One of the major concerns in the COVID-19 pandemic is related to the possible transmission in poorly ventilated spaces of SARS-CoV-2 through aerosol microdroplets, which can remain in the air for long periods of time and be transmitted to others over distances >1 m. Cold atmospheric pressure plasmas can represent a promising solution, thanks to their ability in producing a blend of many reactive species, which can inactivate the airborne aerosolized microorganisms. In this study, a dielectric barrier discharge plasma source is used to directly inactivate suitably produced bioaerosols containing Staphylococcus epidermidis or purified SARS-CoV-2 RNA flowing through it. Results show that for low residence times (<0.2 s) in the plasma region a 3.7 log R on bacterial bioaerosol and degradation of viral RNA can be achieved. K E Y W O R D S bioaerosol, cold plasma, inactivation, indoor airborne transmission, SARS-CoV-2 Alina Bisag and Pasquale Isabelli contributed equally to this study.
This work is focused on the use of non-thermal plasma to improve the electrospinnability of poly(L-lactic acid) (PLLA). The use of toxic high boiling point solvents is minimized to produce high quality solvent free nanofibrous scaffolds for biomedical applications. PLLA polymeric solutions dissolved in pure dichloromethane are exposed to the plasma plume of a jet developed by some of the authors and driven by high voltage pulses with rise rate of several kV ns À1 . The effects of peak voltage, pulse repetition frequency, volume of the solution and treatment time on the morphology of electrospun fibers are investigated by means of scanning electron microscope. Electrospinning is performed at different time lapses after the plasma treatment to study the durability of the induced effects. Figure 10. Spatially resolved optical emission spectrum of the plasma jet, operating conditions: PV ¼ 20 kV, PRF ¼ 330 Hz, Ar flow rate ¼ 1 slpm. V. Colombo et al.
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.
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