V2C MXene-modified g-C3N4 for enhanced visible-light photocatalytic activity

Increasing the efficiency of charge transfer and separation efficiency of photogenerated carriers are still the main challenges in the field of semiconductor-based photocatalysts. Herein, we synthesized g-C3N4@V2C MXene photocatalyst by modifying g-C3N4 using V2C MXene. The prepared photocatalyst exhibited outstanding photocatalytic performance under visible light. The degradation efficiency of methyl orange by g-C3N4@V2C MXene photocatalyst was as high as 94.5%, which is 1.56 times higher than that by g-C3N4. This was attributed to the V2C MXene inhibiting the rapid recombination of photogenerated carriers and facilitating rapid transfer of photogenerated electrons (e) from g-C3N4 to MXene. Moreover, g-C3N4@V2C MXene photocatalyst showed good cycling stability. The photocatalytic performance was higher than 85% after three cycles. Experiments to capture free radicals revealed that superoxide radicals (02) are the main contributors to the photocatalytic activity. Thus, the proposed g-C3N4@V2C MXene photocatalyst is a promising visible-light catalyst.Comment: 20 pages, 9 figure

Comprehensive Analyses of miRNA-mRNA Network and Potential Drugs in Idiopathic Pulmonary Arterial Hypertension

Introduction. Idiopathic pulmonary arterial hypertension (IPAH) is a severe cardiopulmonary disease with a relatively low survival rate. Moreover, the pathogenesis of IPAH has not been fully recognized. Thus, comprehensive analyses of miRNA-mRNA network and potential drugs in IPAH are urgent requirements. Methods. Microarray datasets of mRNA and microRNA (miRNA) in IPAH were searched and downloaded from Gene Expression Omnibus (GEO). Differentially expressed genes (DEGs) and differentially expressed miRNAs (DEMIs) were identified. Then, the DEMI-DEG network was conducted with associated comprehensive analyses including Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, and protein-protein interaction (PPI) network analysis, while potential drugs targeting hub genes were investigated using L1000 platform. Results. 30 DEGs and 6 DEMIs were identified in the lung tissue of IPAH. GO and KEGG pathway analyses revealed that these DEGs were mostly enriched in antimicrobial humoral response and African trypanosomiasis, respectively. The DEMI-DEG network was conducted subsequently with 4 DEMIs (hsa-miR-34b-5p, hsa-miR-26b-5p, hsa-miR-205-5p, and hsa-miR-199a-3p) and 16 DEGs, among which 5 DEGs (AQP9, SPP1, END1, VCAM1, and SAA1) were included in the top 10 hub genes of the PPI network. Nimodipine was identified with the highest CMap connectivity score in L1000 platform. Conclusion. Our study conducted a miRNA-mRNA network and identified 4 miRNAs as well as 5 mRNAs which may play important roles in the pathogenesis of IPAH. Moreover, we provided a new insight for future therapies by predicting potential drugs targeting hub genes

Peroxidasin promotes diabetic vascular endothelial dysfunction induced by advanced glycation end products via NOX2/HOCl/Akt/eNOS pathway

Reactive oxygen species (ROS) derived from NADPH oxidases (NOX) plays an essential role in advanced glycation end products (AGEs)-induced diabetic vascular endothelial dysfunction. Peroxidasin (PXDN, VPO1) is one member of peroxidases family that catalyzes hydrogen peroxide (H2O2) to hypochlorous acid (HOCl). This present study aimed to elucidate the role of PXDN in promoting vascular endothelial dysfunction induced by AGEs in diabetes mellitus. We found that, compared to non-diabetic (db/m) mice, PXDN expression was notably increased in db/db mice with impaired endothelium-dependent relaxation. Knockdown of PXDN in vivo through tail vein injection of siRNA restored the impaired endothelium-dependent relaxation function of db/db mice which is accompanied with up-regulation of eNOS Ser1177 phosphorylation and NO production. AGEs significantly elevated expression of PXDN and 3-Cl-Tyr, but decreased phosphorylation of Akt and eNOS and NO release in HUVECs. All these effects induced by AGEs were remarkable alleviated by silencing PXDN with small interfering RNAs. In addition, HOCl treatment alone as well as HOCl added with Akt inhibitor MK2206 inhibited phosphorylation of Akt and eNOS, reducing NO production. More importantly,AGEs-induced up-regulation of PXDN and 3-Cl-Tyr with endothelial dysfunction were transformed by NOX2 silencing and H2O2 scavengers. Thus, these results support the conclusion that PXDN promotes AGEs-induced diabetic vascular endothelial dysfunction by attenuating eNOS phosphorylation at Ser1177 via NOX2/HOCl/Akt pathway

Distribution and antimicrobial resistance patterns of urinary pathogens in preoperative midstream urine cultures from Chinese patients with urinary calculi: a meta-analysis

Abstract Background and objective This study comprehensively evaluates the distribution patterns and antimicrobial resistance profiles of urinary pathogens in Preoperative midstream urine cultures collected from patients with urinary calculi in China over the last two decades. Methods A cross-sectional analysis of 41 studies was conducted. A systematic search across various databases, including Wanfang Data, CNKI, SinoMed, Embase, PubMed, and Web of Science, was carried out, covering the time period from 2002 to 2022. Using R 4.2.1 software, a meta-analysis was performed to assess heterogeneity using Cochran’s Q test and the I2 statistic. Results In the analysis of preoperative midstream urine cultures from Chinese patients with urinary calculi, gram-negative bacteria dominated at 69%, with Escherichia coli (43%), Klebsiella pneumoniae (8%), Proteus mirabilis (6%), Pseudomonas aeruginosa (5%), Acinetobacter baumannii (3%), and Enterobacter cloacae (4%) being prominent. Gram-positive organisms included Enterococcus faecalis (9%), Enterococcus faecium (5%), and Staphylococcus aureus (4%). Over time, proportions of Proteus mirabilis, Enterococcus faecalis, and Staphylococcus aureus decreased, while Klebsiella pneumoniae and Pseudomonas aeruginosa increased. Notably, Escherichia coli proportion reduced from 37 to 33% within the last two decades. Antimicrobial resistance analysis indicated declining resistance in E. coli (e.g., co-trimoxazole from 73 to 55%, gentamicin from 64 to 40%), but rising resistance in piperacillin and cefotaxime (34–60%). Enterococcus faecalis exhibited increasing resistance to ampicillin (5–69%), gentamicin (59–94%), and tetracycline (77–89%) over time, while resistance to levofloxacin and ciprofloxacin notably decreased (72–16% and 49–8%, respectively). Conclusion Over the past two decades, the proportion of gram-negative bacteria was declined, while the proportion of gram-positive bacteria increased. Escherichia coli remained the most common pathogen in the urine culture of patients with urinary calculi in China and the resistance of Escherichia coli to commonly used antibiotics increased. Clinicians should select appropriate antibiotics according to the results of urine culture and drug sensitivity test to reduce the occurrence of antibiotic resistance

A novel large deletion of the CYLD

Abstract Background CYLD cutaneous syndrome (CCS; syn. Brooke‐Spiegler syndrome) is a rare autosomal dominant hereditary disease characterized by multiple adnexal skin tumors including cylindromas, spiradenomas, and trichoepitheliomas. More than 100 germline mutations of the cylindromatosis (CYLD) gene have been reported in CCS and most of them are frameshift mutations or small alterations. Methods We identified a large, three‐generation Chinese family with CCS, which consisted of 18 living family members, including six affected individuals. To explore the molecular biology of this family, we carried out targeted next‐generation sequencing and Affymetrix CytoScan HD SNP array to analyze the mutation in the CYLD gene. Results A novel large deletion mutation, NC_000016.9:g.(50826498_50827517)_(50963389‐50967346)del was found in the proband of this family. This deletion results in the loss of a nearly 140 kb fragment of the CYLD gene, spanning exons 17 ~ 20, which represent the coding regions of the ubiquitin‐specific protease domain. Further quantitative polymerase chain reaction proved that all patients and two proband‐related family members carried this large deletion. Conclusions Our study expands the types of mutations in CCS and will undoubtedly provide valuable information for genetic counseling for families affected by the condition

Vascular peroxidase 1 is a novel regulator of cardiac fibrosis after myocardial infarction

Cardiac fibrosis is the most important mechanism contributing to cardiac remodeling after myocardial infarction (MI). VPO1 is a heme enzyme that uses hydrogen peroxide (H2O2) to produce hypochlorous acid (HOCl). Our previous study has demonstrated that VPO1 regulates myocardial ischemic reperfusion and renal fibrosis. We investigated the role of VPO1 in cardiac fibrosis after MI. The results showed that VPO1 expression was robustly upregulated in the failing human heart with ischemic cardiomyopathy and in a murine model of MI accompanied by severe cardiac fibrosis. Most importantly, knockdown of VPO1 by tail vein injection of VPO1 siRNA significantly reduced cardiac fibrosis and improved cardiac function and survival rate. In VPO1 knockdown mouse model and cardiac fibroblasts cultured with TGF-β1, VPO1 contributes to cardiac fibroblasts differentiation, migration, collagen I synthesis and proliferation. Mechanistically, the fibrotic effects following MI of VPO1 manifested partially through HOCl formation to activate Smad2/3 and ERK1/2. Thus, we conclude that VPO1 is a crucial regulator of cardiac fibrosis after MI by mediating HOCl/Smad2/3 and ERK1/2 signaling pathways, implying a promising therapeutic target in ischemic cardiomyopathy. Keywords: Cardiac fibrosis, Myocardial infarction, Vascular peroxidase1, Cardiac remodeling, Cardiac fibroblast

DataSheet_2_Outcomes of hyperlactatemia on admission in critically ill patients with acute myocardial infarction: A retrospective study from MIMIC-IV.csv

BackgroundIt has not been verified whether there is a correlation between admission hyperlactatemia and outcomes in critically ill patients with acute myocardial infarction (AMI), especially in large data studies, which we aimed to do in this study.MethodsFor this retrospective study, we extracted analysis data from a famous online intensive care unit database, the Medical Information Mart for Intensive Care (MIMIC)-IV. Included patients were divided into four groups according to the serum lactate level on admission. Hospital mortality and mortality over time were the main outcomes. To explore the relationship between admission hyperlactatemia and outcomes in critically ill patients with AMI, logistic regression, Cox regression, Kaplan-Meier curves, and subgroup analyses were used.Results2171 patients matching the selection criteria were enrolled in this study. After adjusting for potential confounding factors, hyperlactatemia on admission contributed to increased short-term mortality in critically ill patients with AMI. The adjusted odds ratio for hospital mortality were 1.62, 3.46 and 5.28 in the mild, moderate, and severe hyperlactatemia groups (95% CI: 1.20-2.18, 2.15-5.58, and 2.20-12.70, respectively). The adjusted hazard ratio for 7-day and 30-day mortality were 1.99 and 1.35 (95% CI: 1.45-2.73 and 1.09-1.67) in the mild hyperlactatemia group, 3.33 and 2.31 (95% CI: 2.22-4.99 and 1.72-3.10) in the moderate hyperlactatemia group, 4.81 and 2.91 (95% CI: 2.86-8.08 and 1.88-4.50) in the severe hyperlactatemia group. The adjusted hazard ratio for 1-year and 5-year mortality were 2.03 and 1.93 (95% CI: 1.58-2.62 and 1.52-2.47) in the moderate hyperlactatemia group, 1.92 and 1.74 (95% CI: 1.28-2.89 and 1.17-2.59) in the severe hyperlactatemia group. Subgroup analyses indicated that the positive correlation between serum lactate level on admission and short-term mortality of critically ill patients with AMI was similar in the subgroups of cardiogenic shock and acute heart failure (P for interaction > 0.05).ConclusionHyperlactatemia, especially moderate and severe hyperlactatemia, on admission is closely related to higher short-term mortality incidence in critically ill patients with AMI. The relationship between serum lactate level on admission and short-term mortality of critical AMI patients is stable in subgroups of cardiogenic shock and acute heart failure.</p

DataSheet_1_Outcomes of hyperlactatemia on admission in critically ill patients with acute myocardial infarction: A retrospective study from MIMIC-IV.docx

BackgroundIt has not been verified whether there is a correlation between admission hyperlactatemia and outcomes in critically ill patients with acute myocardial infarction (AMI), especially in large data studies, which we aimed to do in this study.MethodsFor this retrospective study, we extracted analysis data from a famous online intensive care unit database, the Medical Information Mart for Intensive Care (MIMIC)-IV. Included patients were divided into four groups according to the serum lactate level on admission. Hospital mortality and mortality over time were the main outcomes. To explore the relationship between admission hyperlactatemia and outcomes in critically ill patients with AMI, logistic regression, Cox regression, Kaplan-Meier curves, and subgroup analyses were used.Results2171 patients matching the selection criteria were enrolled in this study. After adjusting for potential confounding factors, hyperlactatemia on admission contributed to increased short-term mortality in critically ill patients with AMI. The adjusted odds ratio for hospital mortality were 1.62, 3.46 and 5.28 in the mild, moderate, and severe hyperlactatemia groups (95% CI: 1.20-2.18, 2.15-5.58, and 2.20-12.70, respectively). The adjusted hazard ratio for 7-day and 30-day mortality were 1.99 and 1.35 (95% CI: 1.45-2.73 and 1.09-1.67) in the mild hyperlactatemia group, 3.33 and 2.31 (95% CI: 2.22-4.99 and 1.72-3.10) in the moderate hyperlactatemia group, 4.81 and 2.91 (95% CI: 2.86-8.08 and 1.88-4.50) in the severe hyperlactatemia group. The adjusted hazard ratio for 1-year and 5-year mortality were 2.03 and 1.93 (95% CI: 1.58-2.62 and 1.52-2.47) in the moderate hyperlactatemia group, 1.92 and 1.74 (95% CI: 1.28-2.89 and 1.17-2.59) in the severe hyperlactatemia group. Subgroup analyses indicated that the positive correlation between serum lactate level on admission and short-term mortality of critically ill patients with AMI was similar in the subgroups of cardiogenic shock and acute heart failure (P for interaction > 0.05).ConclusionHyperlactatemia, especially moderate and severe hyperlactatemia, on admission is closely related to higher short-term mortality incidence in critically ill patients with AMI. The relationship between serum lactate level on admission and short-term mortality of critical AMI patients is stable in subgroups of cardiogenic shock and acute heart failure.</p

Layer-by-Layer Self-Assembly: Toward Magnetic Films with Tunable Anisotropy

Highly anisotropic magnetic films are possible to fabricate by control of the coupling between individual magnetic particles. Selective control over coupling in the horizontal and vertical directions are of both fundamental and practical interest. Here we show such control in the multiple layer-by-layer (LBL) self-assembly of layered double hydroxide (LDH) nanosheets (<i>x</i> = 1, 2, 3 and 4) with thicknesses of 5–15 nm, co-assembled with 3-aminopropyl-trimethoxysilane (APTS) modified spherical Fe₃O₄ nanoparticles (APTS-Fe₃O₄ NPs) on quartz substrates. The electrostatic charge density on the LDH sheets, controlled by the Mg/Al composition ratio, affects the NP packing in a single horizontal layer, while the thickness of the LDH sheets controls magnetic coupling between layers. The tunable magnetic properties (coercivity <i>H</i>_c, saturation magnetization <i>M</i>_s, anisotropy, and blocking temperatures) are measured as a function of these parameters. The maximum saturation magnetizations <i>M</i>_s, 36.3 and 25.1 emu·g^–1 in the perpendicular and parallel direction, respectively, are found for the sample of <i>x</i> = 3 = Mg/Al ratio in the LDH layer, and 15 nm LDH layer thickness. This work provides a general method to adjust the anisotropy of magnetic films based on directional control of coupling of magnetic nanoparticles between and across, LDH nanosheets. We outline how higher anisotropy and even finer control could be achieved by pH and composition control over the electrostatic charge of the assembly components

Layer-by-Layer Assembly of Carbon Dots-Based Ultrathin Films with Enhanced Quantum Yield and Temperature Sensing Performance

Carbon dots (CDs), an rising kind of fluorescent carbon material, have been extensively studied due to their unique physicochemical properties, but the research on solid state devices and applications is rather lacking. Herein, we report the fabrication of fluorescent ultrathin films (UTFs) by embedding CDs into the 2D layered double hydroxides (LDHs) nanosheets through layer-by-layer assembly. The resulting UTFs present long-range ordered structure and improved luminescent properties compared with the CDs drop-casted films, including quantum yield (57.17% vs 3.04%) and fluorescence lifetime (14.47 ns vs 0.813 ns). This significant enhancement is due to the molecular level dispersion of CDs and the confinement of photoexcited electrons imposed by LDH nanosheets, which is confirmed by both experimental studies and density functional theoretical (DFT) calculations. Moreover, the UTFs display temperature-responsive photoluminescence (PL) and electrochemiluminescence (ECL) performances. Therefore, this work provides a facile method for the design and fabrication of CD UTFs with excellent luminescent properties, which can be potentially used in optical/optoelectronic sensing devices