{"title":"Neuropeptide Y receptor Y8b (npy8br) regulates feeding and digestion in Japanese medaka (Oryzias latipes) larvae: evidence from gene knockout","authors":"Xiaodan Jia, Ke Lu, Xu-Fang Liang","doi":"10.1631/jzus.b2300312","DOIUrl":"https://doi.org/10.1631/jzus.b2300312","url":null,"abstract":"","PeriodicalId":17648,"journal":{"name":"Journal of Zhejiang University-SCIENCE B","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141383847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Seizure as the main presenting manifestation of three patients with acute glufosinate-ammonium poisoning","authors":"Ping Wang, Congying Song, Xuan Lu, Yuanqiang Lu","doi":"10.1631/jzus.B2300469","DOIUrl":"https://doi.org/10.1631/jzus.B2300469","url":null,"abstract":"草铵膦作为谷氨酸(Glu)的结构类似物,可以不可逆地抑制植物中谷氨酰胺合成酶(GS)和谷氨酸脱羧酶活性,从而阻止谷氨酰胺(Gln)生成,最终导致植物因氮代谢紊乱和细胞内氨积累而死亡。人误服草胺磷后也会出现相应的中毒症状,包括胃肠道症状和神经毒性。草铵膦作为最常见的致癫痫类除草剂,且无特定解毒剂,因此支持性治疗至关重要。在临床诊治过程中,如何及时有效识别草铵膦除草剂引起的神经毒性并提供适当治疗尤为关键。本文介绍了我院三名草铵膦中毒患者的主要症状,其中癫痫是主要的神经表现。随后,通过查阅相关文献,对草铵膦引发神经毒性的相关机制进行了总结,并讨论了神经毒性的预测和检测方法。","PeriodicalId":17648,"journal":{"name":"Journal of Zhejiang University-SCIENCE B","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140755920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jinru Weng, Shuo Yang, Jinkang Shen, Hongsen Liu, Yuzi Xu, Dongyun Hao, Shan Wang
The original version of this article (Weng et al., 2023) unfortunately contained a mistake. In Acknowledgments, the number (No. 226-2022-00213) of the Fundamental Research Funds for the Central Universities is wrong. The correct number should be No. 2022FZZX01-33.
本文原版（Weng et al.在 "致谢 "中，中央高校基本科研业务费的编号（编号：226-2022-00213）有误。正确的编号应该是 2022FZZX01-33。
{"title":"Erratum to: Molecular dynamics simulation reveals DNA-specific recognition mechanism via c-Myb in pseudo-palindromic consensus of mim-1 promoter","authors":"Jinru Weng, Shuo Yang, Jinkang Shen, Hongsen Liu, Yuzi Xu, Dongyun Hao, Shan Wang","doi":"10.1631/jzus.B22e0634","DOIUrl":"https://doi.org/10.1631/jzus.B22e0634","url":null,"abstract":"The original version of this article (Weng et al., 2023) unfortunately contained a mistake. In Acknowledgments, the number (No. 226-2022-00213) of the Fundamental Research Funds for the Central Universities is wrong. The correct number should be No. 2022FZZX01-33.","PeriodicalId":17648,"journal":{"name":"Journal of Zhejiang University-SCIENCE B","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140762184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zhibin Yan, Ying Shi, Runling Yang, Jijun Xue, Caiyun Fu
肾脏纤维化是各种慢性肾脏疾病发展为终末期肾病的关键过程。目前尚无针对肾纤维化的特异性治疗方法。ELA13(氨基酸序列:RRCMPLHSRVPFP)是ELABELA在所有脊椎动物中的保守片段,目前对其生物学活性的研究 却很少。本研究评估了ELA13对转化生长因子β1(TGF-β1)处理的NRK-52E细胞和单侧输尿管闭塞(UUO)小鼠的作用效果。首先,体外实验表明在TGF-β1诱导的NRK-52E细胞中,ELA13可以降低纤维化标志物I型胶原 (Collagen I)、纤连蛋白(fibronectin)和α-平滑肌肌动蛋白(α-SMA)的表达水平。随后,在UUO诱导的小鼠肾纤维化模型中,我们发现ELA13可以通过降低血清中肌酐和尿素氮的含量来改善肾功能,并通过Masson染色、免疫组 织化学、实时定量聚合酶链式反应(RT-PCR)和蛋白质印迹(western blot)的结果证实纤维化标志物和炎症标志物的表达降低了。进一步机制研究发现,ELA13处理可抑制Smad和细胞外调节蛋白激酶(ERK)信号通路。综上所述,ELA13通过抑制Smad和ERK信号通路发挥抗肾纤维化的作用,有望成为抗肾纤维化治疗的候选分子。 Kidney fibrosis is an inevitable result of various chronic kidney diseases (CKDs) and significantly contributes to end-stage renal failure. Currently, there is no specific treatment available for renal fibrosis. ELA13 (amino acid sequence: RRCMPLHSRVPFP) is a conserved region of ELABELA in all vertebrates; however, its biological activity has been very little studied. In the present study, we evaluated the therapeutic effect of ELA13 on transforming growth factor-β1 (TGF-β1)-treated NRK-52E cells and unilateral ureteral occlusion (UUO) mice. Our results demonstrated that ELA13 could improve renal function by reducing creatinine and urea nitrogen content in serum, and reduce the expression of fibrosis biomarkers confirmed by Masson staining, immunohistochemistry, real-time polymerase chain reaction (RT-PCR), and western blot. Inflammation biomarkers were increased after UUO and decreased by administration of ELA13. Furthermore, we found that the levels of essential molecules in the mothers against decapentaplegic (Smad) and extracellular signal-regulated kinase (ERK) pathways were reduced by ELA13 treatment in vivo and in vitro. In conclusion, ELA13 protected against kidney fibrosis through inhibiting the Smad and ERK signaling pathways and could thus be a promising candidate for anti-renal fibrosis treatment.
{"title":"ELABELA-derived peptide ELA13 attenuates kidney fibrosis by inhibiting the Smad and ERK signaling pathways","authors":"Zhibin Yan, Ying Shi, Runling Yang, Jijun Xue, Caiyun Fu","doi":"10.1631/jzus.B2300033","DOIUrl":"https://doi.org/10.1631/jzus.B2300033","url":null,"abstract":"肾脏纤维化是各种慢性肾脏疾病发展为终末期肾病的关键过程。目前尚无针对肾纤维化的特异性治疗方法。ELA13(氨基酸序列:RRCMPLHSRVPFP)是ELABELA在所有脊椎动物中的保守片段,目前对其生物学活性的研究 却很少。本研究评估了ELA13对转化生长因子β1(TGF-β1)处理的NRK-52E细胞和单侧输尿管闭塞(UUO)小鼠的作用效果。首先,体外实验表明在TGF-β1诱导的NRK-52E细胞中,ELA13可以降低纤维化标志物I型胶原 (Collagen I)、纤连蛋白(fibronectin)和α-平滑肌肌动蛋白(α-SMA)的表达水平。随后,在UUO诱导的小鼠肾纤维化模型中,我们发现ELA13可以通过降低血清中肌酐和尿素氮的含量来改善肾功能,并通过Masson染色、免疫组 织化学、实时定量聚合酶链式反应(RT-PCR)和蛋白质印迹(western blot)的结果证实纤维化标志物和炎症标志物的表达降低了。进一步机制研究发现,ELA13处理可抑制Smad和细胞外调节蛋白激酶(ERK)信号通路。综上所述,ELA13通过抑制Smad和ERK信号通路发挥抗肾纤维化的作用,有望成为抗肾纤维化治疗的候选分子。 Kidney fibrosis is an inevitable result of various chronic kidney diseases (CKDs) and significantly contributes to end-stage renal failure. Currently, there is no specific treatment available for renal fibrosis. ELA13 (amino acid sequence: RRCMPLHSRVPFP) is a conserved region of ELABELA in all vertebrates; however, its biological activity has been very little studied. In the present study, we evaluated the therapeutic effect of ELA13 on transforming growth factor-β1 (TGF-β1)-treated NRK-52E cells and unilateral ureteral occlusion (UUO) mice. Our results demonstrated that ELA13 could improve renal function by reducing creatinine and urea nitrogen content in serum, and reduce the expression of fibrosis biomarkers confirmed by Masson staining, immunohistochemistry, real-time polymerase chain reaction (RT-PCR), and western blot. Inflammation biomarkers were increased after UUO and decreased by administration of ELA13. Furthermore, we found that the levels of essential molecules in the mothers against decapentaplegic (Smad) and extracellular signal-regulated kinase (ERK) pathways were reduced by ELA13 treatment in vivo and in vitro. In conclusion, ELA13 protected against kidney fibrosis through inhibiting the Smad and ERK signaling pathways and could thus be a promising candidate for anti-renal fibrosis treatment.","PeriodicalId":17648,"journal":{"name":"Journal of Zhejiang University-SCIENCE B","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140767535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Defense and anti-defense mechanisms of bacteria and bacteriophages","authors":"Xiaoqing Wang, S. Leptihn","doi":"10.1631/jzus.b2300101","DOIUrl":"https://doi.org/10.1631/jzus.b2300101","url":null,"abstract":"","PeriodicalId":17648,"journal":{"name":"Journal of Zhejiang University-SCIENCE B","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139779456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：