Antibiotic resistance genes in constructed wetlands: Driving indicators and risk assessment.

Constructed wetlands (CWs) were responsible for the in-depth purification of wastewater, providing an ideal environment for the transport, acquisition, and dissemination of antibiotic resistance genes (ARGs). A better understanding of influencing factors and risks of ARGs in CWs was deemed indispensable. In this research, the abundance of ARGs and mobile genetic elements (MGEs) was determined to be higher in summer and spring, ranging from 53.7 to 8.51 × 106 and 30.9-6.02 × 106 copies/mL, respectively. Seasonal variation significantly influenced the abundance of ARGs and MGEs, as well as the co-occurrence patterns among ARGs, MGEs and bacteria. However, the environmental gradients, from the influent (CW01) to the effluent (CW10), did not impose significant effects on the abundance of ARGs and MGEs. Furthermore, the ratios of pathogenic bacteria to ARG hosts and ARG risks index decreased by 50.4% and 88.54% along with the environmental gradients, indicating that CWs could act as barriers to the transfer of ARGs. Partial least squares-path modeling (PLSPM) revealed that temperature was the main driving factor of ARGs, followed by MGEs, stable and differential bacteria. This finding effectively and innovatively explored the driving indicators for the variations and risks of ARGs caused by spatial-temporal variations, providing new insights into the evaluation and control of ARGs in CWs.

A comparison between partially peeled hulless barley and whole grain hulless barley: beneficial effects on the regulation of serum glucose and the gut microbiota in high-fat diet-induced obese mice.

Though the hypoglycemic effect of whole grain hulless barley (Hordeum vulgare L.) has been documented, whether glucose metabolism would be improved by hulless barley with moderate peeling is still unclear. The purpose of this study was to compare the differences in glucose metabolism and gut microbiota between partially (10%) peeled hulless barley (PHB) and whole grain hulless barley (WHB) intervention in obese mice induced by a high-fat diet. The results showed that both PHB and WHB interventions significantly improved the impaired glucose tolerance, fat accumulation in fat and liver tissues, and the impaired intestinal barrier in mice. The dysbiosis of gut microbiota was improved and the relative abundance of some beneficial bacteria such as genera Lactobacillus, Bifidobacterium, Ileibacterium, and norank_f__Mutibaculaceae was increased by both, PHB and WHB, interventions. Spearman correlation analysis revealed that the abundance of Bifidobacterium was negatively correlated with the area under the blood glucose curve. In conclusion, our results provide evidence that hulless barley improved the gut microbiota and impaired glucose tolerance in mice, and also showed that there was little loss of hypoglycemic effect even when hulless barley was moderately peeled.

Beneficial Effects of Partly Milled Highland Barley on the Prevention of High-Fat Diet-Induced Glycometabolic Disorder and the Modulation of Gut Microbiota in Mice.

The nutritional functions of highland barley (HB) are superior to those of regular cereals and have attracted increasing attention in recent years. The objective of this study was to investigate whether partly milled highland barley (PHB) can regulate the serum glucose and lipid disorders of mice fed a high-fat diet (HFD) and to further explore their potential gut microbiota modulatory effect. Our results showed that PHB supplementation significantly reduced fasting blood glucose (FBG) and improved oral glucose tolerance. Histological observations confirmed the ability of PHB to alleviate liver and intestine damage. Furthermore, the results of 16S amplicon sequencing revealed that PHB prevented a HFD-induced gut microbiota dysbiosis, enriching some beneficial bacteria, such as Lactobacillus, Bifidobacterium, and Ileibacterium, and reducing several HFD-dependent taxa (norank_f_Desulfovibrionaceae, Blautia, norank_f_Lachnospiraceae, unclassified_f_Lachnospiraceae, and Colidextribacter). In addition, the increase of Lactobacillus and Bifidobacterium presence has a slightly dose-dependent relationship with the amount of the added PHB. Spearman correlation analysis revealed that Lactobacillus and Bifidobacterium were negatively correlated with the blood glucose level of the oral glucose tolerance test. Overall, our results provide important information about the processing of highland barley to retain its hypoglycemic effect and improve its acceptability and biosafety.

[Effect of CGMCC No. 8730 Eurotium cristatum fermented dark tea extract on body weight and blood lipid in two dyslipidemia rat models].

OBJECTIVE: To investigate the effect of the CGMCC No. 8730 Eurotium cristatum fermented dark tea on body weight and blood lipid. METHODS: 1. Egg yolk emulsion rat model 40 male Sprague-Dawley( SD) rats were randomly divided into 5groups, given distilled water or the Eurotium cristatum fermented dark tea extract by intragastric administration for 11 days, then fasted and intraperitoneal injected with distilled water or egg yolk emulsion. The next day rats were taken blood and tested for blood lipid. Body weight were recorded regularly. 2. High-fat diet induced rat model 50 male SD rats were randomly divided into 5 groups fed with normal or 60 kcal% high-fat diet, given distilled water or the Eurotium cristatum fermented dark tea extract byintragastric administration for 9 weeks. Blood lipid was tested at baseline( 1st week) and endpoint( 9th week), and body fat ratio was calculated from perirenal and epididymal fat weight at endpoint. Body weight, food intake and energy intake was weekly recorded. RESULTS: 1. Body weight and serum triglycerides of 2500 mg / kg Eurotium cristatum fermented dark tea extract group were significantly decreased foregg yolk emulsion rat model. 2. Body weight, serum triglycerides, food intake and energy intake of 250 mg / kg and 750 mg / kg Eurotium cristatum fermented dark tea extract group were significantly decreased forhigh-fat diet induced rat model. CONCLUSION: The CGMCC No. 8730 Eurotium cristatum fermented dark tea extract decreases body weight andserum triglycerides for SD rats.

ω-3 fatty acid eicosapentaenoic acid attenuates MPP+-induced neurodegeneration in fully differentiated human SH-SY5Y and primary mesencephalic cells.

Eicosapentaenoic acid (EPA), a neuroactive omega-3 fatty acid, has been demonstrated to exert neuroprotective effects in experimental models of Parkinson's disease (PD), but the cellular mechanisms of protection are unknown. Here, we studied the effects of EPA in fully differentiated human SH-SY5Y cells and primary mesencephalic neurons treated with MPP(+) . In both in-vitro models of PD, EPA attenuated an MPP(+) -induced reduction in cell viability. EPA also prevented the presence of electron-dense cytoplasmic inclusions in SH-SY5Y cells. Then, possible mechanisms of the neuroprotection were studied. In primary neurons, EPA attenuated an MPP(+) -induced increase in Tyrosine-related kinase B (TrkB) receptors. In SH-SY5Y cells, EPA down-regulated reactive oxygen species and nitric oxide. This antioxidant effect of EPA may have been mediated by its inhibition of neuronal NADPH oxidase and cyclo-oxygenase-2 (COX-2), as MPP(+) increased the expression of these enzymes. Furthermore, EPA prevented an increase in cytosolic phospholipase A2 (cPLA2), an enzyme linked with COX-2 in the potentially pro-inflammatory arachidonic acid cascade. Lastly, EPA attenuated an increase in the bax:bcl-2 ratio, and cytochrome c release. However, EPA did not prevent mitochondrial enlargement or a decrease in mitochondrial membrane potential. This study demonstrated cellular mechanisms by which EPA provided neuroprotective effects in experimental PD.

Ethyl-eicosapentaenoate modulates changes in neurochemistry and brain lipids induced by parkinsonian neurotoxin 1-methyl-4-phenylpyridinium in mouse brain slices.

Evidence suggests a link between Parkinson's disease and the dietary intake of omega (n)-3 and n-6 polyunsaturated fatty acids (PUFAs). Presently, we investigated whether an acute dose of parkinsonian neurotoxin 1-methyl-4-phenylpyridinium (MPP(+)) affects brain n-3 and n-6 PUFA content and expression of fatty acid metabolic enzymes cytosolic phospholipase A2 (cPLA2) and cyclooxygenase-2 (COX-2) in brain slices from C57Bl/6 mice. Furthermore, we investigated whether feeding a diet of n-3 PUFA ethyl-eicosapentaenoate (E-EPA) to these mice can attenuate the MPP(+) induced changes in brain PUFA content and expression of cPLA2 and COX-2, and attenuate MPP(+) induced changes in neurotransmitters and metabolites and apoptotic markers, bax, bcl-2 and caspase-3. MPP(+) increased brain content of n-6 PUFAs linoleic acid and arachidonic acid, and increased the mRNA expression of cPLA2. MPP(+) also depleted striatal dopamine levels and increased dopamine turnover, and depleted noradrenaline levels in the frontal cortex. The neurotoxin induced increases in bax, bcl-2 and caspase-3 mRNA expression that approached significance. E-EPA by itself increased brain n-3 content, including EPA and docosapentaenoic acid (C22:5, n-3), and increased cortical dopamine. More importantly, E-EPA attenuated the MPP(+) induced increase in n-6 fatty acids content, partially attenuated the striatal dopaminergic turnover, and prevented the increases of pro-apoptotic bax and caspase-3 mRNAs. In conclusion, increases in n-6 PUFAs in the acute stage of exposure to parkinsonian neurotoxins may promote pro-inflammatory conditions. EPA may provide modest beneficial effects in Parkinson's disease, but further investigation is warranted.