Innovative Material-Based Wearable Non-Invasive Electrochemical Sweat Sensors towards Biomedical Applications.

Sweat is an accessible biofluid that provides useful physiological information about the body's biomolecular state and systemic health. Wearable sensors possess various advantageous features, such as lightweight design, wireless connectivity, and compatibility with human skin, that make them suitable for continuous monitoring. Wearable electrochemical sweat sensors can diagnose diseases and monitor health conditions by detecting biomedical signal changes in sweat. This paper discusses the state-of-the-art research in the field of wearable sweat sensors and the materials used in their construction. It covers biomarkers present in sweat, sensing modalities, techniques for sweat collection, and ways to power these sensors. Innovative materials are categorized into three subcategories: sweat collection, sweat detection, and self-powering. These include substrates for sensor fabrication, analyte detection electrodes, absorbent patches, microfluidic devices, and self-powered devices. This paper concludes by forecasting future research trends and prospects in material-based wearable non-invasive sweat sensors.

Mung Bean Starch and Mung Bean Starch Sheet Jelly: NaCl-Based Characteristics Variation.

Empirical evidence indicates that NaCl can improve the quality of mung bean starch sheet jelly (MBSS) when properly incorporated. In this study, by comparison with a sample without NaCl, the influences of NaCl (1.5-8%, w/w) on the physicochemical and structural properties of mung bean starch (MBS) and the quality of MBSS were investigated. MBS with added NaCl had greater gelatinization temperature and pasting parameters but lower gelatinization enthalpy than native MBS. With the addition of NaCl, the drying rate of MBSS first accelerated and then declined in the oven-drying process. The addition of NaCl improved the cooking properties of MBSS but decreased the hardness of cooked MBSS. Rheological results implied that the linear viscoelastic region of cooked MBSS decreased with the NaCl addition, and the storage modulus and tan δ were more frequency-dependent than the loss modulus of cooked MBSS. The addition of NaCl gradually increased the toughness of dried MBSS and the overall acceptability of cooked MBSS. Furthermore, NaCl decreased the structure order degree of starch in MBSS. Correlation analysis demonstrated that the quality of MBSS had a significant correlation with the molecular and lamellar order of starch. Overall, NaCl could improve the quality of MBSS by regulating the thermal, gelatinizing, and structural properties of MBS.

NLRP3 Inflammasome Mediates Silica-induced Lung Epithelial Injury and Aberrant Regeneration in Lung Stem/Progenitor Cell-derived Organotypic Models.

Silica-induced lung epithelial injury and fibrosis are vital pathogeneses of silicosis. Although the NOD-like receptor protein 3 (NLRP3) inflammasome contributes to silica-induced chronic lung inflammation, its role in epithelial injury and regeneration remains unclear. Here, using mouse lung stem/progenitor cell-derived organotypic systems, including 2D air-liquid interface and 3D organoid cultures, we investigated the effects of the NLRP3 inflammasome on airway epithelial phenotype and function, cellular injury and regeneration, and the potential mechanisms. Our data showed that silica-induced NLRP3 inflammasome activation disrupted the epithelial architecture, impaired mucociliary clearance, induced cellular hyperplasia and the epithelial-mesenchymal transition in 2D culture, and inhibited organoid development in 3D system. Moreover, abnormal expression of the stem/progenitor cell markers SOX2 and SOX9 was observed in the 2D and 3D organotypic models after sustained silica stimulation. Notably, these silica-induced structural and functional abnormalities were ameliorated by MCC950, a selective NLRP3 inflammasome inhibitor. Further studies indicated that the NF-κB, Shh-Gli and Wnt/ß-catenin pathways were involved in NLRP3 inflammasome-mediated abnormal differentiation and dysfunction of the airway epithelium. Thus, prolonged NLRP3 inflammasome activation caused injury and aberrant lung epithelial regeneration, suggesting that the NLRP3 inflammasome is a pivotal target for regulating tissue repair in chronic inflammatory lung diseases.

Knockdown of long noncoding RNA MIAT attenuates hypoxia-induced cardiomyocyte injury by regulating the miR-488-3p/Wnt/ß-catenin pathway.

Dysfunction of cardiomyocytes contributes to the development of acute myocardial infarction (AMI). Nonetheless, the regulatory mechanism of lncRNA myocardial infarction-associated transcript (MIAT) in cardiomyocyte injury remains largely unclear. The cardiomyocyte injury was assessed via cell viability and apoptosis using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) and flow cytometry, respectively. The levels of MIAT, microRNA (miR)-488-3p, and Wnt5a were detected via quantitative real-time polymerase chain reaction and Western blot. After bioinformatical analysis, the binding between miR-488-3p and MIAT or Wnt5a was confirmed via dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays. Our results showed that MIAT expression was increased in AC16 cells after hypoxia treatment. Silencing of MIAT alleviated hypoxia-induced viability reduction, apoptosis increase, and Wnt/ß-catenin pathway activation. MIAT directly targeted miR-488-3p. MiR-488-3p might repress hypoxia-induced cardiomyocyte injury, and its knockdown reversed the effect of MIAT depletion on cardiomyocyte injury. Wnt5a was validated as a target of miR-488-3p. Wnt5a expression restoration attenuated the influence of MIAT knockdown on hypoxia-triggered cardiomyocyte injury. Our findings demonstrated that downregulation of MIAT might mitigate hypoxia-induced cardiomyocyte injury partly through miR-488-3p mediated Wnt/ß-catenin pathway.

Acetylene hydrogenation catalyzed by bare and Ni doped CeO2(110): the role of frustrated Lewis pairs.

Ceria (CeO2) has recently been found to catalyze the selective hydrogenation of alkynes, which has stimulated much discussion on the catalytic mechanism on various facets of reducible oxides. In this work, H2 dissociation and acetylene hydrogenation on bare and Ni doped CeO2(110) surfaces are investigated using density functional theory (DFT). Similar to that on the CeO2(111) surface, our results suggest that catalysis is facilitated by frustrated Lewis pairs (FLPs) formed by oxygen vacancies (Ovs) on the oxide surfaces. On bare CeO2(110) with a single Ov (CeO2(110)-Ov), two surface Ce cations with one non-adjacent O anion are shown to form (Ce3+-Ce4+)/O quasi-FLPs, while for the Ni doped CeO2(110) surface with one (Ni-CeO2(110)-Ov) or two (Ni-CeO2(110)-2Ov) Ovs, one Ce and a non-adjacent O counterions are found to form a mono-Ce/O FLP. DFT calculations indicate that Ce/O FLPs facilitate the H2 dissociation via a heterolytic mechanism, while the resulting surface O-H and Ce-H species catalyze the subsequent acetylene hydrogenation. With CeO2(110)-Ov and Ni-CeO2(110)-2Ov, our DFT calculations suggest that the first hydrogenation step is the rate-determining step with a barrier of 0.43 and 0.40 eV, respectively. For Ni-CeO2(110)-Ov, the reaction is shown to be controlled by the H2 dissociation with a barrier of 0.41 eV. These barriers are significantly lower than that (about 0.7 eV) on CeO2(111), explaining the experimentally observed higher catalytic efficiency of the (110) facet of ceria. The change of the rate-determining step is attributed to the different electronic properties of Ce in the Ce/O FLPs - the Ce f states closer to the Fermi level not only facilitate the heterolytic dissociation of H2 but also lead to a higher barrier of acetylene hydrogenation.

Design of Effective Catalysts for Selective Alkyne Hydrogenation by Doping of Ceria with a Single-Atom Promotor.

Since the discovery that ceria is an active catalyst for selective hydrogenation of alkynes, there has been much debate on the catalytic mechanism. In this work, we propose, based on density functional theory (DFT) investigations, a mechanism that involves the heterolytic dissociation of H2 at oxygen vacancies of CeO2(111), facilitated by frustrated Lewis pairs consisting of spatially separated O and Ce sites. The resulting O-H and Ce-H species effectively catalyze the hydrogenation of acetylene, avoiding the overstabilization of the C2H3* intermediate in a previously proposed mechanism. On the basis of our mechanism, we propose the doping of ceria by Ni as a means to create oxygen vacancies. Interestingly, the Ni dopant is not directly involved in the catalytic reaction, but serves as a single-atom promoter. Experimental studies confirm the design principles and demonstrate much higher activity for Ni-doped ceria in selective hydrogenation of acetylene. The combined results from DFT calculations and experiment provide a basis to further develop selective hydrogenation catalysts based on earth-abundant materials.

Inhibition of p38MAPK potentiates mesenchymal stem cell therapy against myocardial infarction injury in rats.

The present study aimed to investigate the protective effect of mesenchymal stem cell (MSC) therapy in combination with p38 mitogen­activated protein (MAPK) inhibition against myocardial infarction (MI) injury in rats, and to elucidate the underlying mechanisms. An MI model was established by ligation of the anterior descending branch of the left coronary artery. The rats were divided into four groups: MSC transplantation, p38MAPK inhibitor (SB203580), MSC + SB203580 and model control group. HE staining and a TUNEL assay were performed to evaluate pathological changes and apoptosis. The expression levels of p38MAPK and transforming growth factor ß­activated kinase 1 (TAK1) were determined using reverse transcription­polymerase chain reaction and western blot analyses. As shown by HE staining, classical morphological changes, including irregular cell arrangement and inflammatory infiltration were observed in the model rats, whereas MSC therapy or injection of the p38MAPK inhibitor ameliorated these pathological changes. Of note, the combined application of MSCs with the p38MAPK inhibitor exerted additive effects. The TUNEL assay showed that the combined application of MSCs with p38MAPK inhibitor also led to potentiation of effects, compared with either MSCs therapy or p38MAPK inhibitor injection alone. Mechanistically, the combined application of MSCs with p38MAPK inhibitor decreased the expression levels of TAK1 and p38MAPK at the mRNA and protein levels. In conclusion, p38MAPK inhibition potentiated the protective effects of MSCs therapy against MI in rats.

Non-Born-Oppenheimer state-to-state dynamics of the N((2)D) + H(2) → NH(X(3)Sigma(-)) + H reaction: influence of the Renner-Teller coupling.

This publication examines the influence of electronically nonadiabatic Renner-Teller coupling between the two lowest-lying electronic states of NH(2) on state-to-state reaction dynamics. The fully Coriolis coupled quantum mechanical calculations were carried out on the recently developed NH(2) potential energy surfaces of both the X̃(2)A″ and Ã(2)A' states. It is shown that the Renner-Teller coupling has a dramatic effect on the low-lying ro-vibrational states on the excited Ã(2)A' potential, but its impact on the differential and integral cross sections of the N((2)D) + H(2) → NH(X(3)Sigma(-)) + H reaction is relatively minor.

An ab initio global potential-energy surface for NH2(A(2)A') and vibrational spectrum of the Renner-Teller A(2)A'-X(2)A" system.

A global potential-energy surface for the first excited electronic state of NH(2)(A(2)A(')) has been constructed by three-dimensional cubic spline interpolation of more than 20,000 ab initio points, which were calculated at the multireference configuration-interaction level with the Davidson correction using the augmented correlation-consistent polarized valence quadruple-zeta basis set. The (J=0) vibrational energy levels for the ground (X(2)A(")) and excited (A(2)A(')) electronic states of NH(2) were calculated on our potential-energy surfaces with the diagonal Renner-Teller terms. The results show a good agreement with the experimental vibrational frequencies of NH(2) and its isotopomers.

State-to-state dynamics of H + O2 reaction, evidence for nonstatistical behavior.

Converged differential and integral cross sections are reported for the H + O2 --> OH + O reaction on an improved potential energy surface of HO2(X2A'') using a dynamically exact quantum wave packet method and Gaussian weighted quasi-classical trajectory method. The complex-forming mechanism is confirmed by strong forward and backward scattering peaks and by highly inverted OH rotational state distributions. Both the quantum and classical results provide strong evidence for nonstatistical behavior in this important reaction.

A new ab initio potential-energy surface for NH2(X 2A") and quantum studies of NH2 vibrational spectrum and rate constant for the N(2D)+H2-->NH+H reaction.

A new global potential-energy surface for the ground electronic state of NH(2)(X (2)A(")) has been constructed by three-dimensional cubic spline interpolation of more than 20 000 ab initio points, which were calculated at the multireference configuration-interaction level with Davidson correction using the augmented correlation-consistent polarized valence quadruple-zeta basis set. The new potential is shown to yield better overall agreement with the experimental vibrational frequencies of NH(2) and its isotopomers. In addition, the rate constant for the N((2)D)+H(2)(X (1)Sigma(g) (+))-->NH(X (3)Sigma(-))+H((2)S) reaction was calculated up to 600 K and the agreement with experimental data is substantially improved over previous results.