80 research outputs found

    Image2_Comprehensive analysis of senescence-associated genes in sepsis based on bulk and single-cell sequencing data.TIF

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    Background: Sepsis is a pathological state resulting from dysregulated immune response in host during severe infection, leading to persistent organ dysfunction and ultimately death. Senescence-associated genes (SAGs) have manifested their potential in controlling the proliferation and dissemination of a variety of diseases. Nevertheless, the correlation between sepsis and SAGs remains obscure and requires further investigation.Methods: Two RNA expression datasets (GSE28750 and GSE57065) specifically related to sepsis were employed to filter hub SAGs, based on which a diagnostic model predictive of the incidence of sepsis was developed. The association between the expression of the SAGs identified and immune-related modules was analyzed employing Cell-type Identification By Estimating Relative Subsets Of RNA Transcripts (CIBERSORT) and Microenvironment Cell Populations-counter (MCP-counter) analysis. The identified genes in each cohort were clustered by unsupervised agreement clustering analysis and weighted gene correlation network analysis (WGCNA).Results: A diagnostic model for sepsis established based on hub genes (IGFBP7, GMFG, IL10, IL18, ETS2, HGF, CD55, and MMP9) exhibited a strong clinical reliability (AUC = 0.989). Sepsis patients were randomly assigned and classified by WGCNA into two clusters with distinct immune statuses. Analysis on the single-cell RNA sequencing (scRNA-seq) data revealed high scores of SAGs in the natural killer (NK) cells of the sepsis cohort than the healthy cohort.Conclusion: These findings suggested a close association between SAGs and sepsis alterations. The identified hub genes had potential to serve as a viable diagnostic marker for sepsis.</p

    Image1_Comprehensive analysis of senescence-associated genes in sepsis based on bulk and single-cell sequencing data.TIF

    No full text
    Background: Sepsis is a pathological state resulting from dysregulated immune response in host during severe infection, leading to persistent organ dysfunction and ultimately death. Senescence-associated genes (SAGs) have manifested their potential in controlling the proliferation and dissemination of a variety of diseases. Nevertheless, the correlation between sepsis and SAGs remains obscure and requires further investigation.Methods: Two RNA expression datasets (GSE28750 and GSE57065) specifically related to sepsis were employed to filter hub SAGs, based on which a diagnostic model predictive of the incidence of sepsis was developed. The association between the expression of the SAGs identified and immune-related modules was analyzed employing Cell-type Identification By Estimating Relative Subsets Of RNA Transcripts (CIBERSORT) and Microenvironment Cell Populations-counter (MCP-counter) analysis. The identified genes in each cohort were clustered by unsupervised agreement clustering analysis and weighted gene correlation network analysis (WGCNA).Results: A diagnostic model for sepsis established based on hub genes (IGFBP7, GMFG, IL10, IL18, ETS2, HGF, CD55, and MMP9) exhibited a strong clinical reliability (AUC = 0.989). Sepsis patients were randomly assigned and classified by WGCNA into two clusters with distinct immune statuses. Analysis on the single-cell RNA sequencing (scRNA-seq) data revealed high scores of SAGs in the natural killer (NK) cells of the sepsis cohort than the healthy cohort.Conclusion: These findings suggested a close association between SAGs and sepsis alterations. The identified hub genes had potential to serve as a viable diagnostic marker for sepsis.</p

    Transformation Mechanism of Magnesium and Aluminum Precursor Solution into Crystallites of Layered Double Hydroxide

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    Layered double hydroxides (LDHs), members of a family of two-dimensional anionic clay with flexibility in composition, have found a wide variety of applications in industry, including as additives in polymers, as precursors to magnetic materials, in biology and medicine, in catalysis, and in environmental remediation. A detailed understanding of the mechanism of the LDH formation should gain deep insight on the synthetic methodologies of the material and further allow the properties of the resulting LDH to be tailored to specific applications. Herein, we report a systematic investigation of the formation mechanism of the typical MgAl-LDH by urea precipitation method from a magnesium and aluminum precursor salt solution. It is revealed that, at the first stage of the synthesis, amorphous colloidal hydroxide aluminum is formed from the aluminum precursor salt solution. Then, the amorphous hydroxides are transformed into the crystallites of oxide-hydroxide aluminum boehmite γ-AlOOH, accompanying the continuous incorporation of surrounding Mg<sup>2+</sup> into the sheet of the lamellar γ-AlOOH, leading to the charge imbalance of the sheet, which destroys the hydrogen bonds existing between the sheets. Subsequently, the carbonate ions in the solution are intercalated into the interlayer galleries by an electrostatic interaction for balancing the sheet charge, resulting in an initial LDH phase with alveolate-like structure. Finally, the main layers stack to build a three-dimensional network with the positive charge being balanced by the carbonate ions arranged in the hydrated interlayer galleries, and the integrated plate-like structure of LDH is formed. Throughout the above-mentioned processes, the incorporation of magnesium ions into the sheet of the lamellar boehmite can play a primary role for the formation of LDH crystallites

    Table1_Comprehensive analysis of senescence-associated genes in sepsis based on bulk and single-cell sequencing data.xlsx

    No full text
    Background: Sepsis is a pathological state resulting from dysregulated immune response in host during severe infection, leading to persistent organ dysfunction and ultimately death. Senescence-associated genes (SAGs) have manifested their potential in controlling the proliferation and dissemination of a variety of diseases. Nevertheless, the correlation between sepsis and SAGs remains obscure and requires further investigation.Methods: Two RNA expression datasets (GSE28750 and GSE57065) specifically related to sepsis were employed to filter hub SAGs, based on which a diagnostic model predictive of the incidence of sepsis was developed. The association between the expression of the SAGs identified and immune-related modules was analyzed employing Cell-type Identification By Estimating Relative Subsets Of RNA Transcripts (CIBERSORT) and Microenvironment Cell Populations-counter (MCP-counter) analysis. The identified genes in each cohort were clustered by unsupervised agreement clustering analysis and weighted gene correlation network analysis (WGCNA).Results: A diagnostic model for sepsis established based on hub genes (IGFBP7, GMFG, IL10, IL18, ETS2, HGF, CD55, and MMP9) exhibited a strong clinical reliability (AUC = 0.989). Sepsis patients were randomly assigned and classified by WGCNA into two clusters with distinct immune statuses. Analysis on the single-cell RNA sequencing (scRNA-seq) data revealed high scores of SAGs in the natural killer (NK) cells of the sepsis cohort than the healthy cohort.Conclusion: These findings suggested a close association between SAGs and sepsis alterations. The identified hub genes had potential to serve as a viable diagnostic marker for sepsis.</p

    Intercalation Pseudocapacitance in Ultrathin VOPO<sub>4</sub> Nanosheets: Toward High-Rate Alkali-Ion-Based Electrochemical Energy Storage

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    There is a growing need for energy storage devices in numerous applications where a large amount of energy needs to be either stored or delivered quickly. The present paper details the study of alkali-ion intercalation pseudocapacitance in ultrathin VOPO<sub>4</sub> nanosheets, which hold promise in high-rate alkali-ion based electrochemical energy storage. Starting from bulk VOPO<sub>4</sub>·2H<sub>2</sub>O chunks, VOPO<sub>4</sub> nanosheets were obtained through simple ultrasonication in 2-propanol. These nanosheets as the cathode exhibit a specific capacity of 154 and 136 mAh/g (close to theoretical value 166 mAh/g) for lithium and sodium storage devices at 0.1 C and 100 and ∼70 mAh/g at 5 C, demonstrating their high rate capability. Moreover, the capacity retention is maintained at 90% for lithium ion storage and 73% for sodium ion storage after 500 cycles, showing their reasonable stability. The demonstrated alkali-ion intercalation pseudocapacitance represents a promising direction for developing battery materials with promising high rate capability

    Layer-by-Layer Assembly of Two-Dimensional Colloidal Cu<sub>2</sub>Se Nanoplates and Their Layer-Dependent Conductivity

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    Colloidal assembly is one of the highly active areas in nanoscale science and technology as it plays an important role in organizing nanoscale building blocks into hierarchical and functional systems for practical applications. Here, we report large scale assemblies of two-dimensional (2D) Cu<sub>2</sub>Se nanoplates synthesized by a microwave-assisted polyol method with careful phase control. Thin films of Cu<sub>2</sub>Se were obtained via the Langmuir–Blodgett (LB) method in a layer-by-layer manner. Interestingly, despite the decrease in volume fraction of Cu<sub>2</sub>Se as layer number increases, the films show an increasing trend in conductivity. We propose a “layer-dependent conducting-bridge” (LDCB) model considering density of conducting points and possible defects, and the simulated trend of conductivity exhibits a corresponding match with experimental measurements. Our study serves as an important extension of colloidal assembly in 2D nanostructures, and the proposed conductivity model provides insights into the understanding of electron transport inside 2D ordered matrix

    Image1_Identification of oncogenes and tumor-suppressor genes with hepatocellular carcinoma: A comprehensive analysis based on TCGA and GEO datasets.TIF

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    Aim: Existing targeted therapies for hepatocellular carcinoma (HCC) are resistant and have limitations. It is crucial to find new HCC-related target genes.Methods: RNA-sequencing data of HCC were gathered from The Cancer Genome Atlas and Gene Expression Omnibus datasets. Initially, differentially expressed genes between normal and tumor tissues were identified from four Gene Expression Omnibus datasets, GSE36376, GSE102079, GSE54236, and GSE45267. GO terms and KEGG pathway enrichment analyses were performed to explore the potential biological functions of differentially expressed genes. A PPI network was constructed by using the STRING database, and up-regulated and down-regulated hub genes were defined through 12 topological approaches. Subsequently, the correlation bounded by up-regulated genes and down-regulated genes in the diagnosis, prognosis, and clinicopathological features of HCC was analyzed. Beyond a shadow of doubt, the key oncogene PBK and tumor suppressor gene F9 were screened out, and the specific mechanism was investigated through GSEA enrichment analysis and immune correlation analysis. The role of PBK in HCC was further verified by western blot, CCK8, transwell, and tube formation experiments.Results:CDCA5, CDC20, PBK, PRC1, TOP2A, and NCAPG are good indicators of HCC diagnosis and prognosis. The low expressions of F9, AFM, and C8B indicate malignant progression and poor prognosis of HCC. PBK was found to be closely related to VEGF, VEGFR, and PDGFR pathways. Experiments showed that PBK promotes HCC cell proliferation, migration, invasion, and tube formation in HUVEC cells. F9 was negatively correlated with the degree of immune infiltration, and low expression of F9 suggested a poor response to immunotherapy.Conclusion: The role of HCC-related oncogenes and tumor-suppressor genes in diagnosis and prognosis was identified. In addition, we have found that PBK may promote tumor proliferation through angiogenesis and F9 may be a predictor of tumor immunotherapy response.</p

    Image2_Identification of oncogenes and tumor-suppressor genes with hepatocellular carcinoma: A comprehensive analysis based on TCGA and GEO datasets.TIF

    No full text
    Aim: Existing targeted therapies for hepatocellular carcinoma (HCC) are resistant and have limitations. It is crucial to find new HCC-related target genes.Methods: RNA-sequencing data of HCC were gathered from The Cancer Genome Atlas and Gene Expression Omnibus datasets. Initially, differentially expressed genes between normal and tumor tissues were identified from four Gene Expression Omnibus datasets, GSE36376, GSE102079, GSE54236, and GSE45267. GO terms and KEGG pathway enrichment analyses were performed to explore the potential biological functions of differentially expressed genes. A PPI network was constructed by using the STRING database, and up-regulated and down-regulated hub genes were defined through 12 topological approaches. Subsequently, the correlation bounded by up-regulated genes and down-regulated genes in the diagnosis, prognosis, and clinicopathological features of HCC was analyzed. Beyond a shadow of doubt, the key oncogene PBK and tumor suppressor gene F9 were screened out, and the specific mechanism was investigated through GSEA enrichment analysis and immune correlation analysis. The role of PBK in HCC was further verified by western blot, CCK8, transwell, and tube formation experiments.Results:CDCA5, CDC20, PBK, PRC1, TOP2A, and NCAPG are good indicators of HCC diagnosis and prognosis. The low expressions of F9, AFM, and C8B indicate malignant progression and poor prognosis of HCC. PBK was found to be closely related to VEGF, VEGFR, and PDGFR pathways. Experiments showed that PBK promotes HCC cell proliferation, migration, invasion, and tube formation in HUVEC cells. F9 was negatively correlated with the degree of immune infiltration, and low expression of F9 suggested a poor response to immunotherapy.Conclusion: The role of HCC-related oncogenes and tumor-suppressor genes in diagnosis and prognosis was identified. In addition, we have found that PBK may promote tumor proliferation through angiogenesis and F9 may be a predictor of tumor immunotherapy response.</p

    SDS-PAGE and Western blot analyses of secreted proteins produced by USA300 and isogenic variants after 8 h of growth in TSB, or TSB supplemented with 25 µM linoleic acid (A), and assay of total protease activity in culture supernatant (B).

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    <p>For (A), protein loading was 2.0 OD<sub>600</sub> units for Coomassie staining, and 0.02 OD<sub>600</sub> units for Western blots, which were developed with primary antibody specific for Aur, and SspA as indicated. Arrows on the Coomassie stained gel indicate the selective induction of secreted proteases in response to linoleic acid. The arrow on the right margin indicates the position of proGeh. In (B), total protease activity in 8 h culture supernatant of USA300 and isogenic variants was determined with FITC-casein substrate. Cultures were grown with 25 µM linoleic acid as indicated, and assay buffer was supplemented with 10 mM EDTA where indicated, to inhibit metalloprotease. Data are reported as fluorescence emission at 535 nm (ε<sub>535</sub>), measured in arbitrary fluorescence units.</p

    SDS-PAGE and Coomassie staining (A and C), or Western blot for detection of SspA (B, D and E), in cultures of <i>S. aureus</i> grown in TSB containing 0 or 25 µM linoleic acid (LA) as indicated.

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    <p>Protein loading was 2.0 OD<sub>600</sub> units for SDS-PAGE, and 0.02 OD<sub>600</sub> units for Western blot. The <i>S. aureus</i> strains are defined in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0045952#pone-0045952-t001" target="_blank">Table 1</a>. Arrows and labels on the right margins of panels A and C indicate the location of 72 kDa glycerol ester hydrolase precursor (proGeh) and mature lipase (Geh), while arrows on the protein gels point to SspA protein that is induced in response to 25 µM LA. SspA exhibits some expected variation in size, being comprised of 327 amino acids in USA400 (MW_0932), 336 amino acids in USA300 (SAUSA300_0951), and 357 amino acids in MRSA252 (SAR_1022) and other CC30 strains, due to variation in a C-terminal disordered segment comprised of tripeptide repeats. Different isomers produced by the same strain as shown on Western blot (5E), and explained in the text, are attributed to varying degrees of processing of the N-terminal propeptide of the SspA precursor, proSspA.</p
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