6 research outputs found

    Table_1_Identification of inflammation-related biomarkers in keloids.xlsx

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    BackgroundThe relationship between inflammation-related genes (IRGs) and keloid disease (KD) is currently unclear. The aim of this study was to identify a new set of inflammation-related biomarkers in KD.MethodsGSE145725 and GSE7890 datasets were used in this study. A list of 3026 IRGs was obtained from the Molecular Signatures Database. Differentially expressed inflammation-related genes (DEGs) were obtained by taking the intersection of DEGs between KD and control samples and the list of IRGs. Candidate genes were selected using least absolute shrinkage and selection operator (LASSO) regression analysis. Candidate genes with consistent expression differences between KD and control in both GSE145725 and GSE7890 datasets were screened as biomarkers. An alignment diagram was constructed and validated, and in silico immune infiltration analysis and drug prediction were performed. Finally, RT-qPCR was performed on KD samples to analyze the expression of the identified biomarkers.ResultsA total of 889 DEGs were identified from the GSE145725 dataset, 169 of which were IRGs. Three candidate genes (TRIM32, LPAR1 and FOXF1) were identified by the LASSO regression analysis, and expression validation analysis suggested that FOXF1 and LPAR1 were down-regulated in KD samples and TRIM32 was up-regulated. All three candidate genes had consistent changes in expression in both the GSE145725 and GSE7890 datasets. An alignment diagram was constructed to predict KD. Effector memory CD4 T cells, T follicular helper cell, Myeloid derived suppressor cell, activated dendritic cell, Immature dendritic cell and Monocyte were differentially expressed between the KD and control group. Sixty-seven compounds that may act on FOXF1, 108 compounds that may act on LPAR1 and 56 compounds that may act on TRIM32 were predicted. Finally, RT-qPCR showed that the expression of LPAR1 was significantly lower in KD samples compared to normal samples whereas TRIM32 was significantly higher, while there was no difference in the expression of FOXF1.ConclusionThis study provides a new perspective to study the relationship between IRGs and KD.</p

    DataSheet_1_Identification of inflammation-related biomarkers in keloids.docx

    No full text
    BackgroundThe relationship between inflammation-related genes (IRGs) and keloid disease (KD) is currently unclear. The aim of this study was to identify a new set of inflammation-related biomarkers in KD.MethodsGSE145725 and GSE7890 datasets were used in this study. A list of 3026 IRGs was obtained from the Molecular Signatures Database. Differentially expressed inflammation-related genes (DEGs) were obtained by taking the intersection of DEGs between KD and control samples and the list of IRGs. Candidate genes were selected using least absolute shrinkage and selection operator (LASSO) regression analysis. Candidate genes with consistent expression differences between KD and control in both GSE145725 and GSE7890 datasets were screened as biomarkers. An alignment diagram was constructed and validated, and in silico immune infiltration analysis and drug prediction were performed. Finally, RT-qPCR was performed on KD samples to analyze the expression of the identified biomarkers.ResultsA total of 889 DEGs were identified from the GSE145725 dataset, 169 of which were IRGs. Three candidate genes (TRIM32, LPAR1 and FOXF1) were identified by the LASSO regression analysis, and expression validation analysis suggested that FOXF1 and LPAR1 were down-regulated in KD samples and TRIM32 was up-regulated. All three candidate genes had consistent changes in expression in both the GSE145725 and GSE7890 datasets. An alignment diagram was constructed to predict KD. Effector memory CD4 T cells, T follicular helper cell, Myeloid derived suppressor cell, activated dendritic cell, Immature dendritic cell and Monocyte were differentially expressed between the KD and control group. Sixty-seven compounds that may act on FOXF1, 108 compounds that may act on LPAR1 and 56 compounds that may act on TRIM32 were predicted. Finally, RT-qPCR showed that the expression of LPAR1 was significantly lower in KD samples compared to normal samples whereas TRIM32 was significantly higher, while there was no difference in the expression of FOXF1.ConclusionThis study provides a new perspective to study the relationship between IRGs and KD.</p

    Image_2_Identification of inflammation-related biomarkers in keloids.tif

    No full text
    BackgroundThe relationship between inflammation-related genes (IRGs) and keloid disease (KD) is currently unclear. The aim of this study was to identify a new set of inflammation-related biomarkers in KD.MethodsGSE145725 and GSE7890 datasets were used in this study. A list of 3026 IRGs was obtained from the Molecular Signatures Database. Differentially expressed inflammation-related genes (DEGs) were obtained by taking the intersection of DEGs between KD and control samples and the list of IRGs. Candidate genes were selected using least absolute shrinkage and selection operator (LASSO) regression analysis. Candidate genes with consistent expression differences between KD and control in both GSE145725 and GSE7890 datasets were screened as biomarkers. An alignment diagram was constructed and validated, and in silico immune infiltration analysis and drug prediction were performed. Finally, RT-qPCR was performed on KD samples to analyze the expression of the identified biomarkers.ResultsA total of 889 DEGs were identified from the GSE145725 dataset, 169 of which were IRGs. Three candidate genes (TRIM32, LPAR1 and FOXF1) were identified by the LASSO regression analysis, and expression validation analysis suggested that FOXF1 and LPAR1 were down-regulated in KD samples and TRIM32 was up-regulated. All three candidate genes had consistent changes in expression in both the GSE145725 and GSE7890 datasets. An alignment diagram was constructed to predict KD. Effector memory CD4 T cells, T follicular helper cell, Myeloid derived suppressor cell, activated dendritic cell, Immature dendritic cell and Monocyte were differentially expressed between the KD and control group. Sixty-seven compounds that may act on FOXF1, 108 compounds that may act on LPAR1 and 56 compounds that may act on TRIM32 were predicted. Finally, RT-qPCR showed that the expression of LPAR1 was significantly lower in KD samples compared to normal samples whereas TRIM32 was significantly higher, while there was no difference in the expression of FOXF1.ConclusionThis study provides a new perspective to study the relationship between IRGs and KD.</p

    Platinum(II)-Catalyzed Asymmetric Ring-Opening Addition of Arylboronic Acids to Oxabenzonorbornadienes

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    A new platinum­(II)-catalyzed asymmetric ring-opening addition of arylboronic acids to oxabenzonorbornadienes was developed, which afforded the corresponding <i>cis</i>-2-aryl-1,2-dihydronaphthalen-1-ol products in high yields (up to 97%) with moderate to good enantioselectivities (up to 89% ee) under very mild conditions. The effects of various ligands, catalyst loading, bases, solvents, and temperatures on the yield and enantioselectivity of the reaction were also investigated. The cis configuration of product <b>2m</b> was confirmed by X-ray diffraction analysis. A potential mechanism for the present catalytic reaction is proposed

    Platinum(II)-Catalyzed Asymmetric Ring-Opening Addition of Arylboronic Acids to Oxabenzonorbornadienes

    No full text
    A new platinum­(II)-catalyzed asymmetric ring-opening addition of arylboronic acids to oxabenzonorbornadienes was developed, which afforded the corresponding <i>cis</i>-2-aryl-1,2-dihydronaphthalen-1-ol products in high yields (up to 97%) with moderate to good enantioselectivities (up to 89% ee) under very mild conditions. The effects of various ligands, catalyst loading, bases, solvents, and temperatures on the yield and enantioselectivity of the reaction were also investigated. The cis configuration of product <b>2m</b> was confirmed by X-ray diffraction analysis. A potential mechanism for the present catalytic reaction is proposed

    Nickel-Catalyzed Asymmetric Ring Opening of Oxa­benzo­norborna­dienes with Arylboronic Acids

    No full text
    A new, versatile, and highly efficient nickel-catalyzed asymmetric ring-opening (ARO) reaction of oxabenzo­norborna­dienes with a wide variety of arylboronic acids has been developed, yielding <i>cis</i>-2-aryl-1,2-dihydro­naph­thalen-1-ols in high yields (up to 99%) with good to excellent enantioselectivities (up to 99% ee) under very mild conditions. The effects of various nickel precursors, chiral bidentate ligands, catalyst loadings, bases, solvents, and temperatures on the yield and enantioselectivity of the reaction were also investigated. A plausible mechanism was proposed to account for the formation of the corresponding <i>cis</i>-ring-opened products based on the X-ray structure of product <b>4b</b>
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