3 results match your criteria: "Department of Life Sciences - University of Parma[Affiliation]"
Rev Saude Publica
April 2017
Evaluative Epidemiology Unit. Fondazione IRCCS Istituto Nazionale dei Tumori. Milano, Italy.
Improvements in the health standards of developed and developing societies depend primarily on the relationships between economy and environment. Recent long-term changes in the chemical composition of man-made environments may be linked to changes in the biology of human beings. Here we argue that children are at the greatest risk of being affected by the dangerous effects of these changes, with particular reference to cancer.
View Article and Find Full Text PDFEcotoxicol Environ Saf
October 2016
Department of Life Sciences - University of Parma, Parco Area delle Scienze 11/A, 43124 Parma, Italy. Electronic address:
The evaluation of toxicity due to persistent pollutants in anoxic aquatic environments has met with various problems, as most test organisms can not withstand oxygen lack and exposure to free sulfide. We evaluated the suitability of the eggs of the brackish copepod Acartia tonsa for bioassays in anoxic/sulfidic conditions: when exposed to deep hypoxia and free sulfide, the eggs become quiescent and are able to resume hatching after restoring normoxic conditions. Tests with cadmium and nickel were performed in normoxic and deeply hypoxic conditions and in anoxic water containing H2S or H2S+FeSO4 on an equimolar basis.
View Article and Find Full Text PDFPLoS One
December 2015
Laboratory of Experimental Oncology, Rizzoli Orthopaedic Institute, Bologna, Italy.
Osteosarcoma (OS) is the most common primary malignant bone tumor and prevalently occurs in the second decade of life. Etoposide, a chemotherapeutic agent used in combined treatments of recurrent human OS, belongs to the topoisomerase inhibitor family and causes DNA breakage. In this study we evaluated the cascade of events determined by etoposide-induced DNA damage in OS cell lines with different p53 status focusing on methylation status and expression of miR-34a that modulate tumor cell growth and cell cycle progression.
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