Potential effects of Cu2+ stress on nitrogen removal performance, microbial characteristics, and metabolism pathways of biofilm reactor.

Sequencing batch biofilm reactors (SBBR) were utilized to investigate the impact of Cu2+ on nitrogen (N) removal and microbial characteristics. The result indicated that the low concentration of Cu2+ (0.5 mg L-1) facilitated the removal of ammonia nitrogen (NH4+-N), total nitrogen (TN), nitrate nitrogen (NO3--N), and chemical oxygen demand (COD). In comparison to the average effluent concentration of the control group, the average effluent concentrations of NH4+-N, NO3--N, COD, and TN were found to decrease by 40.53%, 17.02%, 10.73%, and 15.86%, respectively. Conversely, the high concentration of Cu2+ (5 mg L-1) resulted in an increase of 94.27%, 55.47%, 22.22%, and 14.23% in the aforementioned parameters, compared to the control group. Low concentrations of Cu2+ increased the abundance of nitrifying bacteria (Rhodanobacter, unclassified-o-Sacharimonadales), denitrifying bacteria (Thermomonas, Comamonas), denitrification-associated genes (hao, nosZ, norC, nffA, nirB, nick, and nifD), and heavy-metal-resistant genes related to Cu2+ (pcoB, cutM, cutC, pcoA, copZ) to promote nitrification and denitrification. Conversely, high concentration Cu2+ hindered the interspecies relationship among denitrifying bacteria genera, nitrifying bacteria genera, and other genera, reducing denitrification and nitrification efficiency. Cu2+ involved in the N and tricarboxylic acid (TCA) cycles, as evidenced by changes in the abundance of key enzymes, such as (EC:1.7.99.1), (EC:1.7.2.4), and (EC:1.1.1.42), which initially increased and then decreased with varying concentrations of Cu2+. Conversely, the abundance of EC1.7.2.1, associated with the accumulation of nitrite nitrogen (NO2--N), gradually declined. These findings provided insights into the impact of Cu2+ on biological N removal.

Unraveling the effects and mechanisms of microplastics on anaerobic fermentation: Exploring microbial communities and metabolic pathways.

To investigate the effects of microplastics (MPs) on hydrolysis, acidification and microbial characteristics during waste activated sludge (WAS) anaerobic fermentation process, five different kinds of MPs were added into the WAS fermentation system and results indicated that, compared to the control group, the addition of polyvinyl chloride (PVC)-MPs exhibited the least inhibition on volatile fatty acids (VFAs), reducing them by 13.49 %. Conversely, polyethylene (PE)-MPs resulted in the greatest inhibition, with a reduction of 29.57 %. MPs, while accelerated the dissolution of WAS that evidenced by an increase of lactate dehydrogenase (LDH) release, concurrently inhibited the activities of relevant hydrolytic enzymes (α-Glucosidase, protease). For microbial mechanisms, MPs addition affected the proliferation of key microorganisms (norank_f_Bacteroidetes_vadinHA17, Ottowia, and Propioniclava) and reduced the abundance of genes associated with hydrolysis and acidification (pfkb, gpmI, ilvE, and aces). Additionally, MPs decreased the levels of key hydrolytic and acidogenic enzymes to inhibit hydrolysis and acidification processes. This research provides a basis for understanding and unveils impact mechanisms of the impact of MPs on sludge anaerobic fermentation.

The potential role of GSK-3ß signaling pathway for amelioration actions of ketamine on the PTSD rodent model.

RATIONALE: Post-traumatic stress disorder (PTSD) is a complex, chronic psychiatric disorder typically triggered by life-threatening events and, as yet, lacks a specialized pharmacological treatment. The potential therapeutic role of ketamine, an N-methyl-D-aspartate receptor antagonist, in mitigating PTSD has been the subject of investigation. OBJECTIVE: The aim of this study was to elucidate alterations in the glycogen synthase kinase-3ß (GSK-3ß) signaling pathway in response to ketamine intervention, using the single prolonged stress (SPS) model of PTSD at a molecular level. METHODS: PTSD-like symptoms were simulated using the SPS model. Ketamine (10 mg/kg) and GSK-3ß antagonist SB216763 (5 mg/kg) were then administered intraperitoneally. Stress-related behavior was evaluated through the open field test (OFT) and the elevated plus maze test (EMPT). Additionally, brain activity was analyzed using quantitative electroencephalography (qEEG). Changes in protein and mRNA expressions of glucocorticoid receptor (GR), brain-derived neurotrophic factor (BDNF), GSK-3ß, phosphorylated ser-9 GSK-3ß (p-GSK-3ß), FK506 binding protein 5 (FKBP5), and corticotropin-releasing hormone (CRH) were assessed in the hypothalamus via western blot and qPCR. RESULTS: SPS-exposed rats exhibited reduced distance and time spent in the center of the open arms, a pattern divergent from control rats. qEEG readings revealed SPS-induced increases in alpha power, low gamma and high gamma power. Furthermore, SPS triggered an upregulation in the protein and gene expression of GSK-3ß, GR, BDNF, p-GSK-3ß, and FKBP5, and downregulated CRH expression in the hypothalamus. Ketamine administration following the SPS procedure counteracted these changes by increasing the time spent in the center of the OFT, the distance traversed in the open arms of the EMPT, and mitigating SPS-induced alterations in cerebral cortex oscillations. Moreover, ketamine reduced the protein levels of GSK-3ß, GR, p-GSK-3ß, and altered the ratio of p-GSK-3ß to GSK-3ß. Gene expression of GSK-3ß, GR, BDNF, and FKBP5 decreased in the SPS-Ket group compared to the SPS-Sal group. CONCLUSIONS: Ketamine appeared to remediate the abnormal GSK-3ß signaling pathway induced by SPS. These findings collectively suggest that ketamine could be a promising therapeutic agent for PTSD symptoms, working through the modulation of the GSK-3ß signaling pathway.