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An advanced pod E-cigarette, launched by Shenzhen Woody Vapes Technology Co., Ltd., was researched and analysed in this paper with the help of computational fluid dynamics (CFD) simulation. The standard k-ε turbulent model was introduced to simulate the flow of air, the Broadband Noise Source model adapted to measure the noise and the Discrete Phase Model (DPM) used to calculate the trajectories of the aerosols. The pressure, velocity and noise fields, the trajectories of the aerosols, obtained by Reynolds-Averaged Navier-Stokes (RANS) simulation, were analysed to optimize the structure design of this pod system. Several related experiments were performed and significant improvement was also confirmed.

This study evaluated the initial stress produced in the periodontal ligament (PDL) and the displacements of mandibular incisors under masticatory force in patients with alveolar bone loss (ABL) after orthodontic treatment.Four horizontal absorption models (zero, one third, one half, and two thirds of root length) and 2 labiolingual absorption models (labial two thirds, lingual one third of root length, and vice versa) of the mandibular anterior segment were constructed. A total force of 285.3 N was applied vertically to the edges of incisors. The tooth displacement and principal stresses in the PDL were evaluated in a finite element analysis.In all models, the labial movements of the central incisors ascended more significantly, whereas there was obvious compressive stress and tensile stress concentrated in the labial and lingual cervical margins of the PDL, respectively. For the lateral incisors, augmentation of the distal motions was more evident. Compressive stress was apparent in the labial-distal margin, and tensile stress was concentrated in the lingual-mesial cervical margin. With the same proportion of ABL, more significant displacement and stress concentration in the PDL occurred in the central incisors. In labiolingual absorption models, labial ABL caused greater incisors displacement and periodontal stress concentration. When horizontal ABL extended from one half to two thirds of the root length, mobility of the central incisors and stresses in the PDL increased significantly.Mandibular incisors follow the different movement and stress distribution patterns under occlusal loads. Special consideration should be given to the retention of mandibular incisors when horizontal ABL exceeds half of the root length.

Mitochondrial quality in skeletal muscle is crucial for maintaining energy homeostasis during metabolic stresses. However, how muscle mitochondrial quality is controlled and its physiological impacts remain unclear. Here, we demonstrate that mitoprotease LONP1 is essential for preserving muscle mitochondrial proteostasis and systemic metabolic homeostasis. Skeletal muscle–specific deletion of Lon protease homolog, mitochondrial (LONP1) impaired mitochondrial protein turnover, leading to muscle mitochondrial proteostasis stress. A benefit of this adaptive response was the complete resistance to diet-induced obesity. These favorable metabolic phenotypes were recapitulated in mice overexpressing LONP1 substrate ΔOTC in muscle mitochondria. Mechanistically, mitochondrial proteostasis imbalance elicits an unfolded protein response (UPRmt) in muscle that acts distally to modulate adipose tissue and liver metabolism. Unexpectedly, contrary to its previously proposed role, ATF4 is dispensable for the long-range protective response of skeletal muscle. Thus, these findings reveal a pivotal role of LONP1-dependent mitochondrial proteostasis in directing muscle UPRmtto regulate systemic metabolism.

Due to the complexity of the structure and surface property of metal oxide catalysts, hydrophobization of metal oxide catalysts is a great challenge. The hydrophobization strategy and effects of hy...

Functionalized catalysts with multiple active centers have been studied in direct conversion of ethanol to butadiene (ETB). However, it is still a considerable challenge to control the synergistic effect of multiple active centers. Here, we report that a series of ZnMg/SBA-15-based catalysts were synthesized for the direct ETB process. The non-polar solvent n-hexane is utilized to improve the synergistic effects of ZnO, MgO and SBA-15. The characterization results demonstrate that the ZnMg/SBA-15-hexane catalyst, prepared from n-hexane solvent, can increase dehydrogenation activity and promote synergistic catalysis. The direct ETB performance reveals that it exhibits an excellent selectivity of 70% towards the butadiene product. Further, our in situ DRIFTS analysis indicates that aldol condensation and the MPV reaction are the rate-determining steps of the direct ETB process. The present work offers a simple strategy to optimize synergies of multiple active centers.

Metabolically beneficial beige adipocytes offer tremendous potential to combat metabolic diseases. The folliculin interacting protein 1 (FNIP1) is implicated in controlling cellular metabolism via AMPK and mTORC1. However, whether and how FNIP1 regulates adipocyte browning is unclear. Here, we demonstrate that FNIP1 plays a critical role in controlling adipocyte browning and systemic glucose homeostasis. Adipocyte-specific ablation of FNIP1 promotes a broad thermogenic remodeling of adipocytes, including increased UCP1 levels, high mitochondrial content, and augmented capacity for mitochondrial respiration. Mechanistically, FNIP1 binds to and promotes the activity of SERCA, a main Ca2+ pump responsible for cytosolic Ca2+ removal. Loss of FNIP1 resulted in enhanced intracellular Ca2+ signals and consequential activation of Ca2+-dependent thermogenic program in adipocytes. Furthermore, mice lacking adipocyte FNIP1 were protected against high-fat diet–induced insulin resistance and liver steatosis. Thus, these findings reveal a pivotal role of FNIP1 as a negative regulator of beige adipocyte thermogenesis and unravel an intriguing functional link between intracellular Ca2+ dynamics and adipocyte browning.

High expression of PD-L1 in tumor cells contributes to tumor immune evasion. However, whether PD-L1 expression in tumor cells is regulated by the availability of nutrients is unknown. Here, we show that in human glioblastoma cells, high glucose promotes hexokinase (HK) 2 dissociation from mitochondria and its subsequent binding and phosphorylation of IκBα at T291. This leads to increased interaction between IκBα and μ-calpain protease and subsequent μ-calpain-mediated IκBα degradation and NF-κB activation-dependent transcriptional upregulation of PD-L1 expression. Expression of IκBα T291A in glioblastoma cells blocked high glucose-induced PD-L1 expression and promoted CD8

The complement system is a critical immune component, yet its role in tumor immune evasion and CD8

Periodontitis is a progressive infectious inflammatory disease, which leads to alveolar bone resorption and loss of periodontal attachment. It is imperative for us to develop a therapeutic scaffold to repair the alveolar bone defect of periodontitis. In this study, we designed a new composite scaffold loading metformin (MET) by using the freeze-drying method, which was composed of β-tricalcium phosphate (β-TCP), chitosan (CTS) and the mesoporous silica (SBA-15). The scaffolds were expected to combine the excellent biocompatibility of CTS, the good bioactivity of β-TCP, and the anti-inflammatory properties of MET. The MET-loaded β-TCP/CTS/SBA-15 scaffolds showed improved cell adhesion, appropriate porosity and good biocompatibility in vitro. This MET composite scaffold was implanted in the alveolar bone defects area of rats with periodontitis. After 12 weeks, Micro-CT and histological analysis were performed to evaluate different degrees of healing and mineralization. Results showed that the MET-loaded β-TCP/CTS/SBA-15 scaffolds promoted alveolar bone regeneration in a rat model of periodontitis. To our knowledge, this is the first report that MET-loaded β-TCP/CTS/SBA-15 scaffolds have a positive effect on alveolar bone regeneration in periodontitis. Our findings might provide a new and promising strategy for repairing alveolar bone defects under the condition of periodontitis.

The cytoplasmic coat protein complex-II (COPII) is evolutionarily conserved machinery that is essential for efficient trafficking of protein and lipid cargos. How the COPII machinery is regulated to meet the metabolic demand in response to alterations of the nutritional state remains largely unexplored, however. Here, we show that dynamic changes of COPII vesicle trafficking parallel the activation of transcription factor X-box binding protein 1 (XBP1s), a critical transcription factor in handling cellular endoplasmic reticulum (ER) stress in both live cells and mouse livers upon physiological fluctuations of nutrient availability. Using live-cell imaging approaches, we demonstrate that XBP1s is sufficient to promote COPII-dependent trafficking, mediating the nutrient stimulatory effects. Chromatin immunoprecipitation (ChIP) coupled with high-throughput DNA sequencing (ChIP-seq) and RNA-sequencing analyses reveal that nutritional signals induce dynamic XBP1s occupancy of promoters of COPII traffic-related genes, thereby driving the COPII-mediated trafficking process. Liver-specific disruption of the inositol-requiring enzyme 1α (IRE1α)–XBP1s signaling branch results in diminished COPII vesicle trafficking. Reactivation of XBP1s in mice lacking hepatic IRE1α restores COPII-mediated lipoprotein secretion and reverses the fatty liver and hypolipidemia phenotypes. Thus, our results demonstrate a previously unappreciated mechanism in the metabolic control of liver protein and lipid trafficking: The IRE1α-XBP1s axis functions as a nutrient-sensing regulatory nexus that integrates nutritional states and the COPII vesicle trafficking.

A selective diaminomaleonitrile-based fluorescent probe for Al3+(L) has been synthesized and characterized. The sensing behavior of L towards different metal ions was investigated by fluorescent spectra and competition experiment. The results showed that L exhibited a dual channel emission (λem 522 & 558 nm) with yellow fluorescence in the presence of Al3+ over other metal ions in EtOH solution. The probe L was bound to Al3+ in a 1:2 stoichiometric manner as supported by Job's plot analysis. The binding constant was 9.55 × 108 M−2 with the detection limit of 10.3 nM. The turn-on response was attributed to the inhibition of PET and C N isomerization after binding with Al3+ while the dual emissions were due to ESIPT and ICT processes. In addition, the application of L for imaging Al3+ in living Hela cells was achieved.

C.I.Pigment Yellow 155 (Y 155) is an important bisacetoacetarylide disazo yellow pigment with a unique structure, which has the potential to be an alternative for benzidine yellow pigments due to its superior solvent resistance and light fastness. It is essential to investigate the crystal structure of Y 155 to understand the relationship between the structure and technical performance. Y 155 crystallizes in the triclinic P 1 ( — ) space group. The molecule exists in the bisketohydrazone form which is consistent with that of disazoacetoacetanilide pigments (Diarylide Yellows). Different from the unsubstituted analogue (BADA), Y 155 molecules are approximately planar due to stronger intramolecular hydrogen bonding. In Y 155 crystals, each molecule is interleaved in two adjacent layers above and below. The color and the technical performance are discussed in relation to its crystal structure especially involving in the role of four methyl formate groups.

Cu/ZnO catalysts with varied Cu/(Cu + Zn) molar ratios were prepared by a facile solid-state method. The Cu/(Cu + Zn) molar ratio displayed a significant effect on the oxygen vacancy formation of the calcined catalysts, thereby influencing the CuO-ZnO interaction and the reducibility of CuO. The Cu/(Cu + Zn) molar ratio also exhibited a significant effect on Cu

Objectives To compare the transfer accuracy of two digital transfer trays, the three-dimensional printed (3D printed) tray and the vacuum-formed tray, in the indirect bonding of labial brackets. Materials and Methods Ten digital dental models were constructed by oral scans using an optical scanning system. 3D printed trays and vacuum-formed trays were obtained through the 3Shape indirect bonding system and rapid prototyping technology (10 in each group). Then labial brackets were transferred to 3D printed models, and the models with final bracket positioning were scanned. Linear (mesiodistal, vertical, buccolingual) and angular (angulation, torque, rotation) transfer errors were measured using GOM Inspect software. The mean transfer errors and prevalence of clinically acceptable errors (linear errors of ≤0.5 mm and angular errors of ≤2°) of two digital trays were compared using the Mann-Whitney U-test and the Chi-square test, respectively. Results The 3D printed tray had a lower mean mesiodistal transfer error (P < .01) and a higher prevalence of rotation error within the limit of 2° (P = .03) than did the vacuum-formed tray. Linear errors within 0.5 mm were higher than 90% for both groups, while torque errors within 2° were lowest at 50.9% and 52.9% for the 3D printed tray and vacuum-formed tray, respectively. Both groups had a directional bias toward the occlusal, mesial, and buccal. Conclusions The 3D printed tray generally scored better in terms of transfer accuracy than did the vacuum-formed tray. Both types of trays had better linear control than angular control of brackets.

Skeletal muscle depends on the precise orchestration of contractile and metabolic gene expression programs to direct fiber-type specification and to ensure muscle performance. Exactly how such fiber type-specific patterns of gene expression are established and maintained remains unclear, however. Here, we demonstrate that histone monomethyl transferase MLL4 (KMT2D), an enhancer regulator enriched in slow myofibers, plays a critical role in controlling muscle fiber identity as well as muscle performance. Skeletal muscle-specific ablation of MLL4 in mice resulted in downregulation of the slow oxidative myofiber gene program, decreased numbers of type I myofibers, and diminished mitochondrial respiration, which caused reductions in muscle fatty acid utilization and endurance capacity during exercise. Genome-wide ChIP-Seq and mRNA-Seq analyses revealed that MLL4 directly binds to enhancers and functions as a coactivator of the myocyte enhancer factor 2 (MEF2) to activate transcription of slow oxidative myofiber genes. Importantly, we also found that the MLL4 regulatory circuit is associated with muscle fiber-type remodeling in humans. Thus, our results uncover a pivotal role for MLL4 in specifying structural and metabolic identities of myofibers that govern muscle performance. These findings provide therapeutic opportunities for enhancing muscle fitness to combat a variety of metabolic and muscular diseases.

An efficient colorimetric and absorption ratiometric azo-azomethine receptor N'-((E)-2-hydroxy-5-((E)-(4-nitrophenyl)diazenyl)benzylidene)picolinohydrazide (L) based on phenolic and acyl hydrazine binding units was synthesized and characterized by FT-IR, 1H NMR, 13C NMR and HRMS method. The optical response of L towards different anions was studied by colorimetric, UV–vis and 1H NMR titration method. The results revealed that L had a selective colorimetric sensing ability for biologically important F−, AcO− and H2PO4− by changing color from pale yellow to blue by naked-eye. Interestingly, the sensor L demonstrated an absorption ratiometric response towards F− (1:2 complex) and H2PO4− (1:1 complex) during the recognition process. The detection limit of the sensor L towards F−, AcO− and H2PO4− was estimated to be 2.94 μM, 4.12 μM and 12 μM respectively. The recognition mechanism was attributed to hydrogen bonding and subsequent deprotonation process according to 1H NMR titration experiments.

Summary: The quality of mitochondria in skeletal muscle is essential for maintaining metabolic homeostasis during adaptive stress responses. However, the precise control mechanism of muscle mitochondrial quality and its physiological impacts remain unclear. Here, we demonstrate that FUNDC1, a mediator of mitophagy, plays a critical role in controlling muscle mitochondrial quality as well as metabolic homeostasis. Skeletal-muscle-specific ablation of FUNDC1 in mice resulted in LC3-mediated mitophagy defect, leading to impaired mitochondrial energetics. This caused decreased muscle fat utilization and endurance capacity during exercise. Interestingly, mice lacking muscle FUNDC1 were protected against high-fat-diet-induced obesity with improved systemic insulin sensitivity and glucose tolerance despite reduced muscle mitochondrial energetics. Mechanistically, FUNDC1 deficiency elicited a retrograde response in muscle that upregulated FGF21 expression, thereby promoting the thermogenic remodeling of adipose tissue. Thus, these findings reveal a pivotal role of FUNDC1-dependent mitochondrial quality control in mediating the muscle-adipose dialog to regulate systemic metabolism. : Mitochondrial quality is essential to muscle function. How muscle mitochondrial quality is regulated and its physiological impacts remain unclear. Fu et al. show that loss of FUNDC1-dependent mitochondrial quality control in muscle alleviates high-fat-diet-induced obesity and improves systemic glucose homeostasis through promoting exercise-independent fat burning in adipose tissue. Keywords: muscle, mitochondrial quality control, mitophagy, adaptive thermogenesis, metabolic homeostasis

Purpose Using the combined theoretical umbrella of organizational legitimacy theory, service-dominant logic, fairness heuristic theory and two-factor theory, the purpose of this paper is to investigate the effectiveness of different food recall strategies (recall proactiveness and compensation) in terms of both how consumers react (perceived organizational legitimacy and purchase intention) and how recall norms would influence the effectiveness in three countries. In addition to the reporting of important results, this paper provides implications for food companies to handle effectively the recalls, especially when the recalls are cross-country. Design/methodology/approach A 2 compensation (high vs low) ×2 recall strategy (proactive vs passive) scenario experiment was conducted in Hong Kong, the USA and Mainland China. After checking the effectiveness of manipulation, the paper tested the main effect and interaction effect of recall proactiveness and compensation on perceived organizational legitimacy and purchase intention. In addition, the mediating effect of perceived organizational legitimacy between recall strategies and purchase intention was also tested. Findings Significant main effect, interaction and mediation effect were found across the three countries with a different pattern. For the USA and Mainland China which have strong recall norms, the interaction found followed the predictions of the two-factory theory. However, the pattern found in Hong Kong, which has weak recall norms, followed the predictions of the fairness heuristic theory. Full mediation effect of perceived organizational legitimacy between compensation and purchase intention was found in the USA and Mainland China, while it was only partial in Hong Kong. For the mediation between proactiveness and purchase intention, full mediation was found in Hong Kong and the USA, while it was only partial in Mainland China. Originality/value First, this study differentiated food recall strategy into two dimensions – recall proactiveness and compensation. Second, this study tested the applicability of two-factor theory and fairness heuristic theory in recalls by testing the competing hypotheses proposed according to the two theories. Finally, this study can further help our understanding of the recall effectiveness across different recall norms.

The operating scheme of the Three Gorges Reservoir results in a summer drought in the water-level fluctuation zone during which plants grow vigorously. In the winter inundation season, soaking plants may decompose and release nutrients resulting in water quality deterioration. This study quantifies the contributions of the underwater decomposition of nine dominant plant species in the water-level fluctuation zone to nutrient release. The in-situ litterbag technique was used to study for soaking decomposition over 200days. All soaking plant species decomposed rapidly at an average rate of 1.99±0.33%d-1 in the early stage of soaking (0 to 30days) and at an average rate of only 0.07±0.04%d-1 in the later stage (30 to 200days). After 200days of soaking, the nine plant species released an average of 312.40±39.97gkg-1 organic carbon, 6.71±4.29gkg-1 of nitrogen and 2.25±1.25gkg-1 of phosphorus. A positive relationship was found between soaking plant decomposition rates and initial C/N ratios of 25 to 50, and a negative relationship where the C/N ratios were between 50 and 100. The amounts of total nitrogen or total phosphorus released were significantly negatively correlated with the initial C/N or C/P ratios of the plants. Among the studied plant species, Xanthium sibiricum Patr ex Widder showed high level of nutrient release via soaking decomposition. In contrast, Cynodon dactylon (Linn.) Pers. and Polygonum hydropiper exhibited low levels of nutrient release and are recommended as suitable species for the ecological restoration of the water-level fluctuation zone. Our results demonstrate that after 200days of soaking plant decomposition, the loadings of total organic carbon, nitrogen, and phosphorus in the water-level fluctuation zone of the Three Gorges Reservoir were 2942.1, 81.1, and 24.7kgha-1, respectively and therefore could potentially damage the aquatic environment of the reservoir.

Lactate dehydrogenase (LDH) catalyzes the interconversion of pyruvate and lactate, which are critical fuel metabolites of skeletal muscle particularly during exercise. However, the physiological relevance of LDH remains poorly understood. Here we show that Ldhb expression is induced by exercise in human muscle and negatively correlated with changes in intramuscular pH levels, a marker of lactate production, during isometric exercise. We found that the expression of Ldhb is regulated by exercise-induced peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α). Ldhb gene promoter reporter studies demonstrated that PGC-1α activates Ldhb gene expression through multiple conserved estrogen-related receptor (ERR) and myocyte enhancer factor 2 (MEF2) binding sites. Transgenic mice overexpressing Ldhb in muscle (muscle creatine kinase (MCK)-Ldhb) exhibited increased exercise performance and enhanced oxygen consumption during exercise. MCK-Ldhb muscle was shown to have enhanced mitochondrial enzyme activity and increased mitochondrial gene expression, suggesting an adaptive oxidative muscle transformation. In addition, mitochondrial respiration capacity was increased and lactate production decreased in MCK-Ldhb skeletal myotubes in culture. Together, these results identified a previously unrecognized Ldhb-driven alteration in muscle mitochondrial function and suggested a mechanism for the adaptive metabolic response induced by exercise training.

How to remove P effectively in eutrophic water is an urgent problem to be solved. In this study, a Fe-modified biochar was prepared by pyrolyzed wetland plant Thalia dealbata. The adsorption of P was investigated by using the prepared biochar (TBC-Fe) as an adsorbent. The effects of contact time, initial P concentration, temperature and initial solution pH on adsorption behavior of P on TBC-Fe were studied. The results showed that P adsorption process on TBC-Fe was controlled by internal and external diffusion of particles, due to the adsorption kinetic was better fitted by Intra-particle diffusion model. The adsorption isotherm on TBC-Fe was well performed by Langmuir model, with a maximum P adsorption capacity of 15.86 mg/g. The best adsorption performance was exhibited at 25°C with the initial pH of 10. Overall, the results indicate a promising option of utilizing Fe-modified biochar derived from wetland plants as an efficient remediation adsorbent for phosphorus in water. © The Authors, published by EDP Sciences, 2019.

In sodium ion batteries, heteroatom doping is deemed to be an important way to enhance the electrochemical activity of carbon-based anode materials. In this work, we report 3D nitrogen and sulfur equilibrium co-doping hollow carbon nanosheets for sodium ion battery anode, which can deliver a maximum capacity of 497 mA h g−1 under 0.2 A g−1, good rate capability (260 mA h g−1 under 50 A g−1 and 245 mA h g−1 under 60 A g−1), and good cycling stability (339 mA h g−1 under 5 A g−1 over 5000 cycling and 249 mA h g−1 under 10 A g−1 over 5000 cycling), suggesting wonderful electrochemical performance. To the best of our knowledge, the excellent performance of the long-term cyclability at such high rates is rarely reported for carbon-based sodium ion battery anodes. Meanwhile, the storage mechanism of sodium was studied by in-situ Raman spectroscopy, cyclic/linear sweep voltammetry and electrochemical impedance spectroscopy. Its superior properties can be attributed to the special three-dimensional hollow nanosheets with high specific surface, doping regulation of N and S elements to carbon structure and synergistic effect of nitrogen doping enhancing pseudocapacitive contributions.

Mitochondria are essential for maintaining skeletal muscle metabolic homeostasis during adaptive response to a myriad of physiologic or pathophysiological stresses. The mechanisms by which mitochondrial function and contractile fiber type are concordantly regulated to ensure muscle function remain poorly understood. Evidence is emerging that the Folliculin interacting protein 1 (Fnip1) is involved in skeletal muscle fiber type specification, function, and disease. In this study, Fnip1 was specifically expressed in skeletal muscle in Fnip1-transgenic (Fnip1Tg) mice. Fnip1Tg mice were crossed with Fnip1-knockout (Fnip1KO) mice to generate Fnip1TgKO mice expressing Fnip1 only in skeletal muscle but not in other tissues. Our results indicate that, in addition to the known role in type I fiber program, FNIP1 exerts control upon muscle mitochondrial oxidative program through AMPK signaling. Indeed, basal levels of FNIP1 are sufficient to inhibit AMPK but not mTORC1 activity in skeletal muscle cells. Gain-of-function and loss-of-function strategies in mice, together with assessment of primary muscle cells, demonstrated that skeletal muscle mitochondrial program is suppressed via the inhibitory actions of FNIP1 on AMPK. Surprisingly, the FNIP1 actions on type I fiber program is independent of AMPK and its downstream PGC-1α. These studies provide a vital framework for understanding the intrinsic role of FNIP1 as a crucial factor in the concerted regulation of mitochondrial function and muscle fiber type that determine muscle fitness., Author summary Mitochondria provide an essential source of energy to drive cellular processes and the function of mitochondria is particularly important in skeletal muscle, a metabolically demanding tissue that depends critically on mitochondria, accounting for ~40% of total body mass. In this study, we discovered an essential function of adaptor protein FNIP1 in the coordinated regulation of the mitochondrial and structural programs controlling muscle fitness. Using both gain-of-function and loss-of-function strategies in mice and muscle cells, we provide clear genetic data that demonstrate FNIP1-dependent signaling is crucial for muscle mitochondrial remodeling as well as type I muscle fiber specification. We also uncover that FNIP1 exerts control upon muscle mitochondrial program through AMPK but not mTORC1 signaling. Furthermore, we demonstrate that FNIP1 acts independently of PGC-1α to regulate fiber type specification. Hence, our study emphasizes FNIP1 as a dominant factor that coordinates mitochondrial and muscle fiber type programs that govern muscle fitness.

In this study, a heteroatom-doped porous biochar from waste biomass was prepared via a facile self-sacrificial template strategy for enhanced electrochemical capacitive performance. Numerous narrow pores and carbonized frameworks were formed by hydrothermally decomposing the unstable components in the biomass, which were further broadened to micropores and even larger mesopores through a molten salt activation method. The synthesized porous biochar displayed apparently increased specific surface area, up to 1138 m2 g−1, well-developed porous structure, and moderate heteroatom doping (5.35 at.% O and 1.02 at.% N), which offered more active storage sites and charge capacities. Consequently, the modified biochar exhibited significantly enhanced specific capacitance of 447 F g−1 at 0.2 A g−1, which was 1.6 and 6.0 times higher than that of the samples carbonized directly by molten salt and inert reduction methods, respectively. The findings indicate that the facile self-sacrificial template synthetic route of biochar does not only provide larger pores for reducing the ion diffusion resistance, but also introduces heteroatoms into the carbon frame to increase charge mobility. Moreover, the assembled two-electrode symmetric supercapacitor presented not only a specific capacitance of 367 F g−1 with an energy density of 12.75 Wh∙kg−1 but also an excellent stability after 10000 cycles.

A new benzothiazole-based fluorescent chemosensor (BZDM), namely 2-amino-3-(((E)-3-(benzo[d]thiazol-2-yl)-2-hydroxy-5-methylbenzylidene)amino)maleonitrile, has been designed and synthesized for detection of Al3+/Zn2+ in aqueous medium. The sensing behavior displayed that BZDM possessed an excellent selectivity towards Al3+/Zn2+ with a distinct fluorescence enhancement in DMSO/Tris-HCl buffer solution. The binding stoichiometry was determined to be 1: 1 between BZDM and Al3+/Zn2+ according to Job’s plot method and NMR analysis. The sensing of Al3+/Zn2+ was almost free from interference of other relevant metal ions. Under optimal conditions, the LOD value for Al3+ and Zn2+ was found to be 7.06 μM and 2.98 μM, separately. Notably, the probe was found to have good biological compatibility and was employed to detect Al3+/Zn2+ in living Hela cells.

In order to avoid the secondary pollution caused by the withering of plants, experiments on reasonable harvesting time of emerged plants in the constructed wetland (CWs) was conducted. The results showed that the best plant regrowth and nutrients removal efficiency by harvested plant were happened when plants were harvested at the withering period (January). Whenever plants were harvested, the removal amount of nitrogen and phosphorus in the CWs was greater than that in the non-harvesting CWs. When plants were harvested at the early growing period, the removal of nitrogen and phosphorus by the CWs reached the maximum, which were 92.39 mg·L−1 and 237.17 mg·L−1, respectively. Therefore, based on the plant regrowth and nutrient removal efficiency of the CWs, it is suggested to harvest emerged plants after the growth period (preferably the withering period), which will be most conductive to the long-term effective operation of the CWs.

Molybdenum-zeolite catalysts always suffer from severe carbon deposition and rapid deactivation in the methane dehydroaromatization (MDA) process. Herein, we present a strategy that controls spatial distance between Mo species and HMCM-22 zeolite over Mo/HMCM-22 catalysts, to inhibit the severe carbon deposition. Our characterization analyses demonstrate that the Mo/HMCM-22 catalysts possess the same active components, but the spatial distance plays a key role in determining product selectivity in the MDA process. The MDA performance reveals that Mo/HMCM-22-MM (mechanical milling) catalyst, with a medium spatial distance between Mo species and HMCM-22 zeolite, significantly inhibits carbon deposition and produces high selectivity to benzene. This work shows that spatial distance between molybdenum and zeolite is an important property for suppressing carbon deposition and improving benzene selectivity in MDA process.

Binary Cu/ZnO catalysts were prepared by solid-state method and tested for vapor-phase low-temperature methanol synthesis from CO2-containing syngas. The influence of H2C2O4/(Cu + Zn) molar ratio on the physicochemical properties and the corresponding catalytic activity was systematically studied. The space time yield (STY) of methanol exhibited a linear relationship with the Cu0 surface area, and increased linearly by enhancing the number of strongly acidic sites or moderately basic sites. The effects of various parameters on the methanol synthesis reaction were also investigated. C4-Red catalyst (H2C2O4/(Cu + Zn) = 4/1) exhibited the maximum turnover frequency (TOF, 11.4 × 10−3 s−1) and STY values (456.3 g/kg h−1), due to the larger Cu0 surface area, greater specific surface area, more strongly acidic sites and moderately basic sites. The strengthened Cu-ZnO interaction, superior CO and H2 adsorption capability as well as higher adsorbed CO and H2 amount also contributed to increasing the catalytic performance of C4-Red catalyst.

Upon adaption of skeletal muscle to physiological and pathophysiological stimuli, muscle fiber type and mitochondrial function are coordinately regulated. Recent studies have identified pathways involved in control of contractile proteins of oxidative‐type fibers. However, the mechanism for coupling of mitochondrial function to the muscle contractile machinery during fiber type transition remains unknown. Here, we show that the expression of the genes encoding type I myosins, Myh7/Myh7b and their intronic miR‐208b/miR‐499, parallels mitochondrial function during fiber type transitions. Using in vivo approaches in mice, we found that miR‐499 drives a PGC‐1α‐dependent mitochondrial oxidative metabolism program to match shifts in slow‐twitch muscle fiber composition. Mechanistically, miR‐499 directly targets Fnip1, an AMP‐activated protein kinase (AMPK)‐interacting protein that negatively regulates AMPK, a known activator of PGC‐1α. Inhibition of Fnip1 reactivated AMPK/PGC‐1α signaling and mitochondrial function in myocytes. Restoration of the expression of miR‐499 in the mdx mouse model of Duchenne muscular dystrophy (DMD) reduced the severity of DMD. Thus, we have identified a miR‐499/Fnip1/AMPK circuit that can serve as a mechanism to couple muscle fiber type and mitochondrial function.