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Gliding arc is a promising plasma technology for water activation due to its high energy efficiency for producing reactive nitrogen species (RNS), which is believed as the key agent for the sustained bactericidal effect of plasma-activated water (PAW). Nitric oxide (NO) is the major product of gliding arc and also widely exists in PAW, but the production mechanism of aqueous NO and its role in sterilization have been little investigated before. In this paper, NO-rich plasma effluent gas is produced by gliding arc discharge and introduced into water to produce PAW. The concentrations of gaseous and aqueous reactive species are detected, which decrease with the increasing air flowrate of the gliding arc. To clarify the contribution of plasma-induced RNS on water activation, the NO + air mixed gas is used to simulate the plasma effluent gas, and the results show that the two gases have similar gaseous composition and aqueous NO yield. Compared with the NO + Ar mixed gas with the same NO proportion, the NO + air mixed gas produces much more aqueous NO, implying that the presence of O2 significantly enhances the production of aqueous NO. The sterilization experiments demonstrate the key role of aqueous NO in sterilization, but an acidic environment is necessary for aqueous NO to achieve a potent bactericidal effect. [ABSTRACT FROM AUTHOR]

Air plasma is commonly used to treat water for activation or purification, and plasma-activated water (PAW) is a promising green disinfectant that has attracted much attention in recent years. However, either the O3 discharge mode or the NO x discharge mode of air plasma lacks efficiency for water activation, mainly due to the low solubility of O3, NO and NO2. The transition process between those two modes could produce high-valence NO x such as N2O5 which should be more efficient for water activation, but this process is not easily controlled and water activation by N2O5 has rarely been reported before. In this letter, N2O5 is found to be produced effectively and stably by mixing the effluent gases of a NO x mode air plasma, produced by gliding arc discharge, and an O3 mode air plasma, produced by dielectric barrier discharge. The mixed gas rich in N2O5 is found to be very efficient for water activation. A colony-forming unit reduction of nearly 6 logs was achieved for a methicillin-resistant Staphylococcus aureus suspension by using PAW treated by the mixed gas, and the high bactericidal effect of the PAW could persist for more than 1 h after the plasma activation. The main reactive species for the bactericidal effect in the PAW are discussed, and the chemical pathways for N2O5 production and its usage for water activation are illustrated. [ABSTRACT FROM AUTHOR]

Plasma‐activated media (PAM), the product of cold atmospheric plasma (CAP) acting on aqueous media, has similarly strong biological activity and some unique advantages compared with CAP for biomedical targets. However, no reliable PAM‐preparing device with high safety for medical uses has yet been developed, limiting the advancement of PAM clinical trials. Herein, an integrated device for PAM preparation with a maximum yield of 4.8 L/hr is reported in detail. A large‐area CAP is generated by the plasma‐generating module based on the surface dielectric barrier discharge. Several sensors and controllers are applied in this device to stabilize the discharge environment and PAM consistency. In the in vitro experiments, PAM prepared in this device exhibits the bactericidal property of up to 6 logs reduction against various clinical pathogens with multi‐drug resistance. The high bactericidal effect of PAM can be preserved for ∼10 min. After constructing the mice model by cecal ligation and puncture, it is found that the abdominal injection of PAM can effectively relieve sepsis‐induced systemic toxicity and maintain homeostasis, which is mainly attributed to the anti‐infective efficacy of PAM. The third‐party testing confirms that the soaking bactericidal rates of PAM to S. aureus and E. coli are respectively higher than 99.99% and 99.999%, while the acute oral toxicity, skin irritation, and oral genotoxicity of PAM are negligible. This study provides a practical approach for preparing PAM with high reliability, which shows an excellent prospect of clinical applications and commercialization. [ABSTRACT FROM AUTHOR]

Surface air discharge has been extensively reported to have strong antibacterial and anticancer effects, and these biological effects are more or less attributed to the short-lived aqueous reactive species produced by the air plasma. Insight into the generation mechanism for short-lived species is a key bottleneck in elucidating the antimicrobial and anticancer effects. Although the numerical study has predicted that the dissolution of gaseous NO3 plays a crucial role, but so far without experimental validation. In view of this, cavity ring-down spectroscopy is adopted in this paper to measure the NO3 spatial distribution between the surface air discharge and the solutions to be treated, and the concentrations of short-lived species in the solutions after plasma treatment are also measured for different discharge modes. A simplified chemical pathway for the conversion of gaseous NO3 to aqueous ONOOaq−/ONOOHaq and O2aq− is proposed. Moreover, the inactivation effects for Escherichia coli and A549 lung cancer cells treated by the plasma-activated solutions are measured for different concentrations of short-lived species, and the key species for sterilization and anticancer are identified by chemical scavengers. Finally, a positive correlation chain is found among the inactivation effect, the concentrations of aqueous ONOOaq−/ONOOHaq and O2aq−, and the density of gaseous NO3, implying that NO3 might be very important for the production of aqueous short-lived reactive species as well as the biological effects induced by plasma-activated solutions. [ABSTRACT FROM AUTHOR]

Chronic obstructive pulmonary disease (COPD) is composed of chronic airway inflammation and emphysema. Recent studies show that Class IA phosphatidylinositol 3-kinases (PI3Ks) play an important role in the regulation of inflammation and emphysema. However, there are few studies on their regulatory subunits. p55PIK is a regulatory subunit of Class IA PI3Ks, and its unique NH2-terminal gives it special functions. p55PIK expression in the lungs of nonsmokers, smokers, and patients with COPD was examined. We established a fusion protein TAT-N15 from the NH2-terminal effector sequence of p55PIK and TAT (the transduction domain of HIV transactivator protein) and investigated the effects of silencing p55PIK or adding TAT-N15 on cigarette smoke exposure at the cellular and animal level. p55PIK expression was increased in patients with COPD. p55PIK deficiency and TAT-N15 significantly inhibited the cigarette smoke extract-induced IL-6, IL-8, and activation of the Akt and the NF-κB pathway in BEAS-2B. p55PIK deficiency and TAT-N15 intranasal administration prevented emphysema and the lung function decline in mice exposed to smoke for 6 mo. p55PIK deficiency and TAT-N15 significantly inhibited lung inflammatory infiltration, reduced levels of IL-6 and KC in mice lung homogenate, and inhibited activation of the Akt and the NF-κB signaling in COPD mice lungs. Our studies indicate that p55PIK is involved in the pathogenesis of COPD, and its NH2-terminal derivative TAT-N15 could be an effective drug in the treatment of COPD by inhibiting the activation of the Akt and the NF-κB pathway. [ABSTRACT FROM AUTHOR]

Pulmonary hypertension (PH) is a chronic vascular disease characterized by elevated pulmonary arterial resistance and vascular remodeling, and chronic hypoxia plays an important role in PH. Milk fat globule‐EGF factor 8 (MFG‐E8) is a glycoprotein that regulates cell proliferation and apoptosis, but its role in hypoxia‐induced PH is unknown. The current study aimed to determine the function and fundamental mechanisms of MFG‐E8 in hypoxia‐induced PH. Herein, we exposed mice to hypoxia for 5 weeks, and MFG‐E8 was found to be elevated in mouse lung tissues, arteries, and plasma. Compared with wild‐type littermates, mice lacking MFG‐E8 showed a significant increase in the ratio of pulmonary artery acceleration time to ejection time (PAT/PET), while they showed decreases in right ventricular systolic pressure, the Fulton's Index, percent medial wall thickness (%WT), and vascular muscularization in pulmonary arteries. In addition, MFG‐E8 protein levels were also increased in the serum of patients with chronic PH. Similarly, we observed a higher expression of MFG‐E8 in human pulmonary artery smooth muscle cells (PASMCs) in the presence of hypoxic stimulation than MFG‐E8 in cells in normoxic conditions. Furthermore, MFG‐E8 silencing resulted in partial inhibition of proliferation, migration and cell cycle progression in human PASMCs, and the possible mechanisms might involve the interaction between MFG‐E8 and the p‐Akt/cyclin D1 pathway. Collectively, our study suggests that the absence of MFG‐E8 can attenuate the development of hypoxia‐induced PH and vascular remodeling. MFG‐E8 can be a potential therapeutic target or a biomarker for PH. [ABSTRACT FROM AUTHOR]