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Field-Free Spin-Orbit Torque Switching in Synthetic Ferro and Antiferromagents with Exchange Field Gradient (Adv. Funct. Exchange field gradients, field-free switching, spin-orbit torque, synthetic antiferromagnets Keywords: exchange field gradients; field-free switching; spin-orbit torque; synthetic antiferromagnets EN exchange field gradients field-free switching spin-orbit torque synthetic antiferromagnets 1 1 1 04/20/23 20230418 NES 230418 B Field-Free Switching b In article number 2211953, Tiejun Zhou, Wenjun Li, and co-workers report that field-free switching and high spin-orbit torque efficiency are simultaneously achieved through the introduction of exchange field gradient into perpendicularly magnetized synthetic ferro- and antiferromagnets. [Extracted from the article]

Layered photocatalytic M1/3TiNbO5 (M: Fe, Ce) is prepared by ion-exchange of KTiNbO5 with 2 M M(NO3)3 (96 h). [ABSTRACT FROM AUTHOR]

Dispersion state of inorganic nanoparticles (NPs) in the composite films may significantly influence on the film properties. In the present study, polymer/SiO 2 nanocomposite particles (NCPs) with various SiO 2 grafting states (various grafting ratios, various linking patterns between SiO 2 NPs, and various types of grafted chains), were prepared through in situ emulsion or in situ miniemulsion technique. These NCPs were used as building blocks to prepare composite films. The microscopic observations and surface composition analyses of the composite films manifest that the spatial distribution of SiO 2 NPs in the composite films depends on the baking temperature, SiO 2 grafting state, and the compatibility between SiO 2 NPs and polymer matrix. The SiO 2 NPs might display a cluster-like distribution, homogenous one, or locally aggregated one. The results from this study demonstrate how the grafting state of inorganic NPs is effective in controlling dispersion state of inorganic NPs and further determining the properties of composite films. [ABSTRACT FROM AUTHOR]

Plant terpene synthase genes ( TPSs) have roles in diverse biological processes. Here, we report the functional characterization of one member of the soybean TPS gene family, which was designated Gm AFS. Recombinant Gm AFS produced in Escherichia coli catalysed the formation of a sesquiterpene ( E,E)-α-farnesene. Gm AFS is closely related to ( E,E)-α-farnesene synthase gene from apple, both phylogenetically and structurally. Gm AFS was further investigated for its biological role in defence against nematodes and insects. Soybean cyst nematode ( SCN) is the most important pathogen of soybean. The expression of Gm AFS in a SCN-resistant soybean was significantly induced by SCN infection compared with the control, whereas its expression in a SCN-susceptible soybean was not changed by SCN infection. Transgenic hairy roots overexpressing Gm AFS under the control of the Ca MV 35S promoter were generated in an SCN-susceptible soybean line. The transgenic lines showed significantly higher resistance to SCN, which indicates that Gm AFS contributes to the resistance of soybean to SCN. In soybean leaves, the expression of Gm AFS was found to be induced by Tetranychus urticae (two-spotted spider mites). Exogenous application of methyl jasmonate to soybean plants also induced the expression of Gm AFS in leaves. Using headspace collection combined with gas chromatography-mass spectrometry analysis, soybean plants that were infested with T. urticae were shown to emit a mixture of volatiles with ( E,E)-α-farnesene as one of the most abundant constituents. In summary, this study showed that Gm AFS has defence roles in both below-ground and above-ground organs of soybean against nematodes and insects, respectively. [ABSTRACT FROM AUTHOR]

CeO 2 nanowires were synthesized using a facile hydrothermal process without any surfactant, and their morphological, structural and gas sensing properties were systematically investigated. The CeO 2 nanowires with an average diameter of 12.5 nm had a face-centered cubic fluorite structure and grew along [111] of CeO 2 . At the room temperature of 25 °C, hydrogen sulfide (H 2 S) gas sensor based on the CeO 2 nanowires showed excellent sensitivity, low detection limit (50 ppb), and short response and recovery time (24 s and 15 s for 50 ppb H 2 S, respectively). [ABSTRACT FROM AUTHOR]

Ambient air pollution is one of the most serious public health problems over the last decade. It causes about 4.2 million deaths worldwide each year, and fine particulate matter (PM2.5) is one of the major components of air pollution. Many chronic non-communicable diseases may originate from the early-life environment that alters the development of offspring. Pregnancy and lactation are plastic "window periods" for offspring metabolism, during which PM 2.5 exposure is associated with long-term metabolic dysfunction in offspring. In this review, we summarized the scientific evidence from both epidemiological and toxicological studies, which suggest that perinatal exposure to PM 2.5 causes obesity and metabolic diseases in progeny, including hypertension, cardiometabolic dysfunction, diabetes, and non-alcoholic fatty liver disease (NAFLD). Therefore, prevention strategies are needed to inform government policies and clinical counseling to reduce maternal exposure and its associated health hazards, and ultimately improve the quality of the newborn population. Schematic diagram of the scientific evidence from epidemiological studies and animal models on obesity and long-term metabolic diseases in children following prenatal or perinatal exposure to fine particulate matter (PM 2.5), and potential mechanisms of action. The image was created at BioRender.com. [Display omitted] [ABSTRACT FROM AUTHOR]

• The SOT efficiency and field-free switching are enhanced by the presence of the in-situ field, in perpendicularly coupled Pt/Co and CoFeB bilayers sandwiched by an ultrathin PtMn/Ta layer. • Quantitative characterization indicates that the damping-like field, H DL , is boosted by an amount of up to 45%. • The tilted spin texture at the Co/PtMn interface caused by the presence of the in-situ field may play a role on the enhancement of SOT efficiency and field-free switching. Field-free switching of perpendicular magnetization and improvement of spin-orbit torque (SOT) efficiency are the keys for SOT-based devices towards ultrafast and low-power memory and computing applications. In this letter, we investigated pulse current induced magnetization switching and its efficiency in perpendicularly coupled Pt/Co and CoFeB bilayers sandwiched by an ultrathin PtMn/Ta layer, prepared in the presence/absence of an in-plane in-situ field. It is found that both the SOT efficiency and field-free switching are enhanced by the presence of the in-situ field. Quantitative characterization indicates that the damping-like field, H DL , is boosted by an amount of up to 45%. The tilted spin texture at the Co/PtMn interface caused by the presence of the in-situ field may play a role on the enhancement of SOT efficiency and field-free switching. Our findings not only provide a promising approach for SOT efficiency enhancement but also offer a possible layer stack for the integration of a full magnetic tunnel junction (MTJ) for low power memory and computing. [ABSTRACT FROM AUTHOR]

Manganese (Mn) is an important micronutrient that is not readily available to pathogens during infection. Hosts resist the invasion of pathogens through nutritional immunity and oxidative stress. To overcome this nutrient restriction, bacteria utilize high affinity transporters to compete with nutrient-binding proteins (e.g., calprotectin). Little is known about the role of Mn in the pathophysiology of Streptococcus suis. Here, we revealed that the tolerance of S. suis to calprotectin and oxidative stress was associated with Mn. Inactivation of Mn uptake system, TroABCD, in S. suis decreased the tolerance to calprotectin and oxidative stress. Furthermore, Mn uptake system mutant strains reduced capacity for bacterial cellular survival, and attenuated virulence in a mouse model. To explore the regulatory mechanism, we determined the transcriptional start site of troABCD using capping rapid amplification of cDNA ends. Furthermore, we revealed that TroR was a transcriptional regulatory repressor of troABCD. In the absence of troR , transcription levels of troA , troB , troC , and troD were not inhibited by low or high Mn levels, and intracellular Mn contents of mutant strains were higher than that of the wild-type strain. Finally, we used electrophoretic mobility shift assay to demonstrate that TroR bound the promoter region of troABCD. Collectively, this study revealed that Mn acquisition was essential for pathogenesis of S. suis and Mn uptake systems should be targets for the development of new antimicrobials. • Manganese is an important micronutrient for Streptococcus suis resistance to oxidative stress. • TroABCD manganese import system plays an important role in oxidative stress and virulence of Streptococcus suis. • TroR was a transcriptional regulatory repressor of troABCD and regulated troABCD directly. [ABSTRACT FROM AUTHOR]

Objective. To investigate the role and possible mechanism of α-Klotho in the calcification and the osteogenic transition of cultured VSMCs. Methods. VSMCs were cultured in vitro and divided into 5 groups, each using a different medium: (1) control; (2) β-GP; (3) β-GP + Klotho; (4) β-GP + LiCl; (5) β-GP + Klotho + LiCl. Calcium deposits were visualized using Alizarin Red S staining. The calcium concentrations were determined by the o-cresolphthalein complexone method. BMP2, Runx2 and β-catenin levels were estimated by western blotting, and the level of α-SMA was determined by using immunofluorescence at day 12. Results. β-GP induced an increase in the expression of BMP2, Runx2, and β-catenin. The calcium content increased, and the expression of α-SMA decreased. Alizarin Red S staining was positive under the high phosphorus conditions. BMP2, Runx2, and β-catenin levels and the calcium content decreased when the cells were cultured with rmKlotho; however, the levels of each were upregulated after treatment with the LiCl. Conclusions. Klotho can ameliorate the calcification and osteogenic transition of VSMCs induced by β-GP. The mechanism of Klotho in preventing calcification in VSMCs may be partially mediated by the inhibition of the Wnt/β-catenin signaling pathway. [ABSTRACT FROM AUTHOR]

Background/Aims: Cisplatin is widely used to treat malignancies. However, its major limitation is the development of dose-dependent nephrotoxicity. The precise mechanisms of cisplatin-induced kidney damage remain unclear. Previous study demonstrated the central role of mitochondrial ROS (mtROS) in the pathogenesis of cisplatin nephrotoxicity. The purpose of this study was to explore the mechanism of mtROS regulation in cisplatin nephrotoxicity. Methods: p53, MnSOD and p66shc were detected at mRNA and protein levels by qPCR and western blot in HK2 cells. mtROS levels were determined by DCFDA and MitoSOX staining. Cell viability and cell apoptosis were accessed by CCK-8 assay, TUNEL assay and flow cytometry, respectivesly. siRNAs were used to knock down p53 and p66shc expression and subsequent changes were observed. In vivo assays using a mouse model of cisplatin-induced acute kidney injury were used to validate the in vitro results. Results: In HK2 cells, cisplatin exposure decreased the MnSOD and increased the expression of p53 and p66shc. MnTBAP, a MnSOD mimic, blocked cisplatin-induced the generation of mtROS and cell injury. P66shc and p53 siRNAs rendered renal cells resistant to cisplatin-induced mtROS production and cell death. Furthermore, knockdown of p53 restored MnSOD and inhibiting p66shc. Consistent with these results, we revealed that p53 inhibitor reduced cisplatin-induced oxidative stress and apoptosis by regulating MnSOD and p66shc in the kidney of cisplatin-treated mice. Conclusion: Our study identifies activation of p53 signalling as a potential strategy for reducing the nephrotoxicity associated with cisplatin treatments and, as a result, broadens the therapeutic window of this chemotherapeutic agent. © 2015 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Methyl jasmonate (Me JA) elicits stomatal closure in many plant species. Stomatal closure is accompanied by large ion fluxes across the plasma membrane ( PM). Here, we recorded the transmembrane ion fluxes of H+, Ca2+ and K+ in guard cells of wild-type (Col-0) Arabidopsis, the CORONATINE INSENSITIVE1 ( COI1) mutant coi1-1 and the PM H+- ATPase mutants aha1-6 and aha1-7, using a non-invasive micro-test technique. We showed that Me JA induced transmembrane H+ efflux, Ca2+ influx and K+ efflux across the PM of Col-0 guard cells. However, this ion transport was abolished in coi1-1 guard cells, suggesting that Me JA-induced transmembrane ion flux requires COI1. Furthermore, the H+ efflux and Ca2+ influx in Col-0 guard cells was impaired by vanadate pre-treatment or PM H+- ATPase mutation, suggesting that the rapid H+ efflux mediated by PM H+- ATPases could function upstream of the Ca2+ flux. After the rapid H+ efflux, the Col-0 guard cells had a longer oscillation period than before Me JA treatment, indicating that the activity of the PM H+- ATPase was reduced. Finally, the elevation of cytosolic Ca2+ concentration and the depolarized PM drive the efflux of K+ from the cell, resulting in loss of turgor and closure of the stomata. [ABSTRACT FROM AUTHOR]

Exposure to Di (2-ethylhexyl) phthalate (DEHP) has been associated with toxic effects of the reproductive system. However, the exact mechanism remains to be elucidated. In this study we explored the testicular toxicity induced by DEHP, and the probable molecular mechanism in the process. In vivo, the results demonstrated that DEHP affected testosterone levels and blood-testosterone barrier (BTB) integrity and caused ferroptosis. We further demonstrated that DEHP up-regulated the expression of p38α, p-p38α, p53, p-p53, SAT1, ALOX15. This view has also been confirmed in TM4 cells. After pre-treatment with fer-1 or si-MAPK14, the expression of either p53, p-p53, SAT1 and ALOX15 up-regulated by MEHP was inhibited in vitro. Interestingly, p38α can prevent the accumulation of lipid ROS, and the production of lipid ROS in turn promoted the expression of p38α, thus forming a feedback loop during the ferroptosis. In this process, a vicious cycle consisting of p38α, p53, SAT1, ALOX15, lipid ROS was involved. This study provides new mechanistic insights into DEHP-induced toxicity of the reproductive system. [ABSTRACT FROM AUTHOR]

A variety of polyethylene glycol-400-functionalized dicationic acidic ionic liquids (ILs) (PEG-DAILs) were synthesized and tested in the dehydration of fructose. Among these catalysts, hydrogen sulfate anion-based ILs showed the higher catalytic performance in the conversion of fructose. The highest HMF yield of 96.5 % with 100 % consumption of fructose were obtained after 60 min at 110 °C. The effects of catalyst concentration, reaction time, reaction temperature, and solvents were systematically investigated. In addition, the generality of the catalysts was examined by processing inulin and sucrose to HMF with yield of 71.9 and 52.1 % under certain conditions, respectively. PEG-DAILs possess modified physicochemical properties such as low viscosity, strong hydrophilicity and hydrogen bonding with sugars so as to improve activity for the dehydration of fructose into HMF. The used IL catalyst could be separated and recycled repeatedly without significant loss of catalytic activity. The research emphasizes preparation of the novel catalysts combining polymers with functionalized ILs for conversion of renewable biomass. Graphical abstract: [Figure not available: see fulltext.] [ABSTRACT FROM AUTHOR]

By designing cysteine-containing single-chain peptides and then linking two such molecules with disulfide bond under oxidation, a series of amphiphilic gemini peptides were successfully synthesized. The gemini geometry introduced not only additional constraints in molecular conformations but also the differentiated intra- and intermolecular hydrogen bonding. These aspects result in specific transition of the self-assembly behavior. The single-chain peptides tended to form spherical aggregates, while the gemini molecules all self-assembled into fiber-like structures, especially that I 3 C–CI 3 could form short thin fibers with highly ordered lateral alignments that are rarely found. Moreover, the self-assembly of both the single-chain and the gemini peptides showed great dependence on the side chain groups. With increasing the size of the side chain alkyl groups, the molecules gave decreased critical aggregation concentration (CAC) and were more ready to arrange into ordered assemblies. This should be ascribed to the enhanced hydrophobic interaction and the subsequent force balance shifts. [ABSTRACT FROM AUTHOR]

K 1 − 2x M x TiNbO 5 (M Mn, Ni) photocatalytic material was prepared through a successive ion-exchange reaction of KTiNbO 5 , which was synthesized by a solid-state reaction, with Mn 2 + or Ni 2 + , respectively. The microstructure and the spectral response characteristic of K 1 − 2x M x TiNbO 5 were investigated by means of powder X-ray diffraction (XRD), laser Raman spectroscopy (LRS), and UV–vis diffuse reflectance spectrum (UV–vis DRS). The photocatalytic activities were evaluated by the oxidation of dimethyl sulfide (DMS) and ethyl mercaptan (EM) under natural light (NAT-L) and ultraviolet light (UV-L) irradiation, and the surface species were determined by technology of Fourier-transform infrared (FT-IR) spectroscopy. XRD patterns indicate that ion exchange has changed the interlayer distance. LRS spectra show that there is a significant interaction between the interlayer cation and the terminal Nb O bond. DRS spectra reveal that an additional absorption edge, which locates at a longer wavelength region, can be observed for K 1 − 2x M x TiNbO 5 . For photocatalytic oxidation of DMS and EM, K 1 − 2x Ni x TiNbO 5 has an activity whether under NAT-L or UV-L irradiation. Based on the reactant structure feature and the product distribution, possible reaction pathways of the photocatalytic oxidation for DMS and EM used layered K 1 − 2x M x TiNbO 5 catalyst were proposed. [ABSTRACT FROM AUTHOR]

Accumulating evidence indicates that circular RNAs (circRNAs) play vital roles in tumorigenesis by modulating gene expression. However, the molecular mechanisms underlying the functions of circRNAs remain largely unknown. Here, we demonstrated that a Yes1 associated transcriptional regulator (YAP1)-derived circRNA, circ-LECRC (circRNA low expressed in CRC), was significantly downregulated in colorectal cancer (CRC). High expression of circ-LECRC positively correlated with a lower TNM stage and good prognosis in CRC patients. Circ-LECRC overexpression significantly inhibited CRC cell proliferation, migration, and invasion and promoted apoptosis (P < 0.05). Additionally, we performed xenograft and lung metastasis experiments by injecting CRC cells into nude mice to mechanistically demonstrate that circ-LECRC directly binds to miR-135b-5p and relieve the suppression of its target, Krüppel-like factor 4 (KLF4). Furthermore, we found that both circ-LECRC and KLF4 inhibited YAP1 hyperactivation, which downregulates the expression of the downstream genes of the YAP1 pathway, such as EGFR, MYC, BIRC5, and CTGF. In summary, circ-LECRC regulates KLF4 expression by functioning as a competing endogenous RNA and serves as a "brake signal" to suppress hyperactivation of oncogenic YAP signalling, leading to tumour growth inhibition in CRC. [ABSTRACT FROM AUTHOR]

As an environmental toxicant, arsenic exposure may cause insulin resistance (IR). Previous studies have shown that pyroptosis plays an important role in the occurrence and development of IR. Although gasdermin D (GSDMD) functions as an executor of pyroptosis, the relationship between GSDMD-mediated pyroptosis and hepatic IR remains unclear. Here, we observed that sodium arsenite (NaAsO 2) activated NOD-like receptors containing pyrin domain 3 (NLRP3) inflammasomes, promoted GSDMD activation, induced pyroptosis and hepatic IR, while GSDMD knockdown attenuated pyroptosis and hepatic IR caused by NaAsO 2. However, GSDMD interference did not affect NLRP3 activation. Ubiquitination modification is widely involved in protein regulation and intracellular signal transduction, and whether it regulates GSDMD and affects its degradation, and exerts effects on arsenic-induced pyroptosis remain unclear. We observed that NaAsO 2 reduced the K48- and K63-linked ubiquitination of GSDMD, thereby inhibiting its degradation through the ubiquitin-proteasome system (UPS) and the autophagy-lysosome pathway (ALP), causing GSDMD to accumulate and lyse into GSDMD-N, which promoted pyroptosis. In summary, we demonstrated that GSDMD participated in arsenic-induced hepatic IR. Moreover, NaAsO 2 reduced GSDMD ubiquitination and decreased its intracellular degradation, aggravating pyroptosis and hepatic IR. We have revealed the molecular mechanism underpinning arsenic-induced IR, and we provide potential solutions for the prevention and treatment of type 2 diabetes (T2D). [Display omitted] • The reduction of GSDMD would attenuate the arsenic-induced pyroptosis and insulin resistance. • Exposure to NaAsO 2 would reduce the ubiquitination level of GSDMD. • Ubiquitinated GSDMD would be degraded by ubiquitin-proteasome system and autophagy-lysosome pathway. [ABSTRACT FROM AUTHOR]

A new BF3-mediated cascade reaction yielding the title compounds is presented. [ABSTRACT FROM AUTHOR]

Herbivore-induced plant volatiles (HIPVs) are important compounds to prim neighboring undamaged plants; however, the mechanism for this priming process remains unclear. To reveal metabolic changes in plants exposed to HIPVs, metabolism of leaves and roots of Ammopiptanthus mongolicus seedlings exposed to HIPVs released from conspecific plants infested with larvae of Orgyia ericae were analyzed together with control and infested seedlings using nuclear magnetic resonance (NMR)-based metabolic technology and multi variate data analysis. Results presented showed that HIPVs exposure led to similar but specific metabolic changes compared with those induced by infestation in both leaves and roots. Furthermore, both HIPVs exposure and herbivore attack resulted in metabolic changes involving a series of primary and secondary metabolites in both leaves and roots. Taken together, these results suggested that priming of yet-damaged plants may be achieved by reconfiguring metabolic pathways in leaves and roots to make similar concentrations for all metabolites as those in seedlings infested. Therefore, we propose that improved readiness of defense induction of primed plants toward subsequent herbivore attack may be based on the similar metabolic profiling induced by HIPVs exposure as those caused by herbivore. [ABSTRACT FROM AUTHOR]

9,11,12,14-Tetraaryldibenzo[ f, h]imidazo[1,2- b]isoquinolines 3a- h were synthesized in moderate yields through the reaction of benzils with 1,3-diphenyl-2 H-cyclopenta[ l]phenanthren-2-ones and ammonium acetate. The photophysical properties of the products in solutions and in thin films were investigated, and strong emissions ranging from 492 to 516 nm were observed in cyclohexane solutions. Moreover, 3h exhibited potential as a versatile fluorescent chemosensor for the detection of solvent polarity, acidity, or trace amounts of nitroaromatics. [ABSTRACT FROM AUTHOR]

Microfabricated inductors experience increasing interest and research activity because of their high potential in buck converters for power supply in package and power supply on chip applications. This paper details the modeling and optimization of microfabricated racetrack inductors. The analytical expressions derived characterize inductance, efficiency, and power density based on geometrical parameters, inductor current, and switching frequency. An accurate analysis of the inductor current that includes the impact of losses is performed to determine the switching frequency, the ac copper losses, and the core losses. The presented model is compared to finite element method simulations and reported results of three microfabricated inductors. Finally, the optimum tradeoff between efficiency and power density is identified using the Pareto front, which results from the evaluation of a large number of microfabricated inductors in the design space defined by the application. [ABSTRACT FROM AUTHOR]

• Acrolein induced ferroptosis and insulin secretion dysfunction in MIN6 cells. • Acrolein activated the ER stress and caused the PPARγ decrease. • Acrolein-induced ferroptosis via PERK-CHOP-PPARγ pathway. • Resveratrol improved the ferroptosis and insulin secretion dysfunction induced by acrolein. Acrolein is a typical food and environmental pollutant and a risk factor for diabetes. The primary pathogenesis of diabetes is insulin deficiency and resistance. Ferroptosis is an iron-dependent cell death type, accompanying by lipid peroxide accumulation. Here, 25 μM acrolein-induced ferroptosis is observed in mouse pancreatic β-cell MIN6 cells as indicated by ferroptosis-related indicators, including GPX4 exhaustion, lipid peroxides accumulation, and insulin secretion impairment. Additionally, acrolein-induced ferroptosis could be reversed by Ferrostatin-1. Furthermore, endoplasmic reticulum stress (ER stress) is involved in acrolein-induced ferroptosis. The ER stress inhibits the expression of PPARγ, an essential gene in glucose and lipid metabolism, and facilitates lipid peroxide accumulation, leading to MIN6 cells ferroptosis and dysfunction. Moreover, resveratrol, an antioxidant natural product, may relieve ER stress and upregulate PPARγ expression, thereby inhibiting acrolein-induced ferroptosis. Thus, this study demonstrated a new perspective for the cytotoxic mechanism of acrolein on pancreatic β-cell and the protective effect of resveratrol. [ABSTRACT FROM AUTHOR]

Interface modification plays an important role in improving the efficiency of organic solar cells (OSCs). Here, disodium 4, 4'-(1,10-phenanthroline-4,7-diyl) dibenzenesulfonate (Phen-1) and disodium 4,7-diphenyl-1,10-phenanthroline 4′,4″-disulfonate (Phen-2) was successfully introduced into OSCs as cathode interface layers (CILs) using environment-friendly methanol as solvent. As contrasted with devices without (w/o) CILs, when Phen-2 as CIL, V OC of the devices increases from 0.73 V to 0.79 V, FF increases from 52.49% to 67.17%, respectively. Foremost, the power conversion efficiency (PCE) of the device has been improved from 5.56% to 8.58%. It was found that the surface of the active layer with CILs exhibited a smoother interface and better hydrophilicity, which facilitated the contact between the cathode and the active layer as well as the extraction and transport of electrons. This indicates that the use water-soluble phen series materials as CILs can improve device performance and provide an effective method for the preparation of environmentally friendly OSCs. [Display omitted] • Phenanthroline derivatives have been successfully exploited in OSCs as electron transport layer. • The electron transport layer of phenanthroline derivatives has high conductivity. • In the fullerene system, Phen-1 and Phen-2 achieved the PCE of 8.01% and 8.58%, respectively. [ABSTRACT FROM AUTHOR]

A phosphane-free, highly atom-efficient, and mild basic method for the synthesis of the title compounds is developed. [ABSTRACT FROM AUTHOR]

Under a nitrogen atmosphere, the palladium-catalyzed reaction of o-haloacetophenones (I) with terminal alkynes in the presence of wet secondary cyclic amines gives β-arylnaphthalenes. [ABSTRACT FROM AUTHOR]

Ethylene plays an important role in the regulation of many growth and developmental processes of higher plants. In tomato, Le-ACS6, a member of the ACC synthase multigene family involved in system 1 ethylene biosynthesis during fruit ripening, is subject to negative feedback regulation by ethylene. To identify the cis-elements that are responsible for the negative feedback control, we established an in vitro transient assay system employing particle bombardment on mature-green tomato fruit pericarp to examine the expression of a luciferase (LUC) reporter gene driven by a 5'-serially deleted Le-ACS6 promoter. The results localized putative cis-elements required for negative ethylene-response between -347 and -266 upstream from the translational start site ATG. Several lines of stable transformation of the Le-ACS6 promoter and GUS reporter fusion gene containing internal deletion from -347 to -266 were generated. The expression pattern of the GUS reporter showed that removal of the nucleotides from -347 to -266 completely eliminated the response of the Le-ACS6 promoter to exogenous ethylene. [ABSTRACT FROM AUTHOR]

Abstract The full length cDNA coding for a novel vacuolar Na+/H+ antiporter (GmNHX1) was cloned from soybean and determined to consist of 2591 bp with a 5′-untranslated region of 464 bp, an open reading frame (ORF) of 1641 bp, and a 3′-untranslated region of 466 bp. The deduced protein sequence contains 546 aa with the typical characters of the vacuolar Na+/H+ antiporters, and shares high similarity with that of AtNHX1, OsNHX1 and AgNHX1. The soybean genome showed a single copy of the GmNHX1 gene. Northern blot analysis demonstrated that the expression of the GmNHX1 was tissue-specific, increased by ABA treatment, NaCl, KCl, LiCl and dehydration stress, and lower in leaves but higher in roots and hypocotyls of salt-tolerant than salt-sensitive cultivars. The GmNHX1 was overexpressed under the control of a tandem cauliflower mosaic virus (CaMV) 35S promoter in the model leguminous plant Lotus corniculatus L. and conferred salt-tolerance of the transgenic plants. Measurements of Na+ and K+ contents in both roots and shoots demonstrated that the plantlets of GmNHX1-overexpressing lines had lower Na+ and K+ content, and higher K+/Na+ ratio than the controlled lines that were transformed with the empty vector, which indicates that the salt-tolerance conferred by GmNHX1 is closely related with decreased accumulation of Na+ in the transgenic plants. [ABSTRACT FROM AUTHOR]

Maize Lis1 (lethal leaf-spot 1) gene and its Arabidopsis orthologue AtAcd1 have been suggested to encode pheide a oxygenase (PaO), a key enzyme catalyzing chlorophyll breakdown. To further elucidate the molecular mechanism that regulates chlorophyll catabolism during soybean leaf senescence, a soybean Lis1 homolog was cloned and designated as GmLis1 (GenBank Accession No. DQ154009). Database searches using the deduced protein sequence revealed that it was highly homologous to Lis1 genes or Lis1 orthologues in Arabidopsis, maize, cowpea and tomato. Structural analysis of the predicted GmLLS1 protein revealed typical Rieske [2Fe-2S] and mononuclear iron-binding domains as well as the C-terminus CxxC motif that were conserved in and featured PaO homologues. RT-PCR results showed that the transcription of GmLis1 was up-regulated in all the three tested senescence systems: the natural leaf senescence process, the dark-induced primary leaf senescence and senescing cotyledons. We have previously described the involvement of an LRR receptor-like kinase (RLK), RLPK2 in regulation of soybean leaf senescence. Here we report that the expression of GmLis1 gene was dramatically down-regulated by the RNAi-mediated suppression of rlpk2 and, as expected, greatly up regulated by the CaMV 35S promoter derived overexpression of this RLK gene. These results suggested that the expression of GmLis1 was controlled by the RLPK2-mediated senescence signaling pathway. The observation that the detached rlpk2-RNAi transgenic leaves exhibited light-dependent necrotic lesions, which featured the [ABSTRACT FROM AUTHOR]

Leaf senescence that occurs in the last stage of left development is a genetically programmed process. It is very significant to elucidate the molecular mechanisms that control the initiation and progression of leaf senescence and the way the senescence signal is transduced. In a previous study an artificially induced soybean leaf senescence, we cloned a novel gene designated rlpk2 (Genbank Accession No. AY687391) that encodes a leucine-rich repeat (LRR) receptor like protein kinase. The expression level of rlpk2 gene was shown to he strongly up-regulated during both the natural leaf senescence process in this report and the artificially induced primary-leaf-senescence process in our previous work. The RNA interference (RNAi)-mediated knocking-down of rlpk2 dramatically retarded both the natural and nutrient deficiency-induced leaf senescence in transgenic soybean. The transgenic leaves showed more cell-aggregated surface structure and higher content of chlorophyll. [ABSTRACT FROM AUTHOR]

• Study on effectiveness of seal coat pavement treatments and the influencing factors. • Performance based study aimed at evaluating effectiveness of seal coat treatments. • Random forests method employed to investigate influencing factors. • Influencing factors in construction, environment, and existing pavement conditions. Seal coat or chip seal treatment is a cost-effective preventive pavement maintenance technique frequently used by highway agencies to extend asphalt pavement service life. Many studies were conducted to understand the best practice for a seal coat treatment. However, a lot of the studies focused on the material side and in the laboratory test stage, while there is a great need for field performance based studies to evaluate the effectiveness of seal coat treatments. The performance of seal coats depends on construction techniques, adhesive characteristics of asphalt emulsion, and properties of aggregates, and hence, many factors during the seal coat construction can impact the effectiveness of a seal coat treatment. The main purpose of this study is to evaluate the effectiveness of seal coat treatments and analyze the effects of influencing factors on the seal coat construction. The data employed are 28 pavement sections in Texas with relatively complete records of pavement performance from 2000 to 2016, which are retrieved from the Long-Term Pavement Performance (LTPP) database. Statistical analyses and visualization methods are applied to compare the performance before and after the treatment of a seal coat. Random forests are conducted to identify the effects of selected variables using an importance score indicator. The results show that seal coat treatments have an effect on reducing the cracking of pavement surfaces. The average air temperature and the shortwave surface value are important to the cracking performance. The pavement condition and seal coat thickness are vital to the rutting and IRI performance. [ABSTRACT FROM AUTHOR]

• A micro-inductor has been fabricated using a MEMS process. • The device has a single layer copper winding sandwiched between two layers of core. • The micro-inductor has a footprint area of 2.9 mm2. • The measured inductance is 204 nH at 21.7 MHz and DC resistance is 470 m Ω. • The peak quality factor of the micro-inductor is 9.23 at 9.2 MHz. • The micro-inductor has been applied in a buck converter. • The achieved maximum converter efficiency is 81.74% at 20 MHz. • The micro-inductor has also been compared with an air core inductor embedded in PCB. • The 220 nH air core inductor has a large footprint area of 32 mm2. • The maximum converter efficiency is 85.47% when the air core inductor is applied. A micro-inductor has been fabricated on silicon substrate using a Micro-Electromechanical Systems (MEMS) process. The micro-inductor has a single layer copper winding sandwiched between two layers of electroplated NiFe core. It has a footprint area of 2.9 mm2, an inductance of 204 nH at 21.7 MHz, a DC resistance of 470 m Ω , and a peak quality factor of 9.23 at 9.2 MHz. The micro-inductor has been applied in a buck converter and achieved a maximum converter efficiency of 81.74% at 20 MHz. The performance of the micro-inductor has also been compared with an air-core inductor embedded in PCB. The air core inductor has a similar inductance of 220 nH, but with a large footprint area of 32 mm2. The maximum buck converter efficiency is 85.47% when the air core inductor is applied. [ABSTRACT FROM AUTHOR]

Emerging studies have pointed to a significant relationship between exposure to ambient fine particulate matter (aerodynamic diameter < 2.5 μm, PM2.5) and the incidence of non-alcoholic fatty liver disease (NAFLD). By referring to previous studies on the pathogenesis of NAFLD and PM2.5 exposure-induced metabolic damage, we summarized the possible mediating pathways through which PM2.5 exposure can cause the phenotype and progression of NAFLD. Crucially, PM2.5 exposure is considered to have an impact on the classic hypothesis "multiple hits" of NAFLD. In addition, we also concluded that exposure to PM2.5 can promote the development of NAFLD by destroying the intestinal epithelium and microbiotic homeostasis, triggering endoplasmic reticulum stress, inducing abnormal expression of specific microRNA or inflammatory factors. Unlabelled Image [ABSTRACT FROM AUTHOR]

Interface modification makes an important contribution to improving the optoelectronic performance and stability of polymer solar cells (PSCs). Here, the hexamethylenetetramine (C 6 H 12 N 4) was successfully introduced into PSCs as cathode interface layers (CILs) using environmental-friendly methanol as solvent. Compared to the PSCs without CILs, the open circuit voltage (V OC) and short-circuit current density (J SC) of the device with C 6 H 12 N 4 CILs was increased from 0.44 V to 12.73 mA cm−2 to 0.77 V and 15.89 mA cm−2, respectively. More importantly, under the same experimental conditions, the optimal power conversion efficiency (PCE) of the device with C 6 H 12 N 4 CILs was improved to 7.79%, which is 185% higher than that of the device without C 6 H 12 N 4 CILs (2.73%). We found that the active layer PTB7-Th:PC 71 BM showed a smoother interface morphology and better hydrophilicity after insertion of CILs, which facilitated enhance the physical contact between active layers and cathode as well as electron extraction and transport. The results show that the introduction of C 6 H 12 N 4 as CILs provides an effective method for preparing high-performance PSCs. • C 6 H 12 N 4 has been successfully exploited in PSCs as electron transfer layer. • C 6 H 12 N 4 can reduce cathode work function and efficiently extract electrons. • C 6 H 12 N 4 modifies the active layer to exhibit a smoother interfacial topography, which reduces contact resistance of PSCs. [ABSTRACT FROM AUTHOR]

Patulin (PAT), a kind of mycotoxin, is produced by many common fungi in fruit and vegetable-based products. It has been shown to cause hepatotoxicity. However, the possible mechanisms are not completely elucidated. The present study aimed to characterize the role of autophagic-inflammasomal pathway on pyroptosis induced by PAT. In mouse livers, PAT induced pyroptosis, and increased inflammation through the activation of NLRP3 inflammasome. In liver cells, we noticed that PAT induced pyroptotic cell death, which was confirmed by the activation of GSDMD, caspase-1, the release of LDH, and the result of PI/Hoechst assay. In addition, PAT-induced pyroptosis was dependent upon the activation of NLRP3 inflammasome and the release of cathepsin B. Cells had less expression of caspase-1 and IL-1β protein levels after treated by NLRP3 inhibitor MCC950 or cathepsin B inhibitor CA-074Me. The expression of GSDMD and IL-1β protein levels were also decrease after treated by caspase-1 inhibitor Ac-YVAD-cmk. Moreover, autophagy inhibitor 3-methyladenine (3-MA) attenuated PAT-induced increase in cytoplasmic cathepsin B expression, and subsequent LDH release, the activation of NLRP3 inflamosomes, pyroptotic cell death, and inflammation. These findings suggested that PAT-induced pyroptosis maybe through autophagy-cathepsin B-inflammasomal pathway in the liver. These results provide new mechanistic insights into PAT-induced hepatotoxicity. • PAT could induce pyroptosis in mice liver and liver cells. • Autophagy may play an important role in PAT-induced pyroptosis. • PAT-induced pyroptosis maybe through autophagy-cathepsin B-inflammasomal pathway. [ABSTRACT FROM AUTHOR]

Aims: Diabetes mellitus and hypertension are both complex diseases that are caused by interactions among multiple genetic and physiological factors. To investigate the association of common single-nucleotide polymorphisms (SNPs) of SUCNR1, GRK4 and CAMK1D genes with the susceptibility of the two diseases in a northern Chinese Han population.Methods: 36 SNPs were genotyped in 2304 clinical patients (1152 type 2 diabetes mellitus, 1152 essential hypertension) and 1152 health controls by Sequenom Mass-ARRAY RS1000.Results: In this study, we found that BMI, blood press, pulse pressure, FBG, total cholesterol and triglycerides were associated with an increased risk of type 2 diabetes mellitus (T2DM) and essential hypertension (EH). Three SNPs (SUCNR1: rs73168929; GRK4: rs1557213; CAMK1D: rs17151584) significantly associated with the susceptibility of T2DM and EH at the same time. Also, the susceptibility genotypes of 3 SNPs were significantly correlated with liver and renal function parameters.Conclusion: To the best of our knowledge, the present study is the first to report that three SNPs (SUCNR1: rs73168929; GRK4: rs1557213; CAMK1D: rs17151584) contributed to the risk of T2DM and EH in a northern Chinese Han population. These results provide a favourable evidence for better understand of the underlying common mechanism of these two diseases. [ABSTRACT FROM AUTHOR]

• MtROS-NLRP3 inflammasome pathway plays an important role in arsenic-induced hepatic insulin resistance (IR). • Activation of NLRP3 inflammasome in arsenic-induced hepatic IR is dependent on mitophagy. • Arsenic-induced mtROS primarily triggered ox-mtDNA and mitophagy. Hepatic insulin resistance (IR) is the key event for arsenic-caused type 2 diabetes (T2D). However, the unequivocal mechanism of arsenic-induced hepatic IR remains unclear. The current study determined the role of NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation in arsenic-induced IR and revealed the underlying mechanism. Three-month NaAsO 2 gavage led to glucose intolerance and insulin insensitivity, impaired hepatic insulin signaling. Additionally, NaAsO 2 upregulated the level of oxidized mitochondrial DNA (ox-mtDNA) and mitophagy, thereby activating the NLRP3 inflammasome in SD rat liver. In vitro , we demonstrated that NaAsO 2 -induced IR depended upon the NLRP3 inflammasome activation. Moreover, inhibiting mitophagy mitigated the NLRP3 inflammasome activation and impaired insulin signaling induced by NaAsO 2. Furthermore, mitochondrial reactive oxygen species (mtROS) scavenger alleviated the upregulated ox-mtDNA and mitophagy, thereby inhibiting the NLRP3 inflammasome activation, and improving insulin signaling. Taken together, these data demonstrated that mtROS-triggered ox-mtDNA, mitophagy, and the activation of NLRP3 inflammasome was involved in arsenic-induced hepatic IR. [ABSTRACT FROM AUTHOR]

Cannabinoid receptor 2 (CB2R) is an important regulator of immunoinflammatory responses. Interestingly, studies have demonstrated that CB2R was expressed in metabolically active tissue, so we speculated that CB2R might have a crucial impact on energy balance. We thus examined the anti-inflammatory activities of CB2R and a CB2R agonist, JWH-133, in diet-induced obese in mice as well as in cultured macrophages. We evaluated the in vivo effect of JWH-133 on diet-induced adipose tissue inflammation. We also assessed the in vitro effects of JWH-133 on lipopolysaccharide (LPS)-induced inflammation in RAW264.7 macrophages, with a focus on the nuclear factor E2-related factor 2/heme oxygenase 1 (Nrf2/HO-1) signaling pathway. We found that JWH-133 reduced body weight gain, relieved glucose tolerance, and enhanced insulin sensitivity in a mouse model. It also down-regulated the expression of M1 macrophage biomarkers (tumor necrosis factor-α, interleukin (IL)-6, inducible nitric oxide synthase (iNOS), IL-1β, C C motif chemokine ligand 2, and C-X-C motif chemokine 10) in vivo and in vitro, but up-regulated levels of M2 macrophage biomarkers (IL-10 and arginase-1) in both mice and cultured macrophages. Furthermore, the underlying mechanisms were studied in an LPS-treated RAW264.7 cell line. We found a role for JWH-133 in controlling M1 macrophage polarization by activating the Nrf2/HO-1 pathway, while the effect of JWH-133 was diminished by a HO-1 inhibitor, Sn(IV) protoporphyrin IX dichloride. JWH-133 showed anti-obesity effects that ameliorated pro-inflammatory M1 macrophage polarization through the Nrf2/HO-1 pathway. Therefore, our results provide a new proof for the potential use of the CB2R agonist, JWH-133, in the treatment of obesity. • The present study revealed beneficial effects of JWH-133 on weight gain, glucose tolerance and insulin insensitivity; • JWH-133 orchestrate anti-inflammatory activities by regulating macrophage M1/M2 polarization via the Nrf2/HO-1 pathway; • CB2R may play a therapeutic role in obesity and associated metabolic disorders. [ABSTRACT FROM AUTHOR]

Novel H7N9 influenza virus transmitted from birds to human and, since March 2013, it has caused five epidemic waves in China. Although the evolution of H7N9 viruses has been investigated, the evolutionary changes associated with codon usage are still unclear. Herein, the codon usage pattern of two surface glycoproteins, hemagglutinin (HA) and neuraminidase (NA), was studied to understand the evolutionary changes in relation to host, epidemic wave, and pathogenicity. Both genes displayed a low codon usage bias, with HA higher than NA. The codon usage was driven by mutation pressure and natural selection, although the main contributing factor was natural selection. Additionally, the codon adaptation index (CAI) and deoptimization (RCDI) illustrated the strong adaptability of H7N9 to Gallus gallus. Similarity index (SiD) analysis showed that Homo sapiens posed a stronger selection pressure than Gallus gallus. Thus, we assume that this may be related to the gradual adaptability of the virus to human. In addition, the host strong selection pressure was validated based on CpG dinucleotide content. In conclusion, this study analyzed the usage of codons of two genes of H7N9 and expanded our understanding of H7N9 host specificity. This aids into the development of control measures against H7N9 influenza virus. [ABSTRACT FROM AUTHOR]

Error-related potentials (ErrPs) have provided technical support for the brain-computer interface. However, different visual stimulations may affect the ErrPs, and furthermore, affect the error recognition based on ErrPs. Therefore, the study aimed to investigate how people respond to different visual stimulations (static and dynamic) and find the best time window for different stimulation. Nineteen participants were recruited in the ErrPs-based tasks with static and dynamic visual stimulations. Five ErrPs were statistically compared, and the classification accuracies were obtained through linear discriminant analysis (LDA) with nine different time windows. The results showed that the P3, N6, and P8 with correctness were significantly different from those with error in both stimulations, while N1 only existed in static. The differences between dynamic and static errors existed in N1 and P2. The highest accuracy was obtained in the time window related to N1, P3, N6, and P8 for the static condition, and in the time window related to P3, N6, and P8 for the dynamic. In conclusion, the early components of ErrPs may be affected by stimulation modes, and the late components are more sensitive to errors. The error recognition with static stimulation requires information from the entire epoch, while the late windows should be focused more within the dynamic case. [ABSTRACT FROM AUTHOR]

Glioma is the most common type of malignant tumor of the nervous system, and aggressiveness and recurrence are major obstacles for treatment. This study is designed to explore the effects of amentoflavone (AF) on glioma, and to investigate the underlying mechanism of the anti-cancer activities of AF. Cell morphology was recorded under microscopy. Cell viability and cell death ratio were determined by CCK-8 assay and lactate dehydrogenase (LDH) release assay, respectively. Cell cycle progression was assessed by flow cytometry. The levels of iron, MDA (malondialdehyde), lipid ROS, and GSH (reduced glutathione) were assessed by ELISA kit. The cycle-related proteins, ferroptosis-related protein, autophagy-related protein, and the phosphorylation of AMPK, mTOR and p70S6K were analyzed by western blotting. The autophagic flux was observed by transfecting cells with mRFP-GFP-LC3 plasmids. The xenograft murine models were established to analyze the effects of amentoflavone in vivo. The immunohistochemistry assay was performed to analyze the expression of LC3B, Beclin1, ATG5, ATG7, and ferritin heavy chain (FTH). Our results showed that AF treatment led to reduction in cell viability and cell death. In addition, AF was found to block cell cycle progression in a dose-dependent manner in vitro. Following treatment with AF, the intracellular levels of iron, MDA, and lipid OS were increased, and the levels of GSH and the mitochondrial membrane potential were reduced. In addition, our results showed that AF promoted the autophagic by regulating autophagy-relevant proteins. Our results also showed that the autophagy-induction by AF was associated with regulation of AMPK/mTOR signaling. Mechanistically, the inhibition effects of AF on glioma cell were reversed by DFO, ferreostatin-1 as well as upregulation of FTH. Meanwhile, the FTH levels were increased by compound C and knockdown of ATG7. Moreover, both autophagy inhibitor Baf A1 and knockdown of ATG7 were able to compromising AF-induce ferroptosis and cell death. In vivo , the tumor growth was suppressed by AF in a dose-dependent manner. The level of MDA in the tumor tissue was increased while the level of GSH in tumor tissue was decreased by AF in a dose-dependent manner. Furthermore, the expression of LC3B, Beclin1, ATG5, ATG7 were increased, and the expression of FTH were decreased by AF in a dose-dependent manner in vivo. Conclusion These results demonstrate that AF triggered ferroptosis in autophagy-dependent manner. Our results suggest that AF has the potential to be considered as a novel treatment agent in glioma. [ABSTRACT FROM AUTHOR]

Long-term exposure to arsenic can cause liver injury and fibrosis. The activation of hepatic stellate cells (HSCs) plays an essential role in the process of liver fibrosis. We found that NaAsO 2 caused liver damage and fibrosis in vivo , accompanied by excessive collagen deposition and HSCs activation. In addition, NaAsO 2 upregulated autophagy flux, elevated the level of cytoplasmic cathepsin B (CTSB), and activated the NOD-like receptors containing pyrin domain 3 (NLRP3) inflammasome in a subtle way. Consistent with these findings in vivo , we demonstrated that NaAsO 2 -induced activation of HSCs depended on CTSB-mediated NLRP3 inflammasome activation in HSC-t6 cells and rats primary HSCs. Moreover, inhibition of autophagy decreased the cytoplasmic CTSB and alleviated the activation of the NLRP3 inflammasome, thereby attenuating the NaAsO 2 -induced HSCs activation. In summary, these results indicated that NaAsO 2 induced HSCs activation via autophagic-CTSB-NLRP3 inflammasome pathway. These findings may provide a novel insight into the potential mechanism of NaAsO 2 -induced liver fibrosis. Image 1 • Chronic arsenic exposure leads to inflammation and fibrosis in livers. • NLRP3 inflammasome plays a crucial role in the activation of HSCs induced by arsenic. • Autophagy and lysosomal rupture are involved in the arsenic-activated of NLRP3 inflammasome. [ABSTRACT FROM AUTHOR]

• Ferroptosis existed in animal models of NaAsO 2 -induced pancreatic dysfunction. • NaAsO 2 -induced ferroptotic cell death is relied on the MtROS-dependent autophagy. • NaAsO 2 -induced ferroptosis involves MtROS, autophagy, ferritin. Chronic arsenic exposure is a significantly risk factor for pancreatic dysfunction and type 2 diabetes (T2D). Ferroptosis is a newly identified iron-dependent form of oxidative cell death that relies on lipid peroxidation. Previous data have indicated that ferroptosis is involved in various diseases, including cancers, neurodegenerative diseases, and T2D. However, the concrete effect and mechanism of ferroptosis on pancreatic dysfunction triggered by arsenic remains unknown. In this study, we verified that ferroptosis occurred in animal models of arsenic-induced pancreatic dysfunction through assessing proferroptotic markers and morphological changes in mitochondria. In vitro, arsenic caused execution of ferroptosis in a dose-dependent manner, which could be significantly reduced by ferrostatin-1. Additionally, arsenic damaged mitochondria manifested as diminishing of mitochondrial membrane potential, reduced cytochrome c level and production of mitochondrial reactive oxygen species (MtROS) in MIN6 cells. Using the Mito-TEMPO, we found the autophagy level and subsequent ferroptotic cell death induced by arsenic were both alleviated. With autophagy inhibitor chloroquine, we further revealed that ferritin regulated ferroptosis through the MtROS-autophagy pathway. Collectively, NaAsO 2 -induced ferroptotic cell death is relied on the MtROS-dependent autophagy by regulating the iron homeostasis. Ferroptosis is involved in pancreatic dysfunction triggered by arsenic, and arsenic-induced ferroptosis involves MtROS, autophagy, ferritin. [ABSTRACT FROM AUTHOR]

Ionic liquids (ILs) can be recycled as extractants for their low vapor pressure and volatility. More and more applications are applied to the separation of industrial organic matter. The industrial production of ILs has gradually been realized, which also widens the way for the application of ILs. In this work, the liquid-liquid extraction of cyclohexane-acetone azeotropic mixture with different ILs {1-butyl-3-methylimidazolium bis(trifluormethylsulfonyl), 1-butyl-3-methylimidazolium trifluoromethansulfonate and 1-butyl-3-methylimidazolium dicyanamide} is studied. The extraction mechanism is discussed based on the molecular scale. The relationship between hydrogen bond donor and acceptor between ILs and acetone is analyzed by COSMO-SAC. The interaction between molecules is optimized and calculated by Materials Studio 7.0. The extraction ability of ILs is analyzed by radial distribution function, and the experimental results are verified. The liquid-liquid equilibrium test is carried out at 298.15 K. Distribution and selectivity are indices used to judge the extraction efficiency of ILs. The NRTL model and UNIQUAC model are adopted to correlate the liquid-liquid equilibrium data. The results show that all of the two models can well correlate the experimental. • The extraction process was studied by using quantum chemical calculation and RDF. • LLE data of cyclohexane + acetone + IL systems were measured. • The NRTL and UNIQUAC models were applied to correlate the studied system. [ABSTRACT FROM AUTHOR]

• ZEA triggered pyroptosis in INS-1 cells. • ZEA-induced pyroptosis was NLRP3 inflammasome-dependent. • ZEA-induced activation of NLRP3 inflammasome was regulated by autophagy. • ZEA-triggered NF-κB p65 activation was involved in NLRP3 inflammasome activation. Zearalenone (ZEA), one of the mycotoxins widely found in food and feed, can stimulate an inflammatory reaction. In the present study, we demonstrated that ZEA induced the activation of NLRP3 inflammasome even pyroptotic cell death in rat Insulinoma Cell Line (INS-1). Meanwhile, according to the results of western blot and TEM, the level of autophagy was elevated by ZEA, which protected against the activation of NLRP3 inflammasome and inflammatory response caused by ZEA. Furthermore, we indicated that ZEA-induced NF-κB p65 activation contributed to the activation of the NLRP3 inflammasome, inflammatory response, and pyroptosis in INS-1 cells, which were indicated by western blot and immunofluorescence, and the activation of NF-κB p65 induced by ZEA was autophagy-dependent. This study demonstrates that ZEA induces NLRP3-dependent pyroptosis via activation of NF-κB modulated by autophagy in INS-1 cells. [ABSTRACT FROM AUTHOR]

• DOX induced autophagy-depending apoptosis in HUVECs. • DOX-induced apoptosis was via lysosomal-mitochondrial axis to some extent. • PQQ protected HUVECs from autophagy-dependent apoptosis induced by DOX. The cardiotoxicity of doxorubicin (DOX) limits its clinical use in the treatment of a variety of solid tumors and malignant hematologic disease. However, the mechanism by which it causes cardiotoxicity is not fully understood. Apoptosis has been regarded as one of mechanisms underlying the cardiotoxic effects of DOX. In our study, we found that treatment of human umbilical vein endothelial cells (HUVECs) with DOX induced autophagy and apoptosis in a dose- and time-dependent manner. Treatment with DOX induced autophagy at earlier time (3 h), then lysosomal membrane permeabilization (LMP) altered after treatment for 12 h which followed by the release of cathepsin D (CTSD). Lysosome-associated membrane proteins-1 and -2 (LAMP1 and LAMP2) were decreased in DOX-treated cells. Additionally, DOX induced the collapse of mitochondrial transmembrane potential, reduction of translocase of the outer mitochondrial membrane-20 (TOM-20), and release of cytochrome c. Furthermore, autophagy inhibitor 3-MA relieved DOX-induced apoptosis as assessed by the expression of cleaved caspase-3, cleaved caspase-9 and TUNEL assay. CTSD inhibitor, pepstatin A, upregulated TOM-20 and suppressed the mitochondria release of cytochrome c as well as apoptosis under DOX stress. Pyrroloquinoline quinine (PQQ), a new B vitamin, ameliorated aforementioned phenomenon. In conclusion, our results suggested that DOX-induced apoptosis was autophagy-dependent via lysosomal-mitochondrial axis. PQQ had an ability to protect cell from autophagy-dependent apoptosis induced by DOX via lysosomal-mitochondrial axis to some extent. This study provided new mechanistic insight toward understanding the pathogenesis of DOX-induced cardiotoxicity and the protection effect of PQQ. [ABSTRACT FROM AUTHOR]

Presents the electrical performance of fabricated E-core microtransformers and their use in a direct current-direct current converter. Design and fabrication of microtransfomers; Electrical parameters of the packaged transformers; Model of microtransformers.