An integrated meta-omics approach reveals the different response mechanisms of two anammox bacteria towards fluoroquinolone antibiotics.

The emerging fluoroquinolone antibiotics (FQs) are highly influential in nitrogen removal from livestock wastewater. However, beyond the capability of nitrogen removal, little is known about the molecular mechanisms (e.g., shift of core metabolism and energy allocation) of different anaerobic ammonium-oxidizing bacteria (AnAOB) under continuous FQ stress. This study investigated the effects of ciprofloxacin, ofloxacin and their mixture at concentrations detected in livestock wastewater on two key anammox species in membrane bioreactors. It was found 20 µg/L FQs promoted nitrogen removal efficiency and community stability, and42-51 % of FQs were removed simultaneously. Integrated meta-omics analysis revealed varied gene expression patterns between the two dominant AnAOB, Candidatus Brocadia sapporoensis (B AnAOB) and Candidatus Kuenenia stuttgartiensis (K AnAOB). The nitrogen metabolic processes were bolstered in B AnAOB, while those involved in anammox pathway of K AnAOB were inhibited. This difference was tentatively attributed to the up-regulation of reactive oxygen species scavenger genes (ccp and dxf) and FQ resistance gene (qnrB72) in B AnAOB. Importantly, most enhanced core biosynthesis/metabolism of AnAOB and close cross-feeding with accompanying bacteria were also likely to contribute to their higher levels of biomass yield and metabolism activity under FQ stress. This finding suggests that B AnAOB has the advantage of higher nitrogen metabolism capacity over K AnAOB in livestock wastewater containing FQs, which is helpful for efficient and stable nitrogen removal by the functional anammox species.

Sustainable treatment of nitrate-containing wastewater by an autotrophic hydrogen-oxidizing bacterium.

Bacteria are key denitrifiers in the reduction of nitrate (NO3 --N), which is a contaminant in wastewater treatment plants (WWTPs). They can also produce carbon dioxide (CO2) and nitrous oxide (N2O). In this study, the autotrophic hydrogen-oxidizing bacterium Rhodoblastus sp. TH20 was isolated for sustainable treatment of NO3 --N in wastewater. Efficient removal of NO3 --N and recovery of biomass nitrogen were achieved. Up to 99% of NO3 --N was removed without accumulation of nitrite and N2O, consuming CO2 of 3.25 mol for each mole of NO3 --N removed. The overall removal rate of NO3 --N reached 1.1 mg L-1 h-1 with a biomass content of approximately 0.71 g L-1 within 72 h. TH20 participated in NO3 --N assimilation and aerobic denitrification. Results from 15N-labeled-nitrate test indicated that removed NO3 --N was assimilated into organic nitrogen, showing an assimilation efficiency of 58%. Seventeen amino acids were detected, accounting for 43% of the biomass. Nitrogen loss through aerobic denitrification was only approximately 42% of total nitrogen. This study suggests that TH20 can be applied in WWTP facilities for water purification and production of valuable biomass to mitigate CO2 and N2O emissions.

Protective effect of L-carnitine on myocardial injury in rats with heatstroke.

PURPOSE: To investigate the protective effect of L-carnitine on myocardial injury in rats with heatstroke. METHODS: orty-eight rats were randomly divided into control, heatstroke and 25, 50 and 100 mg/kg L-carnitine groups. The last three groups were treated with 25, 50 and 100 mg/kg L-carnitine, respectively, for seven successive days. Then, except for the control group, the other four groups were transferred into the environment with ambient temperature of (39.5 ± 0.4 °C) and relative humidity of (13.5 ± 2.1%) for 2 h. The core temperature (Tc), mean arterial pressure (MAP), heart rate (HR) and serum and myocardial indexes were detected. RESULTS: Compared with the heatstroke group, in the 100 mg/kg L-carnitine group, the Tc was significantly decreased, the MAP and HR were significantly increased, the serum creatine kinase, lactate dehydrogenase, alkaline phosphatase, aspartate aminotransferase, tumor necrosis factor α and interleukin 1ß levels were significantly decreased, the myocardial superoxide dismutase and glutathione peroxidase levels were significantly increased, the myocardial malondialdehyde level was significantly decreased and the cardiomyocyte apoptosis index and myocardial caspase-3 protein expression level were remarkably decreased (p < 0.05). CONCLUSIONS: The L-carnitine pretreatment can alleviate the myocardial injury in heatstroke rats through reducing the inflammatory response, oxidative stress and cardiomyocyte apoptosis.

Protective effect of L-carnitine on myocardial injury in rats with heatstroke

Abstract Purpose: To investigate the protective effect of L-carnitine on myocardial injury in rats with heatstroke. Methods: orty-eight rats were randomly divided into control, heatstroke and 25, 50 and 100 mg/kg L-carnitine groups. The last three groups were treated with 25, 50 and 100 mg/kg L-carnitine, respectively, for seven successive days. Then, except for the control group, the other four groups were transferred into the environment with ambient temperature of (39.5 ± 0.4 °C) and relative humidity of (13.5 ± 2.1%) for 2 h. The core temperature (Tc), mean arterial pressure (MAP), heart rate (HR) and serum and myocardial indexes were detected. Results: Compared with the heatstroke group, in the 100 mg/kg L-carnitine group, the Tc was significantly decreased, the MAP and HR were significantly increased, the serum creatine kinase, lactate dehydrogenase, alkaline phosphatase, aspartate aminotransferase, tumor necrosis factor α and interleukin 1β levels were significantly decreased, the myocardial superoxide dismutase and glutathione peroxidase levels were significantly increased, the myocardial malondialdehyde level was significantly decreased and the cardiomyocyte apoptosis index and myocardial caspase-3 protein expression level were remarkably decreased (p < 0.05). Conclusions: The L-carnitine pretreatment can alleviate the myocardial injury in heatstroke rats through reducing the inflammatory response, oxidative stress and cardiomyocyte apoptosis.

Wood-based biochar as an excellent activator of peroxydisulfate for Acid Orange 7 decolorization.

Wood-based biochar, as a metal-free heterogeneous activator of peroxydisulfate (PDS), was successfully prepared by pyrolysis of polar sawdust for efficient removal of Acid Orange 7 (AO7). The results demonstrate PDS could be effectively activated by wood-based biochar, and AO7 was rapidly eliminated in a wide range of pH value (3.0-10.0) with AO7 removal achieved ≥ 99.3% after 14 min reaction. The dominant reactive species in the biochar/PDS system were verified via radical quenching tests and electron paramagnetic resonance (EPR) technique. It is speculated that sulfate radicals (SO4•-) and hydroxyl radicals (•OH) were formed on the surface of biochar. Based on the results of X-ray photoelectron spectroscopy (XPS), π-electron density and oxygen-containing functional groups (especially C-OH) on biochar surface were active centers for the catalytic reaction. Recycle experiments of biochar for 4 runs were carried out and the regeneration method of the catalyst was also studied.

Mst1 regulates post-infarction cardiac injury through the JNK-Drp1-mitochondrial fission pathway.

BACKGROUND: Post-infarction cardiac injury is closely associated with cardiac remodeling and heart dysfunction. Mammalian STE20-like kinase 1 (Mst1), a regulator of cellular apoptosis, is involved in cardiac remodeling in post-infarction heart, but the mechanisms remain poorly defined. We aimed to explore the role of Mst1 in regulating chronic post-infarction cardiac injury, with a focus on mitochondrial homoeostasis. METHODS: Wild-type (WT) and Mst1-knockout mice were as the cardiac myocardial infarction model. Cardiac fibrosis, myocardial inflammation response, heart dysfunction and cardiomyocyte death were measured in vivo using immunohistochemistry, immunofluorescence, western blot, qPCR and TUNEL assays. Cardiomyocytes were isolated from WT and Mst1-knockout mice, and a chronic hypoxia model was used to induce damage. Mitochondrial function was determined via JC1 staining, ROS measurement, cyt-c leakage detection and mitochondrial apoptotic pathways analysis. Mitochondrial fission was observed using immunofluorescence. A pathway activator and inhibitor were applied to establish the signaling pathways involved in regulating mitochondrial homeostasis. RESULTS: Our study demonstrated that Mst1 expression was significantly upregulated in the heart post-infarction. Activated Mst1 induced cardiac fibrosis, an excessive inflammatory response, and cardiomyocyte death, whereas the genetic ablation of Mst1 protected the myocardium against chronic post-infarction injury. Function assays showed that upregulation of Mst1 activity contributed to JNK pathway activation, which led to Drp1 migration from the cytoplasm onto the surface of the mitochondria, indicative of mitochondrial fission activation. Excessive mitochondrial fission caused mitochondrial fragmentation, resulting in mitochondrial potential collapse, ROS overproduction, mitochondrial pro-apoptotic leakage into the cytoplasm, and the initiation of caspase-9-mediated mitochondrial apoptosis. By contrast, Mst1 deletion helped to maintain mitochondrial structure and function, sending pro-survival signals to the cardiomyocytes. CONCLUSIONS: Our results identify Mst1 as a malefactor in the development of post-infarction cardiac injury and that it acts through the JNK-Drp1-mitochondrial fission pathway.