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sst2 dst200  (R&D Systems)


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    Structured Review

    R&D Systems sst2 dst200
    Effect of obesity and sex on the circulating levels of interleukin (IL)-33 and soluble suppression of tumorigenicity 2 <t>(sST2).</t> Fasting serum concentrations of ( A ) IL-33, ( C ) sST2 and ( E ) IL-33/sST2 in normal-weight (NW-NG) volunteers ( n = 22), patients with obesity with normoglycemia (OB-NG) ( n = 24) and with obesity-associated type 2 diabetes (OB-T2D) ( n = 27). Circulating concentrations of ( B ) IL-33, ( D ) sST2 and ( F ) IL-33/sST2 in males ( n = 26) and females ( n = 47) volunteers. Data are mean ± SEM. Differences between groups were analyzed by one-way ANOVA followed by Tukey’s tests or by unpaired two-tailed Student’s t test as appropriate. * P < 0.05, ** P < 0.01 and *** P < 0.001
    Sst2 Dst200, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 54 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/sst2 dst200/product/R&D Systems
    Average 95 stars, based on 54 article reviews
    sst2 dst200 - by Bioz Stars, 2026-06
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    1) Product Images from "Dual and context-dependent role of the interleukin-33/soluble suppression of tumorigenicity 2 axis in obesity and adipose tissue inflammation"

    Article Title: Dual and context-dependent role of the interleukin-33/soluble suppression of tumorigenicity 2 axis in obesity and adipose tissue inflammation

    Journal: Molecular Medicine

    doi: 10.1186/s10020-026-01454-z

    Effect of obesity and sex on the circulating levels of interleukin (IL)-33 and soluble suppression of tumorigenicity 2 (sST2). Fasting serum concentrations of ( A ) IL-33, ( C ) sST2 and ( E ) IL-33/sST2 in normal-weight (NW-NG) volunteers ( n = 22), patients with obesity with normoglycemia (OB-NG) ( n = 24) and with obesity-associated type 2 diabetes (OB-T2D) ( n = 27). Circulating concentrations of ( B ) IL-33, ( D ) sST2 and ( F ) IL-33/sST2 in males ( n = 26) and females ( n = 47) volunteers. Data are mean ± SEM. Differences between groups were analyzed by one-way ANOVA followed by Tukey’s tests or by unpaired two-tailed Student’s t test as appropriate. * P < 0.05, ** P < 0.01 and *** P < 0.001
    Figure Legend Snippet: Effect of obesity and sex on the circulating levels of interleukin (IL)-33 and soluble suppression of tumorigenicity 2 (sST2). Fasting serum concentrations of ( A ) IL-33, ( C ) sST2 and ( E ) IL-33/sST2 in normal-weight (NW-NG) volunteers ( n = 22), patients with obesity with normoglycemia (OB-NG) ( n = 24) and with obesity-associated type 2 diabetes (OB-T2D) ( n = 27). Circulating concentrations of ( B ) IL-33, ( D ) sST2 and ( F ) IL-33/sST2 in males ( n = 26) and females ( n = 47) volunteers. Data are mean ± SEM. Differences between groups were analyzed by one-way ANOVA followed by Tukey’s tests or by unpaired two-tailed Student’s t test as appropriate. * P < 0.05, ** P < 0.01 and *** P < 0.001

    Techniques Used: Two Tailed Test

    The increased circulating levels of IL-33 in obesity together the decrease in its soluble decoy receptor sST2 may be potentially enhancing IL-33 bioactivity. In addition, gene and protein expression levels of IL-33 in visceral adipose tissue (VAT) are upregulated in obesity in both adipocytes and stromal vascular fraction cells. IL-33 modulates adipocyte function by upregulating both anti-inflammatory mediators ( ADIPOQ , ITLN1 and IL13 ) and pro-inflammatory cytokines ( TNF , IL8 ). Under inflammatory conditions, such as LPS stimulation, IL-33 attenuates excessive pro-inflammatory responses and promotes protective adipokine expression in visceral adipocytes. In THP-1-derived macrophages, adipocyte-derived factors suppress IL33 expression, whereas IL-33 attenuates macrophage pro-inflammatory activation and enhances IL4 expression only in the context of adipocyte-conditioned medium. Together, these findings suggest the dual and context-dependent nature of IL-33 in obesity, acting as a compensatory mediator to maintain tissue homeostasis while potentially contributing to chronic low-grade inflammation when elevated chronically. ADIPOQ, adiponectin; IL , interleukin; ITLN1 , omentin; TNF , tumor necrosis factor α
    Figure Legend Snippet: The increased circulating levels of IL-33 in obesity together the decrease in its soluble decoy receptor sST2 may be potentially enhancing IL-33 bioactivity. In addition, gene and protein expression levels of IL-33 in visceral adipose tissue (VAT) are upregulated in obesity in both adipocytes and stromal vascular fraction cells. IL-33 modulates adipocyte function by upregulating both anti-inflammatory mediators ( ADIPOQ , ITLN1 and IL13 ) and pro-inflammatory cytokines ( TNF , IL8 ). Under inflammatory conditions, such as LPS stimulation, IL-33 attenuates excessive pro-inflammatory responses and promotes protective adipokine expression in visceral adipocytes. In THP-1-derived macrophages, adipocyte-derived factors suppress IL33 expression, whereas IL-33 attenuates macrophage pro-inflammatory activation and enhances IL4 expression only in the context of adipocyte-conditioned medium. Together, these findings suggest the dual and context-dependent nature of IL-33 in obesity, acting as a compensatory mediator to maintain tissue homeostasis while potentially contributing to chronic low-grade inflammation when elevated chronically. ADIPOQ, adiponectin; IL , interleukin; ITLN1 , omentin; TNF , tumor necrosis factor α

    Techniques Used: Expressing, Derivative Assay, Activation Assay



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    Effect of obesity and sex on the circulating levels of interleukin (IL)-33 and soluble suppression of tumorigenicity 2 <t>(sST2).</t> Fasting serum concentrations of ( A ) IL-33, ( C ) sST2 and ( E ) IL-33/sST2 in normal-weight (NW-NG) volunteers ( n = 22), patients with obesity with normoglycemia (OB-NG) ( n = 24) and with obesity-associated type 2 diabetes (OB-T2D) ( n = 27). Circulating concentrations of ( B ) IL-33, ( D ) sST2 and ( F ) IL-33/sST2 in males ( n = 26) and females ( n = 47) volunteers. Data are mean ± SEM. Differences between groups were analyzed by one-way ANOVA followed by Tukey’s tests or by unpaired two-tailed Student’s t test as appropriate. * P < 0.05, ** P < 0.01 and *** P < 0.001
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    Effect of obesity and sex on the circulating levels of interleukin (IL)-33 and soluble suppression of tumorigenicity 2 <t>(sST2).</t> Fasting serum concentrations of ( A ) IL-33, ( C ) sST2 and ( E ) IL-33/sST2 in normal-weight (NW-NG) volunteers ( n = 22), patients with obesity with normoglycemia (OB-NG) ( n = 24) and with obesity-associated type 2 diabetes (OB-T2D) ( n = 27). Circulating concentrations of ( B ) IL-33, ( D ) sST2 and ( F ) IL-33/sST2 in males ( n = 26) and females ( n = 47) volunteers. Data are mean ± SEM. Differences between groups were analyzed by one-way ANOVA followed by Tukey’s tests or by unpaired two-tailed Student’s t test as appropriate. * P < 0.05, ** P < 0.01 and *** P < 0.001
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    Effect of obesity and sex on the circulating levels of interleukin (IL)-33 and soluble suppression of tumorigenicity 2 <t>(sST2).</t> Fasting serum concentrations of ( A ) IL-33, ( C ) sST2 and ( E ) IL-33/sST2 in normal-weight (NW-NG) volunteers ( n = 22), patients with obesity with normoglycemia (OB-NG) ( n = 24) and with obesity-associated type 2 diabetes (OB-T2D) ( n = 27). Circulating concentrations of ( B ) IL-33, ( D ) sST2 and ( F ) IL-33/sST2 in males ( n = 26) and females ( n = 47) volunteers. Data are mean ± SEM. Differences between groups were analyzed by one-way ANOVA followed by Tukey’s tests or by unpaired two-tailed Student’s t test as appropriate. * P < 0.05, ** P < 0.01 and *** P < 0.001
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    R&D Systems human r d systems sst2 elisa kit
    Serum <t>sST2</t> increased in CVDs. Serum sST2 levels in (A) men and women (black), (B) women only (peach), or (C) men only (blue) were compared between control patients without known CVDs (white) to those with myocarditis (Myo), cardiomyopathy (Card), coronary artery disease (CAD), myocardial infarct (MI), or congestive heart failure (CHF). Violin plots denote data distribution for each group with p -value calculated using Welch’s t -test: *, p < 0.05; ** , p < 0.01; *** , p < 0.001; **** , p < 0.0001; ns, not significant.
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    Effect of obesity and sex on the circulating levels of interleukin (IL)-33 and soluble suppression of tumorigenicity 2 (sST2). Fasting serum concentrations of ( A ) IL-33, ( C ) sST2 and ( E ) IL-33/sST2 in normal-weight (NW-NG) volunteers ( n = 22), patients with obesity with normoglycemia (OB-NG) ( n = 24) and with obesity-associated type 2 diabetes (OB-T2D) ( n = 27). Circulating concentrations of ( B ) IL-33, ( D ) sST2 and ( F ) IL-33/sST2 in males ( n = 26) and females ( n = 47) volunteers. Data are mean ± SEM. Differences between groups were analyzed by one-way ANOVA followed by Tukey’s tests or by unpaired two-tailed Student’s t test as appropriate. * P < 0.05, ** P < 0.01 and *** P < 0.001

    Journal: Molecular Medicine

    Article Title: Dual and context-dependent role of the interleukin-33/soluble suppression of tumorigenicity 2 axis in obesity and adipose tissue inflammation

    doi: 10.1186/s10020-026-01454-z

    Figure Lengend Snippet: Effect of obesity and sex on the circulating levels of interleukin (IL)-33 and soluble suppression of tumorigenicity 2 (sST2). Fasting serum concentrations of ( A ) IL-33, ( C ) sST2 and ( E ) IL-33/sST2 in normal-weight (NW-NG) volunteers ( n = 22), patients with obesity with normoglycemia (OB-NG) ( n = 24) and with obesity-associated type 2 diabetes (OB-T2D) ( n = 27). Circulating concentrations of ( B ) IL-33, ( D ) sST2 and ( F ) IL-33/sST2 in males ( n = 26) and females ( n = 47) volunteers. Data are mean ± SEM. Differences between groups were analyzed by one-way ANOVA followed by Tukey’s tests or by unpaired two-tailed Student’s t test as appropriate. * P < 0.05, ** P < 0.01 and *** P < 0.001

    Article Snippet: Circulating concentrations of IL-33 (D3300B) and sST2 (DST200) were quantified using commercial ELISA kits (R&D Systems, Minneapolis, MN) according to manufacturer’s instructions.

    Techniques: Two Tailed Test

    The increased circulating levels of IL-33 in obesity together the decrease in its soluble decoy receptor sST2 may be potentially enhancing IL-33 bioactivity. In addition, gene and protein expression levels of IL-33 in visceral adipose tissue (VAT) are upregulated in obesity in both adipocytes and stromal vascular fraction cells. IL-33 modulates adipocyte function by upregulating both anti-inflammatory mediators ( ADIPOQ , ITLN1 and IL13 ) and pro-inflammatory cytokines ( TNF , IL8 ). Under inflammatory conditions, such as LPS stimulation, IL-33 attenuates excessive pro-inflammatory responses and promotes protective adipokine expression in visceral adipocytes. In THP-1-derived macrophages, adipocyte-derived factors suppress IL33 expression, whereas IL-33 attenuates macrophage pro-inflammatory activation and enhances IL4 expression only in the context of adipocyte-conditioned medium. Together, these findings suggest the dual and context-dependent nature of IL-33 in obesity, acting as a compensatory mediator to maintain tissue homeostasis while potentially contributing to chronic low-grade inflammation when elevated chronically. ADIPOQ, adiponectin; IL , interleukin; ITLN1 , omentin; TNF , tumor necrosis factor α

    Journal: Molecular Medicine

    Article Title: Dual and context-dependent role of the interleukin-33/soluble suppression of tumorigenicity 2 axis in obesity and adipose tissue inflammation

    doi: 10.1186/s10020-026-01454-z

    Figure Lengend Snippet: The increased circulating levels of IL-33 in obesity together the decrease in its soluble decoy receptor sST2 may be potentially enhancing IL-33 bioactivity. In addition, gene and protein expression levels of IL-33 in visceral adipose tissue (VAT) are upregulated in obesity in both adipocytes and stromal vascular fraction cells. IL-33 modulates adipocyte function by upregulating both anti-inflammatory mediators ( ADIPOQ , ITLN1 and IL13 ) and pro-inflammatory cytokines ( TNF , IL8 ). Under inflammatory conditions, such as LPS stimulation, IL-33 attenuates excessive pro-inflammatory responses and promotes protective adipokine expression in visceral adipocytes. In THP-1-derived macrophages, adipocyte-derived factors suppress IL33 expression, whereas IL-33 attenuates macrophage pro-inflammatory activation and enhances IL4 expression only in the context of adipocyte-conditioned medium. Together, these findings suggest the dual and context-dependent nature of IL-33 in obesity, acting as a compensatory mediator to maintain tissue homeostasis while potentially contributing to chronic low-grade inflammation when elevated chronically. ADIPOQ, adiponectin; IL , interleukin; ITLN1 , omentin; TNF , tumor necrosis factor α

    Article Snippet: Circulating concentrations of IL-33 (D3300B) and sST2 (DST200) were quantified using commercial ELISA kits (R&D Systems, Minneapolis, MN) according to manufacturer’s instructions.

    Techniques: Expressing, Derivative Assay, Activation Assay

    Serum sST2 increased in CVDs. Serum sST2 levels in (A) men and women (black), (B) women only (peach), or (C) men only (blue) were compared between control patients without known CVDs (white) to those with myocarditis (Myo), cardiomyopathy (Card), coronary artery disease (CAD), myocardial infarct (MI), or congestive heart failure (CHF). Violin plots denote data distribution for each group with p -value calculated using Welch’s t -test: *, p < 0.05; ** , p < 0.01; *** , p < 0.001; **** , p < 0.0001; ns, not significant.

    Journal: Frontiers in Cardiovascular Medicine

    Article Title: Sex and age differences in sST2 in cardiovascular disease

    doi: 10.3389/fcvm.2022.1073814

    Figure Lengend Snippet: Serum sST2 increased in CVDs. Serum sST2 levels in (A) men and women (black), (B) women only (peach), or (C) men only (blue) were compared between control patients without known CVDs (white) to those with myocarditis (Myo), cardiomyopathy (Card), coronary artery disease (CAD), myocardial infarct (MI), or congestive heart failure (CHF). Violin plots denote data distribution for each group with p -value calculated using Welch’s t -test: *, p < 0.05; ** , p < 0.01; *** , p < 0.001; **** , p < 0.0001; ns, not significant.

    Article Snippet: As this kit was not available when myocarditis samples were initially analyzed, the human R&D Systems sST2 ELISA kit (Cat# DST200, Minneapolis, MN, USA) was used for myocarditis samples.

    Techniques: Control

    Sex differences in sST2 in controls and CVDs. sST2 levels compared women (peach) vs. men (blue) for (A) controls, (B) myocarditis (Myo), (C) cardiomyopathy (Card), (D) coronary artery disease (CAD), (E) myocardial infarction (MI), or (F) congestive heart failure (CHF). Violin plots denote data distribution for each group with p -value calculated using unpaired Student’s t -test: ** , p < 0.01; **** , p < 0.0001; ns, not significant.

    Journal: Frontiers in Cardiovascular Medicine

    Article Title: Sex and age differences in sST2 in cardiovascular disease

    doi: 10.3389/fcvm.2022.1073814

    Figure Lengend Snippet: Sex differences in sST2 in controls and CVDs. sST2 levels compared women (peach) vs. men (blue) for (A) controls, (B) myocarditis (Myo), (C) cardiomyopathy (Card), (D) coronary artery disease (CAD), (E) myocardial infarction (MI), or (F) congestive heart failure (CHF). Violin plots denote data distribution for each group with p -value calculated using unpaired Student’s t -test: ** , p < 0.01; **** , p < 0.0001; ns, not significant.

    Article Snippet: As this kit was not available when myocarditis samples were initially analyzed, the human R&D Systems sST2 ELISA kit (Cat# DST200, Minneapolis, MN, USA) was used for myocarditis samples.

    Techniques:

    Sex and age differences in sST2 in CVDs. sST2 levels compared women (peach) vs. men (blue) that were <50 vs. ≥50 years of age for (A) myocarditis (Myo), (B) cardiomyopathy (Card), (C) coronary artery disease (CAD), (D) myocardial infarction (MI), or (E) congestive heart failure (CHF). Violin plots denote data distribution for each group. One-way ANOVA: (A) p = 0.0043, (B) p = 0.035, (C) p = 0.94, (D) p = 0.16, and (E) p = 0.70 with two-way comparisons analyzed using unpaired Student’s t -test: *, p < 0.05; *** , p < 0.001; ns, not significant. (A) Two-way ANOVA p -values indicate no interaction between sex and age in patients with myo ( p = 0.11), but interactions between sex and sST2 ( p = 0.0047) and age and sST2 ( p = 0.0496). (B) Two-way ANOVA p -values indicate no interactions between sex and age ( p = 0.43) or age and sST2 ( p = 0.99) in patients with card, but interaction between sex and sST2 ( p = 0.04). (C) Two-way ANOVA p -values indicate no interactions between sex and age ( p = 0.60), age and sST2 ( p = 0.79), or sex and sST2 ( p = 0.79) in patients with CAD. (D) Two-way ANOVA p -values indicate no interactions between sex and age ( p = 0.32), age and sST2 ( p = 0.25), or sex and sST2 ( p = 0.92) in patients with MI. (E) Two-way ANOVA p -values indicate no interactions between sex and age ( p = 0.87), age and sST2 ( p = 0.54), or sex and sST2 ( p = 0.57) in patients with CHF.

    Journal: Frontiers in Cardiovascular Medicine

    Article Title: Sex and age differences in sST2 in cardiovascular disease

    doi: 10.3389/fcvm.2022.1073814

    Figure Lengend Snippet: Sex and age differences in sST2 in CVDs. sST2 levels compared women (peach) vs. men (blue) that were <50 vs. ≥50 years of age for (A) myocarditis (Myo), (B) cardiomyopathy (Card), (C) coronary artery disease (CAD), (D) myocardial infarction (MI), or (E) congestive heart failure (CHF). Violin plots denote data distribution for each group. One-way ANOVA: (A) p = 0.0043, (B) p = 0.035, (C) p = 0.94, (D) p = 0.16, and (E) p = 0.70 with two-way comparisons analyzed using unpaired Student’s t -test: *, p < 0.05; *** , p < 0.001; ns, not significant. (A) Two-way ANOVA p -values indicate no interaction between sex and age in patients with myo ( p = 0.11), but interactions between sex and sST2 ( p = 0.0047) and age and sST2 ( p = 0.0496). (B) Two-way ANOVA p -values indicate no interactions between sex and age ( p = 0.43) or age and sST2 ( p = 0.99) in patients with card, but interaction between sex and sST2 ( p = 0.04). (C) Two-way ANOVA p -values indicate no interactions between sex and age ( p = 0.60), age and sST2 ( p = 0.79), or sex and sST2 ( p = 0.79) in patients with CAD. (D) Two-way ANOVA p -values indicate no interactions between sex and age ( p = 0.32), age and sST2 ( p = 0.25), or sex and sST2 ( p = 0.92) in patients with MI. (E) Two-way ANOVA p -values indicate no interactions between sex and age ( p = 0.87), age and sST2 ( p = 0.54), or sex and sST2 ( p = 0.57) in patients with CHF.

    Article Snippet: As this kit was not available when myocarditis samples were initially analyzed, the human R&D Systems sST2 ELISA kit (Cat# DST200, Minneapolis, MN, USA) was used for myocarditis samples.

    Techniques:

    Soluble ST2 (sST2) in pre- vs. post-menopausal women with CVDs. sST2 levels compared pre-menopausal women (light peach) to post-menopausal women (dark peach) for (A) cardiomyopathy (Card), (B) coronary artery disease (CAD), (C) myocardial infarction (MI), or (D) congestive heart failure (CHF). Violin plots denote data distribution for each group with p -value calculated using unpaired Student’s t -test: *, p < 0.05; ns, not significant.

    Journal: Frontiers in Cardiovascular Medicine

    Article Title: Sex and age differences in sST2 in cardiovascular disease

    doi: 10.3389/fcvm.2022.1073814

    Figure Lengend Snippet: Soluble ST2 (sST2) in pre- vs. post-menopausal women with CVDs. sST2 levels compared pre-menopausal women (light peach) to post-menopausal women (dark peach) for (A) cardiomyopathy (Card), (B) coronary artery disease (CAD), (C) myocardial infarction (MI), or (D) congestive heart failure (CHF). Violin plots denote data distribution for each group with p -value calculated using unpaired Student’s t -test: *, p < 0.05; ns, not significant.

    Article Snippet: As this kit was not available when myocarditis samples were initially analyzed, the human R&D Systems sST2 ELISA kit (Cat# DST200, Minneapolis, MN, USA) was used for myocarditis samples.

    Techniques:

    Soluble ST2 (sST2) levels in women with early menopause. sST2 levels compared women with early menopause (Early, magenta) vs. those with normal menopause (peach) for (A) cardiomyopathy (Card), (B) coronary artery disease (CAD), (C) myocardial infarction (MI), or (D) congestive heart failure (CHF). Violin plots denote data distribution for each group with p -value calculated using unpaired Student’s t -test: *, p < 0.05; ns, not significant.

    Journal: Frontiers in Cardiovascular Medicine

    Article Title: Sex and age differences in sST2 in cardiovascular disease

    doi: 10.3389/fcvm.2022.1073814

    Figure Lengend Snippet: Soluble ST2 (sST2) levels in women with early menopause. sST2 levels compared women with early menopause (Early, magenta) vs. those with normal menopause (peach) for (A) cardiomyopathy (Card), (B) coronary artery disease (CAD), (C) myocardial infarction (MI), or (D) congestive heart failure (CHF). Violin plots denote data distribution for each group with p -value calculated using unpaired Student’s t -test: *, p < 0.05; ns, not significant.

    Article Snippet: As this kit was not available when myocarditis samples were initially analyzed, the human R&D Systems sST2 ELISA kit (Cat# DST200, Minneapolis, MN, USA) was used for myocarditis samples.

    Techniques:

    Sex differences in LVEF and sST2. sST2 levels compared women (peach) vs. men (blue) with a left ventricular ejection fraction (LVEF) of ≥45% vs. <45% for (A) myocarditis (Myo), (B) cardiomyopathy (Card), (C) coronary artery disease (CAD), (D) myocardial infarction (MI), or (E) congestive heart failure (CHF). Violin plots denote data distribution for each group. One-way ANOVA: (A) p = 0.024, (B) p = 0.023, (C) p = 0.79, (D) p = 0.17, and (E) p = 0.36 with two-way comparisons analyzed using unpaired Student’s t -test: *, p < 0.05; ns, not significant. (A) Two-way ANOVA p -values indicate no interaction between EF and sex ( p = 0.59) in patients with myocarditis, but interactions between LVEF and sST2 ( p = 0.04) and sex and sST2 ( p = 0.0036). (B) Two-way ANOVA p -values indicate no interactions between EF and sex ( p = 0.81) or EF and sST2 ( p = 0.22) in patients with cardiomyopathy, but interactions between sex and sST2 ( p = 0.01). (C) Two-way ANOVA p -values indicate no interactions between EF and sex ( p = 0.34), EF and sST2 ( p = 0.48), or sex and sST2 ( p = 0.40) in patients with CAD. (D) Two-way ANOVA p -values indicate no interactions between EF and sex ( p = 0.77), EF and sST2 ( p = 0.23), or sex and sST2 ( p = 0.39) in patients with MI. (E) Two-way ANOVA p -values indicate no interactions between EF and sex ( p = 0.21), EF and sST2 ( p = 0.87), or sex and sST2 ( p = 0.85) in patients with CHF.

    Journal: Frontiers in Cardiovascular Medicine

    Article Title: Sex and age differences in sST2 in cardiovascular disease

    doi: 10.3389/fcvm.2022.1073814

    Figure Lengend Snippet: Sex differences in LVEF and sST2. sST2 levels compared women (peach) vs. men (blue) with a left ventricular ejection fraction (LVEF) of ≥45% vs. <45% for (A) myocarditis (Myo), (B) cardiomyopathy (Card), (C) coronary artery disease (CAD), (D) myocardial infarction (MI), or (E) congestive heart failure (CHF). Violin plots denote data distribution for each group. One-way ANOVA: (A) p = 0.024, (B) p = 0.023, (C) p = 0.79, (D) p = 0.17, and (E) p = 0.36 with two-way comparisons analyzed using unpaired Student’s t -test: *, p < 0.05; ns, not significant. (A) Two-way ANOVA p -values indicate no interaction between EF and sex ( p = 0.59) in patients with myocarditis, but interactions between LVEF and sST2 ( p = 0.04) and sex and sST2 ( p = 0.0036). (B) Two-way ANOVA p -values indicate no interactions between EF and sex ( p = 0.81) or EF and sST2 ( p = 0.22) in patients with cardiomyopathy, but interactions between sex and sST2 ( p = 0.01). (C) Two-way ANOVA p -values indicate no interactions between EF and sex ( p = 0.34), EF and sST2 ( p = 0.48), or sex and sST2 ( p = 0.40) in patients with CAD. (D) Two-way ANOVA p -values indicate no interactions between EF and sex ( p = 0.77), EF and sST2 ( p = 0.23), or sex and sST2 ( p = 0.39) in patients with MI. (E) Two-way ANOVA p -values indicate no interactions between EF and sex ( p = 0.21), EF and sST2 ( p = 0.87), or sex and sST2 ( p = 0.85) in patients with CHF.

    Article Snippet: As this kit was not available when myocarditis samples were initially analyzed, the human R&D Systems sST2 ELISA kit (Cat# DST200, Minneapolis, MN, USA) was used for myocarditis samples.

    Techniques:

    Sex differences in LVEF and sST2 using ESC guidelines. sST2 levels compared women (peach) vs. men (blue) in patients with HFrEF, HFmrEF, or HFpEF for (A) myocarditis (Myo), (B) cardiomyopathy (Card), (C) coronary artery disease (CAD), (D) myocardial infarction (MI), or (E) congestive heart failure (CHF). Violin plots denote data distribution for each group. One-way ANOVA: (A) p = 0.053, (B) p = 0.032, (C) p = 0.72, (D) p = 0.093, and (E) p = 0.89 with two-way comparisons analyzed using unpaired Student’s t -test: *, p < 0.05; ns, not significant. (A) Two-way ANOVA p -values indicate no interaction between sex and ejection fraction (EF) in patients with myocarditis ( p = 0.51), or EF and sST2 ( p = 0.29), but interaction between and sex and sST2 ( p = 0.025). (B) Two-way ANOVA p -values indicate no interactions between sex and EF ( p = 0.69), EF and sST2 ( p = 0.16), or sex and sST2 ( p = 0.15) in patients with cardiomopathy. (C) Two-way ANOVA p -values indicate no interactions between sex and EF ( p = 0.89), EF and sST2 ( p = 0.20) or sex and sST2 ( p = 0.81) in patients with CAD. (D) Two-way ANOVA p -values indicate no interactions between sex and EF ( p = 0.42) and EF and sST2 ( p = 0.77), but interaction between sex and sST2 ( p = 0.032) in patients with MI. (E) Two-way ANOVA p -values indicate no interactions between sex and EF ( p = 0.95), EF and sST2 ( p = 0.68), or sex and sST2 ( p = 0.84) in patients with CHF.

    Journal: Frontiers in Cardiovascular Medicine

    Article Title: Sex and age differences in sST2 in cardiovascular disease

    doi: 10.3389/fcvm.2022.1073814

    Figure Lengend Snippet: Sex differences in LVEF and sST2 using ESC guidelines. sST2 levels compared women (peach) vs. men (blue) in patients with HFrEF, HFmrEF, or HFpEF for (A) myocarditis (Myo), (B) cardiomyopathy (Card), (C) coronary artery disease (CAD), (D) myocardial infarction (MI), or (E) congestive heart failure (CHF). Violin plots denote data distribution for each group. One-way ANOVA: (A) p = 0.053, (B) p = 0.032, (C) p = 0.72, (D) p = 0.093, and (E) p = 0.89 with two-way comparisons analyzed using unpaired Student’s t -test: *, p < 0.05; ns, not significant. (A) Two-way ANOVA p -values indicate no interaction between sex and ejection fraction (EF) in patients with myocarditis ( p = 0.51), or EF and sST2 ( p = 0.29), but interaction between and sex and sST2 ( p = 0.025). (B) Two-way ANOVA p -values indicate no interactions between sex and EF ( p = 0.69), EF and sST2 ( p = 0.16), or sex and sST2 ( p = 0.15) in patients with cardiomopathy. (C) Two-way ANOVA p -values indicate no interactions between sex and EF ( p = 0.89), EF and sST2 ( p = 0.20) or sex and sST2 ( p = 0.81) in patients with CAD. (D) Two-way ANOVA p -values indicate no interactions between sex and EF ( p = 0.42) and EF and sST2 ( p = 0.77), but interaction between sex and sST2 ( p = 0.032) in patients with MI. (E) Two-way ANOVA p -values indicate no interactions between sex and EF ( p = 0.95), EF and sST2 ( p = 0.68), or sex and sST2 ( p = 0.84) in patients with CHF.

    Article Snippet: As this kit was not available when myocarditis samples were initially analyzed, the human R&D Systems sST2 ELISA kit (Cat# DST200, Minneapolis, MN, USA) was used for myocarditis samples.

    Techniques:

    Soluble ST2 (sST2) relationship to LVEF by sex. sST2 levels in men and women (black), women only (peach), or men only (blue) were correlated to % left ventricular ejection fraction (LVEF) for (A) myocarditis (Myo), (B) cardiomyopathy (Card), (C) coronary artery disease (CAD), (D) myocardial infarction (MI), or (E) congestive heart failure (CHF). P -values were calculated using 2-tailed Pearson correlation.

    Journal: Frontiers in Cardiovascular Medicine

    Article Title: Sex and age differences in sST2 in cardiovascular disease

    doi: 10.3389/fcvm.2022.1073814

    Figure Lengend Snippet: Soluble ST2 (sST2) relationship to LVEF by sex. sST2 levels in men and women (black), women only (peach), or men only (blue) were correlated to % left ventricular ejection fraction (LVEF) for (A) myocarditis (Myo), (B) cardiomyopathy (Card), (C) coronary artery disease (CAD), (D) myocardial infarction (MI), or (E) congestive heart failure (CHF). P -values were calculated using 2-tailed Pearson correlation.

    Article Snippet: As this kit was not available when myocarditis samples were initially analyzed, the human R&D Systems sST2 ELISA kit (Cat# DST200, Minneapolis, MN, USA) was used for myocarditis samples.

    Techniques:

    Sex differences in NYHA class and sST2 levels. sST2 levels compared women and men (gray), women (peach), or men (blue) to New York Heart Association (NYHA) class I–II vs. III–IV heart failure for (A) myocarditis (Myo), (B) cardiomyopathy (Card), (C) coronary artery disease (CAD), (D) myocardial infarction (MI), or (E) congestive heart failure (CHF). Violin plots denote data distribution for each group. One-way ANOVA: (A) p = 0.0002, (B) p = 0.66, (C) p = 0.64, (D) p = 0.55, and (E) p = 0.28. (A) Two-way ANOVA p -values indicate no interaction between NYHA Class and sex ( p = 0.59) in patients with myocarditis, but interactions between NYHA Class and sST2 ( p = 0.04) and sex and sST2 ( p = 0.0002). (B) Two-way ANOVA p -values indicate no interactions between NYHA Class and sex ( p = 0.94), NYHA Class and sST2 ( p = 0.74), or sex and sST2 ( p = 0.22) in patients with cardiomyopathy. (C) Two-way ANOVA p -values indicate no interactions between NYHA Class and sex ( p = 0.63), NYHA Class and sST2 ( p = 0.32), or sex and sST2 ( p = 0.52) in patients with CAD. (D) Two-way ANOVA p -values indicate no interactions between NYHA Class and sex ( p = 0.75), NYHA Class and sST2 ( p = 0.80), or sex and sST2 ( p = 0.20) in patients with MI. (E) Two-way ANOVA p -values indicate no interactions between NYHA Class and sex ( p = 0.12), NYHA Class and sST2 ( p = 0.72), or sex and sST2 ( p = 0.40) in patients with CHF. *, p < 0.05; **, p < 0.01.

    Journal: Frontiers in Cardiovascular Medicine

    Article Title: Sex and age differences in sST2 in cardiovascular disease

    doi: 10.3389/fcvm.2022.1073814

    Figure Lengend Snippet: Sex differences in NYHA class and sST2 levels. sST2 levels compared women and men (gray), women (peach), or men (blue) to New York Heart Association (NYHA) class I–II vs. III–IV heart failure for (A) myocarditis (Myo), (B) cardiomyopathy (Card), (C) coronary artery disease (CAD), (D) myocardial infarction (MI), or (E) congestive heart failure (CHF). Violin plots denote data distribution for each group. One-way ANOVA: (A) p = 0.0002, (B) p = 0.66, (C) p = 0.64, (D) p = 0.55, and (E) p = 0.28. (A) Two-way ANOVA p -values indicate no interaction between NYHA Class and sex ( p = 0.59) in patients with myocarditis, but interactions between NYHA Class and sST2 ( p = 0.04) and sex and sST2 ( p = 0.0002). (B) Two-way ANOVA p -values indicate no interactions between NYHA Class and sex ( p = 0.94), NYHA Class and sST2 ( p = 0.74), or sex and sST2 ( p = 0.22) in patients with cardiomyopathy. (C) Two-way ANOVA p -values indicate no interactions between NYHA Class and sex ( p = 0.63), NYHA Class and sST2 ( p = 0.32), or sex and sST2 ( p = 0.52) in patients with CAD. (D) Two-way ANOVA p -values indicate no interactions between NYHA Class and sex ( p = 0.75), NYHA Class and sST2 ( p = 0.80), or sex and sST2 ( p = 0.20) in patients with MI. (E) Two-way ANOVA p -values indicate no interactions between NYHA Class and sex ( p = 0.12), NYHA Class and sST2 ( p = 0.72), or sex and sST2 ( p = 0.40) in patients with CHF. *, p < 0.05; **, p < 0.01.

    Article Snippet: As this kit was not available when myocarditis samples were initially analyzed, the human R&D Systems sST2 ELISA kit (Cat# DST200, Minneapolis, MN, USA) was used for myocarditis samples.

    Techniques:

    Soluble ST2 (sST2) relationship to NYHA class by sex. sST2 levels compared women (peach) vs. men (blue) with New York Heart Association (NYHA) class I–II vs. III–IV heart failure for (A) myocarditis (Myo), (B) cardiomyopathy (Card), (C) coronary artery disease (CAD), (D) myocardial infarction (MI), or (E) congestive heart failure (CHF). Data show simple linear regression of data for each group with 95% confidence intervals showing spread of certainty in the model. P -values were calculated using 2-tailed Pearson correlation.

    Journal: Frontiers in Cardiovascular Medicine

    Article Title: Sex and age differences in sST2 in cardiovascular disease

    doi: 10.3389/fcvm.2022.1073814

    Figure Lengend Snippet: Soluble ST2 (sST2) relationship to NYHA class by sex. sST2 levels compared women (peach) vs. men (blue) with New York Heart Association (NYHA) class I–II vs. III–IV heart failure for (A) myocarditis (Myo), (B) cardiomyopathy (Card), (C) coronary artery disease (CAD), (D) myocardial infarction (MI), or (E) congestive heart failure (CHF). Data show simple linear regression of data for each group with 95% confidence intervals showing spread of certainty in the model. P -values were calculated using 2-tailed Pearson correlation.

    Article Snippet: As this kit was not available when myocarditis samples were initially analyzed, the human R&D Systems sST2 ELISA kit (Cat# DST200, Minneapolis, MN, USA) was used for myocarditis samples.

    Techniques: