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The significance of bound states in the continuum (BICs) lies in their potential for theoretically infinite quality factors. However, their actual quality factors are limited by imperfections in fabrication, which lead to coupling with the radiation continuum. In this study, we present a novel approach to address this issue by introducing a merging BIC regime based on a Lieb lattice. By utilizing this approach, we effectively suppress the out-of-plane scattering loss, thereby enhancing the robustness of the structure against fabrication artifacts. Notably, unlike previous merging systems, our design does not rely on the up-down symmetry of metasurfaces. This characteristic grants more flexibility in applications that involve substrates and superstrates with different optical properties, such as microfluidic devices. Furthermore, we incorporate a lateral band gap mirror into the design to encapsulate the BIC structure. This mirror serves to suppress the in-plane radiation resulting from finite-size effects, leading to a remarkable ten-fold improvement in the quality factor. Consequently, our merged BIC metasurface, enclosed by the Lieb lattice photonic crystal mirror, achieves an exceptionally high-quality factor of 105 while maintaining a small footprint of 26.6 × 26.6 μm. Our findings establish an appealing platform that capitalizes on the topological nature of BICs within compact structures. This platform holds great promise for various applications, including optical trapping, optofluidics, and high-sensitivity biodetection, opening up new possibilities in these fields.

An aptasensor with dual-outputs was developed for malathion detection. Fe-MOF was synthesized to design favorable signal probes for catalytic amplification. Owing to the excellent peroxidase-like activity of Fe-MOF, the redox reaction was catalyzed to produce the dual-outputs of colorimetric and electrochemical. In this sensing strategy, malathion was captured by the aptamer on sensing interface, leading to the release of signal probe. Thanks to the catalytic amplification of Fe-MOF and the high capture effect of aptamer, the aptasensor produced a sensitive response for malathion. Based on the dual-signals of absorbance and current, the detection method for malathion was developed ranging from 10 ng/mL to 500 ng/mL. The detection limit of malathion was 5.8 ng/mL for colorimetric output and 4.6 ng/mL for electrochemical output. Furthermore, the aptasensor exhibited high specificity and good repeatability in malathion detection. Finally, the aptasensor was applied to detect malathion in fruit and vegetable samples with satisfactory recovery.

Morphing aircraft can change its aerodynamic configurations to obtain optimized aerodynamic performance. Smart material actuator and flexible skin are the key technologies of morphing aircraft. Smart materials have the advantages of light weight，simple structure，and large driving force. Flexible skin can meet the requirements of large deformation and withstand local aerodynamic loads，both of which have very good application prospects. In this paper，the research of actuators made of shape memory alloys，piezoelectric materials and magneto strictive materials is introduced. The development of flexible skin based on material elasticity and structure design is analyzed. The related research issue and interests are summarized and prospected.

BackgroundThe two-step approach, as the major method in reactor numerical calculation, faces the challenge of accuracy in calculating high-fidelity models because of limitations imposed by simplified assumptions such as assembly homogenization and the core diffusion calculation.PurposeThis study aims to validate the applicability of the two-step method in high-fidelity numerical simulation calculations and homogenization scheme of asymmetrical assemblies.MethodsBased on the Benchmark for Evaluation And Validation of Reactor Simulations Rev.2.0.2 (BEAVRS 2.02), the deterministic codes DRAGON5 and DONION5 were used to calculate the BEAVRS benchmark in the hot zero-power state. Firstly, a transport calculation was performed with DRAGON5 on the fuel assemblies. Then, the complete core calculation was done with DONJON5 using diffusion theory. Finally, the calculation errors of traditional homogenization, one-time multi zone homogenization, and multiple multi zone homogenization schemes were compared.ResultsThe results show that these calculations are comparable to the accuracy of the benchmark, with the deviation of critical boron concentration being less than 5×10-5 and the error of the control rod value calculation being within 5×10-4. Comparison results of the fission rate indicate that the average deviation of the assemblies near the asymmetric fuel assemblies is reduced from 5.62% to 3.345% using one-time multi zone homogenization scheme.ConclusionsThis study verifies the applicability of the two-step approach in high-fidelity numerical simulation calculations.

A variety of mouse models have been used to study the pathogenesis of pulmonary emphysema/ chronic obstructive pulmonary disease. The effect of cigarette smoke (CS) is believed to be strain dependent, because certain mouse strains are more susceptible or resistant to development of emphysema. However, the molecular basis of susceptibility of mouse strains to effects of CS is not known. We investigated the effect of CS on lungs of most of the commonly used mouse strains to study the molecular mechanism of susceptibility to effects of CS. C57BL/6J, A/J, AKR/J, CD-1, and 129SvJ mice were exposed to CS for 3 consecutive days, and various parameters of inflammatory and oxidative responses were assessed in lungs of these mice. We found that the C57BL/6J strain was highly susceptible, the A/J, AKR/J, and CD-I strains were moderately susceptible, and the 129SvJ strain was resistant to lung inflammatory and oxidant responses to CS exposure. The mouse strain that was more susceptible to effects of CS showed augmented lung inflammatory cell influx, activation of NF-[kappa]B and p38 MAPK, and increased levels of matrix metalloproteinase-9 and NF-[kappa]B-dependent proinflammatory cytokines compared with resistant mouse strains. Similarly, decreased levels of glutathione were associated with increased levels of lipid peroxidation products in susceptible mouse strains compared with resistant strains. Hence, we identified the susceptible and resistant mouse strains on the basis of the pattern of inflammatory and oxidant responses. Identification of sensitive and resistant mouse strains could be useful for studying the molecular mechanisms of effects of CS on inflammation and pharmacological interventional studies in CS-exposure mouse models. nuclear factor-[kappa]B; histone deacetylase-2; p38 MAPK; lipid peroxides; glutathione; chronic obstructive pulmonary disease

Nuclear erythroid-related factor 2 (Nrf2), a redox-sensitive transcription factor, is involved in transcriptional regulation of many antioxidant genes, including glutamate-cysteine ligase (GCL). Cigarette smoke (CS) is known to cause oxidative stress and deplete glutathione (GSH) levels in alveolar epithelial cells. We hypothesized that resveratrol, a polyphenolic phytoalexin, has antioxidant signaling properties by inducing GSH biosynthesis via the activation of Nrf2 and protects lung epithelial cells against CS-mediated oxidative stress. Treatment of human primary small airway epithelial and human alveolar epithelial (A549) cells with CS extract (CSE) dose dependently decreased GSH levels and GCL activity, effects that were associated with enhanced production of reactive oxygen species. Resveratrol restored CSE-depleted GSH levels by upregulation of GCL via activation of Nrf2 and also quenched CSE-induced release of reactive oxygen species. Interestingly, CSE failed to induce nuclear translocation of Nrf2 in A549 and small airway epithelial cells. On the contrary, Nrf2 was localized in the cytosol of alveolar and airway epithelial cells due to CSE-mediated posttranslational modifications such as aldehyde/carbonyl adduct formation and nitration. On the other hand, resveratrol attenuated CSE-mediated Nrf2 modifications, thereby inducing its nuclear translocation associated with GCL gene transcription, as demonstrated by GCL-promoter reporter and Nrf2 small interfering RNA approaches. Thus resveratrol attenuates CSE-mediated GSH depletion by inducing GSH synthesis and protects epithelial cells by reversing CSE-induced posttranslational modifications of Nrf2. These data may have implications in dietary modulation of antioxidants in treatment of chronic obstructive pulmonary disease. glutamate-cysteine ligase; 4-hydroxy-2-nonenal; chronic obstructive pulmonary disease; polyphenols; reactive oxygen species

The silent information regulator 2 (Sir2) family of proteins (sirtuins or SIRTs), which belong to class III histone/protein deacetylases, have been implicated in calorie restriction, aging, and inflammation. We hypothesized that cigarette smoke-mediated proinflammatory cytokine release is regulated by SIRT1 by its interaction with NF-[kappa]B in a monocyte-macrophage cell line (MonoMac6) and in inflammatory cells of rat lungs. Cigarette smoke extract (CSE) exposure to MonoMac6 cells caused dose- and time-dependent decreases in SIRT1 activity and levels, which was concomitant to increased NF-[kappa]B-dependent proinflammatory mediator release. Similar decrements in SIRT1 were also observed in inflammatory cells in the lungs of rats exposed to cigarette smoke as well as with increased levels of several NF-[kappa]B-dependent proinflammatory mediators in bronchoalveolar lavage fluid and in lungs. Sirtinol, an inhibitor of SIRT1, augmented, whereas resveratrol, an activator of SIRT1, inhibited CSE-mediated proinflammatory cytokine release. CSE-mediated inhibition of SIRT1 was associated with increased NF-[kappa]B levels. Furthermore, we showed that SIRT1 interacts with the RelA/p65 subunit of NF-[kappa]B, which was disrupted by cigarette smoke, leading to increased acetylation RelA/ p65 in MonoMac6 cells. Thus our data show that SIRT1 regulates cigarette smoke-mediated proinflammatory mediator release via NF[kappa]B, implicating a role of SIRT1 in sustained inflammation and aging of the lungs. oxidants; resveratrol; MonoMac6 cells; chronic obstructive pulmonary disease; histone; acetylation; deacetylase

Cigarette smoke-mediated oxidative stress induces an inflammatory response in the lungs by stimulating the release of proinflammatory cytokines. Chromatin remodeling due to histone acetylation and deacetylation is known to play an important role in transcriptional regulation of proinflammatory genes. The aim of this study was to investigate the molecular mechanism(s) of inflammatory responses caused by cigarette smoke extract (CSE) in the human macrophage-like cell line MonoMac6 and whether the treatment of these cells with the antioxidant glutathione (GSH) monoethyl ester, or modulation of the thioredoxin redox system, can attenuate cigarette smoke-mediated IL-8 release. Exposure of MonoMac6 cells to CSE (1% and 2.5%) increased IL-8 and TNF-[alpha] production vs. control at 24 h and was associated with significant depletion of GSH levels associated with increased reactive oxygen species release in addition to activation of NF-[kappa]B. Inhibition of IKK ablated the CSE-mediated IL-8 release, suggesting that this process is dependent on the NF-[kappa]B pathway. CSE also reduced histone deacetylase (HDAC) activity and HDAC1, HDAC2, and HDAC3 protein levels. This was associated with posttranslational modification of HDAC1, HDAC2, and HDAC3 protein by nitrotyrosine and aldehyde-adduct formation. Pretreatment of cells with GSH monoethyl ester, but not thioredoxin/thioredoxin reductase, reversed cigarette smoke-induced reduction in HDAC levels and significantly inhibited IL-8 release. Thus cigarette smoke-induced release of IL-8 is associated with activation of NF-[kappa]B via IKK and reduction in HDAC levels/activity in macrophages. Moreover, cigarette smoke-mediated proinflammatory events are regulated by the redox status of the cells. oxidants; glutathione; MonoMac6 cells; I[kappa]B kinase; chronic obstructive pulmonary disease