aida two-dimensional densitometry software, version 2.11 Search Results


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Mice treated with DS-IkL exhibited reduced infarct size and improved cardiac function after I/R. (A) After 24 h of reperfusion, we assessed size of myocardial infarction using TTC staining. Representative sections are shown. (B) Quantification revealed an increase in infarct size with saline-treated mice. (C) Cardiac injury was also assessed using cardiac troponin I. After 2 weeks of reperfusion, mice were subjected to conscious <t>echocardiography</t> to examine the cardiac structure and function. (D) Representative M-mode images at the parasternal short-axis for all four groups are depicted. (E) Heart rate was not significantly different in these conscious mice. (F) I/R induced an increase in left ventricular mass, and (G) reduced fractional shortening and (H) global radial strain. (I) Summary data of region-specific radial strain and (J) circumferential strain are displayed. (K) Diastolic function was assessed by blood flow velocity through the mitral valve, as shown in representative images in all four groups. (L) The E/A ratio was significantly decreased in both groups but was more obvious in the saline I/R group. (M) Although the isovolumetric relaxation time (IVRT) was not significantly different in all four groups, (N) there was a difference in the mitral valve (MV) deceleration time in the saline I/R group vs. the saline sham group. In each graph, data are represented as means ± SEM of n = 5–7 mice per group. * P < 0.05, ** P < 0.01 by one-way ANOVA with post hoc Tukey test.
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Mice treated with DS-IkL exhibited reduced infarct size and improved cardiac function after I/R. (A) After 24 h of reperfusion, we assessed size of myocardial infarction using TTC staining. Representative sections are shown. (B) Quantification revealed an increase in infarct size with saline-treated mice. (C) Cardiac injury was also assessed using cardiac troponin I. After 2 weeks of reperfusion, mice were subjected to conscious <t>echocardiography</t> to examine the cardiac structure and function. (D) Representative M-mode images at the parasternal short-axis for all four groups are depicted. (E) Heart rate was not significantly different in these conscious mice. (F) I/R induced an increase in left ventricular mass, and (G) reduced fractional shortening and (H) global radial strain. (I) Summary data of region-specific radial strain and (J) circumferential strain are displayed. (K) Diastolic function was assessed by blood flow velocity through the mitral valve, as shown in representative images in all four groups. (L) The E/A ratio was significantly decreased in both groups but was more obvious in the saline I/R group. (M) Although the isovolumetric relaxation time (IVRT) was not significantly different in all four groups, (N) there was a difference in the mitral valve (MV) deceleration time in the saline I/R group vs. the saline sham group. In each graph, data are represented as means ± SEM of n = 5–7 mice per group. * P < 0.05, ** P < 0.01 by one-way ANOVA with post hoc Tukey test.
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Mice treated with DS-IkL exhibited reduced infarct size and improved cardiac function after I/R. (A) After 24 h of reperfusion, we assessed size of myocardial infarction using TTC staining. Representative sections are shown. (B) Quantification revealed an increase in infarct size with saline-treated mice. (C) Cardiac injury was also assessed using cardiac troponin I. After 2 weeks of reperfusion, mice were subjected to conscious <t>echocardiography</t> to examine the cardiac structure and function. (D) Representative M-mode images at the parasternal short-axis for all four groups are depicted. (E) Heart rate was not significantly different in these conscious mice. (F) I/R induced an increase in left ventricular mass, and (G) reduced fractional shortening and (H) global radial strain. (I) Summary data of region-specific radial strain and (J) circumferential strain are displayed. (K) Diastolic function was assessed by blood flow velocity through the mitral valve, as shown in representative images in all four groups. (L) The E/A ratio was significantly decreased in both groups but was more obvious in the saline I/R group. (M) Although the isovolumetric relaxation time (IVRT) was not significantly different in all four groups, (N) there was a difference in the mitral valve (MV) deceleration time in the saline I/R group vs. the saline sham group. In each graph, data are represented as means ± SEM of n = 5–7 mice per group. * P < 0.05, ** P < 0.01 by one-way ANOVA with post hoc Tukey test.
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Mice treated with DS-IkL exhibited reduced infarct size and improved cardiac function after I/R. (A) After 24 h of reperfusion, we assessed size of myocardial infarction using TTC staining. Representative sections are shown. (B) Quantification revealed an increase in infarct size with saline-treated mice. (C) Cardiac injury was also assessed using cardiac troponin I. After 2 weeks of reperfusion, mice were subjected to conscious <t>echocardiography</t> to examine the cardiac structure and function. (D) Representative M-mode images at the parasternal short-axis for all four groups are depicted. (E) Heart rate was not significantly different in these conscious mice. (F) I/R induced an increase in left ventricular mass, and (G) reduced fractional shortening and (H) global radial strain. (I) Summary data of region-specific radial strain and (J) circumferential strain are displayed. (K) Diastolic function was assessed by blood flow velocity through the mitral valve, as shown in representative images in all four groups. (L) The E/A ratio was significantly decreased in both groups but was more obvious in the saline I/R group. (M) Although the isovolumetric relaxation time (IVRT) was not significantly different in all four groups, (N) there was a difference in the mitral valve (MV) deceleration time in the saline I/R group vs. the saline sham group. In each graph, data are represented as means ± SEM of n = 5–7 mice per group. * P < 0.05, ** P < 0.01 by one-way ANOVA with post hoc Tukey test.
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Mice treated with DS-IkL exhibited reduced infarct size and improved cardiac function after I/R. (A) After 24 h of reperfusion, we assessed size of myocardial infarction using TTC staining. Representative sections are shown. (B) Quantification revealed an increase in infarct size with saline-treated mice. (C) Cardiac injury was also assessed using cardiac troponin I. After 2 weeks of reperfusion, mice were subjected to conscious <t>echocardiography</t> to examine the cardiac structure and function. (D) Representative M-mode images at the parasternal short-axis for all four groups are depicted. (E) Heart rate was not significantly different in these conscious mice. (F) I/R induced an increase in left ventricular mass, and (G) reduced fractional shortening and (H) global radial strain. (I) Summary data of region-specific radial strain and (J) circumferential strain are displayed. (K) Diastolic function was assessed by blood flow velocity through the mitral valve, as shown in representative images in all four groups. (L) The E/A ratio was significantly decreased in both groups but was more obvious in the saline I/R group. (M) Although the isovolumetric relaxation time (IVRT) was not significantly different in all four groups, (N) there was a difference in the mitral valve (MV) deceleration time in the saline I/R group vs. the saline sham group. In each graph, data are represented as means ± SEM of n = 5–7 mice per group. * P < 0.05, ** P < 0.01 by one-way ANOVA with post hoc Tukey test.
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Mice treated with DS-IkL exhibited reduced infarct size and improved cardiac function after I/R. (A) After 24 h of reperfusion, we assessed size of myocardial infarction using TTC staining. Representative sections are shown. (B) Quantification revealed an increase in infarct size with saline-treated mice. (C) Cardiac injury was also assessed using cardiac troponin I. After 2 weeks of reperfusion, mice were subjected to conscious <t>echocardiography</t> to examine the cardiac structure and function. (D) Representative M-mode images at the parasternal short-axis for all four groups are depicted. (E) Heart rate was not significantly different in these conscious mice. (F) I/R induced an increase in left ventricular mass, and (G) reduced fractional shortening and (H) global radial strain. (I) Summary data of region-specific radial strain and (J) circumferential strain are displayed. (K) Diastolic function was assessed by blood flow velocity through the mitral valve, as shown in representative images in all four groups. (L) The E/A ratio was significantly decreased in both groups but was more obvious in the saline I/R group. (M) Although the isovolumetric relaxation time (IVRT) was not significantly different in all four groups, (N) there was a difference in the mitral valve (MV) deceleration time in the saline I/R group vs. the saline sham group. In each graph, data are represented as means ± SEM of n = 5–7 mice per group. * P < 0.05, ** P < 0.01 by one-way ANOVA with post hoc Tukey test.
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Mice treated with DS-IkL exhibited reduced infarct size and improved cardiac function after I/R. (A) After 24 h of reperfusion, we assessed size of myocardial infarction using TTC staining. Representative sections are shown. (B) Quantification revealed an increase in infarct size with saline-treated mice. (C) Cardiac injury was also assessed using cardiac troponin I. After 2 weeks of reperfusion, mice were subjected to conscious <t>echocardiography</t> to examine the cardiac structure and function. (D) Representative M-mode images at the parasternal short-axis for all four groups are depicted. (E) Heart rate was not significantly different in these conscious mice. (F) I/R induced an increase in left ventricular mass, and (G) reduced fractional shortening and (H) global radial strain. (I) Summary data of region-specific radial strain and (J) circumferential strain are displayed. (K) Diastolic function was assessed by blood flow velocity through the mitral valve, as shown in representative images in all four groups. (L) The E/A ratio was significantly decreased in both groups but was more obvious in the saline I/R group. (M) Although the isovolumetric relaxation time (IVRT) was not significantly different in all four groups, (N) there was a difference in the mitral valve (MV) deceleration time in the saline I/R group vs. the saline sham group. In each graph, data are represented as means ± SEM of n = 5–7 mice per group. * P < 0.05, ** P < 0.01 by one-way ANOVA with post hoc Tukey test.
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Mice treated with DS-IkL exhibited reduced infarct size and improved cardiac function after I/R. (A) After 24 h of reperfusion, we assessed size of myocardial infarction using TTC staining. Representative sections are shown. (B) Quantification revealed an increase in infarct size with saline-treated mice. (C) Cardiac injury was also assessed using cardiac troponin I. After 2 weeks of reperfusion, mice were subjected to conscious <t>echocardiography</t> to examine the cardiac structure and function. (D) Representative M-mode images at the parasternal short-axis for all four groups are depicted. (E) Heart rate was not significantly different in these conscious mice. (F) I/R induced an increase in left ventricular mass, and (G) reduced fractional shortening and (H) global radial strain. (I) Summary data of region-specific radial strain and (J) circumferential strain are displayed. (K) Diastolic function was assessed by blood flow velocity through the mitral valve, as shown in representative images in all four groups. (L) The E/A ratio was significantly decreased in both groups but was more obvious in the saline I/R group. (M) Although the isovolumetric relaxation time (IVRT) was not significantly different in all four groups, (N) there was a difference in the mitral valve (MV) deceleration time in the saline I/R group vs. the saline sham group. In each graph, data are represented as means ± SEM of n = 5–7 mice per group. * P < 0.05, ** P < 0.01 by one-way ANOVA with post hoc Tukey test.
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Mice treated with DS-IkL exhibited reduced infarct size and improved cardiac function after I/R. (A) After 24 h of reperfusion, we assessed size of myocardial infarction using TTC staining. Representative sections are shown. (B) Quantification revealed an increase in infarct size with saline-treated mice. (C) Cardiac injury was also assessed using cardiac troponin I. After 2 weeks of reperfusion, mice were subjected to conscious <t>echocardiography</t> to examine the cardiac structure and function. (D) Representative M-mode images at the parasternal short-axis for all four groups are depicted. (E) Heart rate was not significantly different in these conscious mice. (F) I/R induced an increase in left ventricular mass, and (G) reduced fractional shortening and (H) global radial strain. (I) Summary data of region-specific radial strain and (J) circumferential strain are displayed. (K) Diastolic function was assessed by blood flow velocity through the mitral valve, as shown in representative images in all four groups. (L) The E/A ratio was significantly decreased in both groups but was more obvious in the saline I/R group. (M) Although the isovolumetric relaxation time (IVRT) was not significantly different in all four groups, (N) there was a difference in the mitral valve (MV) deceleration time in the saline I/R group vs. the saline sham group. In each graph, data are represented as means ± SEM of n = 5–7 mice per group. * P < 0.05, ** P < 0.01 by one-way ANOVA with post hoc Tukey test.
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Mice treated with DS-IkL exhibited reduced infarct size and improved cardiac function after I/R. (A) After 24 h of reperfusion, we assessed size of myocardial infarction using TTC staining. Representative sections are shown. (B) Quantification revealed an increase in infarct size with saline-treated mice. (C) Cardiac injury was also assessed using cardiac troponin I. After 2 weeks of reperfusion, mice were subjected to conscious <t>echocardiography</t> to examine the cardiac structure and function. (D) Representative M-mode images at the parasternal short-axis for all four groups are depicted. (E) Heart rate was not significantly different in these conscious mice. (F) I/R induced an increase in left ventricular mass, and (G) reduced fractional shortening and (H) global radial strain. (I) Summary data of region-specific radial strain and (J) circumferential strain are displayed. (K) Diastolic function was assessed by blood flow velocity through the mitral valve, as shown in representative images in all four groups. (L) The E/A ratio was significantly decreased in both groups but was more obvious in the saline I/R group. (M) Although the isovolumetric relaxation time (IVRT) was not significantly different in all four groups, (N) there was a difference in the mitral valve (MV) deceleration time in the saline I/R group vs. the saline sham group. In each graph, data are represented as means ± SEM of n = 5–7 mice per group. * P < 0.05, ** P < 0.01 by one-way ANOVA with post hoc Tukey test.
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Image Search Results


Mice treated with DS-IkL exhibited reduced infarct size and improved cardiac function after I/R. (A) After 24 h of reperfusion, we assessed size of myocardial infarction using TTC staining. Representative sections are shown. (B) Quantification revealed an increase in infarct size with saline-treated mice. (C) Cardiac injury was also assessed using cardiac troponin I. After 2 weeks of reperfusion, mice were subjected to conscious echocardiography to examine the cardiac structure and function. (D) Representative M-mode images at the parasternal short-axis for all four groups are depicted. (E) Heart rate was not significantly different in these conscious mice. (F) I/R induced an increase in left ventricular mass, and (G) reduced fractional shortening and (H) global radial strain. (I) Summary data of region-specific radial strain and (J) circumferential strain are displayed. (K) Diastolic function was assessed by blood flow velocity through the mitral valve, as shown in representative images in all four groups. (L) The E/A ratio was significantly decreased in both groups but was more obvious in the saline I/R group. (M) Although the isovolumetric relaxation time (IVRT) was not significantly different in all four groups, (N) there was a difference in the mitral valve (MV) deceleration time in the saline I/R group vs. the saline sham group. In each graph, data are represented as means ± SEM of n = 5–7 mice per group. * P < 0.05, ** P < 0.01 by one-way ANOVA with post hoc Tukey test.

Journal: Cardiovascular Research

Article Title: Selectin-targeting glycosaminoglycan-peptide conjugate limits neutrophil-mediated cardiac reperfusion injury

doi: 10.1093/cvr/cvaa312

Figure Lengend Snippet: Mice treated with DS-IkL exhibited reduced infarct size and improved cardiac function after I/R. (A) After 24 h of reperfusion, we assessed size of myocardial infarction using TTC staining. Representative sections are shown. (B) Quantification revealed an increase in infarct size with saline-treated mice. (C) Cardiac injury was also assessed using cardiac troponin I. After 2 weeks of reperfusion, mice were subjected to conscious echocardiography to examine the cardiac structure and function. (D) Representative M-mode images at the parasternal short-axis for all four groups are depicted. (E) Heart rate was not significantly different in these conscious mice. (F) I/R induced an increase in left ventricular mass, and (G) reduced fractional shortening and (H) global radial strain. (I) Summary data of region-specific radial strain and (J) circumferential strain are displayed. (K) Diastolic function was assessed by blood flow velocity through the mitral valve, as shown in representative images in all four groups. (L) The E/A ratio was significantly decreased in both groups but was more obvious in the saline I/R group. (M) Although the isovolumetric relaxation time (IVRT) was not significantly different in all four groups, (N) there was a difference in the mitral valve (MV) deceleration time in the saline I/R group vs. the saline sham group. In each graph, data are represented as means ± SEM of n = 5–7 mice per group. * P < 0.05, ** P < 0.01 by one-way ANOVA with post hoc Tukey test.

Article Snippet: 2.11 Echocardiography Cardiac structure and function were monitored using 2D echocardiography (VisualSonic Vevo 2100 with a MS 550 D probe).

Techniques: Staining, Saline