthy controls (CTRs) and patients with chronic kidney disease undergoing HD or PD. Key findings were validated in an independent cohort using standardized biomolecular techniques. Bioinformatic analysis identified 36 differentially expressed proteins and 19 transcripts between HD and PD according to the predefined FDR-adjusted significance threshold. Functional enrichment analysis revealed that these factors were primarily involved in cellular senescence, aging, and stress-response pathways. Among the identified molecules, interferon regulatory factor 8 (IRF8) was the only factor consistently upregulated in HD compared with PD in both omics analyses. This finding was confirmed by ELISA in an independent cohort (p < 0.0001). Kinase enrichment analysis prioritized Checkpoint Kinase 2 (CHEK2), which was also identified by proteomics, as a predicted upstream regulator and warrants further investigation. Overall, these findings identify distinct molecular signatures in PBMCs from HD and PD patients and suggest a potential association between HD and increased PBMC IRF8 abundance and a senescence-related signature, which requires validation in larger and longitudinal cohorts.