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Eutrophication can stimulate the emissions of volatile sulfur compounds (VSCs) accompanied by variations in environmental variables in lakes. However, the effects of eutrophication on VSC emissions from lake sediments as well as the underlying mechanisms remain unclear. In this study, depth gradient sediments at different eutrophication levels and seasons were collected from Lake Taihu to investigate the response of sulfur biotransformation in the sediments to eutrophication based on the analysis of environmental variables, microbial activity, abundance and community structure. H 2 S and CS 2 were the main VSCs produced from the lake sediments, with the production rates of 2.3-7.9 and 1.2-3.9 ng g -1  h -1 in August, respectively, which were higher than those in March, mainly due to the increasing activity and abundance of sulfate-reducing bacteria (SRB) at high temperatures. The VSC production rates from the sediments increased with lake eutrophication level. Higher VSC production rates were detected in surface sediments in eutrophic regions but in deep sediments in oligotrophic regions. Sulfuricurvum, Thiobacillus and Sulfuricella were the main sulfur-oxidizing bacteria (SOB) in the sediments, while Desulfatiglans and Desulfobacca were the predominant SRB. Organic matter, Fe 3+ , NO 3 - -N and total sulfur had significant influences on the microbial communities in the sediments. Partial least squares path modelling showed that the trophic level index could stimulate VSC emissions from lake sediments by influencing the activities and abundances of SOB and SRB. These findings indicated that sediments contributed substantially to VSC emissions from eutrophic lakes, especially surface sediments, and sediment dredging might be an effective way to mitigate VSC emissions from eutrophic lakes., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Algae decay is an important process influencing environmental variables and emissions of volatile sulfur compounds (VSCs) in eutrophic lakes. However, effects of algae decay on VSC emissions from eutrophic lakes as well as fate of algae-derived sulfur remain poorly understood. In this study, simulated algae-sediment systems were used to explore the flow and distribution of sulfur during algae decay. VSCs including hydrogen sulfide (H 2 S), methanethiol (CH 3 SH), carbon disulfide (CS 2 ) and dimethyl sulfide ((CH 3 ) 2 S) were detected during algae decay, which increased with algae biomass and eutrophic levels in lakes. During algae decay, the highest H 2 S, CH 3 SH and (CH 3 ) 2 S emission rates of 10.45, 21.82 and 43.26 μg d -1 occurred in the first 1-2 days, respectively, while the highest CS 2 emission rates were observed between days 8 and 11. The maximum emissions of H 2 S and CS 2 from algae decay were estimated at 0.51 and 0.35 mg m -2 d -1 in Lake Taihu, accounting for 1.57% and 0.69% of the total H 2 S and CS 2 emissions of in situ, respectively. Algae decay could significantly increase the contents of total sulfur and total carbon in sediments by 2.90%-21.11% and 4.23%-45.05%, respectively. The VSC emissions during algae decay could be predicted using the multiple regression models with the contents of total carbon, total nitrogen and sulfur-containing compounds in sediments. Partial least squares path modelling demonstrated that algae decay had a low direct effect on VSC emissions with a strength of 0.06, while it had a significant influence on environmental variables with a strength of 0.63, which could affect VSC emissions with a strength of 0.85, indicating VSC emissions from eutrophic lakes were affected by the environmental variables rather than the direct influence of algae decay. These findings illustrated the mechanisms of VSC emissions during algae decay and provided insights into VSC control and mitigation for eutrophic lakes., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Landfills are the third largest source of anthropogenic CH 4 emissions. Anaerobic oxidation of methane (AOM) activity and communities of methane-oxidizing bacteria were investigated in three informal landfills in this study, namely, BJ, CH and SZ landfills, among which BJ and CH represent traditional anaerobic landfills, while the SZ landfill was subjected to aeration to accelerate waste stabilization. The AOM rates of the investigated landfilled wastes ranged from 3.66 to 23.91 nmol g -1 h -1 . Among the three landfills, the AOM rate was highest in the SZ-1-Top sample, which was closest to the aeration pipe. Among the possible electron acceptors for AOM, including NO 3 - , NO 2 - , SO 4 2- and Fe 3+ , the NO 2 - -N content was the only variable that was positively correlated with the AOM rate. Compared with α-Proteobacteria methanotrophs, γ-Proteobacteria methanotrophs were more abundant in the landfilled waste, especially Methylobacter, which was detected in nearly all samples. Members of the family Methylomirabilaceae, including Candidatus Methylomirabilis, were also detected in the SZ-1 and SZ-2-Bot samples. The relative abundance of the main methanotrophs in the families Methylomonadaceae, Methylococcaceae, Rokubacteriales and Methylomirabilaceae, the genus Methylocystis and the phylum NC10 were all positive correlations with the contents of NO 2 - -N in the landfilled waste samples. Additionally, significantly positive correlations were observed between the AOM rates and the relative abundance of the main methanotrophs except for the family Methylococcaceae. This indicated that aeration could enhance the conversion of nitrogen compounds in the landfilled waste, in which the high contents of NO 2 - -N could stimulate the growth of methanotrophs and increase AOM rate. These findings are helpful for understanding the mechanisms of CH 4 oxidation in landfills and for taking effective measures to mitigate CH 4 emissions from landfills., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Lakes are important methane (CH 4 ) sources to the atmosphere, especially eutrophic lakes with cyanobacterial blooms accompanied by volatile sulfur compound (VSC) emissions. CH 4 oxidation is a key strategy to mitigate CH 4 emission from lakes. In this study, we characterized the fate of CH 4 -derived carbon and active microbial communities in lake sediments with CS 2 used as a typical VSC, based on the investigation of CH 4 and VSC fluxes from Meiliang Bay in Lake Taihu. Stable isotope probing microcosm incubation showed that the efficiency of CH 4 -derived carbon incorporated into organic matter was 21.1% in the sediment with CS 2 existence, which was lower than that without CS 2 (27.3%). SO 4 2- -S was the main product of CS 2 oxidation under aerobic condition, accounting for 59.3-62.7% of the input CS 2 -S. CS 2 and CH 4 coexistence led to a decrease of methanotroph and methylotroph abundances and stimulated the production of extracellular polymeric substances. CS 2 and its metabolites including total sulfur, SO 4 2- and acid volatile sulfur acted as the main drivers influencing the active microbial community structure in the sediments. Compared with α-proteobacteria methanotrophs, γ-proteobacteria methanotrophs Methylomicrobium, Methylomonas, Crenothrix and Methylosarcina were more dominant in the sediments. CH 4 -derived carbon mainly flowed into methylotrophs in the first stage. With CH 4 consumption, more CH 4 -derived carbon flowed into non-methylotrophs. CS 2 could prompt more CH 4 -derived carbon flowing into non-methanotrophs and non-methylotrophs, such as sulfur-metabolizing bacteria. These findings can help elucidate the influence of VSCs on microorganisms and provide insights to carbon fluxes from eutrophic lake systems., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Aerobic methane (CH 4 ) oxidation coupled to denitrification (AME-D) can not only mitigate CH 4 emission into the atmosphere, but also potentially alleviate nitrogen pollution in surface waters and engineered ecosystems, and it has attracted substantial research interest. O 2 concentration plays a key role in AME-D, yet little is understood about how it impacts microbial interactions. Here, we applied isotopically labeled K 15 NO 3 and 13 CH 4 and metagenomic analyses to investigate the metabolic and microbial link of AME-D at different O 2 levels. Among the four experimental O 2 levels of 21%,10%, 5% and 2.5% and a CH 4 concentration of 8% (i.e., the O 2 /CH 4 ratios of 2.62, 1.26, 0.63 and 0.31), the highest NO 3 - -N removal occurred in the AME-D system incubated at the O 2 concentration of 10%. Methanol and acetate may serve as the trophic linkage between aerobic methanotrophs and denitrifers in the AME-D systems. Methylotrophs including Methylophilus, Methylovorus, Methyloversatilis and Methylotenera were abundant under the O 2 -sufficient condition with the O 2 concentration of 21%, while denitrifiers such as Azoarcus, Thauera and Thiobacillus dominated in the O 2 -limited environment with the O 2 concentration of 10%. The competition of denitrifiers and methylotrophs in the AME-D system for CH 4 -derived carbon, such as methanol and acetate, might be influenced by chemotactic responses. More methane-derived carbon flowed into methylotrophs under the O 2 -sufficient condition, while more methane-derived carbon was used for denitrification in the O 2 -limited environment. These findings can aid in evaluating the distribution and contribution of AME-D and in developing strategies for mitigating CH 4 emission and nitrogen pollution in natural and engineered ecosystems., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Topographical structures and bioactive surface coatings are effective in improving the biological function for bone regeneration. However, the simultaneous introduction of these benefits into three-dimensional (3D) porous scaffolds poses a daunting challenge. In this study, we proposed a simple yet effective approach to decorate 3D-printed polylactic acid (PLA) scaffolds with chemically modified nanotopographical patterns. The nanotopography was produced by etching the amorphous phase of PLA in an alcohol/alkali solution to expose dense lamellae. Subsequently, conformal decoration of polydopamine (PDA) was realized via self-assembly of catecholamines without changing the surface nanotopography. In vitro cell experiments including live and dead staining, cell morphology, cell growth, and alkaline phosphatase showed that the combination of nanotopography and PDA-coating led to a favorable enhancement of osteoblasts adhesion, spread and proliferation in 3D-printed scaffolds. The contribution of integrated patterns to bone regeneration was evaluated using a rat femur critical-sized defect model in vivo. Micro-CT evaluation and histological analysis demonstrated that the scaffold decorated with integrated pattens promoted osteogenesis more than the bare scaffolds and the scaffolds decorated with only nanotopography. Our proposed approach offers a promising method for improving bioactivity of 3D polymer scaffolds for bone tissue regeneration., (Copyright © 2020. Published by Elsevier B.V.)

Objective: Thoracic aortic dissection (TAD) is associated with matrix changes, biochemical changes, and inflammatory markers like interleukin-1 beta (IL-1β). However, the exact mechanism remains unknown. This study aimed to investigate the role of IL-1β, matrix metalloproteinase (MMP)-2, MMP-9, smooth muscle cell apoptosis, and elastic fibre fracture in the development of TAD in a rat model., Methods: The TAD rat model was induced by β-aminopropionitrile (BAPN). TAD was investigated in 112 male Sprague-Dawley rats, which were equally divided into four groups of 28 rats (Control, BAPN, BAPN + IL-1β, and BAPN + IL-1β antibody). Systolic blood pressure, survival, and the development of TAD were measured after six weeks. Expression of IL-1β, MMP-2, and MMP-9 was measured by Western blot. Apoptosis, aortic elastin concentration, and biomechanical characteristics were measured by the TdT mediated dUTP nick end labelling assay, Victoria blue staining, and in vitro testing., Results: During six weeks, the mortality was 0% (0/28) in the control group, 53.6% (15/28) in the BAPN group (p < .001 compared with the control group), 75.0% (21/28) in the BAPN + IL-1β group (p = .007 compared with the BAPN group), and 35.7% (10/28) in the BAPN + IL-1β antibody group (p = .023 compared with BAPN group and p < .001 compared with the BAPN + IL-1β group). IL-1β treatment deteriorates BAPN induced mortality and aneurysm expansion, which were attenuated by anti-IL-1β treatment. In BAPN + IL-1β group, stress and strain parameters were decreased by 13.5%-53.5% and elastin content was decreased by 14%, and IL-1β, MMP-2, and MMP-9 were expressed higher by 117%, 108%, and 75% when compared with the rats in the BAPN group. Contrarily, in the BAPN + IL-1β antibody group, the above changes could be completely (strain, elastin content, and expression of MMP-2) or partly (elasticity modulus, stress, and expression of MMP-9) blocked by anti-IL-1β treatment., Conclusion: IL-1β plays a critical role in TAD formation by altering the expression of MMP-2 and MMP-9, degrading the aortic wall matrix, causing elastic fibre rupture, and changing the stress or strain of the aortic wall. Anti-IL-1β reduces the later effects and could be one of the molecular targets for prognosis and drug treatment of TAD in the future., (Copyright © 2020 European Society for Vascular Surgery. Published by Elsevier B.V. All rights reserved.)

Trigeminal neuralgia is characterized by extensive spreading of pain, referred to as ectopic pain, which describes the phenomenon of the pain passing from the injured regions to uninjured regions. Patients with orofacial pain often show no response to commonly used analgesics, and the exact mechanism of ectopic pain remains unclear, which restricts the development of specific drugs. The present review aims to summarize the contribution of the two families of transmembrane proteins, connexins (Cxs) and pannexins (Panxs), to the induction and spreading of orofacial pain and to provide potential targets for orofacial pain treatment. Cxs and Panxs have recently been shown to play essential roles in intercellular signal propagation in sensory ganglia, and previous studies have provided evidence for the contribution of several subtypes of Cxs and Panxs in various orofacial pain models. Upregulation of the expression of Cxs and Panxs in the trigeminal ganglia is observed in most cases after trigeminal injury, and regulating their expression or activity can improve pain-like behaviors in animals. It is speculated that after trigeminal injury, pain-related signals are transmitted to adjacent neurons and satellite glial cells in the trigeminal ganglia directly through gap junctions and simultaneously through hemichannels and pannexons through both autocrine and paracrine mechanisms. This review highlights recent discoveries in the regulation of Cxs and Panxs in different orofacial pain models and presents a hypothetical mechanism of ectopic pain in trigeminal neuralgia. In addition, the existing problems in current research are discussed., Competing Interests: Declaration of competing interest All authors claim that there is no conflict of interest., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Chemotherapy-induced peripheral neuropathy (CIPN) is a common adverse side effect of many antineoplastic agents. Patients treated with chemotherapy often report pain and paresthesias in a "glove-and-stocking" distribution. Diverse mechanisms contribute to the development and maintenance of CIPN. However, the role of spinal microglia in CIPN is not completely understood. In this study, cisplatin-treated mice displayed persistent mechanical allodynia, sensory deficits and decreased density of intraepidermal nerve fibers (IENFs). In the spinal cord, activation of microglia, but not astrocyte, was persistently observed until week five after the first cisplatin injection. Additionally, mRNA levels of inflammation related molecules including IL-1β, IL-6, tumor necrosis factor (TNF)-α, inducible nitric oxide synthase (iNOS) and CD16, were increased after cisplatin treatment. Intraperitoneal (i.p.) or intrathecal (i.t.) injection with minocycline both alleviated cisplatin-induced mechanical allodynia and sensory deficits, and prevented IENFs loss. Furthermore, cisplatin enhanced triggering receptor expressed on myeloid cells 2 (TREM2) /DNAX-activating protein of 12 kDa (DAP12) signaling in the spinal cord microglia. The blockage of TREM2 by i.t. injecting anti-TREM2 neutralizing antibody significantly attenuated cisplatin-induced mechanical allodynia, sensory deficits and IENFs loss. Meanwhile, anti-TREM2 neutralizing antibody prominently suppressed the spinal IL-6, TNF-α, iNOS and CD16 mRNA level, but it dramatically up-regulated the anti-inflammatory cytokines IL-4 and IL-10. The data demonstrated that cisplatin triggered persistent activation of spinal cord microglia through strengthening TREM2/DAP12 signaling, which further resulted in CIPN. Functional blockage of TREM2 or inhibition of microglia both benefited for cisplatin-induced peripheral neuropathy. Microglial TREM2/DAP12 may serve as a potential target for CIPN intervention., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Lanthanum (La) is an important rare earth element in the ecological environment of plant. The proteins on the plasma membrane control the transport of molecules into and out of cell. It is very important to investigate the effect of La(III) on the proteins on the plasma membrane in the plant cell. In the present work, the interaction between La(III) and proteins on the plasma membrane of horseradish was investigated using optimization of the fluorescence microscopy and fluorescence spectroscopy. It is found that the fluorescence of the complex system of protoplasts and 1-aniline Kenai-8-sulfonic acid in horseradish treated with the low concentration of La(III) is increased compared with that of the control horseradish. The opposite effect is observed in horseradish treated with the high concentration of La(III). These results indicated that the low concentration of La(III) can interact with the proteins on the plasma membrane of horseradish, causing the improvement in the structure of proteins on the plasma membrane. The high concentration of La(III) can also interact with the proteins on the plasma membrane of horseradish, leading to the destruction of the structure of proteins on the plasma membrane. We demonstrate that the proteins on the plasma membrane are the targets of La(III) action on plant cell., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Tetanic stimulation of the sciatic nerve (TSS) produces long-term potentiation (LTP) of C-fiber-evoked field potentials in the spinal cord. This potentiation is considered to be a substrate for long-lasting sensitization in the spinal pain pathway. Because microglia have previously been shown to regulate the induction of spinal LTP, we hypothesize that P2X7 receptors (P2X7R), which are predominantly expressed in microglia and participate in the communication between microglia and neurons, may play a role in this induction. This study investigated the potential roles of P2X7Rs in spinal LTP and persistent pain induced by TSS in rats. OxATP or BBG, a P2X7R antagonist, prevented the induction of spinal LTP both in vivo and in spinal cord slices in vitro and alleviated mechanical allodynia. Down-regulation of P2X7Rs with P2X7-siRNA blocked the induction of spinal LTP and inhibited mechanical allodynia. Double immunofluorescence showed colocalization of P2X7Rs with the microglial marker OX-42, but not with the astrocytic marker GFAP or the neuronal marker NeuN. Intrathecal injection of BBG suppressed the up-regulation of microglial P2X7Rs and increased expression of Fos in the spinal superficial dorsal horn. Further, pre-administration of BBG inhibited increased expression of the microglial marker Iba-1, phosphorylated p38 (p-p38), interleukin 1β (IL-1β) and GluR1 following TSS. Pre-administration of the IL-1 receptor antagonist (IL-1ra) blocked both the induction of spinal LTP and the up-regulation of GluR1. These results suggest that microglial P2X7Rs and its downstream signaling pathways play a pivotal role in the induction of spinal LTP and persistent pain induced by TSS., (Copyright © 2010 Elsevier Inc. All rights reserved.)