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Human and mouse inflammatory markers in arthritic joints and plasma are increased in NSG-RA mice. Mice were treated as described in <xref ref-type=Fig. 1 . (A) RT-PCR expression analysis of IFNG , TNFA , Saa1 and Cxcl13 depicted as Cumming plots. CT values over 40 cycles and undetermined values were considered as not expressed and set to zero. (B) Plasma expression levels of human IFNγ, IL-17A, IL12p70 and TNFα detected by Luminex assay and displayed as Cumming plots. The upper part of the plot presents each data point in a swarmplot. The mean and s.d. of each group is plotted as a gapped line, where the vertical lines correspond to the mean±s.d. and the mean itself is depicted as a gap in the line (*** P ≤0.001, ** P ≤0.01, * P ≤0.05). Statistical analysis was performed with R (Kruskal–Wallis test). mRNA levels are depicted as lg(−deltaCT). RA, N =3, n =17; RA+, N =4, n =27; nonRA, N =1, n =6; nonRA+, N =1, n =6. Variations in sample sizes can be attributed to challenges encountered during RNA isolation and the exclusion of outliers during data processing. Values deviating more than sixfold from the mean were considered outliers. As indicated in the key to the right of the lower plot in B, plasma from the RA5 samples was not included in the human TNFα analysis, resulting in a decreased sample size for that plot. N =number of donors, n =total number of mice. Mice were reconstituted with PBMCs from patients with RA (RA3, n =6; RA4, n =6; RA5, n =11; RA7, n =6; RA8, n =15) and an unaffected individual (RA6, n =12). " width="250" height="auto" />
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R&D Systems anti saa1 2 antibody
Human and mouse inflammatory markers in arthritic joints and plasma are increased in NSG-RA mice. Mice were treated as described in <xref ref-type=Fig. 1 . (A) RT-PCR expression analysis of IFNG , TNFA , Saa1 and Cxcl13 depicted as Cumming plots. CT values over 40 cycles and undetermined values were considered as not expressed and set to zero. (B) Plasma expression levels of human IFNγ, IL-17A, IL12p70 and TNFα detected by Luminex assay and displayed as Cumming plots. The upper part of the plot presents each data point in a swarmplot. The mean and s.d. of each group is plotted as a gapped line, where the vertical lines correspond to the mean±s.d. and the mean itself is depicted as a gap in the line (*** P ≤0.001, ** P ≤0.01, * P ≤0.05). Statistical analysis was performed with R (Kruskal–Wallis test). mRNA levels are depicted as lg(−deltaCT). RA, N =3, n =17; RA+, N =4, n =27; nonRA, N =1, n =6; nonRA+, N =1, n =6. Variations in sample sizes can be attributed to challenges encountered during RNA isolation and the exclusion of outliers during data processing. Values deviating more than sixfold from the mean were considered outliers. As indicated in the key to the right of the lower plot in B, plasma from the RA5 samples was not included in the human TNFα analysis, resulting in a decreased sample size for that plot. N =number of donors, n =total number of mice. Mice were reconstituted with PBMCs from patients with RA (RA3, n =6; RA4, n =6; RA5, n =11; RA7, n =6; RA8, n =15) and an unaffected individual (RA6, n =12). " width="250" height="auto" />
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Human and mouse inflammatory markers in arthritic joints and plasma are increased in NSG-RA mice. Mice were treated as described in <xref ref-type=Fig. 1 . (A) RT-PCR expression analysis of IFNG , TNFA , Saa1 and Cxcl13 depicted as Cumming plots. CT values over 40 cycles and undetermined values were considered as not expressed and set to zero. (B) Plasma expression levels of human IFNγ, IL-17A, IL12p70 and TNFα detected by Luminex assay and displayed as Cumming plots. The upper part of the plot presents each data point in a swarmplot. The mean and s.d. of each group is plotted as a gapped line, where the vertical lines correspond to the mean±s.d. and the mean itself is depicted as a gap in the line (*** P ≤0.001, ** P ≤0.01, * P ≤0.05). Statistical analysis was performed with R (Kruskal–Wallis test). mRNA levels are depicted as lg(−deltaCT). RA, N =3, n =17; RA+, N =4, n =27; nonRA, N =1, n =6; nonRA+, N =1, n =6. Variations in sample sizes can be attributed to challenges encountered during RNA isolation and the exclusion of outliers during data processing. Values deviating more than sixfold from the mean were considered outliers. As indicated in the key to the right of the lower plot in B, plasma from the RA5 samples was not included in the human TNFα analysis, resulting in a decreased sample size for that plot. N =number of donors, n =total number of mice. Mice were reconstituted with PBMCs from patients with RA (RA3, n =6; RA4, n =6; RA5, n =11; RA7, n =6; RA8, n =15) and an unaffected individual (RA6, n =12). " width="250" height="auto" />
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Enhanced <t>SAA1</t> expression and NET formation in plasma of MS patients. (A) SAA1 protein expression was quantified by ELISA in plasma samples collected from MS patients and HC. (B) H3.1-nucleosome expression was quantified by ELISA in plasma samples collected from MS patients and HC
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Verification of potential biomarkers for AS. (A) Expression levels of <t>SAA1,</t> FERMT3, ILK, and TLN1 in plasma samples from active-stage AS patients, stable-stage AS patients, and healthy controls measured by proteomics. ROC curves for the individual protein (SAA1, FERMT3, ILK, and TLN1) as a predictor to classify AS patients from healthy controls (B), and active-stage AS patients from stable-stage AS patients (C). (D) ELISA analysis of SAA1, FERMT3, ILK, and TLN1 expressions in the plasma samples from an independent validation cohort of healthy controls (N, n = 24), active-stage AS (A, n = 27), and stable-stage AS patients (S, n = 28). Statistical analyses employed Wilcoxon rank-sum test for intergroup comparisons, with results reported as mean ± SEM. Significance thresholds based on BH-adjusted p -values were defined as: *, <0.05; **, <0.01; ***, <0.001.
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(A) Expression of thyroid hormone receptor-β ( THR-β ) and thyroid hormone receptor-α ( THR-α ) in human liver tissue across MASLD progression stages (GSE213621). (B) Experimental design: male C57BL/6J mice were fed a fructose, palmitate, and cholesterol (FPC) diet for 12 weeks. Therapeutic Resmetirom (Rem) (5 mg/kg/day) or vehicle (0.5% carboxymethyl cellulose-sodium + 0.4% Tween-80) was administered intraperitoneally from week 4 to week 12. (C) Body weight changes over the 12-week period. (D) Representative images and quantification of hepatic lipid accumulation by Nile Red, BODIPY, and hematoxylin & eosin (H&E) staining. Scale bar: 50 μm for Nile Red and BODIPY; Scale bar: 100 μm for H&E. (E–F) Serum biochemical analyses, including total cholesterol (TC), triglycerides (TG), high-density-lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C), alanine aminotransferase (ALT) and aspartate aminotransferase (AST). (G) Total cholesterol and triglyceride content in liver. (H) Immunofluorescence analysis of macrophage infiltration (CD68). Scale bar: 50 μm. (I-J) Serum levels of systemic inflammation markers (CRP and <t>SAA1).</t> (K–L) Sirius Red and immunofluorescence staining of α-smooth muscle actin (α-SMA) indicating fibrosis. Scale bar: 100 μm for Sirius Red; Scale bar: 50 μm for α-SMA. (M) TUNEL assay for hepatocyte apoptosis. Scale bar: 100 μm. (N) Principal component analysis (PCA) of hepatic transcriptome showing distinct clustering between vehicle- and Resmetirom-treated groups (n=4). (O) Volcano plot depicting differentially expressed genes (DEGs) between groups (p < 0.05, |log 2 FC| > 0.5). (P) Pathway enrichment analysis of DEGs highlighting key biological processes. (Q) Heatmap of representative DEGs associated with hepatic steatosis, inflammation, fibrosis, and cell death. Statistical significance: p < 0.05.
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Human and mouse inflammatory markers in arthritic joints and plasma are increased in NSG-RA mice. Mice were treated as described in <xref ref-type=Fig. 1 . (A) RT-PCR expression analysis of IFNG , TNFA , Saa1 and Cxcl13 depicted as Cumming plots. CT values over 40 cycles and undetermined values were considered as not expressed and set to zero. (B) Plasma expression levels of human IFNγ, IL-17A, IL12p70 and TNFα detected by Luminex assay and displayed as Cumming plots. The upper part of the plot presents each data point in a swarmplot. The mean and s.d. of each group is plotted as a gapped line, where the vertical lines correspond to the mean±s.d. and the mean itself is depicted as a gap in the line (*** P ≤0.001, ** P ≤0.01, * P ≤0.05). Statistical analysis was performed with R (Kruskal–Wallis test). mRNA levels are depicted as lg(−deltaCT). RA, N =3, n =17; RA+, N =4, n =27; nonRA, N =1, n =6; nonRA+, N =1, n =6. Variations in sample sizes can be attributed to challenges encountered during RNA isolation and the exclusion of outliers during data processing. Values deviating more than sixfold from the mean were considered outliers. As indicated in the key to the right of the lower plot in B, plasma from the RA5 samples was not included in the human TNFα analysis, resulting in a decreased sample size for that plot. N =number of donors, n =total number of mice. Mice were reconstituted with PBMCs from patients with RA (RA3, n =6; RA4, n =6; RA5, n =11; RA7, n =6; RA8, n =15) and an unaffected individual (RA6, n =12). " width="100%" height="100%">

Journal: Disease Models & Mechanisms

Article Title: Validation of a model of rheumatoid arthritis using mice reconstituted with patient peripheral blood mononuclear cells

doi: 10.1242/dmm.052294

Figure Lengend Snippet: Human and mouse inflammatory markers in arthritic joints and plasma are increased in NSG-RA mice. Mice were treated as described in Fig. 1 . (A) RT-PCR expression analysis of IFNG , TNFA , Saa1 and Cxcl13 depicted as Cumming plots. CT values over 40 cycles and undetermined values were considered as not expressed and set to zero. (B) Plasma expression levels of human IFNγ, IL-17A, IL12p70 and TNFα detected by Luminex assay and displayed as Cumming plots. The upper part of the plot presents each data point in a swarmplot. The mean and s.d. of each group is plotted as a gapped line, where the vertical lines correspond to the mean±s.d. and the mean itself is depicted as a gap in the line (*** P ≤0.001, ** P ≤0.01, * P ≤0.05). Statistical analysis was performed with R (Kruskal–Wallis test). mRNA levels are depicted as lg(−deltaCT). RA, N =3, n =17; RA+, N =4, n =27; nonRA, N =1, n =6; nonRA+, N =1, n =6. Variations in sample sizes can be attributed to challenges encountered during RNA isolation and the exclusion of outliers during data processing. Values deviating more than sixfold from the mean were considered outliers. As indicated in the key to the right of the lower plot in B, plasma from the RA5 samples was not included in the human TNFα analysis, resulting in a decreased sample size for that plot. N =number of donors, n =total number of mice. Mice were reconstituted with PBMCs from patients with RA (RA3, n =6; RA4, n =6; RA5, n =11; RA7, n =6; RA8, n =15) and an unaffected individual (RA6, n =12).

Article Snippet: Single-tube TaqMan gene expression assays (Thermo Fisher Scientific) included the housekeeping gene Gapdh (Mm99999915_g1) and the markers TNFA (Hs01113624_g1), IFNG (Hs00989291_m1), Cxcl13 (Mm04214185_s1) and Saa1 (Mm00656927_g1).

Techniques: Clinical Proteomics, Reverse Transcription Polymerase Chain Reaction, Expressing, Luminex, Isolation

Cytokine concentration in plasma and expression of human and mouse proinflammatory cytokines in arthritic joints are decreased in response to treatment with prednisolone or infliximab. Mice were treated as described in <xref ref-type=Fig. 7 . (A) Plasma levels of human TNFα, human IL12p70 and murine Cxcl9 presented as Cumming plots. Challenged, non-treated NSG-RA mice ( N =2, n =15 in total) were compared to challenged, infliximab-treated ( N =2, n =15 in total) or challenged, prednisolone-treated ( N =2, n =12 in total) mice. Outliers (values above 44,000 for Luminex) or undetermined values were removed for data analysis. (B) RT-PCR expression analysis of TNFA , Cxcl13 , Saa1 and IFNG calculated as lg(-deltaCT) and presented as Cumming plots. Challenged, non-treated NSG-RA mice ( N =3, n =21 in total) were compared to challenged, infliximab-treated ( N =3, n =15 in total) or challenged, prednisolone-treated ( N =2, n =11 in total) mice. The upper part of the plot presents each data point in a swarmplot. The mean and s.d. of each group is plotted as a gapped line, where the vertical lines correspond to the mean±s.d., and the mean itself is depicted as a gap in the line (*** P ≤0.001, * P ≤0.05). N =number of donors, n =total number of mice. Statistical analysis was performed with R (Mann–Whitney U -test). For raw data, see Table S7 . Mice were reconstituted with PBMCs from patients with RA (RA5, n =12; RA7, n =18; RA8, n =18). " width="100%" height="100%">

Journal: Disease Models & Mechanisms

Article Title: Validation of a model of rheumatoid arthritis using mice reconstituted with patient peripheral blood mononuclear cells

doi: 10.1242/dmm.052294

Figure Lengend Snippet: Cytokine concentration in plasma and expression of human and mouse proinflammatory cytokines in arthritic joints are decreased in response to treatment with prednisolone or infliximab. Mice were treated as described in Fig. 7 . (A) Plasma levels of human TNFα, human IL12p70 and murine Cxcl9 presented as Cumming plots. Challenged, non-treated NSG-RA mice ( N =2, n =15 in total) were compared to challenged, infliximab-treated ( N =2, n =15 in total) or challenged, prednisolone-treated ( N =2, n =12 in total) mice. Outliers (values above 44,000 for Luminex) or undetermined values were removed for data analysis. (B) RT-PCR expression analysis of TNFA , Cxcl13 , Saa1 and IFNG calculated as lg(-deltaCT) and presented as Cumming plots. Challenged, non-treated NSG-RA mice ( N =3, n =21 in total) were compared to challenged, infliximab-treated ( N =3, n =15 in total) or challenged, prednisolone-treated ( N =2, n =11 in total) mice. The upper part of the plot presents each data point in a swarmplot. The mean and s.d. of each group is plotted as a gapped line, where the vertical lines correspond to the mean±s.d., and the mean itself is depicted as a gap in the line (*** P ≤0.001, * P ≤0.05). N =number of donors, n =total number of mice. Statistical analysis was performed with R (Mann–Whitney U -test). For raw data, see Table S7 . Mice were reconstituted with PBMCs from patients with RA (RA5, n =12; RA7, n =18; RA8, n =18).

Article Snippet: Single-tube TaqMan gene expression assays (Thermo Fisher Scientific) included the housekeeping gene Gapdh (Mm99999915_g1) and the markers TNFA (Hs01113624_g1), IFNG (Hs00989291_m1), Cxcl13 (Mm04214185_s1) and Saa1 (Mm00656927_g1).

Techniques: Concentration Assay, Clinical Proteomics, Expressing, Luminex, Reverse Transcription Polymerase Chain Reaction, MANN-WHITNEY

Enhanced SAA1 expression and NET formation in plasma of MS patients. (A) SAA1 protein expression was quantified by ELISA in plasma samples collected from MS patients and HC. (B) H3.1-nucleosome expression was quantified by ELISA in plasma samples collected from MS patients and HC

Journal: Journal of Neuroinflammation

Article Title: Single-cell RNA sequencing uncovers neutrophil clusters associated with autoimmune neuroinflammation

doi: 10.1186/s12974-026-03772-9

Figure Lengend Snippet: Enhanced SAA1 expression and NET formation in plasma of MS patients. (A) SAA1 protein expression was quantified by ELISA in plasma samples collected from MS patients and HC. (B) H3.1-nucleosome expression was quantified by ELISA in plasma samples collected from MS patients and HC

Article Snippet: The human SAA1 ELISA kit (DY3019-05; R & D Systems, Minneapolis, MN) detected human SAA1 in plasma samples from MS patients and HC.

Techniques: Expressing, Clinical Proteomics, Enzyme-linked Immunosorbent Assay

Verification of potential biomarkers for AS. (A) Expression levels of SAA1, FERMT3, ILK, and TLN1 in plasma samples from active-stage AS patients, stable-stage AS patients, and healthy controls measured by proteomics. ROC curves for the individual protein (SAA1, FERMT3, ILK, and TLN1) as a predictor to classify AS patients from healthy controls (B), and active-stage AS patients from stable-stage AS patients (C). (D) ELISA analysis of SAA1, FERMT3, ILK, and TLN1 expressions in the plasma samples from an independent validation cohort of healthy controls (N, n = 24), active-stage AS (A, n = 27), and stable-stage AS patients (S, n = 28). Statistical analyses employed Wilcoxon rank-sum test for intergroup comparisons, with results reported as mean ± SEM. Significance thresholds based on BH-adjusted p -values were defined as: *, <0.05; **, <0.01; ***, <0.001.

Journal: Journal of Advanced Research

Article Title: Characterization of immune features and discovery of potential biomarkers for ankylosing spondylitis using deep plasma proteomics

doi: 10.1016/j.jare.2025.05.052

Figure Lengend Snippet: Verification of potential biomarkers for AS. (A) Expression levels of SAA1, FERMT3, ILK, and TLN1 in plasma samples from active-stage AS patients, stable-stage AS patients, and healthy controls measured by proteomics. ROC curves for the individual protein (SAA1, FERMT3, ILK, and TLN1) as a predictor to classify AS patients from healthy controls (B), and active-stage AS patients from stable-stage AS patients (C). (D) ELISA analysis of SAA1, FERMT3, ILK, and TLN1 expressions in the plasma samples from an independent validation cohort of healthy controls (N, n = 24), active-stage AS (A, n = 27), and stable-stage AS patients (S, n = 28). Statistical analyses employed Wilcoxon rank-sum test for intergroup comparisons, with results reported as mean ± SEM. Significance thresholds based on BH-adjusted p -values were defined as: *, <0.05; **, <0.01; ***, <0.001.

Article Snippet: The human serum amyloid A (SAA1) ELISA kit (#OKIA00083) was purchased from Aviva Systems Biology Company (San Diego, CA, USA).

Techniques: Expressing, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Biomarker Discovery

(A) Expression of thyroid hormone receptor-β ( THR-β ) and thyroid hormone receptor-α ( THR-α ) in human liver tissue across MASLD progression stages (GSE213621). (B) Experimental design: male C57BL/6J mice were fed a fructose, palmitate, and cholesterol (FPC) diet for 12 weeks. Therapeutic Resmetirom (Rem) (5 mg/kg/day) or vehicle (0.5% carboxymethyl cellulose-sodium + 0.4% Tween-80) was administered intraperitoneally from week 4 to week 12. (C) Body weight changes over the 12-week period. (D) Representative images and quantification of hepatic lipid accumulation by Nile Red, BODIPY, and hematoxylin & eosin (H&E) staining. Scale bar: 50 μm for Nile Red and BODIPY; Scale bar: 100 μm for H&E. (E–F) Serum biochemical analyses, including total cholesterol (TC), triglycerides (TG), high-density-lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C), alanine aminotransferase (ALT) and aspartate aminotransferase (AST). (G) Total cholesterol and triglyceride content in liver. (H) Immunofluorescence analysis of macrophage infiltration (CD68). Scale bar: 50 μm. (I-J) Serum levels of systemic inflammation markers (CRP and SAA1). (K–L) Sirius Red and immunofluorescence staining of α-smooth muscle actin (α-SMA) indicating fibrosis. Scale bar: 100 μm for Sirius Red; Scale bar: 50 μm for α-SMA. (M) TUNEL assay for hepatocyte apoptosis. Scale bar: 100 μm. (N) Principal component analysis (PCA) of hepatic transcriptome showing distinct clustering between vehicle- and Resmetirom-treated groups (n=4). (O) Volcano plot depicting differentially expressed genes (DEGs) between groups (p < 0.05, |log 2 FC| > 0.5). (P) Pathway enrichment analysis of DEGs highlighting key biological processes. (Q) Heatmap of representative DEGs associated with hepatic steatosis, inflammation, fibrosis, and cell death. Statistical significance: p < 0.05.

Journal: bioRxiv

Article Title: Modulation of metabolic, inflammatory, fibrotic and cell death pathways by Resmetirom in metabolic dysfunction-associated steatohepatitis (MASH): A transcriptomic profiling study

doi: 10.1101/2025.11.26.690715

Figure Lengend Snippet: (A) Expression of thyroid hormone receptor-β ( THR-β ) and thyroid hormone receptor-α ( THR-α ) in human liver tissue across MASLD progression stages (GSE213621). (B) Experimental design: male C57BL/6J mice were fed a fructose, palmitate, and cholesterol (FPC) diet for 12 weeks. Therapeutic Resmetirom (Rem) (5 mg/kg/day) or vehicle (0.5% carboxymethyl cellulose-sodium + 0.4% Tween-80) was administered intraperitoneally from week 4 to week 12. (C) Body weight changes over the 12-week period. (D) Representative images and quantification of hepatic lipid accumulation by Nile Red, BODIPY, and hematoxylin & eosin (H&E) staining. Scale bar: 50 μm for Nile Red and BODIPY; Scale bar: 100 μm for H&E. (E–F) Serum biochemical analyses, including total cholesterol (TC), triglycerides (TG), high-density-lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C), alanine aminotransferase (ALT) and aspartate aminotransferase (AST). (G) Total cholesterol and triglyceride content in liver. (H) Immunofluorescence analysis of macrophage infiltration (CD68). Scale bar: 50 μm. (I-J) Serum levels of systemic inflammation markers (CRP and SAA1). (K–L) Sirius Red and immunofluorescence staining of α-smooth muscle actin (α-SMA) indicating fibrosis. Scale bar: 100 μm for Sirius Red; Scale bar: 50 μm for α-SMA. (M) TUNEL assay for hepatocyte apoptosis. Scale bar: 100 μm. (N) Principal component analysis (PCA) of hepatic transcriptome showing distinct clustering between vehicle- and Resmetirom-treated groups (n=4). (O) Volcano plot depicting differentially expressed genes (DEGs) between groups (p < 0.05, |log 2 FC| > 0.5). (P) Pathway enrichment analysis of DEGs highlighting key biological processes. (Q) Heatmap of representative DEGs associated with hepatic steatosis, inflammation, fibrosis, and cell death. Statistical significance: p < 0.05.

Article Snippet: To assess systemic inflammatory markers, serum concentrations of C-reactive protein (CRP; #KE10128, Proteintech) and serum amyloid A1 (SAA1; #CSB-EL020656MO, CUSABIO) were determined using specific ELISA kits following the manufacturers’ instructions.

Techniques: Expressing, Staining, Immunofluorescence, TUNEL Assay