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Foodborne pathogens and biofilm formation pose a critical threat to food safety. Pseudomonas aeruginosa is a pathogen of interest in the food industry. High-power pulsed microwave (HPPM) is a non-thermal technology with proven efficacy towards bacterial inactivation. This study investigated the inactivation mechanisms and performance of different HPPM treatments (50, 100, 150, 200, and 250 Hz for 3, 5, 7, 9, and 11 min, respectively) to identify the optimum conditions to inactivate P. aeruginosa PAO1 biofilms. The results showed significant cell inactivation at increasing frequency/time (p < 0.05). Hence, HPPM treatment (200 Hz, 9 min) was selected following its efficacy and limited thermal sublethal effects to elucidate further the inactivation mechanisms against P. aeruginosa and its biofilm-forming ability. Cell viability, scanning (SEM) and transmission electron microscopy (TEM) results demonstrated severe morphological disruptions, cell disintegration, and cell lysis in the treated cells. From the confocal laser scanning micrographs (CLSM), biofilm thickness was calculated, showing a significant reduction after treatment (17.56 vs. 42.16 μm in the treated and untreated groups, respectively), indicating that HPPM effectively compromised the integrity of the biofilm envelope. This study outlines useful insights into better understanding HPPM's efficacy on microbial inactivation and biofilm proliferation in the food industry. • High-power pulse microwave (HPPM) demonstrated significant cell inactivation at increasing frequency/time (p < 0.05). • Treated cells demonstrated severe cell deformation, membrane shriveling, and cell lysis. • It showed a marked reduction in biofilm thickness than untreated cells (17.56 ± 1.51vs. 42.16 ± 1.23 μm). • This study provides useful insights into validating HPPM's efficacy against bacterial biofilm formation. [ABSTRACT FROM AUTHOR]

Opioid withdrawal generates extremely unpleasant physical symptoms and negative affective states. A rapid relief of opioid withdrawal-induced anxiety has obvious clinical relevance but has been rarely reported. We have shown that injection of ketamine metabolite (2 R ,6 R)-hydroxynorketamine (HNK) leads to a rapid alleviation of anxiety-like behaviors in male mice undergoing chronic morphine withdrawal. Here we investigated the contribution of nucleus accumbens shell (sNAc) parvalbumin (PV)-neurons to this process. Chronic morphine withdrawal was associated with higher intrinsic excitability of sNAc PV-neurons via reduced voltage-dependent potassium currents. Chemogenetic inhibition of sNAc PV-neurons reversed the enhanced excitability of PV-neurons and anxiety-like behaviors in these morphine withdrawal male mice, while activation of sNAc PV-neurons induced anxiety-like behaviors in naive male mice. (2 R ,6 R)-HNK reversed the altered potassium currents and intrinsic excitability of sNAc PV-neurons. Our findings demonstrate an important contribution of sNAc PV-neurons to modulating morphine withdrawal-induced anxiety-like behaviors and rapid relief of anxiety-like behaviors by (2 R ,6 R)-HNK, this newly identified target may have therapeutic potentials in treating opioid addiction and anxiety disorders. • sNAc PV-neuron excitability is higher in mice undergoing morphine withdrawal. • Inhibiting sNAc PV-neurons improves morphine withdrawal-induced anxiety-like behaviors. • Activating sNAc PV-neurons elicits anxiety-like behaviors in naïve mice. • (2 R ,6 R)-HNK alleviates morphine withdrawal-induced anxiety-like behaviors in mice. • (2 R ,6 R)-HNK increases K+ currents and reduces excitability of sNAc PV-neurons. [ABSTRACT FROM AUTHOR]