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A deployable structure can significantly change its geometric shape by switching lattice configurations. Using compliant mechanisms as the lattice units can prevent wear and friction among multi-part mechanisms. This work presents two distinctive deployable structures based on a programmable compliant bistable lattice. Several novel parameters are introduced into the bistable mechanism to better control the behaviour of bistable mechanisms. By adjusting the defined geometry parameters, the programmable bistable lattices can be optimized for specific targets such as a larger deformation range or higher stability. The first structure is designed to perform 1D deployable movement. This structure consists of multi-series-connected bistable lattices. In order to explore the 3D bistable characteristic, a cylindrical deployable mechanism is designed based on the curved double tensural bistable lattice. The investigation of bistable lattices mainly involves four types of bistable mechanisms. These bistable mechanisms are obtained by dividing the long segment of traditional compliant bistable mechanisms into two equal parts and setting a series of angle data to them, respectively. The experiment and FEA simulation results confirm the feasibility of the compliant deployable structures.

A conventional linear guiding mechanism refers to the slide rail guides composed of multiple assemble parts. These guiding mechanisms suffer from many adverse effects, including lubrication, wear and assembly issues. A novel compliant guiding mechanism is proposed in this paper to address these common problems, and this mechanism transfers or transforms motion, force and energy via the deformation of flexible members. This linear guide is designed in a cylindrical shape, and the centre platform moves along its axis (i.e., the motion direction). The proposed linear guide consists of several in-parallel curved compound double parallelogram mechanisms (CDPMs) connected by the same number of decoupling parallelogram mechanisms. Nonlinear finite element analysis (FEA) is used for stiffness analysis and shows that applying the decoupling mechanisms to the detached linear guide (the in-parallel curved CDPMs only) can dramatically improve the stiffness in undesired movement (bearing) directions while keeping its original stiffness along its axis. The nonlinear FEA can capture the stiffness variation by considering all the structural deformation. The issue of bearing-direction stiffness degradation of the detached linear guide is dealt with by applying decoupling mechanisms. The static experimental test is conducted on a 3D printed prototype and shows that the stiffness in the motion direction is nearly constant (linear). The results obtained from the experimental test show good agreement with those obtained from the nonlinear FEA with a maximum error of 9.76%.

Hyperspectral anomaly detection is used to recognize unusual patterns or anomalies in hyperspectral data. Currently, many spectral–spatial detection methods have been proposed with a cascaded manner; however, they often neglect the complementary characteristics between the spectral and spatial dimensions, which easily leads to yield high false alarm rate. To alleviate this issue, a spectral–spatial information fusion (SSIF) method is designed for hyperspectral anomaly detection. First, an isolation forest is exploited to obtain spectral anomaly map, in which the object-level feature is constructed with an entropy rate segmentation algorithm. Then, a local spatial saliency detection scheme is proposed to produce the spatial anomaly result. Finally, the spectral and spatial anomaly scores are integrated together followed by a domain transform recursive filtering to generate the final detection result. Experiments on five hyperspectral datasets covering ocean and airport scenes prove that the proposed SSIF produces superior detection results over other state-of-the-art detection techniques.

Molybdenum oxide (MoOX) has been widely utilized as a hole transport layer (HTL) in crystalline silicon (c-Si) solar cells, owing to characteristics such as a wide bandgap and high work function. However, the relatively low conductivity of MoOX films and their poor contact performance at the MoOX-based hole-selective contact severely degrade device performance, particularly because they limit the fill factor (FF). Oxygen vacancies are of paramount importance in governing the conductivity of MoOX films. In this work, MoOX films were modified through ultraviolet irradiation (UV-MoOX), resulting in MoOX films with tunable oxygen vacancies. Compared to untreated MoOX films, UV-MoOX films contain a higher density of oxygen vacancies, leading to an enhancement in conductivity (2.124 × 10−3 S/m). In addition, the UV-MoOX rear contact exhibits excellent contact performance, with a contact resistance of 20.61 mΩ·cm2, which is significantly lower than that of the untreated device. Consequently, the application of UV-MoOX enables outstanding hole selectivity. The power conversion efficiency (PCE) of the solar cell with an n-Si/i-a-Si:H/UV-MoOX/Ag rear contact reaches 24.15%, with an excellent FF of 84.82%.

Fibroblast growth factor 21 (FGF21) has been only reported to prevent type 1 diabetic nephropathy (DN) in the streptozotocin-induced type 1 diabetes mellitus (T1DM) mouse model. However, the FVB (Cg)-Tg (Cryaa-Tag, Ins2-CALM1) 26OVE/PneJ (OVE26) transgenic mouse is a widely recommended mouse model to recapture the most important features of T1DM nephropathy that often occurs in diabetic patients. In addition, most previous studies focused on exploring the preventive effect of FGF21 on the development of DN. However, in clinic, development of therapeutic strategy has much more realistic value compared with preventive strategy since the onset time of DN is difficult to be accurately predicted. Therefore, in the present study OVE26 mice were used to investigate the potential therapeutic effects of FGF21 on DN. Four-month-old female OVE26 mice were intraperitoneally treated with recombinant FGF21 at a dose of 100 μg/kg/day for 3 months. The diabetic and non-diabetic control mice were treated with phosphate-buffered saline at the same volume. Renal functions, pathological changes, inflammation, apoptosis, oxidative stress and fibrosis were examined in mice of all groups. The results showed that severe renal dysfunction, morphological changes, inflammation, apoptosis, and fibrosis were observed in OVE26 mice. However, all the renal abnormalities above in OVE26 mice were significantly attenuated by 3-month FGF21 treatment associated with improvement of renal adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) activity and sirtuin 1 (SIRT1) expression. Therefore, this study demonstrated that FGF21 might exert therapeutic effects on DN through AMPK-SIRT1 pathway.

Zinc is an essential trace element that is often reduced under the type 1 diabetic condition. Previous studies demonstrated that zinc deficiency enhanced type 1 diabetes-induced liver injury and that zinc supplementation significantly helped to prevent this. Due to the differences in pathogenesis between type 1 and type 2 diabetes, it is unknown whether zinc supplementation can induce a beneficial effect on type 2 diabetes-induced liver injury. This possible protective mechanism was investigated in the present study. A high-fat diet, along with a one-time dose of streptozotocin, was applied to metallothionein (MT) knockout mice, nuclear factor-erythroid 2-related factor (Nrf) 2 knockout mice, and age-matched wild-type (WT) control mice, in order to induce type 2 diabetes. This was followed by zinc treatment at 5 mg/kg body weight given every other day for 3 months. Global metabolic disorders of both glucose and lipids were unaffected by zinc supplementation. This induced preventive effects on conditions caused by type 2 diabetes like oxidative stress, apoptosis, the subsequent hepatic inflammatory response, fibrosis, hypertrophy, and hepatic dysfunction. Additionally, we also observed that type 2 diabetes reduced hepatic MT expression, while zinc supplementation induced hepatic MT expression. This is a crucial antioxidant. A mechanistic study showed that MT deficiency blocked zinc supplementation-induced hepatic protection under the condition of type 2 diabetes. This suggested that endogenous MT is involved in the hepatic protection of zinc supplementation in type 2 diabetic mice. Furthermore, zinc supplementation-induced hepatic MT increase was unobserved once Nrf2 was deficient, indicating that Nrf2 mediated the upregulation of hepatic MT in response to zinc supplementation. Results of this study indicated that zinc supplementation prevented type 2 diabetes-induced liver injury through the activation of the Nrf2-MT-mediated antioxidative pathway.

Acute alcoholism commonly targets the myocardium, triggering acute alcoholic cardiomyopathy (ACM). Strong evidence suggested that mitochondrial dysfunction‐induced myocardial oxidative stress is involved in the subcellular pathogenesis of acute ACM. We investigated whether astaxanthin (AST), an antioxidant lutein carotenoid, prevents acute ACM and explored the underlying mechanisms. C57BL/6J mice were used to model ethanol‐induced ACM and were treated with AST (100 mg/kg/day) alongside the autophagy inhibitor, 3‐methyladenine (10 mg/kg/day). Cardiac function, heart pathology, cardiac hypertrophy, cardiomyocyte apoptosis, oxidative stress and mitochondrial function were evaluated, respectively in response to ethanol and/or AST. The in vivo study showed that ethanol‐induced cardiac dysfunction, morphological injury, cardiomyocyte apoptosis and oxidative stress were mitigated by AST. AST's anti‐apoptotic effects against ethanol were confirmed in vitro. Ethanol‐induced cardiac apoptosis is closely associated with mitochondrial dysfunction which was attenuated by AST characterised by inhibiting fission and promoting fusion, as well as maintaining stable mitochondrial membrane potential, increased ATP production, enhanced biogenesis and restored mitophagy. Autophagy inhibition suppressed AST‐induced myocardial protection, indicating that myocardial mitophagy mediates AST effects. The present study demonstrates that AST induces cardiac protection against acute ACM by improving cardiac function, reducing pathological changes, and inhibiting oxidative stress, inflammation and apoptosis through preserved myocardial mitophagy‐mediated mitochondrial homeostasis.

Molybdenum oxide (MoO ) has been widely utilized as a hole transport layer (HTL) in crystalline silicon ( -Si) solar cells, owing to characteristics such as a wide bandgap and high work function. However, the relatively low conductivity of MoO films and their poor contact performance at the MoO -based hole-selective contact severely degrade device performance, particularly because they limit the fill factor (FF). Oxygen vacancies are of paramount importance in governing the conductivity of MoO films. In this work, MoO films were modified through ultraviolet irradiation (UV-MoO ), resulting in MoO films with tunable oxygen vacancies. Compared to untreated MoO films, UV-MoO films contain a higher density of oxygen vacancies, leading to an enhancement in conductivity (2.124 × 10 S/m). In addition, the UV-MoO rear contact exhibits excellent contact performance, with a contact resistance of 20.61 mΩ·cm , which is significantly lower than that of the untreated device. Consequently, the application of UV-MoO enables outstanding hole selectivity. The power conversion efficiency (PCE) of the solar cell with an n-Si/i-a-Si:H/UV-MoO /Ag rear contact reaches 24.15%, with an excellent FF of 84.82%.

Molybdenum oxide (MoO[sub.X]) has been widely utilized as a hole transport layer (HTL) in crystalline silicon (c-Si) solar cells, owing to characteristics such as a wide bandgap and high work function. However, the relatively low conductivity of MoO[sub.X] films and their poor contact performance at the MoO[sub.X]-based hole-selective contact severely degrade device performance, particularly because they limit the fill factor (FF). Oxygen vacancies are of paramount importance in governing the conductivity of MoO[sub.X] films. In this work, MoO[sub.X] films were modified through ultraviolet irradiation (UV-MoO[sub.X]), resulting in MoO[sub.X] films with tunable oxygen vacancies. Compared to untreated MoO[sub.X] films, UV-MoO[sub.X] films contain a higher density of oxygen vacancies, leading to an enhancement in conductivity (2.124 × 10[sup.−3] S/m). In addition, the UV-MoO[sub.X] rear contact exhibits excellent contact performance, with a contact resistance of 20.61 mΩ·cm[sup.2], which is significantly lower than that of the untreated device. Consequently, the application of UV-MoO[sub.X] enables outstanding hole selectivity. The power conversion efficiency (PCE) of the solar cell with an n-Si/i-a-Si:H/UV-MoO[sub.X]/Ag rear contact reaches 24.15%, with an excellent FF of 84.82%.

We assessed whether concomitant exposure of human monocytes to bacterial agents and different engineered nanoparticles can affect the induction of protective innate memory, an immune mechanism that affords better resistance to diverse threatening challenges. Monocytes were exposed in vitro to nanoparticles of different chemical nature, shape and size either alone or admixed with LPS, and cell activation was assessed in terms of production of inflammatory (TNFα, IL-6) and anti-inflammatory cytokines (IL-10, IL-1Ra). After return to baseline conditions, cells were re-challenged with LPS and their secondary “memory” response measured. Results show that nanoparticles alone are essentially unable to generate memory, while LPS induced a tolerance memory response (less inflammatory cytokines, equal or increased anti-inflammatory cytokines). LPS-induced tolerance was not significantly affected by the presence of nanoparticles during the memory generation phase, although with substantial donor-to-donor variability. This suggests that, despite the overall lack of significant effects on LPS-induced innate memory, nanoparticles may have donor-specific effects. Thus, future nanosafety assessment and nanotherapeutic strategies will need a personalized approach in order to ensure both the safety and efficacy of nano medical compounds for individual patients.