Department of Industrial Engineering (DIN) & Advanced Mechanics and Materials, Interdepartmental Center for Industrial Research (AMM-ICIR), Via Saragozza 8, 40123, Alma Mater Studiorum-Università di Bologna, Italy
Dr. Vittorio Colombo
Department of Industrial Engineering (DIN) & Advanced Mechanics and Materials, Interdepartmental Center for Industrial Research (AMM-ICIR), Via Saragozza 8, 40123, Alma Mater Studiorum-Università di Bologna, Italy
This white paper considers the future of plasma science and technology related to the manufacturing and modifications of plastics and textiles, summarizing existing efforts and the current state‐of‐art for major topics related to plasma processing techniques. It draws on the frontier of plasma technologies in order to see beyond and identify the grand challenges which we face in the following 5–10 years. To progress and move the frontier forward, the paper highlights the major enabling technologies and topics related to the design of surfaces, coatings and materials with non‐equilibrium plasmas. The aim is to progress the field of plastics and textile production using advanced plasma processing as the key enabling technology which is environmentally friendly, cost‐efficient, and offers high‐speed processing.
1 January 2017 in Oxidative Medicine and Cellular Longevity
Cold atmospheric plasma (CAP) has shown its antitumor activity in both in vitro and in vivo systems. However, the mechanisms at the basis of CAP‐cell interaction are not yet completely understood. The aim of this study is to investigate CAP proapoptotic effect and identify some of the molecular mechanisms triggered by CAP in human T‐lymphoblastoid leukemia cells. CAP treatment was performed by means of a wand electrode DBD source driven by nanosecond high‐voltage pulses under different operating conditions. The biological endpoints were assessed through flow cytometry and real‐time PCR. CAP caused apoptosis in Jurkat cells mediated by p53 upregulation. To test the involvement of intrinsic and/or extrinsic pathway, the expression of Bax/Bcl‐2 and caspase‐8 was analyzed. The activation of caspase‐8 and the upregulation of Bax and Bcl‐2 were observed. Moreover, CAP treatment increased ROS intracellular level. The situation reverts after a longer time of treatment. This is probably due to compensatory cellular mechanisms such as the posttranscriptional upregulation of SOD1, CAT, and GSR2. According to ROS increase, CAP induced a significant increase in DNA damage at all treatment conditions. In conclusion, our results provide a deeper understanding of CAP potential in the oncological field and pose the basis for the evaluation of its toxicological profile.