Properties and Photocatalytic Activity of β

β-Ga2O3 nanorods are prepared by hydrothermal method and characterized by X-ray diffraction, high-resolution transmission electron microscopy, Raman spectroscopy, X-ray photoelectron spectroscopy, and photoluminescence spectra. The results reveal that high crystallinity, monoclinic phase of β-Ga2O3 nanorods were prepared with a diameter of about 60 nm and length of 500 nm. Photoluminescence study indicates that the β-Ga2O3 nanorods exhibit a broad blue light emission at room temperature. The β-Ga2O3 nanorods displayed high photocatalytic activity under simulated solar irradiation; after 2 h irradiation, over 95% of methylene blue solution and over 90% of methyl orange solution were decolorized. Since this process does not require additional hydrogen peroxide and uses solar light, it can be developed as an economically feasible and environmentally friendly method to treat dye effluent

Sema3A inactivates the ERK/JNK signalling pathways to alleviate inflammation and oxidative stress in lipopolysaccharide-stimulated rat endothelial cells and lung tissues

Semaphorin 3A (Sema3A) is a secretory member of the semaphorin family of immune response regulators. This research focuses on its effects on inflammation and oxidative stress in acute respiratory distress syndrome (ARDS). By analysing the GEO dataset GSE57011, we obtained Sema3A as the most downregulated gene in ARDS samples. Lipopolysaccharide (LPS) was used to stimulate rat pulmonary microvascular endothelial cells (PMVECs) and rats to induce ARDS-like symptoms in vitro and in vivo, respectively. LPS induced severe damage in rat lung tissues, in which reduced immunohistochemical staining of Sema3A was detected. Sema3A overexpression reduced apoptosis and angiogenesis of LPS-induced PMVECs and alleviated lung injury and pulmonary edoema of rats. Moreover, ELISA results showed that Sema3A overexpression downregulated the levels of inflammatory cytokines and oxidative stress markers both in PMVECs and the rat lung. Activation of ERK/JNK signalling aggravated LPS-induced damage on PMVECs; however, the aggravation was partly blocked by Sema3A, which suppressed phosphorylation of ERK/JNK. Overall, this study demonstrates that Sema3A inactivates the ERK/JNK signalling to ameliorate inflammation and oxidative stress in LPS-induced ARDS models. Sema3A might therefore represent a candidate option for ARDS treatment

Anticancer Activity and Mode of Action of Cu(II), Zn(II), and Mn(II) Complexes with 5-Chloro-2-<i>N</i>-(2-quinolylmethylene)aminophenol

Developing a new generation of anticancer metal-based drugs that can both kill tumor cells and inhibit cell migration is a promising strategy. Herein, we synthesized three Cu(II), Zn(II), and Mn(II) complexes derived from 5-chloro-2-N-(2-quinolylmethylene)aminophenol (C1–C3). Among these complexes, the Cu(II) complex (C1) showed significantly greater cytotoxicity toward lung cancer cell lines than cisplatin. C1 inhibited A549 cell metastasis and suppressed the growth of the A549 tumor in vivo. In addition, we confirmed the anticancer mechanism of C1 by triggering multiple mechanisms, including inducing mitochondrial apoptosis, acting on DNA, blocking cell cycle arrest, inducing cell senescence, and inducing DNA damage

Thermal Catalytic Decomposition of Dimethyl Methyl Phosphonate Using CuO-CeO2/&gamma;-Al2O3

Chemical warfare agents (CWAs) are highly toxic and fast-acting and are easy to cause large-scale poisoning to humans and livestock after being released. The activated carbon used for CWAs adsorption has disadvantages of limited adsorption capacity, easy aging and deactivation. Metal oxides have environmental stability, and they are characterized by long lasting and broad spectrum when used for thermal catalytic decomposition. Therefore, in this study, the supported copper&ndash;cerium catalyst CuO-CeO2/&gamma;-Al2O3 was prepared using an equal volume impregnation method. The thermal catalytic decomposition performance was studied using sarin CWAs simulant dimethyl methyl phosphonate (DMMP) as the target compound. The results show that the CuO-CeO2/&gamma;-Al2O3 catalyst with a CeO2 loading of 5% exhibited better thermal catalytic decomposition performance of DMMP. The catalyst provided protection against DMMP for 237 min at 350 &deg;C; CuO was highly dispersed on CuO-5% CeO2/&gamma;-Al2O3, and there was a strong interaction between Cu and Ce on CuO-5% CeO2/&gamma;-Al2O3, which promoted the generation of surface-adsorbed oxygen, leading to a better thermal catalytic decomposition performance of DMMP. This study is expected to provide a reference for the study of catalysts for the thermal catalytic decomposition of CWAs

Thermal Catalytic Decomposition of Dimethyl Methyl Phosphonate Using CuO-CeO₂/<i>γ</i>-Al₂O₃

Chemical warfare agents (CWAs) are highly toxic and fast-acting and are easy to cause large-scale poisoning to humans and livestock after being released. The activated carbon used for CWAs adsorption has disadvantages of limited adsorption capacity, easy aging and deactivation. Metal oxides have environmental stability, and they are characterized by long lasting and broad spectrum when used for thermal catalytic decomposition. Therefore, in this study, the supported copper–cerium catalyst CuO-CeO2/γ-Al2O3 was prepared using an equal volume impregnation method. The thermal catalytic decomposition performance was studied using sarin CWAs simulant dimethyl methyl phosphonate (DMMP) as the target compound. The results show that the CuO-CeO2/γ-Al2O3 catalyst with a CeO2 loading of 5% exhibited better thermal catalytic decomposition performance of DMMP. The catalyst provided protection against DMMP for 237 min at 350 °C; CuO was highly dispersed on CuO-5% CeO2/γ-Al2O3, and there was a strong interaction between Cu and Ce on CuO-5% CeO2/γ-Al2O3, which promoted the generation of surface-adsorbed oxygen, leading to a better thermal catalytic decomposition performance of DMMP. This study is expected to provide a reference for the study of catalysts for the thermal catalytic decomposition of CWAs

Catalytic Oxidative Decomposition of Dimethyl Methyl Phosphonate over CuO/CeO₂ Catalysts Prepared Using a Secondary Alkaline Hydrothermal Method

Bimetallic synergism plays an important role in lattice-doped catalysts. Therefore, lattice-doped bimetallic CuO/CeO2 catalysts were prepared by secondary alkaline hydrothermal reaction. During this process, the CeO2 nanomaterials were partially dissolved and recrystallized; thus, Cu ions were doped into the CeO2 lattice. The physical and chemical properties of CeO2, CuO/CeO2, and CuO were investigated. H2 temperature-programmed reduction characterization showed that the oxidation activity of CuO/CeO2 was significantly improved. X-ray photoelectron spectroscopy results showed that electron transfer occurred between Ce and Cu in the CuO/CeO2 catalyst. Additionally, Raman characterization confirmed the strong interaction between Cu and Ce. After CuO was loaded, the thermal catalytic decomposition performance of the catalyst was significantly improved with respect to the sarin simulant dimethyl methyl phosphonate (DMMP); with an increase in the Cu/Ce ratio, the performance first strengthened and then weakened. Additionally, the reaction tail gas and catalyst surface products were analyzed using mass spectrometry and ion chromatography, and the changes in the surface products during the thermal catalytic decomposition of DMMP were characterized at different temperatures using in situ diffuse reflectance infrared Fourier transform spectroscopy. Finally, the catalytic reaction pathways of DMMP on CeO2, CuO/CeO2, and CuO were inferred. The study results not only demonstrate an effective catalyst for the removal of nerve agent but also a feasible preparation method for lattice-doped bimetallic catalysts in the field of environmental protection

Metabolic heterogeneity in clear cell renal cell carcinoma revealed by single-cell RNA sequencing and spatial transcriptomics

Abstract Background Clear cell renal cell carcinoma is a prototypical tumor characterized by metabolic reprogramming, which extends beyond tumor cells to encompass diverse cell types within the tumor microenvironment. Nonetheless, current research on metabolic reprogramming in renal cell carcinoma mostly focuses on either tumor cells alone or conducts analyses of all cells within the tumor microenvironment as a mixture, thereby failing to precisely identify metabolic changes in different cell types within the tumor microenvironment. Methods Gathering 9 major single-cell RNA sequencing databases of clear cell renal cell carcinoma, encompassing 195 samples. Spatial transcriptomics data were selected to conduct metabolic activity analysis with spatial localization. Developing scMet program to convert RNA-seq data into scRNA-seq data for downstream analysis. Results Diverse cellular entities within the tumor microenvironment exhibit distinct infiltration preferences across varying histological grades and tissue origins. Higher-grade tumors manifest pronounced immunosuppressive traits. The identification of tumor cells in the RNA splicing state reveals an association between the enrichment of this particular cellular population and an unfavorable prognostic outcome. The energy metabolism of CD8+ T cells is pivotal not only for their cytotoxic effector functions but also as a marker of impending cellular exhaustion. Sphingolipid metabolism evinces a correlation with diverse macrophage-specific traits, particularly M2 polarization. The tumor epicenter is characterized by heightened metabolic activity, prominently marked by elevated tricarboxylic acid cycle and glycolysis while the pericapsular milieu showcases a conspicuous enrichment of attributes associated with vasculogenesis, inflammatory responses, and epithelial–mesenchymal transition. The scMet facilitates the transformation of RNA sequencing datasets sourced from TCGA into scRNA sequencing data, maintaining a substantial degree of correlation. Conclusions The tumor microenvironment of clear cell renal cell carcinoma demonstrates significant metabolic heterogeneity across various cell types and spatial dimensions. scMet exhibits a notable capability to transform RNA sequencing data into scRNA sequencing data with a high degree of correlation

A case study on the bearing characteristics of a bottom uplift pile in a layered foundation

Abstract The bottom uplift pile, which has been applied in practical projects, has the following advantages: the pile body is not easy to crack, good bearing characteristics, and small displacement of the pile top. Based on the bearing capacity test of foundation piles in the third stage expansion project of Lanzhou Zhongchuan International Airport, the upper part pile of the self-balancing test method was used to simulate the bottom uplift pile, and the anchor piles in the anchor pile method were regarded as normal uplift piles. The bearing characteristics of the bottom uplift pile in a layered foundation were studied by comparing these two kinds of piles. The results show that under the same displacement of the pile top, the ultimate uplift bearing capacity of the bottom uplift pile can be more than twice that of the normal uplift pile because of the fully exerted frictional resistance of the soil at the bottom of the pile, the Poisson effect of the pile body and the avoidance of the influence of pile body deformation on the pile top displacement. The maximum axial force of the bottom uplift pile appears at the bottom of the pile and gradually decreases from the bottom to the top, which is opposite to that of the normal uplift pile. The properties and thickness of the soil layers around the pile have a great influence on the distribution curves of the frictional resistance along the pile length of the two kinds of uplift piles. With changing soil layer conditions, the distribution curve may be a "parabola", a "straight line" or a "double line". The soil property plays a decisive role in the frictional resistance, which may cause softening. The influence of the pile diameter on the ultimate uplift bearing capacity is greater than that of the pile length, while the elastic modulus of the pile has little influence

Myocardial Injection of Apelin-Overexpressing Bone Marrow Cells Improves Cardiac Repair via Upregulation of Sirt3 after Myocardial Infarction

<div><p>Our previous study shows that treatment with apelin increases bone marrow cells (BMCs) recruitment and promotes cardiac repair after myocardial infarction (MI). The objective of this study was to investigate whether overexpression of apelin in BMCs improved cell therapy and accelerated cardiac repair and functional recovery in post-MI mice. Mouse myocardial infarction was achieved by coronary artery ligation and BMCs overexpressing apelin (apelin-BMCs) or GFP (GFP-BMCs) were injected into ischemic area immediately after surgery. <i>In vitro</i>, exposure of cultured BMCs to apelin led to a gradual increase in SDF-1á and CXCR4 expression. Intramyocardial delivery of apelin-BMCs in post-MI mice resulted in a significant increase number of APJ⁺/c-kit⁺/Sca1⁺ cells in the injected area compared to GFP-BMCs treated post-MI mice. Treatment with apelin-BMCs increased expression of VEGF, Ang-1 and Tie-2 in post-MI mice. Apelin-BMCs treatment also significantly increased angiogenesis and attenuated cardiac fibrosis formation in post-MI mice. Most importantly, treatment with apelin-BMCs significantly improved left ventricular (LV) systolic function in post-MI mice. Mechanistically, Apelin-BMCs treatment led to a significant increase in Sirtuin3 (Sirt3) expression and reduction of reactive oxygen species (ROS) formation. Treatment of cultured BMCs with apelin also increased Notch3 expression and Akt phosphorylation. Apelin treatment further attenuated stress-induced apoptosis whereas knockout of Sirt3 abolished anti-apoptotic effect of apelin in cultured BMCs. Moreover, knockout of Sirt3 significantly attenuated apelin-BMCs-induced VEGF expression and angiogenesis in post-MI mice. Knockout of Sirt3 further blunted apelin-BMCs-mediated improvement of cardiac repair and systolic functional recovery in post-MI mice. These data suggest that apelin improves BMCs therapy on cardiac repair and systolic function in post-MI mice. Upregulation of Sirt3 may contribute to the protective effect of apelin-BMCs therapy.</p></div