Project description:Human mercury (Hg) exposure is mostly caused by eating fish. However, there are major differences between the measured and predicted mercury concentration on Hg bioavailability. This study investigated the effects of cooking (steaming, baking, frying, marinating, and smoking) and selected components' co-ingestion on Hg bioaccessibility. Baking and frying reduced Hg bioaccessibility compared to the raw sample. The bioaccessible Hg fraction in fish was assessed through in vitro digestion method. Hg bioaccessibility varied from 4.31 to nearly 24.95% and the Hg recovery rate varied from 63.44 to 78.74%. Co-ingested garlic and broccoli with pontic shad had a positive effect on decreasing fish Hg bioaccessibility. The antioxidant activity of co-ingested food items was also calculated and correlated with mercury bioaccessibility. These results highlighted a possible positive role of plant-based foods and other food processing techniques in the bioaccessibility reduction of other chemical contaminants found in food sources.
Project description:The DNA isolated from 44 either frozen or FFPE Neuroendocrine Neoplasm (NEN) was analysed by NGS, to identify genes more likely to be subject to sequence variations among 523 cancer-related ones.
Project description:Plasma DNA from 558 malignancies, 263 benign and borderline tumors and 367 healthy control samples were collected and subjected to random short-gun whole genome sequencing.
Project description:This study aims to investigate the DNA methylation patterns at transcription factor binding regions and their evolutionary conservation with respect to binding activity divergence. We combined newly generated bisulfite-sequencing experiments in livers of five mammals (human, macaque, mouse, rat and dog) and matched publicly available ChIP-sequencing data for five transcription factors (CEBPA, HNF4a, CTCF, ONECUT1 and FOXA1). To study the chromatin contexts of TF binding subjected to distinct evolutionary pressures, we integrated publicly available active promoter, active enhancer and primed enhancer calls determined by profiling genome wide patterns of H3K27ac, H3K4me3 and H3K4me1.
