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Mercury (Hg) is a persistent environmental and industrial pollutant that accumulated in the body and induces oxidative stress and inflammation damage. Selenium (Se) has been reported to antagonize immune organs damage caused by heavy metals. Here, we aimed to investigate the prevent effect of Se on mercuric chloride (HgCl2)‐induced thymus and bursa of Fabricius (BF) damage in chickens. The results showed that HgCl2 caused immunosuppression by reducing the relative weight, cortical area of the thymus and BF, and the number of peripheral blood lymphocytes. Meanwhile, HgCl2 induced oxidative stress and imbalance in cytokines expression in the thymus and BF. Further, we found that thioredoxin‐interacting protein (TXNIP) and the NOD‐like receptor pyrin domain containing 3 (NLRP3) inflammasome mediated HgCl2‐induced oxidative stress and inflammation. Mechanically, the targeting and inhibitory effect of microRNA (miR)‐135b/183 on forkhead box O1 (FOXO1) were an upstream event for HgCl2‐activated TXNIP/NLRP3 inflammasome pathway. Most importantly, Se effectively attenuated the aforementioned damage in the thymus and BF caused by HgCl2 and inhibited the TXNIP/NLRP3 inflammasome pathway by reversing the expression of FOXO1 through inhibiting miR‐135b/183. In conclusion, the miR‐135b/183‐FOXO1/TXNIP/NLRP3 inflammasome axis might be a novel mechanism for Se to antagonize HgCl2‐induced oxidative stress and inflammation in the central immune organs of chickens. [ABSTRACT FROM AUTHOR]

Summary: miRNAs contribute to plant resistance against pathogens. Previously, we found that the function of miR398b in immunity in rice differs from that in Arabidopsis. However, the underlying mechanisms are unclear.In this study, we characterized the mutants of miR398b target genes and demonstrated that multiple superoxide dismutase genes contribute to miR398b‐regulated rice immunity against the blast fungus Magnaporthe oryzae.Out of the four target genes of miR398b, mutations in Cu/Zn‐Superoxidase Dismutase1 (CSD1), CSD2 and Os11g09780 (Superoxide DismutaseX,SODX) led to enhanced resistance to M. oryzae and increased hydrogen peroxide (H2O2) accumulation. By contrast, mutations in Copper Chaperone for Superoxide Dismutase (CCSD) resulted in enhanced susceptibility. Biochemical studies revealed that csd1, csd2 and sodx displayed altered expression of CSDs and other superoxide dismutase (SOD) family members, leading to increased total SOD enzyme activity that positively contributed to higher H2O2 production. By contrast, the ccsd mutant showed CSD protein deletion, resulting in decreased CSD and total SOD enzyme activity.Our results demonstrate the roles of different SODs in miR398b‐regulated resistance to rice blast disease, and uncover an integrative regulatory network in which miR398b boosts total SOD activity to upregulate H2O2 concentration and thereby improve disease resistance. [ABSTRACT FROM AUTHOR]

The cosmopolitan pest Aphis gossypii (Glover) causes considerable economic losses on various crops by its feeding damage and transmitting diseases around the world. Flupyradifurone is a novel butenolide pesticide; its toxicity on A. gossypii parent generation (F0) was estimated following treatment with LC25 concentration for 48 h. The adult longevity and fecundity of the F0 individuals treated by flupyradifurone showed no significant decrease in comparison with the control. Life table method was used to evaluate the sublethal effects on progeny population (F1). Results showed that the development time of the fourth instar and the preadult as well as the total pre-reproductive period were significantly prolonged, while their fecundity was significantly decreased compared with the control. Additionally, the intrinsic rate of increase (r), the finite rate of increase (λ), and the net reproductive rate (R 0) of F1 were all significantly lower in the group treated by LC25 than in the control group. These results reveal that the sublethal concentration of flupyradifurone could suppress the population growth of A. gossypii and indicate that this novel insecticide may be as a useful tool in pest management. [ABSTRACT FROM AUTHOR]

Objective: To investigate the alleviating effect of hydrogen (H 2 ) on homocysteine (Hcy) levels and non alcoholic fatty liver in rats with hyperhomocysteinemia (HHcy). Methods: After one week of adaptive feeding, Wistar rats were randomly divided into three groups: the general diet group (CHOW), the high methionine group (HMD), and the high methionine plus hydrogen rich water group (HMD+HRW), with 8 rats in each group. The CHOW group was fed with AIN-93G feed, while the HMD and HMD+HRW groups were fed with AIN-93G+2% methionine feed to construct an HHcy model. The HMD+HRW group was also gavaged with hydrogen rich water (3 ml/animal, twice a day, with a hydrogen concentration of 0.8 mmol/L), and body weight data were recorded. After 6 weeks of feeding, the plasma and liver samples were processed and collected. The plasma homocysteine (Hcy) and lipid contents of each group were measured, and the histological morphology of the liver was observed. The activities of key enzymes in the Hcy metabolism pathway and mRNA expression were detected in the liver. Results: Compared with the CHOW group rats, the Hcy level in the blood of HMD rats was significantly increased significantly ( P ＜0.05). Pathological tissue sections showed liver enlargement, injury, and fatty liver in the rats; Compared with the HMD group rats, the HMD+HRW group rats showed a significant decrease in Hcy in the blood, reduced liver damage, and increased Hcy metabolism key enzyme activity and mRNA expression in the liver, with statistical differences ( P ＜0.05). Conclusion: Hydrogen has a significant improvement effect on liver injury induced by HMD diet in HHcy rats, possibly by enhancing the three metabolic pathways of Hcy to reduce excessive Hcy in the body, thereby improving liver metabolic function and symptoms of non-alcoholic fatty liver disease.

Objective: To investigate the effects of 36 h total sleep deprivation (TSD) on object working memory by event related potential(ERP). Methods: We used a pre-post-design, sixteen healthy college students (age range: 21-28 years, mean age: 23 years) received object working memory tasks while awake and after 36 hours of TSD and simultaneously recording electroencephalograph (EEG) data while completing 2-back object working memory tasks. ERP data were statistically analyzed using repeated measurements analysis of variance to observe the changes in the working memory-related P2, N2 and P3 components. Results: After 36 h TSD, the latency of N2 waves related to object working memory significantly was prolonged ( P ＜0.05), and the amplitude was decreased, but difference did not reach statistical significance ( P ＞0.05). The latency of P2 was significantly prolonged after TSD ( P ＜0.05). There was no significant difference in the change of latency and amplitude of P3 waves ( P ＞0.05). Conclusion: 36 h of total sleep deprivation affected working memory-related components and impaired object working memory capacity.