kaplan-meier cumulative plot Search Results


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Table 1b IMPROVE-VTE <t> RAM </t> used in medical inpatients a
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Baseline patient characteristics by angiotensin-converting enzyme <t> (ACE) </t> inhibitor use before and after propensity score matching
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Baseline patient characteristics by angiotensin-converting enzyme <t> (ACE) </t> inhibitor use before and after propensity score matching
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Baseline patient characteristics by angiotensin-converting enzyme <t> (ACE) </t> inhibitor use before and after propensity score matching
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Baseline patient characteristics by angiotensin-converting enzyme <t> (ACE) </t> inhibitor use before and after propensity score matching
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Overview of the 37,498 single cells from extrahepatic <t>cholangiocarcinoma</t> <t>(eCCA)</t> and nonmalignant bile duct samples. ( a ) Workflow of sample composition, processing and bioinformatic analyses for eight samples in the present study. Five primary tumor and three paired adjacent normal tissues were collected from five patients. Single cell suspension was prepared for single-cell RNA sequencing. ( b ) t-SNE of the 37,498 cells profiled here, with each cell color coded for (left to right): its sample type of origin (tumor or nonmalignant sample), the corresponding sample, the associated cell type and the number of transcripts (UMIs) detected in that cell. k, thousand. ( c ) Violin plots showing marker genes for nine major cell types including B, endothelial, epithelial, fibroblast, HPLC, mast, myeloid, <t>Schwann</t> and T cells. ( d ) Bubble plot depicting the differences in transcriptional activity between tumor and adjacent normal tissues across nine cell types. Fold changes and P values are depicted for each cell type. ( e ) For each of the 39 stromal cell subclusters and the 7 subclusters of cancer cells (left to right): the fraction of cells originating from the three adjacent normal (non-malignant) and five tumor samples (tumor), the fraction of cells originating from each of the eight samples, the number of cells and box plots of the number of transcripts (with plot center, box and whiskers corresponding to median, IQR and 1.5 IQR, respectively; n per boxplot is shown in the ‘number of cells’ panel, and is specified in Supplementary Table )
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Overview of the 37,498 single cells from extrahepatic <t>cholangiocarcinoma</t> <t>(eCCA)</t> and nonmalignant bile duct samples. ( a ) Workflow of sample composition, processing and bioinformatic analyses for eight samples in the present study. Five primary tumor and three paired adjacent normal tissues were collected from five patients. Single cell suspension was prepared for single-cell RNA sequencing. ( b ) t-SNE of the 37,498 cells profiled here, with each cell color coded for (left to right): its sample type of origin (tumor or nonmalignant sample), the corresponding sample, the associated cell type and the number of transcripts (UMIs) detected in that cell. k, thousand. ( c ) Violin plots showing marker genes for nine major cell types including B, endothelial, epithelial, fibroblast, HPLC, mast, myeloid, <t>Schwann</t> and T cells. ( d ) Bubble plot depicting the differences in transcriptional activity between tumor and adjacent normal tissues across nine cell types. Fold changes and P values are depicted for each cell type. ( e ) For each of the 39 stromal cell subclusters and the 7 subclusters of cancer cells (left to right): the fraction of cells originating from the three adjacent normal (non-malignant) and five tumor samples (tumor), the fraction of cells originating from each of the eight samples, the number of cells and box plots of the number of transcripts (with plot center, box and whiskers corresponding to median, IQR and 1.5 IQR, respectively; n per boxplot is shown in the ‘number of cells’ panel, and is specified in Supplementary Table )
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Overview of the 37,498 single cells from extrahepatic <t>cholangiocarcinoma</t> <t>(eCCA)</t> and nonmalignant bile duct samples. ( a ) Workflow of sample composition, processing and bioinformatic analyses for eight samples in the present study. Five primary tumor and three paired adjacent normal tissues were collected from five patients. Single cell suspension was prepared for single-cell RNA sequencing. ( b ) t-SNE of the 37,498 cells profiled here, with each cell color coded for (left to right): its sample type of origin (tumor or nonmalignant sample), the corresponding sample, the associated cell type and the number of transcripts (UMIs) detected in that cell. k, thousand. ( c ) Violin plots showing marker genes for nine major cell types including B, endothelial, epithelial, fibroblast, HPLC, mast, myeloid, <t>Schwann</t> and T cells. ( d ) Bubble plot depicting the differences in transcriptional activity between tumor and adjacent normal tissues across nine cell types. Fold changes and P values are depicted for each cell type. ( e ) For each of the 39 stromal cell subclusters and the 7 subclusters of cancer cells (left to right): the fraction of cells originating from the three adjacent normal (non-malignant) and five tumor samples (tumor), the fraction of cells originating from each of the eight samples, the number of cells and box plots of the number of transcripts (with plot center, box and whiskers corresponding to median, IQR and 1.5 IQR, respectively; n per boxplot is shown in the ‘number of cells’ panel, and is specified in Supplementary Table )
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Image Search Results


Table 1b IMPROVE-VTE  RAM  used in medical inpatients a

Journal: Annals of Vascular Diseases

Article Title: External Validation of the Padua and IMPROVE-VTE Risk Assessment Models for Predicting Venous Thromboembolism in Hospitalized Adult Medical Patients: A Retrospective Single-Center Study in Japan

doi: 10.3400/avd.oa.22-00108

Figure Lengend Snippet: Table 1b IMPROVE-VTE RAM used in medical inpatients a

Article Snippet: Similarly, the originally proposed three-group IMPROVE-VTE RAM had excellent discriminative performance (Log-rank Chi-squared=16.59; P<0.001); however, two of the three-risk groups (high- and intermediate-risk groups) showed overlapping cumulative incidence curves according to the Kaplan–Meier plots ( ).

Techniques:

Baseline patient characteristics by angiotensin-converting enzyme  (ACE)  inhibitor use before and after propensity score matching

Journal:

Article Title: Effects of ACE Inhibitors in Systolic Heart Failure Patients with Chronic Kidney Disease

doi: 10.1016/j.cardfail.2006.05.008

Figure Lengend Snippet: Baseline patient characteristics by angiotensin-converting enzyme (ACE) inhibitor use before and after propensity score matching

Article Snippet: Compared with 31 (29.8%) deaths in patients receiving ACE inhibitors, 41 (39.4%) of those not receiving ACE inhibitors died (9.6% absolute risk reduction; Chi-square p =0.145). displays Kaplan-Meier plots for unadjusted 2-year cumulative mortality for patients receiving versus not receiving ACE inhibitor therapy.

Techniques: Medications, Activity Assay, Functional Assay

Overview of the 37,498 single cells from extrahepatic cholangiocarcinoma (eCCA) and nonmalignant bile duct samples. ( a ) Workflow of sample composition, processing and bioinformatic analyses for eight samples in the present study. Five primary tumor and three paired adjacent normal tissues were collected from five patients. Single cell suspension was prepared for single-cell RNA sequencing. ( b ) t-SNE of the 37,498 cells profiled here, with each cell color coded for (left to right): its sample type of origin (tumor or nonmalignant sample), the corresponding sample, the associated cell type and the number of transcripts (UMIs) detected in that cell. k, thousand. ( c ) Violin plots showing marker genes for nine major cell types including B, endothelial, epithelial, fibroblast, HPLC, mast, myeloid, Schwann and T cells. ( d ) Bubble plot depicting the differences in transcriptional activity between tumor and adjacent normal tissues across nine cell types. Fold changes and P values are depicted for each cell type. ( e ) For each of the 39 stromal cell subclusters and the 7 subclusters of cancer cells (left to right): the fraction of cells originating from the three adjacent normal (non-malignant) and five tumor samples (tumor), the fraction of cells originating from each of the eight samples, the number of cells and box plots of the number of transcripts (with plot center, box and whiskers corresponding to median, IQR and 1.5 IQR, respectively; n per boxplot is shown in the ‘number of cells’ panel, and is specified in Supplementary Table )

Journal: BMC Gastroenterology

Article Title: Single-cell transcriptomic analysis reveals prognosis-related stromal signatures that potentiate stratification of patients with extrahepatic cholangiocarcinoma

doi: 10.1186/s12876-025-03829-8

Figure Lengend Snippet: Overview of the 37,498 single cells from extrahepatic cholangiocarcinoma (eCCA) and nonmalignant bile duct samples. ( a ) Workflow of sample composition, processing and bioinformatic analyses for eight samples in the present study. Five primary tumor and three paired adjacent normal tissues were collected from five patients. Single cell suspension was prepared for single-cell RNA sequencing. ( b ) t-SNE of the 37,498 cells profiled here, with each cell color coded for (left to right): its sample type of origin (tumor or nonmalignant sample), the corresponding sample, the associated cell type and the number of transcripts (UMIs) detected in that cell. k, thousand. ( c ) Violin plots showing marker genes for nine major cell types including B, endothelial, epithelial, fibroblast, HPLC, mast, myeloid, Schwann and T cells. ( d ) Bubble plot depicting the differences in transcriptional activity between tumor and adjacent normal tissues across nine cell types. Fold changes and P values are depicted for each cell type. ( e ) For each of the 39 stromal cell subclusters and the 7 subclusters of cancer cells (left to right): the fraction of cells originating from the three adjacent normal (non-malignant) and five tumor samples (tumor), the fraction of cells originating from each of the eight samples, the number of cells and box plots of the number of transcripts (with plot center, box and whiskers corresponding to median, IQR and 1.5 IQR, respectively; n per boxplot is shown in the ‘number of cells’ panel, and is specified in Supplementary Table )

Article Snippet: Fig. 5 SLIT2 + Schwann cells were associated with tumor restriction in eCCA. ( a ) Enriched biological pathways in Schwann cells compared to the remaining cell populations ( p < 0.05, cumulative hypergeometric test). ( b ) UMAP plot, color-coded for the expression (gray to red) of marker genes for Schwann cells, as indicated ( c ) Kaplan-Meier analysis of overall survival in eCCA patients, stratified by the median GSVA score of Schwann cell signature genes, with statistical significance assessed using the log-rank test ( p = 0.004). ( d ) UMAP plot of 664 Schwann cells, color-coded by their associated cluster. ( e ) Top, Dot plot showing the expression of the top ten marker genes in each subcluster of Schwann cells.

Techniques: Suspension, RNA Sequencing, Marker, Activity Assay

SLIT2 + Schwann cells were associated with tumor restriction in eCCA. ( a ) Enriched biological pathways in Schwann cells compared to the remaining cell populations ( p < 0.05, cumulative hypergeometric test). ( b ) UMAP plot, color-coded for the expression (gray to red) of marker genes for Schwann cells, as indicated ( c ) Kaplan-Meier analysis of overall survival in eCCA patients, stratified by the median GSVA score of Schwann cell signature genes, with statistical significance assessed using the log-rank test ( p = 0.004). ( d ) UMAP plot of 664 Schwann cells, color-coded by their associated cluster. ( e ) Top, Dot plot showing the expression of the top ten marker genes in each subcluster of Schwann cells. Bottom, Violin plots showing the smoothened expression distribution of specific genes identifying myelinating and repair Schwann cell subtypes. ( f ) Enriched biological pathways in each Schwann cell subtype compared to other subtypes ( P < 0.05, cumulative hypergeometric test)

Journal: BMC Gastroenterology

Article Title: Single-cell transcriptomic analysis reveals prognosis-related stromal signatures that potentiate stratification of patients with extrahepatic cholangiocarcinoma

doi: 10.1186/s12876-025-03829-8

Figure Lengend Snippet: SLIT2 + Schwann cells were associated with tumor restriction in eCCA. ( a ) Enriched biological pathways in Schwann cells compared to the remaining cell populations ( p < 0.05, cumulative hypergeometric test). ( b ) UMAP plot, color-coded for the expression (gray to red) of marker genes for Schwann cells, as indicated ( c ) Kaplan-Meier analysis of overall survival in eCCA patients, stratified by the median GSVA score of Schwann cell signature genes, with statistical significance assessed using the log-rank test ( p = 0.004). ( d ) UMAP plot of 664 Schwann cells, color-coded by their associated cluster. ( e ) Top, Dot plot showing the expression of the top ten marker genes in each subcluster of Schwann cells. Bottom, Violin plots showing the smoothened expression distribution of specific genes identifying myelinating and repair Schwann cell subtypes. ( f ) Enriched biological pathways in each Schwann cell subtype compared to other subtypes ( P < 0.05, cumulative hypergeometric test)

Article Snippet: Fig. 5 SLIT2 + Schwann cells were associated with tumor restriction in eCCA. ( a ) Enriched biological pathways in Schwann cells compared to the remaining cell populations ( p < 0.05, cumulative hypergeometric test). ( b ) UMAP plot, color-coded for the expression (gray to red) of marker genes for Schwann cells, as indicated ( c ) Kaplan-Meier analysis of overall survival in eCCA patients, stratified by the median GSVA score of Schwann cell signature genes, with statistical significance assessed using the log-rank test ( p = 0.004). ( d ) UMAP plot of 664 Schwann cells, color-coded by their associated cluster. ( e ) Top, Dot plot showing the expression of the top ten marker genes in each subcluster of Schwann cells.

Techniques: Expressing, Marker

Stromal features potentiated the stratification of eCCA into three phenotypes. ( a ) Unsupervised hierarchical clustering of six stromal cell subtypes across 43 eCCA tumor samples. The heatmap displays the expression activity of the six survival-related stromal cell subtypes, including HPLCs, Treg, C3-iCAF, C2-mast cells (MC), C3-MC, and Schwann cells (Sch). Patients were stratified into three distinct groups based on clustering results: Group 1 (proliferative), Group 2 (inflammatory and fibrotic), and Group 3 (neuronal). The annotation bars indicate survival status, follow-up time, and patient grouping. ( b ) Left, Correlogram of the expression activity of the six survival-related stromal cell subtypes in tumor samples from 43 eCCA patients. Pearson’s R coefficients are shown from blue (− 1.0) to red (1.0); R values are indicated by color and circle size. Right, correlation between the expression activity of selected related cell subtypes. ( c ) Kaplan-Meier analysis of overall survival in eCCA patients, stratified by the three groups identified in (a), with statistical significance assessed using the log-rank test ( p = 0.011). ( d ) Significantly upregulated (NES > 1.50 and FDR < 0.25) pathways identified by GSEA in each group compared to the remaining groups in eCCA tumors ( n = 43). ( e ) Predicted intercellular communication among the six survival-related stromal subtypes. The network plot illustrates potential ligand-receptor interactions between stromal subtypes. Nodes represent cell subtypes, and edges denote ligand-receptor interactions, with line thickness corresponding to the interaction strength (based on the number and expression level of ligand-receptor pairs). ( f ) Overview of the ligand-receptor pairs between C2-MC, C3-iCAF and Treg cells. The color indicates the interaction probability, and the dot size represents the statistical significance of the interactive molecular pairs

Journal: BMC Gastroenterology

Article Title: Single-cell transcriptomic analysis reveals prognosis-related stromal signatures that potentiate stratification of patients with extrahepatic cholangiocarcinoma

doi: 10.1186/s12876-025-03829-8

Figure Lengend Snippet: Stromal features potentiated the stratification of eCCA into three phenotypes. ( a ) Unsupervised hierarchical clustering of six stromal cell subtypes across 43 eCCA tumor samples. The heatmap displays the expression activity of the six survival-related stromal cell subtypes, including HPLCs, Treg, C3-iCAF, C2-mast cells (MC), C3-MC, and Schwann cells (Sch). Patients were stratified into three distinct groups based on clustering results: Group 1 (proliferative), Group 2 (inflammatory and fibrotic), and Group 3 (neuronal). The annotation bars indicate survival status, follow-up time, and patient grouping. ( b ) Left, Correlogram of the expression activity of the six survival-related stromal cell subtypes in tumor samples from 43 eCCA patients. Pearson’s R coefficients are shown from blue (− 1.0) to red (1.0); R values are indicated by color and circle size. Right, correlation between the expression activity of selected related cell subtypes. ( c ) Kaplan-Meier analysis of overall survival in eCCA patients, stratified by the three groups identified in (a), with statistical significance assessed using the log-rank test ( p = 0.011). ( d ) Significantly upregulated (NES > 1.50 and FDR < 0.25) pathways identified by GSEA in each group compared to the remaining groups in eCCA tumors ( n = 43). ( e ) Predicted intercellular communication among the six survival-related stromal subtypes. The network plot illustrates potential ligand-receptor interactions between stromal subtypes. Nodes represent cell subtypes, and edges denote ligand-receptor interactions, with line thickness corresponding to the interaction strength (based on the number and expression level of ligand-receptor pairs). ( f ) Overview of the ligand-receptor pairs between C2-MC, C3-iCAF and Treg cells. The color indicates the interaction probability, and the dot size represents the statistical significance of the interactive molecular pairs

Article Snippet: Fig. 5 SLIT2 + Schwann cells were associated with tumor restriction in eCCA. ( a ) Enriched biological pathways in Schwann cells compared to the remaining cell populations ( p < 0.05, cumulative hypergeometric test). ( b ) UMAP plot, color-coded for the expression (gray to red) of marker genes for Schwann cells, as indicated ( c ) Kaplan-Meier analysis of overall survival in eCCA patients, stratified by the median GSVA score of Schwann cell signature genes, with statistical significance assessed using the log-rank test ( p = 0.004). ( d ) UMAP plot of 664 Schwann cells, color-coded by their associated cluster. ( e ) Top, Dot plot showing the expression of the top ten marker genes in each subcluster of Schwann cells.

Techniques: Expressing, Activity Assay