Water pollution caused by organic wastewater has become a serious concern worldwide. Fenton oxidation process is one of the most effective and suitable methods for the abatement of organic ...pollutants. However, the process has three obvious shortcomings: the narrow working pH range, the high costs and risks associated with handling, transportation and storage of reagents (H2O2 and catalyst), the significant iron sludge related second pollution. In order to overcome these shortcomings, various optimized Fenton processes have been widely studied. Therefore, a summary of the study status of Fenton optimization processes is necessary to develop a novel and high efficiency organic wastewater treatment method. Based on the optimization perspective, taking shortcomings of Fenton process as a breakthrough, the fundamentals, advantages and disadvantages of single Fenton optimization processes (heterogeneous Fenton, photo-Fenton and electro-Fenton) for organic wastewater treatment were reviewed and the corresponding reaction mechanism diagrams were drawn in this paper. Then, the feasibility and application of the coupled Fenton optimization processes (photoelectro-Fenton, heterogeneous electro-Fenton, heterogeneous photoelectro-Fenton, three-dimensional electro-Fenton) for organic wastewater treatment were discussed in depth. Additionally, the effect of some important operation parameters (pH and catalyst, H2O2, organic pollutants concentration) on the degradation efficiency of organic pollutants was studied to provide guidance for the optimization of operation parameters. Finally, the possible future research directions for optimized Fenton processes were given. The review aims to assist researchers and engineers to gain fundamental understandings and critical view of Fenton process and its optimization processes, and hopefully with the knowledge it could bring new opportunities for the optimization and future development of Fenton process.
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•Review of single Fenton optimization processes for organic wastewater treatment.•Review of coupled Fenton optimization processes for organic wastewater treatment.•Key operational parameters are discussed.•Insights into future research directions for optimized Fenton processes.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Brassinosteroids (BRs) play essential roles in modulating plant growth, development and stress responses. Here, involvement of BRs in plant systemic resistance to virus was studied. Treatment of ...local leaves in Nicotiana benthamiana with BRs induced virus resistance in upper untreated leaves, accompanied by accumulations of H₂O₂ and NO. Scavenging of H₂O₂ or NO in upper leaves blocked BR‐induced systemic virus resistance. BR‐induced systemic H₂O₂ accumulation was blocked by local pharmacological inhibition of NADPH oxidase or silencing of respiratory burst oxidase homolog gene NbRBOHB, but not by systemic NADPH oxidase inhibition or NbRBOHA silencing. Silencing of the nitrite‐dependent nitrate reductase gene NbNR or systemic pharmacological inhibition of NR compromised BR‐triggered systemic NO accumulation, while local inhibition of NR, silencing of NbNOA1 and inhibition of NOS had little effect. Moreover, we provide evidence that BR‐activated H₂O₂ is required for NO synthesis. Pharmacological scavenging or genetic inhibiting of H₂O₂ generation blocked BR‐induced systemic NO production, but BR‐induced H₂O₂ production was not sensitive to NO scavengers or silencing of NbNR. Systemically applied sodium nitroprusside rescued BR‐induced systemic virus defense in NbRBOHB‐silenced plants, but H₂O₂ did not reverse the effect of NbNR silencing on BR‐induced systemic virus resistance. Finally, we demonstrate that the receptor kinase BRI1(BR insensitive 1) is an upstream component in BR‐mediated systemic defense signaling, as silencing of NbBRI1 compromised the BR‐induced H₂O₂ and NO production associated with systemic virus resistance. Together, our pharmacological and genetic data suggest the existence of a signaling pathway leading to BR‐mediated systemic virus resistance that involves local Respiratory Burst Oxidase Homolog B (RBOHB)‐dependent H₂O₂ production and subsequent systemic NR‐dependent NO generation.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
Systemic resistance is induced by pathogens and confers protection against a broad range of pathogens. Recent studies have indicated that salicylic acid (SA) derivative methyl salicylate (MeSA) ...serves as a long-distance phloem-mobile systemic resistance signal in tobacco, Arabidopsis, and potato. However, other experiments indicate that jasmonic acid (JA) is a critical mobile signal. Here, we present evidence suggesting both MeSA and methyl jasmonate (MeJA) are essential for systemic resistance against Tobacco mosaic virus (TMV), possibly acting as the initiating signals for systemic resistance. Foliar application of JA followed by SA triggered the strongest systemic resistance against TMV. Furthermore, we use a virus-induced gene-silencing-based genetics approach to investigate the function of JA and SA biosynthesis or signaling genes in systemic response against TMV infection. Silencing of SA or JA biosynthetic and signaling genes in Nicotiana benthamiana plants increased susceptibility to TMV. Genetic experiments also proved the irreplaceable roles of MeSA and MeJA in systemic resistance response. Systemic resistance was compromised when SA methyl transferase or JA carboxyl methyltransferase, which are required for MeSA and MeJA formation, respectively, were silenced. Moreover, high-performance liquid chromatography-mass spectrometry analysis indicated that JA and MeJA accumulated in phloem exudates of leaves at early stages and SA and MeSA accumulated at later stages, after TMV infection. Our data also indicated that JA and MeJA could regulate MeSA and SA production. Taken together, our results demonstrate that (Me)JA and (Me)SA are required for systemic resistance response against TMV.
Cardiac macrophage contributes to the development of cardiac fibrosis, but factors that regulate cardiac macrophages transition and activation during this process remains elusive. Here we show, by ...single-cell transcriptomics, lineage tracing and parabiosis, that cardiac macrophages from circulating monocytes preferentially commit to macrophage-to-myofibroblast transition (MMT) under angiotensin II (Ang II)-induced hypertension, with accompanying increased expression of the RNA N6-methyladenosine demethylases, ALKBH5. Meanwhile, macrophage-specific knockout of ALKBH5 inhibits Ang II-induced MMT, and subsequently ameliorates cardiac fibrosis and dysfunction. Mechanistically, RNA immunoprecipitation sequencing identifies interlukin-11 (IL-11) mRNA as a target for ALKBH5-mediated m6A demethylation, leading to increased IL-11 mRNA stability and protein levels. By contrast, overexpression of IL11 in circulating macrophages reverses the phenotype in ALKBH5-deficient mice and macrophage. Lastly, targeted delivery of ALKBH5 or IL-11 receptor α (IL11RA1) siRNA to monocytes/macrophages attenuates MMT and cardiac fibrosis under hypertensive stress. Our results thus suggest that the ALKBH5/IL-11/IL11RA1/MMT axis alters cardiac macrophage and contributes to hypertensive cardiac fibrosis and dysfunction in mice, and thereby identify potential targets for cardiac fibrosis therapy in patients.
This paper presents the behavior of six tests of planar prestressed concrete frames under the loss of a middle column. The six tests consist of two non-prestressed reinforced concrete (RC) specimens ...and four prestressed concrete (PC) specimens with bonded post-tensioning tendons (BPT). The structural response of the specimens with different flexural reinforcement ratio, span-depth ratio, and effective prestress level has been reported. In addition, the impact of parabolic BPT on the behavior of RC frames to resist progressive collapse is also evaluated. Experimental results indicated that the BPT cannot only increase the initial stiffness and yielding load of the RC counterparts, but also increase the ultimate load capacity in the catenary action stage. Moreover, it will impact the load-resisting mechanisms and the failure modes. Contrary to the commonly accepted sequential mobilization of compressive arch action and catenary action to resist progressive collapse of RC frames, no effective compressive arch action is developed in PC frames to mitigate progressive collapse risk. Based on experimental observations, it is found that higher effective prestress in BPT results in enhanced initial stiffness and yielding load but less deformation capacity and ultimate load capacity. It is also found that higher non-prestressed flexural tensile reinforcement ratio could improve the behavior of PC specimens to resist progressive collapse. Keywords: bonded; catenary action; compressive arch action; mechanism; post-tensioning tendon; prestressed concrete; progressive collapse.
This randomised phase III study was conducted to investigate the efficacy of extended nodal irradiation (ENI) and/or erlotinib in inoperable oesophageal squamous cell cancer (ESCC).
Patients with ...histologically confirmed locally advanced ESCC or medically inoperable disease were randomly assigned (ratio 1:1:1:1) to one of four treatment groups: group A, radiotherapy adoption of ENI with two cycles of concurrent TP chemotherapy (paclitaxel 135 mg/m2 day 1 and cisplatin 20 mg/m2 days 1–3, every 4 weeks) plus erlotinib (150 mg per day during chemoradiotherapy); group B, radiotherapy adoption of ENI with two cycles of concurrent TP; group C, radiotherapy adoption of conventional field irradiation (CFI) with two cycles of concurrent TP plus erlotinib; group D, radiotherapy adoption of CFI with two cycles of concurrent TP.
A total of 352 patients (88 assigned to each treatment group) were enrolled. The 2-year overall survival rates of group A, B, C and D were 57.8%, 49.9%, 44.9% and 38.7%, respectively (P = 0.015). Group A significantly improved 2-year overall survival compared with group D. The ENI significantly improved overall survival in patients with inoperable ESCC (P = 0.014). The addition of erlotinib significantly decreased loco-regional recurrence (P = 0.042). Aside from rash and radiation oesophagitis, the incidence of grade 3 or greater toxicities did not differ among 4 groups.
Chemoradiotherapy with ENI and erlotinib might represent a substantial improvement on the standard of care for inoperable ESCC. ENI alone should be adopted in concurrent chemoradiotherapy for ESCC patients.
•Chemotherapy with extended nodal irradiation and erlotinib improve survival for inoperable oesophageal squamous cell cancer.•Chemoradiotherapy with ENI alone can significantly improve 2-year overall survival to 54.0% and reduce 31.2% risk of death.•ENI alone should be adopted in concurrent chemoradiotherapy for inoperable ESCC.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK, ZRSKP
A new metal–organic framework (MOF), Co2(L)2(azpy)n (compound 1, H2L = 5-(pyridin-4-ylmethoxy)-isophthalic acid, azpy = 4,4′-azopyridine), was synthesized by a solvothermal method and further ...characterized by elemental analysis, IR spectra, thermogravimetric analysis, single-crystal and powder X-ray diffraction. The X-ray single-crystal diffraction analysis for compound 1 indicated that two cis L22− ligands connected to two cobalt atoms resulted in a macrocycle structure. Through a series of adsorption tests, we found that compound 1 exhibited a high capacity of CO2, and the adsorption capacity could reach 30.04 cm3/g. More interestingly, under 273 K conditions, the adsorption of CO2 was 41.33 cm3/g. In addition, when the Co-MOF was irradiated by a 730 nm laser, rapid temperature increases for compound 1 were observed (temperature variation in 169 s: 26.6 °C), showing an obvious photothermal conversion performance. The photothermal conversion efficiency reached 20.3%, which might be due to the fact that the parallel arrangement of azo units inhibited non-radiative transition and promoted photothermal conversion. The study provides an efficient strategy for designing MOFs for the adsorption of CO2 and with good photothermal conversion performance.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
Diabetic cardiomyopathy (DCM) causes the myocardium to rely on fatty acid β-oxidation for energy. The accumulation of intracellular lipids and fatty acids in the myocardium usually results in ...lipotoxicity, which impairs myocardial function. Adipsin may play an important protective role in the pathogenesis of DCM. The aim of this study is to investigate the regulatory effect of Adipsin on DCM lipotoxicity and its molecular mechanism.
A high-fat diet (HFD)-induced type 2 diabetes mellitus model was constructed in mice with adipose tissue-specific overexpression of Adipsin (Adipsin-Tg). Liquid chromatography-tandem mass spectrometry (LC-MS/MS), glutathione-S-transferase (GST) pull-down technique, Co-immunoprecipitation (Co-IP) and immunofluorescence colocalization analyses were used to investigate the molecules which can directly interact with Adipsin. The immunocolloidal gold method was also used to detect the interaction between Adipsin and its downstream modulator.
The expression of Adipsin was significantly downregulated in the HFD-induced DCM model (P < 0.05). Adipose tissue-specific overexpression of Adipsin significantly improved cardiac function and alleviated cardiac remodeling in DCM (P < 0.05). Adipsin overexpression also alleviated mitochondrial oxidative phosphorylation function in diabetic stress (P < 0.05). LC-MS/MS analysis, GST pull-down technique and Co-IP studies revealed that interleukin-1 receptor-associated kinase-like 2 (Irak2) was a downstream regulator of Adipsin. Immunofluorescence analysis also revealed that Adipsin was co-localized with Irak2 in cardiomyocytes. Immunocolloidal gold electron microscopy and Western blotting analysis indicated that Adipsin inhibited the mitochondrial translocation of Irak2 in DCM, thus dampening the interaction between Irak2 and prohibitin (Phb)-optic atrophy protein 1 (Opa1) on mitochondria and improving the structural integrity and function of mitochondria (P < 0.05). Interestingly, in the presence of Irak2 knockdown, Adipsin overexpression did not further alleviate myocardial mitochondrial destruction and cardiac dysfunction, suggesting a downstream role of Irak2 in Adipsin-induced responses (P < 0.05). Consistent with these findings, overexpression of Adipsin after Irak2 knockdown did not further reduce the accumulation of lipids and their metabolites in the cardiac myocardium, nor did it enhance the oxidation capacity of cardiomyocytes expose to palmitate (PA) (P < 0.05). These results indicated that Irak2 may be a downstream regulator of Adipsin.
Adipsin improves fatty acid β-oxidation and alleviates mitochondrial injury in DCM. The mechanism is related to Irak2 interaction and inhibition of Irak2 mitochondrial translocation.
Plant steroid hormones, brassinosteroids (BRs), play essential roles in plant growth, development and stress responses. However, mechanisms by which BRs interfere with plant resistance to virus ...remain largely unclear. In this study, we used pharmacological and genetic approaches in combination with infection experiments to investigate the role of BRs in plant defense against Tobacco Mosaic Virus (TMV) in Nicotiana benthamiana. Exogenous applied BRs enhanced plant resistance to virus infection, while application of Bikinin (inhibitor of glycogen synthase kinase-3), which activated BR signaling, increased virus susceptibility. Silencing of NbBRI1 and NbBSK1 blocked BR-induced TMV resistance, and silencing of NbBES1/BZR1 blocked Bikinin-reduced TMV resistance. Silencing of NbMEK2, NbSIPK and NbRBOHB all compromised BR-induced virus resistance and defense-associated genes expression. Furthermore, we found MEK2-SIPK cascade activated while BES1/BZR1 inhibited RBOHB-dependent ROS production, defense gene expression and virus resistance induced by BRs. Thus, our results revealed BR signaling had two opposite effects on viral defense response. On the one hand, BRs enhanced virus resistance through MEK2-SIPK cascade and RBOHB-dependent ROS burst. On the other hand, BES1/BZR1 inhibited RBOHB-dependent ROS production and acted as an important mediator of the trade-off between growth and immunity in BR signaling.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
Hepatocellular carcinoma (HCC) is the most common liver cancer with high mortality. Here, we found that hnRNPU is overexpressed in HCC tissues and is correlated with the poor prognosis of HCC ...patients. Besides, hnRNPU is of high significance in regulating the proliferation, apoptosis, self‐renewal, and tumorigenic potential of HCC cells. Mechanismly, c‐Myc regulates hnRNPU expression at the transcriptional level, and meanwhile, hnRNPU stabilizes the mRNA of c‐MYC. We found that the hnRNPU and c‐Myc regulatory loop exerts a synergistic effect on the proliferation and self‐renewal of HCC, and promotes the HCC progression. Taken together, hnRNPU functions as a novel transcriptional target of c‐Myc and promotes HCC progression, which may become a promising target for the treatment of c‐Myc‐driven HCC.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
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