Bismuth oxide modified V₂C MXene as a Schottky catalyst with enhanced photocatalytic oxidation for photo-denitration activities

In this work, a new composite photocatalyst was synthesized by flower-like Bi2O3 and two-dimensional multilayer V2C using a facile hydrothermal method. Compared with the pristine sample, the specific surface area of Bi2O3/V2C MXene composite is significantly increased, which is favorable to improve the photocatalytic efficiency. The analysis of the UV-vis absorption spectrum and band gap energy shows that the construction of heterojunction broadens the light response range, improves the light absorption capacity, and obtains a narrower band gap than any of the single component, which is beneficial to the utilization of light. PL, TPC and EIS analysis revealed that Bi2O3/V2C MXene composite had stronger carrier mobility, which further confirmed that the photocatalytic oxidation performance of the system was the dominant reason in the photocatalytic NO pollutant removal process. This study provides a new idea for better understanding the two-dimensional MXene material-based photocatalyst and improving the NO removal efficiency.</p

Identifying the Ground State Geometry of a MoN₂ Sheet through a Global Structure Search and Its Tunable p‑Electron Half-Metallicity

MoN₂ and MoS₂ sheets are representatives of two-dimensional transition metal dinitrides and dichalcogenides, respectively. Their similarity in atomic ratios misled people to make an incorrect assumption in previous studies that the former adopts the geometry of the latter. However, compared with S, N is smaller and has fewer valence electrons, and N is more effective in mediating magnetic couplings; therefore, a different geometry and different properties can be expected for the MoN₂ sheet. Here using a global structure search, for the first time we have identified the ground state geometry of this sheet named Tetra-MoN₂ that is much more stable than the H phase proposed previously. Different from the metallic nature of H-MoN₂, Tetra-MoN₂ is a semiconductor having an indirect band gap of 1.41 eV with a flexible strain tunability. In particular, Tetra-MoN₂ can exhibit rich half-metallic behaviors mediated by the polarized p electron of N and induced by low-concentration hole doping and small strains that are readily achievable experimentally

DataSheet1_The serum soluble scavenger with 5 domains levels: A novel biomarker for individuals with heart failure.PDF

Background: We aimed to explore the relationship between the serum Soluble Scavenger with 5 Domains (SSC5D) levels and heart failure (HF).Methods and Results: We retrospectively enrolled 276 patients diagnosed with HF or normal during hospitalization in Shanghai General Hospital between September 2020 and December 2021. Previously published RNA sequencing data were re-analyzed to confirm the expression profile of SSC5D in failing and non-failing human and mouse heart tissues. Quantitative real-time polymerase chain reaction assay was used to quantify Ssc5d mRNA levels in murine heart tissue after myocardial infarction and transverse aortic constriction surgery. To understand the HF-induced secreted proteins profile, 1,755 secreted proteins were investigated using human dilated cardiomyopathy RNA-seq data, and the results indicated that SSC5D levels were significantly elevated in failing hearts compared to the non-failing. Using single-cell RNA sequencing data, we demonstrated that Ssc5d is predominantly expressed in cardiac fibroblasts. In a murine model of myocardial infarction or transverse aortic constriction, Ssc5d mRNA levels were markedly increased compared with those in the sham group. Similarly, serum SSC5D levels were considerably elevated in the HF group compared with the control group [15,789.35 (10,745.32–23,110.65) pg/mL, 95% CI (16,263.01–19,655.43) vs. 8,938.72 (6,154.97–12,778.81) pg/mL, 95% CI (9,337.50–11,142.93); p Conclusion: We concluded that SSC5D was a specific response to HF. Serum SSC5D may function as a novel biomarker and therapeutic target for patients with HF.</p

DataSheet1_SLC2A9 rs16890979 reduces uric acid absorption by kidney organoids.docx

Introduction: The excretion and absorption of uric acid (UA) by the kidneys helps regulate serum UA levels. GLUT9, encoded by SLC2A9, is mainly expressed in the renal tubules responsible for UA absorption. SLC2A9 polymorphisms are associated with different serum UA levels. However, the lack of proper in vitro models has stalled research on the mechanisms of single nucleotide polymorphisms (SNPs) that affect UA metabolism in human urate transporters.Methods: In this study, we constructed a gene-edited human embryonic stem cells-9 (ESC-H9) derived kidney organoid bearing rs16890979, an SLC2A9 missense mutation with undetermined associations with hyperuricemia or hypouricemia. Kidney organoids derived from ESC-H9 with genetical overexpression (OE) and low expression (shRNA) of SLC2A9 to serve as controls to study the function of SLC2A9. The function of rs16890979 on UA metabolism was evaluated after placing the organoids to urate-containing medium and following histopathological analysis.Results: The kidney organoids with heterozygous or homozygous rs16890979 mutations showed normal SLC2A9 expression levels and histological distribution, phenotypically similar to the wild-type controls. However, reduced absorption of UA by the kidney organoids with rs16890979 mutants was observed. This finding together with the observation that UA absorption is increased in organoids with SLC2A9 overexpression and decreased in those with SLC2A9 knockdown, suggest that GLUT9 is responsible for UA absorption, and the rs16890979 SNP may compromise this functionality. Moreover, epithelial-mesenchymal transition (EMT) was detected in organoids after UA treatment, especially in the kidney organoid carrying GLUT9OE, suggesting the cytobiological mechanism explaining the pathological features in hyperuricosuria-related renal injury.Discussion: This study showing the transitional value of kidney organoid modeling the function of SNPs on UA metabolism. With a defined genetic background and a confirmed UA absorption function should be useful for studies on renal histological, cellular, and molecular mechanisms with this organoid model.</p

Design, Synthesis, and Biological Evaluation of (<i>E</i>)‑3,4-Dihydroxystyryl Aralkyl Sulfones and Sulfoxides as Novel Multifunctional Neuroprotective Agents

Novel (<i>E</i>)-3,4-dihydroxystyryl aralkyl sulfones and sulfoxides were designed and synthesized as new analogues of <b>1</b>, which showed interesting multifunctional neuroprotective effects, including antioxidative and antineuroinflammatory properties. Specifically, target compounds display excellent potency in scavenging reactive free radicals and demonstrate potent effects against various kinds of toxicities, including H₂O₂, 6-hydroxydopamine, and lipopolysaccharide in different types of neuronal cells. The antioxidative properties of the target compounds are more potent than that of <b>1</b>, and the antineuroinflammatory properties are less strong than that of <b>1</b>. According to the parallel artificial membrane permeation assay for the blood–brain barrier, target compounds possess greater blood–brain barrier (BBB) permeability than <b>1</b>. In short, due to improvement of the antioxidative effect, stability, and BBB permeability, (<i>E</i>)-3,4-dihydroxystyryl aralkyl sulfones and sulfoxides can thus be considered as potential multifunctional neuroprotective agents and serve as new lead candidates in the treatment of neurodegenerative diseases

Table1_Differential expression of cyclins CCNB1 and CCNG1 is involved in the chondrocyte damage of kashin-beck disease.DOCX

The purpose of this study was clarify the relationship between the differential expression of cyclins CCNB1 and CCNG1 and chondrocyte damage in Kashin-Beck disease. Systematic review and high-throughput sequencing of chondrocytes derived from Kashin-Beck disease patients were combined to identify the differentially expressed cyclins and cyclin-dependent kinase genes. In parallel, weaned SD rats were treated with low selenium for 4 weeks and then T-2 toxin for 4 weeks. Knee cartilage was collected to harvest chondrocytes for gene expression profiling. Finally, the protein expression levels of CCNB1 and CCNG1 were verified in knee cartilage tissue of Kashin-Beck disease patients and normal controls by immunohistochemical staining. The systematic review found 52 cartilage disease-related cyclins and cyclin-dependent kinase genes, 23 of which were coexpressed in Kashin-Beck disease, including 15 upregulated and 8 downregulated genes. Under the intervention of a low selenium diet and T-2 toxin exposure, CCNB1 (FC = 0.36) and CCNG1 (FC = 0.73) showed a downward expression trend in rat articular cartilage. Furthermore, compared to normal controls, CCNB1 protein in Kashin-Beck disease articular cartilage was 71.98% and 66.27% downregulated in the superficial and middle zones, respectively, and 12.06% upregulated in the deep zone. CCNG1 protein was 45.66% downregulated in the superficial zone and 12.19% and 9.13% upregulated in the middle and deep zones, respectively. The differential expression of cyclins CCNB1 and CCNG1 may be related to articular cartilage damage in Kashin-Beck disease.</p

Novel Pyridinone Derivatives As Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs) with High Potency against NNRTI-Resistant HIV‑1 Strains

Novel 6-substituted-4-cycloalkyloxy-pyridin-2­(1<i>H</i>)-ones were synthesized as non-nucleoside reverse transcriptase inhibitors (NNRTIs), and their biological activity was evaluated. Most of the compounds, especially <b>26</b> and <b>22</b>, bearing a 3-isopropyl and 3-iodine group, respectively, exhibited highly potent activity against wild-type HIV-1 strains and those resistant to reverse transcriptase inhibitors (RTIs). The diastereoisomers of <b>26</b>-<i>trans</i> and <b>26</b>-<i>cis</i> were synthesized separately and confirmed with HPLC and NOESY spectra. The <b>26</b>-<i>trans</i> isomers had an activity about 400-fold more potent than that of <b>26</b>-<i>cis</i>. The pair of <b>26</b>-<i>trans</i> enantiomers, one of the most potent inhibitors with EC₅₀ of 4 nM and selectivity index (SI) of 75000, was highly effective against a panel of RTIs-resistant strains with single (Y181C and K103N) or double (A17) mutations in reverse transcriptase. The results suggest that these novel pyridinone derivatives have the potential to be further developed as new antiretroviral drugs with improved antiviral efficacy and drug resistance profile

Image1_Differential expression of cyclins CCNB1 and CCNG1 is involved in the chondrocyte damage of kashin-beck disease.JPEG

The purpose of this study was clarify the relationship between the differential expression of cyclins CCNB1 and CCNG1 and chondrocyte damage in Kashin-Beck disease. Systematic review and high-throughput sequencing of chondrocytes derived from Kashin-Beck disease patients were combined to identify the differentially expressed cyclins and cyclin-dependent kinase genes. In parallel, weaned SD rats were treated with low selenium for 4 weeks and then T-2 toxin for 4 weeks. Knee cartilage was collected to harvest chondrocytes for gene expression profiling. Finally, the protein expression levels of CCNB1 and CCNG1 were verified in knee cartilage tissue of Kashin-Beck disease patients and normal controls by immunohistochemical staining. The systematic review found 52 cartilage disease-related cyclins and cyclin-dependent kinase genes, 23 of which were coexpressed in Kashin-Beck disease, including 15 upregulated and 8 downregulated genes. Under the intervention of a low selenium diet and T-2 toxin exposure, CCNB1 (FC = 0.36) and CCNG1 (FC = 0.73) showed a downward expression trend in rat articular cartilage. Furthermore, compared to normal controls, CCNB1 protein in Kashin-Beck disease articular cartilage was 71.98% and 66.27% downregulated in the superficial and middle zones, respectively, and 12.06% upregulated in the deep zone. CCNG1 protein was 45.66% downregulated in the superficial zone and 12.19% and 9.13% upregulated in the middle and deep zones, respectively. The differential expression of cyclins CCNB1 and CCNG1 may be related to articular cartilage damage in Kashin-Beck disease.</p