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concentrated rabbit anti-human polyclonal ccn5  (OriGene)


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    OriGene concentrated rabbit anti-human polyclonal ccn5
    Concentrated Rabbit Anti Human Polyclonal Ccn5, supplied by OriGene, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/concentrated rabbit anti-human polyclonal ccn5/product/OriGene
    Average 90 stars, based on 1 article reviews
    concentrated rabbit anti-human polyclonal ccn5 - by Bioz Stars, 2026-06
    90/100 stars

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    Expression of <t>CCN5</t> is significantly increased in endometriosis. A The mRNA expression of CCN5 in ectopic lesions of patients with endometriosis and control eutopic endometrial tissues measured by RT-qPCR (n = 15, **** p < 0.0001). B Protein expression of CCN5 in ectopic lesions of patients with endometriosis and control eutopic endometrial tissues determined by western blotting. C IHC assay of CCN5 protein expression in control eutopic endometrial tissues and ectopic lesions of patients with endometriosis. Scale bar: 100 μm; 50 μm. D Immunofluorescent staining assay of CCN5 protein expression in control eutopic endometrial tissues and ectopic lesions of patients with endometriosis. Scale bar: 50 μm; 20 μm. Data are presented as mean ± SD. Statistical analysis was performed using an unpaired student’s t-test, **** p < 0.0001
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    Expression of CCN5 is significantly increased in endometriosis. A The mRNA expression of CCN5 in ectopic lesions of patients with endometriosis and control eutopic endometrial tissues measured by RT-qPCR (n = 15, **** p < 0.0001). B Protein expression of CCN5 in ectopic lesions of patients with endometriosis and control eutopic endometrial tissues determined by western blotting. C IHC assay of CCN5 protein expression in control eutopic endometrial tissues and ectopic lesions of patients with endometriosis. Scale bar: 100 μm; 50 μm. D Immunofluorescent staining assay of CCN5 protein expression in control eutopic endometrial tissues and ectopic lesions of patients with endometriosis. Scale bar: 50 μm; 20 μm. Data are presented as mean ± SD. Statistical analysis was performed using an unpaired student’s t-test, **** p < 0.0001

    Journal: Journal of Translational Medicine

    Article Title: CCN5 negatively regulates TGF-β-induced endometriosis associated fibrosis through Wnt/β-catenin signaling via Smad3-dependent mechanism

    doi: 10.1186/s12967-025-06804-9

    Figure Lengend Snippet: Expression of CCN5 is significantly increased in endometriosis. A The mRNA expression of CCN5 in ectopic lesions of patients with endometriosis and control eutopic endometrial tissues measured by RT-qPCR (n = 15, **** p < 0.0001). B Protein expression of CCN5 in ectopic lesions of patients with endometriosis and control eutopic endometrial tissues determined by western blotting. C IHC assay of CCN5 protein expression in control eutopic endometrial tissues and ectopic lesions of patients with endometriosis. Scale bar: 100 μm; 50 μm. D Immunofluorescent staining assay of CCN5 protein expression in control eutopic endometrial tissues and ectopic lesions of patients with endometriosis. Scale bar: 50 μm; 20 μm. Data are presented as mean ± SD. Statistical analysis was performed using an unpaired student’s t-test, **** p < 0.0001

    Article Snippet: Furthermore, C57BL/6JCya- Ccn5 em1 /Cya mice (#S-KO-16036), which have a knockout of the CCN5 gene, were also acquired from Cyagen Biosciences (Guangzhou, China).

    Techniques: Expressing, Control, Quantitative RT-PCR, Western Blot, Staining

    Decreased CCN5 promotes TGF- β -induced proliferation and pro-fibrotic markers expression of primary HESCs in vitro. A The proliferation ability of shCCN5-HESCs and shNC-HESCs treated with TGF-β or not by CCK-8 assay. Data are presented as mean ± SD. Statistical analysis was conducted using one-way ANOVA for the optical density (OD) values at 72 h. * p < 0.05. B EdU assay was performed to reveal the effects of CCN5 knockdown on the proliferation of CCN5-knockdown HESCs and WT-HESCs treated with TGF-β or without TGF-β. Scale bar, 100 μm. C The mRNA expression levels of CCN5, COL1A1 and α-SMA in shCCN5-HESCs and shNC-HESCs treated with TGF-β or without TGF-β. Data are presented as the mean ± SEM. Statistical analysis was performed using one-way ANOVA. * p < 0.05, ** p < 0.01. D Expression of CCN5, α-SMA, Collagen Ι in shCCN5-HESCs and shNC-HESCs treated with TGF-β or without TGF-β. E Immunofluorescence for α-SMA in shCCN5-HESCs and shNC-HESCs treated with TGF-β or without TGF-β. Scale bar, 25 μm (red α-SMA, blue DAPI)

    Journal: Journal of Translational Medicine

    Article Title: CCN5 negatively regulates TGF-β-induced endometriosis associated fibrosis through Wnt/β-catenin signaling via Smad3-dependent mechanism

    doi: 10.1186/s12967-025-06804-9

    Figure Lengend Snippet: Decreased CCN5 promotes TGF- β -induced proliferation and pro-fibrotic markers expression of primary HESCs in vitro. A The proliferation ability of shCCN5-HESCs and shNC-HESCs treated with TGF-β or not by CCK-8 assay. Data are presented as mean ± SD. Statistical analysis was conducted using one-way ANOVA for the optical density (OD) values at 72 h. * p < 0.05. B EdU assay was performed to reveal the effects of CCN5 knockdown on the proliferation of CCN5-knockdown HESCs and WT-HESCs treated with TGF-β or without TGF-β. Scale bar, 100 μm. C The mRNA expression levels of CCN5, COL1A1 and α-SMA in shCCN5-HESCs and shNC-HESCs treated with TGF-β or without TGF-β. Data are presented as the mean ± SEM. Statistical analysis was performed using one-way ANOVA. * p < 0.05, ** p < 0.01. D Expression of CCN5, α-SMA, Collagen Ι in shCCN5-HESCs and shNC-HESCs treated with TGF-β or without TGF-β. E Immunofluorescence for α-SMA in shCCN5-HESCs and shNC-HESCs treated with TGF-β or without TGF-β. Scale bar, 25 μm (red α-SMA, blue DAPI)

    Article Snippet: Furthermore, C57BL/6JCya- Ccn5 em1 /Cya mice (#S-KO-16036), which have a knockout of the CCN5 gene, were also acquired from Cyagen Biosciences (Guangzhou, China).

    Techniques: Expressing, In Vitro, CCK-8 Assay, EdU Assay, Knockdown, Immunofluorescence

    Overexpression of CCN5 attenuates TGF-β-induced proliferation and pro-fibrotic markers expression of primary HESCs in vitro. A The proliferation ability of CCN5-overexpression HESCs (CCN5) and control-HESCs (Vector) treated with TGF-β or without TGF-β by CCK-8 assay. Data are presented as mean ± SD. Statistical analysis was conducted using one-way ANOVA for the optical density values at 72 h. * p < 0.05. B EdU assay was performed to reveal the effects of CCN5 knockdown on the proliferation of CCN5-overexpression HESCs and control-HESCs treated with TGF-β or without TGF-β. Scale bar, 100 μm. C The mRNA expression levels of CCN5 , COL1A1 and α-SMA in CCN5-overexpression HESCs and control-HESCs treated with TGF-β or without TGF-β. Data are presented as the mean ± SEM. Statistical analysis was performed using one-way ANOVA for each target gene. * p < 0.05, ** p < 0.01. D Expression of CCN5, α-SMA, Collagen Ι in CCN5-overexpression HESCs and control-HESCs treated with TGF-β or without TGF-β. E. Immunofluorescence for α-SMA in CCN5-overexpression HESCs and control-HESCs treated with TGF-β or without TGF-β. Scale bar, 25 μm (red α-SMA, blue DAPI)

    Journal: Journal of Translational Medicine

    Article Title: CCN5 negatively regulates TGF-β-induced endometriosis associated fibrosis through Wnt/β-catenin signaling via Smad3-dependent mechanism

    doi: 10.1186/s12967-025-06804-9

    Figure Lengend Snippet: Overexpression of CCN5 attenuates TGF-β-induced proliferation and pro-fibrotic markers expression of primary HESCs in vitro. A The proliferation ability of CCN5-overexpression HESCs (CCN5) and control-HESCs (Vector) treated with TGF-β or without TGF-β by CCK-8 assay. Data are presented as mean ± SD. Statistical analysis was conducted using one-way ANOVA for the optical density values at 72 h. * p < 0.05. B EdU assay was performed to reveal the effects of CCN5 knockdown on the proliferation of CCN5-overexpression HESCs and control-HESCs treated with TGF-β or without TGF-β. Scale bar, 100 μm. C The mRNA expression levels of CCN5 , COL1A1 and α-SMA in CCN5-overexpression HESCs and control-HESCs treated with TGF-β or without TGF-β. Data are presented as the mean ± SEM. Statistical analysis was performed using one-way ANOVA for each target gene. * p < 0.05, ** p < 0.01. D Expression of CCN5, α-SMA, Collagen Ι in CCN5-overexpression HESCs and control-HESCs treated with TGF-β or without TGF-β. E. Immunofluorescence for α-SMA in CCN5-overexpression HESCs and control-HESCs treated with TGF-β or without TGF-β. Scale bar, 25 μm (red α-SMA, blue DAPI)

    Article Snippet: Furthermore, C57BL/6JCya- Ccn5 em1 /Cya mice (#S-KO-16036), which have a knockout of the CCN5 gene, were also acquired from Cyagen Biosciences (Guangzhou, China).

    Techniques: Over Expression, Expressing, In Vitro, Control, Plasmid Preparation, CCK-8 Assay, EdU Assay, Knockdown, Immunofluorescence

    CCN5 regulates activation of TGF-β/Smad and Wnt/β-catenin signaling pathways. A , B Luciferase reporter assays in primary HESCs transfected with the indicated plasmids and treated with the vehicle, TGF-β or prifenidone. FLuc/RLuc activity was determined as mean ± SEM. Statistical analysis was performed using one-way ANOVA. * p < 0.05, ** p < 0.01. C, D. The mRNA expression of downstream target genes of TGF-β/Smad and Wnt/β-catenin signaling pathways in CCN5-overexpression HESCs ( C ) or CCN5-knockdown HESCs ( D ) treated with TGF-β or without TGF-β. Data are presented as the mean ± SEM. Statistical analysis was performed using one-way ANOVA for each target gene. * p < 0.05, ** p < 0.01. E, F. The protein expression of p-Smad3, Smad3, p-β-catenin and β-catenin in CCN5-overexpression HESCs ( E ) or CCN5-knockdown HESCs ( F ) treated with TGF-β or without TGF-β. G. The protein expression of β-catenin in cytoplasmic and nuclear part of CCN5-overexpression HESCs or CCN5-knockdown HESCs was measured by western blotting

    Journal: Journal of Translational Medicine

    Article Title: CCN5 negatively regulates TGF-β-induced endometriosis associated fibrosis through Wnt/β-catenin signaling via Smad3-dependent mechanism

    doi: 10.1186/s12967-025-06804-9

    Figure Lengend Snippet: CCN5 regulates activation of TGF-β/Smad and Wnt/β-catenin signaling pathways. A , B Luciferase reporter assays in primary HESCs transfected with the indicated plasmids and treated with the vehicle, TGF-β or prifenidone. FLuc/RLuc activity was determined as mean ± SEM. Statistical analysis was performed using one-way ANOVA. * p < 0.05, ** p < 0.01. C, D. The mRNA expression of downstream target genes of TGF-β/Smad and Wnt/β-catenin signaling pathways in CCN5-overexpression HESCs ( C ) or CCN5-knockdown HESCs ( D ) treated with TGF-β or without TGF-β. Data are presented as the mean ± SEM. Statistical analysis was performed using one-way ANOVA for each target gene. * p < 0.05, ** p < 0.01. E, F. The protein expression of p-Smad3, Smad3, p-β-catenin and β-catenin in CCN5-overexpression HESCs ( E ) or CCN5-knockdown HESCs ( F ) treated with TGF-β or without TGF-β. G. The protein expression of β-catenin in cytoplasmic and nuclear part of CCN5-overexpression HESCs or CCN5-knockdown HESCs was measured by western blotting

    Article Snippet: Furthermore, C57BL/6JCya- Ccn5 em1 /Cya mice (#S-KO-16036), which have a knockout of the CCN5 gene, were also acquired from Cyagen Biosciences (Guangzhou, China).

    Techniques: Activation Assay, Protein-Protein interactions, Luciferase, Transfection, Activity Assay, Expressing, Over Expression, Knockdown, Western Blot

    CCN5 regulates TGF-β induced proliferation and pro-fibrotic transition in HESCs through phosphorylation of Smad3. A Proliferative capability of primary HESCs in shCCN5-HESCs or shNC-HESCs treated with or without SIS3 assessed by CCK8 assay. Data are presented as mean ± SD. Statistical analysis was conducted using one-way ANOVA for the optical density values at 72 h. * p < 0.05. B The mRNA expression of downstream target genes of TGF-β/Smad and Wnt/β-catenin signaling in shCCN5-HESCs or shNC-HESCs treated with SIS3 or without SIS3. Data are presented as the mean ± SEM. Statistical analysis was performed using one-way ANOVA for each target gene. ns, non-significant, * p < 0.05, ** p < 0.01. C The protein expression of α-SMA and Collagen Ι in shCCN5-HESCs or shNC-HESCs treated with SIS3 or without SIS3. D The HE, Masson and Sirius red staining of the endometriosis tissues from the endometriosis mice constructed based on CCN5 knockout mice and combined SIS3 treatment, along with the expression of α-SMA in the endometriosis tissues. Scale bar, 100 μm

    Journal: Journal of Translational Medicine

    Article Title: CCN5 negatively regulates TGF-β-induced endometriosis associated fibrosis through Wnt/β-catenin signaling via Smad3-dependent mechanism

    doi: 10.1186/s12967-025-06804-9

    Figure Lengend Snippet: CCN5 regulates TGF-β induced proliferation and pro-fibrotic transition in HESCs through phosphorylation of Smad3. A Proliferative capability of primary HESCs in shCCN5-HESCs or shNC-HESCs treated with or without SIS3 assessed by CCK8 assay. Data are presented as mean ± SD. Statistical analysis was conducted using one-way ANOVA for the optical density values at 72 h. * p < 0.05. B The mRNA expression of downstream target genes of TGF-β/Smad and Wnt/β-catenin signaling in shCCN5-HESCs or shNC-HESCs treated with SIS3 or without SIS3. Data are presented as the mean ± SEM. Statistical analysis was performed using one-way ANOVA for each target gene. ns, non-significant, * p < 0.05, ** p < 0.01. C The protein expression of α-SMA and Collagen Ι in shCCN5-HESCs or shNC-HESCs treated with SIS3 or without SIS3. D The HE, Masson and Sirius red staining of the endometriosis tissues from the endometriosis mice constructed based on CCN5 knockout mice and combined SIS3 treatment, along with the expression of α-SMA in the endometriosis tissues. Scale bar, 100 μm

    Article Snippet: Furthermore, C57BL/6JCya- Ccn5 em1 /Cya mice (#S-KO-16036), which have a knockout of the CCN5 gene, were also acquired from Cyagen Biosciences (Guangzhou, China).

    Techniques: Phospho-proteomics, CCK-8 Assay, Expressing, Staining, Construct, Knock-Out

    CCN5 prohibited Smad3 shuttle into nucleus by forming complex in cytosol. A Immunofluorescence for CCN5 and Smad3 in HESCs treated with TGF-β or without TGF-β. Scale bar, 20 μm (green CCN5, red Smad3, blue DAPI). B The distribution of Smad3 in the nucleus and cytoplasm in CCN5-overexpression HESCs (CCN5) and control-HESCs treated with TGF-β or without TGF-β was detected by WB. C Co-immunoprecipitation assay of endogenous CCN5 and Smad3 in HESCs treated with or without TGF-β specific inhibitor TGF-β-IN-1. D Co-immunoprecipitation assay of CCN5 and Smad3 in cytoplasm or nucleus in HESCs treated with or without TGF-β specific inhibitor TGF-β-IN-1. E. Molecular docking of CCN5 with Smad3

    Journal: Journal of Translational Medicine

    Article Title: CCN5 negatively regulates TGF-β-induced endometriosis associated fibrosis through Wnt/β-catenin signaling via Smad3-dependent mechanism

    doi: 10.1186/s12967-025-06804-9

    Figure Lengend Snippet: CCN5 prohibited Smad3 shuttle into nucleus by forming complex in cytosol. A Immunofluorescence for CCN5 and Smad3 in HESCs treated with TGF-β or without TGF-β. Scale bar, 20 μm (green CCN5, red Smad3, blue DAPI). B The distribution of Smad3 in the nucleus and cytoplasm in CCN5-overexpression HESCs (CCN5) and control-HESCs treated with TGF-β or without TGF-β was detected by WB. C Co-immunoprecipitation assay of endogenous CCN5 and Smad3 in HESCs treated with or without TGF-β specific inhibitor TGF-β-IN-1. D Co-immunoprecipitation assay of CCN5 and Smad3 in cytoplasm or nucleus in HESCs treated with or without TGF-β specific inhibitor TGF-β-IN-1. E. Molecular docking of CCN5 with Smad3

    Article Snippet: Furthermore, C57BL/6JCya- Ccn5 em1 /Cya mice (#S-KO-16036), which have a knockout of the CCN5 gene, were also acquired from Cyagen Biosciences (Guangzhou, China).

    Techniques: Immunofluorescence, Over Expression, Control, Co-Immunoprecipitation Assay

    Basic properties of anthropometrical and biochemical in the studied groups.

    Journal: Biochemistry and Biophysics Reports

    Article Title: CCN5/WISP2 serum levels in patients with coronary artery disease and type 2 diabetes and its correlation with inflammation and insulin resistance; a machine learning approach

    doi: 10.1016/j.bbrep.2024.101857

    Figure Lengend Snippet: Basic properties of anthropometrical and biochemical in the studied groups.

    Article Snippet: In addition, the ELISA method utilized to measure the circulating levels of CCN5 (MyBioSource, United States) and adiponectin (Adipogen, South Korea), with an analytical sensitivity of 156 pg/ml and 100 pg/ml.

    Techniques: Control

    Alteration of CCN5 serum concentration. a) The patient groups had significantly higher level of CCN5 compared the controls (P < 0.001). Furthermore, its level was higher in the CAD-T2DM patients than the CAD group (P < 0.05). b) The patients in the CAD groups (CAD and CAD-T2DM) with three vessel disease showed significantly higher levels of CCN5 compared to those with single vessel disease, 1-VD (Single-Vessel Disease), 2-VD (Double-Vessel Disease), 3VD (Triple-Vessel Disease). C) There were no remarkable differences between males and females in term of CCN5 in the patients (CAD, T2DM and CAD-T2DM) (P < 0.05).

    Journal: Biochemistry and Biophysics Reports

    Article Title: CCN5/WISP2 serum levels in patients with coronary artery disease and type 2 diabetes and its correlation with inflammation and insulin resistance; a machine learning approach

    doi: 10.1016/j.bbrep.2024.101857

    Figure Lengend Snippet: Alteration of CCN5 serum concentration. a) The patient groups had significantly higher level of CCN5 compared the controls (P < 0.001). Furthermore, its level was higher in the CAD-T2DM patients than the CAD group (P < 0.05). b) The patients in the CAD groups (CAD and CAD-T2DM) with three vessel disease showed significantly higher levels of CCN5 compared to those with single vessel disease, 1-VD (Single-Vessel Disease), 2-VD (Double-Vessel Disease), 3VD (Triple-Vessel Disease). C) There were no remarkable differences between males and females in term of CCN5 in the patients (CAD, T2DM and CAD-T2DM) (P < 0.05).

    Article Snippet: In addition, the ELISA method utilized to measure the circulating levels of CCN5 (MyBioSource, United States) and adiponectin (Adipogen, South Korea), with an analytical sensitivity of 156 pg/ml and 100 pg/ml.

    Techniques: Concentration Assay

    The spearman correlation analysis of various variables with  CCN5.

    Journal: Biochemistry and Biophysics Reports

    Article Title: CCN5/WISP2 serum levels in patients with coronary artery disease and type 2 diabetes and its correlation with inflammation and insulin resistance; a machine learning approach

    doi: 10.1016/j.bbrep.2024.101857

    Figure Lengend Snippet: The spearman correlation analysis of various variables with CCN5.

    Article Snippet: In addition, the ELISA method utilized to measure the circulating levels of CCN5 (MyBioSource, United States) and adiponectin (Adipogen, South Korea), with an analytical sensitivity of 156 pg/ml and 100 pg/ml.

    Techniques: Control

    Odd ratio of the diseases based on 10-unit change in  CCN5.

    Journal: Biochemistry and Biophysics Reports

    Article Title: CCN5/WISP2 serum levels in patients with coronary artery disease and type 2 diabetes and its correlation with inflammation and insulin resistance; a machine learning approach

    doi: 10.1016/j.bbrep.2024.101857

    Figure Lengend Snippet: Odd ratio of the diseases based on 10-unit change in CCN5.

    Article Snippet: In addition, the ELISA method utilized to measure the circulating levels of CCN5 (MyBioSource, United States) and adiponectin (Adipogen, South Korea), with an analytical sensitivity of 156 pg/ml and 100 pg/ml.

    Techniques:

    a) ROC analysis for CCN5 in the CAD patients and the healthy individuals. For CAD prediction, the CCN5 threshold value was 244.24 pg/ml with a percent of 70 and 90, specificity and sensitivity, respectively. The area under the curve was estimated to be 0.865, with a 95 % confidence interval of 0.788–0.942 and a significance level of P < 0.001. b) ROC analysis for CCN5 in the T2DM patients and the healthy individuals. For T2DM prediction, the CCN5 threshold value was 244.24 pg/ml with a percent of 77.5 and 82.5 specificity and sensitivity respectively. The area under the curve was estimated to be 0.916, with a 95 % confidence interval of 0.853–0.979 and a significance level of P < 0.001. c) ROC analysis for CCN5 in the CAD-T2DM patients and the healthy individuals. For CAD-T2DM prediction, the CCN5 threshold value was 245.19 pg/ml with a percent of 70 and 90, specificity and sensitivity respectively. The area under the curve was estimated to be 0.932, with a 95 % confidence interval of 0.882–0.983 and a significance level of P < 0.001.

    Journal: Biochemistry and Biophysics Reports

    Article Title: CCN5/WISP2 serum levels in patients with coronary artery disease and type 2 diabetes and its correlation with inflammation and insulin resistance; a machine learning approach

    doi: 10.1016/j.bbrep.2024.101857

    Figure Lengend Snippet: a) ROC analysis for CCN5 in the CAD patients and the healthy individuals. For CAD prediction, the CCN5 threshold value was 244.24 pg/ml with a percent of 70 and 90, specificity and sensitivity, respectively. The area under the curve was estimated to be 0.865, with a 95 % confidence interval of 0.788–0.942 and a significance level of P < 0.001. b) ROC analysis for CCN5 in the T2DM patients and the healthy individuals. For T2DM prediction, the CCN5 threshold value was 244.24 pg/ml with a percent of 77.5 and 82.5 specificity and sensitivity respectively. The area under the curve was estimated to be 0.916, with a 95 % confidence interval of 0.853–0.979 and a significance level of P < 0.001. c) ROC analysis for CCN5 in the CAD-T2DM patients and the healthy individuals. For CAD-T2DM prediction, the CCN5 threshold value was 245.19 pg/ml with a percent of 70 and 90, specificity and sensitivity respectively. The area under the curve was estimated to be 0.932, with a 95 % confidence interval of 0.882–0.983 and a significance level of P < 0.001.

    Article Snippet: In addition, the ELISA method utilized to measure the circulating levels of CCN5 (MyBioSource, United States) and adiponectin (Adipogen, South Korea), with an analytical sensitivity of 156 pg/ml and 100 pg/ml.

    Techniques:

    a) Factors weight on T2DM calculated by Gini Index. CCN5, TNF, and HOMAIR were found to have the highest weights in relation to diabetes. b) Decision Tree model classifier of T2DM cases. c) Factors weight on CAD calculated by Gini Index. CCN5, IL6, and TNF were observed to have the most significant effects on CAD. d) Decision Tree model classifier of CAD cases. e) Factors weight on CAD-T2DM calculated by Gini Index. f) Decision Tree model classifier of CAD-T2DM cases.

    Journal: Biochemistry and Biophysics Reports

    Article Title: CCN5/WISP2 serum levels in patients with coronary artery disease and type 2 diabetes and its correlation with inflammation and insulin resistance; a machine learning approach

    doi: 10.1016/j.bbrep.2024.101857

    Figure Lengend Snippet: a) Factors weight on T2DM calculated by Gini Index. CCN5, TNF, and HOMAIR were found to have the highest weights in relation to diabetes. b) Decision Tree model classifier of T2DM cases. c) Factors weight on CAD calculated by Gini Index. CCN5, IL6, and TNF were observed to have the most significant effects on CAD. d) Decision Tree model classifier of CAD cases. e) Factors weight on CAD-T2DM calculated by Gini Index. f) Decision Tree model classifier of CAD-T2DM cases.

    Article Snippet: In addition, the ELISA method utilized to measure the circulating levels of CCN5 (MyBioSource, United States) and adiponectin (Adipogen, South Korea), with an analytical sensitivity of 156 pg/ml and 100 pg/ml.

    Techniques: