Analysis on the causes of massive stranding of Yellow Sea green tide on Lianyungang and Rizhao coasts in 2022

In 2022,Yellow Sea green tide caused by Ulva prolifera reached a historic minimum and the coastal areas of Shandong Peninsula were less affected.However,the largest amount of seaweed biomass has been washed ashore on Lianyungang and Rizhao coasts since 2015.We studied the development pattern of Yellow Sea green tide in 2022,and analyzed the key environmental factors on the growth and drifting,then discussed the possible reasons that resulted in the massive stranding of green tide biomass in Lianyungang and Rizhao.Results show under the combined influence of the east to southeast winds and currents with shoreward anomalies,green tide drifted to the coastal waters between Shandong and Jiangsu provinces and the distribution areas located westward compared with previous years(2008–2021).Floating U.prolifera rafts from the coastal waters of Binhai and Sheyang drifted continuously into the coastal waters of Lianyungang and Rizhao,providing important supplements for Yellow Sea green tide.Because green tide in 2022 distributed close to the coastal waters,the abundant nutrients might support their continuous high growth rate.In addition,the amount of rainfall around Shandong Peninsula from late June to early July were significantly higher than in previous years,which might promote the development of green tide to some extent.

Argonaute protein as a linker to command center of physiological processes

MicroRNAs （miRNAs） post-transcriptionally regulate gene expression by binding to target mRNAs with perfect or imperfect complementarity, recruiting an Argonaute （AGO） protein complex that usually results in degradation or translational repression of the target mRNA. AGO proteins function as the Slicer enzyme in miRNA and small interfering RNA （siRNA） pathways involved in human physiological and pathophysiological processes, such as antiviral responses and disease formation. Although the past decade has witnessed rapid advancement in studies of AGO protein functions, to further elucidate the molecular mechanism of AGO proteins in cellular function and biochemical process is really a challenging area for researchers. In order to understand the molecular causes underlying the pathological processes, we mainly focus on five fundamental problems of AGO proteins, including evolution, functional domain, subcellular location, post-translational modification and protein-protein interactions. Our discussion highlight their roles in early diagnosis, disease prevention, drug target identification, drug response, etc.

A novel mechanism of inhibiting in-stent restenosis with arsenic trioxide drug-eluting stent: Enhancing contractile phenotype of vascular smooth muscle cells via YAP pathway

Objective:Arsenic trioxide(ATO or As2O3)has beneficial effects on suppressing neointimal hyperplasia and restenosis,but the mechanism is still unclear.The goal of this study is to further understand the mechanism of ATO's inhibitory effect on vascular smooth muscle cells(VSMCs).Methods and results:Through in vitro cell culture and in vivo stent implanting into the carotid arteries of rabbit,a synthetic-to-contractile phenotypic transition was induced and the proliferation of VSMCs was inhibited by ATO.F-actin filaments were clustered and the elasticity modulus was increased within the phenotypic modulation of VSMCs induced by ATO in vitro.Meanwhile,Yes-associated protein(YAP)nuclear translocation was inhibited by ATO both in vivo and in vitro.It was found that ROCK inhibitor or YAP inactivator could partially mask the phenotype modulation of ATO on VSMCs.Conclusions:The interaction of YAP with the ROCK pathway through ATO seems to mediate the contractile phenotype of VSMCs.This provides an indication of the clinical therapeutic mechanism for the beneficial bioactive effect of ATO-drug eluting stent(AES)on in-stent restenosis(ISR).

Corrigendum to“A novel mechanism of inhibiting in-stent restenosis with arsenic trioxide drug-eluting stent:Enhancing contractile phenotype of vascular smooth muscle cells via YAP pathway”[Bioact.Mater.62(February 2021)375-385]

The authors regret the publication of incorrect fund numbers in the acknowledgment section of the article.The number“cstc2019jcyj-zdxm0033”has been updated as“cstc2019jcyj-zdxmX0028”.The corrected acknowledgment section is as follows:This study was supported in part by grants from the National Natural Science Foundation,China(31971242,31701275),the Natural Science Foundation of Chongqing,China(cstc2020jcjy-msxmX0189),the Chongqing Research Program of Basic Research and Frontier Technology,China(cstc2019jcjy-dxmX0028),Open Fund for Key Laboratory of Biorheological Science and Technology,Ministry of Education,China(CQKLBST-2019-010),Innovation Talent Project of 2020 for Chongqing Primary and secondary School,China(CY200405)and the National Key R&D Program,China(2016YFC1102305).The support from the Chongqing Engineering Laboratory in Vascular Implants,China,the Public Experiment Centre of State Bioindustrial Base(Chongqing)and the National“111 Plan”,China(B06023)are gratefully acknowledged.