log rank tests Search Results


log rank chi square  (CH Instruments)
90
CH Instruments log rank chi square
Log Rank Chi Square, supplied by CH Instruments, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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log-rank test  (CH Instruments)
90
CH Instruments log-rank test
A) Domain organization of ADAMTS17 shows location and targeting of exon 3 by CRISPR/Cas9 gRNA to induce non-homologous end joining. The nucleotide and amino acid sequence of the ADAMTS17 WT allele (green) and after AT insertion (red) are indicated. The dinucleotide insertion induced a frameshift, which resulted in a premature stop codon after 12 amino acids. B) Sanger sequencing traces of a PCR product generated with primers flanking exon 3 showing the AT insertion (underlined) in the Adamts17 KO. C) Micrographs of ADAMTS17 immunostaining of sections through WT and Adamts17 KO skin (left), <t>DKO</t> growth plates (middle), and of primary DKO mouse skin fibroblasts (right). The signal in the dermis around hair follicles, in growth plate chondrocytes, and in fibroblasts and their ECM originating from the monoclonal ADAMTS17 antibody was strongly reduced in KO and DKO tissues and cells, indicating lack of ADAMTS17 protein in Adamts17 KO mice. D) Pie chart showing Mendelian distribution of genotypes recovered from Adamts17 Het intercrosses at the time of genotyping (P7-P10) (n=94 mice). E) Breeding scheme to generate WT, Adamts10 KO (10KO), Adamts17 KO (17KO), and DKO mice. F) Pie chart showing distribution of genotypes recovered from Adamts10 Het;Adamts17 Het intercrosses at P7-P10 (n=180 mice). Statistical analysis was performed using Chi square calculation. <t>G)</t> <t>Kaplan-Meier</t> survival analysis of DKO mice. The numbers of observed dead/total mice for the individual genotypes are indicated in brackets. Statistical significance was determined using a log-rank test. H) Whole mount images of WT, 10KO, 10KO;17Het mice at 4 weeks of age shows progressive reduction in body size. I) Bar graphs showing body weights of 4-week-old mice of the indicated genotypes. The number of mice is indicated below the genotypes. J) Bar graphs showing body weight normalized to average femur length for the genotypes that were significantly different in I. In I, J floating bars indicate the 25 th – 75 th percentile range, lines the mean value, and whiskers the standard deviation. Statistical differences in I, J were determined using a one-way ANOVA with post-hoc Tukey test. a, p<0.05 compared to WT.
Log Rank Test, supplied by CH Instruments, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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log-rank mantel–cox test  (GraphPad Software Inc)
90
GraphPad Software Inc log-rank mantel–cox test
A) Domain organization of ADAMTS17 shows location and targeting of exon 3 by CRISPR/Cas9 gRNA to induce non-homologous end joining. The nucleotide and amino acid sequence of the ADAMTS17 WT allele (green) and after AT insertion (red) are indicated. The dinucleotide insertion induced a frameshift, which resulted in a premature stop codon after 12 amino acids. B) Sanger sequencing traces of a PCR product generated with primers flanking exon 3 showing the AT insertion (underlined) in the Adamts17 KO. C) Micrographs of ADAMTS17 immunostaining of sections through WT and Adamts17 KO skin (left), <t>DKO</t> growth plates (middle), and of primary DKO mouse skin fibroblasts (right). The signal in the dermis around hair follicles, in growth plate chondrocytes, and in fibroblasts and their ECM originating from the monoclonal ADAMTS17 antibody was strongly reduced in KO and DKO tissues and cells, indicating lack of ADAMTS17 protein in Adamts17 KO mice. D) Pie chart showing Mendelian distribution of genotypes recovered from Adamts17 Het intercrosses at the time of genotyping (P7-P10) (n=94 mice). E) Breeding scheme to generate WT, Adamts10 KO (10KO), Adamts17 KO (17KO), and DKO mice. F) Pie chart showing distribution of genotypes recovered from Adamts10 Het;Adamts17 Het intercrosses at P7-P10 (n=180 mice). Statistical analysis was performed using Chi square calculation. <t>G)</t> <t>Kaplan-Meier</t> survival analysis of DKO mice. The numbers of observed dead/total mice for the individual genotypes are indicated in brackets. Statistical significance was determined using a log-rank test. H) Whole mount images of WT, 10KO, 10KO;17Het mice at 4 weeks of age shows progressive reduction in body size. I) Bar graphs showing body weights of 4-week-old mice of the indicated genotypes. The number of mice is indicated below the genotypes. J) Bar graphs showing body weight normalized to average femur length for the genotypes that were significantly different in I. In I, J floating bars indicate the 25 th – 75 th percentile range, lines the mean value, and whiskers the standard deviation. Statistical differences in I, J were determined using a one-way ANOVA with post-hoc Tukey test. a, p<0.05 compared to WT.
Log Rank Mantel–Cox Test, supplied by GraphPad Software Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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log-rank (mantel-cox) test  (GraphPad Software Inc)
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GraphPad Software Inc log-rank (mantel-cox) test
A) Domain organization of ADAMTS17 shows location and targeting of exon 3 by CRISPR/Cas9 gRNA to induce non-homologous end joining. The nucleotide and amino acid sequence of the ADAMTS17 WT allele (green) and after AT insertion (red) are indicated. The dinucleotide insertion induced a frameshift, which resulted in a premature stop codon after 12 amino acids. B) Sanger sequencing traces of a PCR product generated with primers flanking exon 3 showing the AT insertion (underlined) in the Adamts17 KO. C) Micrographs of ADAMTS17 immunostaining of sections through WT and Adamts17 KO skin (left), <t>DKO</t> growth plates (middle), and of primary DKO mouse skin fibroblasts (right). The signal in the dermis around hair follicles, in growth plate chondrocytes, and in fibroblasts and their ECM originating from the monoclonal ADAMTS17 antibody was strongly reduced in KO and DKO tissues and cells, indicating lack of ADAMTS17 protein in Adamts17 KO mice. D) Pie chart showing Mendelian distribution of genotypes recovered from Adamts17 Het intercrosses at the time of genotyping (P7-P10) (n=94 mice). E) Breeding scheme to generate WT, Adamts10 KO (10KO), Adamts17 KO (17KO), and DKO mice. F) Pie chart showing distribution of genotypes recovered from Adamts10 Het;Adamts17 Het intercrosses at P7-P10 (n=180 mice). Statistical analysis was performed using Chi square calculation. <t>G)</t> <t>Kaplan-Meier</t> survival analysis of DKO mice. The numbers of observed dead/total mice for the individual genotypes are indicated in brackets. Statistical significance was determined using a log-rank test. H) Whole mount images of WT, 10KO, 10KO;17Het mice at 4 weeks of age shows progressive reduction in body size. I) Bar graphs showing body weights of 4-week-old mice of the indicated genotypes. The number of mice is indicated below the genotypes. J) Bar graphs showing body weight normalized to average femur length for the genotypes that were significantly different in I. In I, J floating bars indicate the 25 th – 75 th percentile range, lines the mean value, and whiskers the standard deviation. Statistical differences in I, J were determined using a one-way ANOVA with post-hoc Tukey test. a, p<0.05 compared to WT.
Log Rank (Mantel Cox) Test, supplied by GraphPad Software Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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logrank test graphpad prism version 6.0  (GraphPad Software Inc)
90
GraphPad Software Inc logrank test graphpad prism version 6.0
A) Domain organization of ADAMTS17 shows location and targeting of exon 3 by CRISPR/Cas9 gRNA to induce non-homologous end joining. The nucleotide and amino acid sequence of the ADAMTS17 WT allele (green) and after AT insertion (red) are indicated. The dinucleotide insertion induced a frameshift, which resulted in a premature stop codon after 12 amino acids. B) Sanger sequencing traces of a PCR product generated with primers flanking exon 3 showing the AT insertion (underlined) in the Adamts17 KO. C) Micrographs of ADAMTS17 immunostaining of sections through WT and Adamts17 KO skin (left), <t>DKO</t> growth plates (middle), and of primary DKO mouse skin fibroblasts (right). The signal in the dermis around hair follicles, in growth plate chondrocytes, and in fibroblasts and their ECM originating from the monoclonal ADAMTS17 antibody was strongly reduced in KO and DKO tissues and cells, indicating lack of ADAMTS17 protein in Adamts17 KO mice. D) Pie chart showing Mendelian distribution of genotypes recovered from Adamts17 Het intercrosses at the time of genotyping (P7-P10) (n=94 mice). E) Breeding scheme to generate WT, Adamts10 KO (10KO), Adamts17 KO (17KO), and DKO mice. F) Pie chart showing distribution of genotypes recovered from Adamts10 Het;Adamts17 Het intercrosses at P7-P10 (n=180 mice). Statistical analysis was performed using Chi square calculation. <t>G)</t> <t>Kaplan-Meier</t> survival analysis of DKO mice. The numbers of observed dead/total mice for the individual genotypes are indicated in brackets. Statistical significance was determined using a log-rank test. H) Whole mount images of WT, 10KO, 10KO;17Het mice at 4 weeks of age shows progressive reduction in body size. I) Bar graphs showing body weights of 4-week-old mice of the indicated genotypes. The number of mice is indicated below the genotypes. J) Bar graphs showing body weight normalized to average femur length for the genotypes that were significantly different in I. In I, J floating bars indicate the 25 th – 75 th percentile range, lines the mean value, and whiskers the standard deviation. Statistical differences in I, J were determined using a one-way ANOVA with post-hoc Tukey test. a, p<0.05 compared to WT.
Logrank Test Graphpad Prism Version 6.0, supplied by GraphPad Software Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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log-rank (mantel-cox) test that compares kaplan–meier survival curves graphpad prism windows version 6.01  (GraphPad Software Inc)
90
GraphPad Software Inc log-rank (mantel-cox) test that compares kaplan–meier survival curves graphpad prism windows version 6.01
A) Domain organization of ADAMTS17 shows location and targeting of exon 3 by CRISPR/Cas9 gRNA to induce non-homologous end joining. The nucleotide and amino acid sequence of the ADAMTS17 WT allele (green) and after AT insertion (red) are indicated. The dinucleotide insertion induced a frameshift, which resulted in a premature stop codon after 12 amino acids. B) Sanger sequencing traces of a PCR product generated with primers flanking exon 3 showing the AT insertion (underlined) in the Adamts17 KO. C) Micrographs of ADAMTS17 immunostaining of sections through WT and Adamts17 KO skin (left), <t>DKO</t> growth plates (middle), and of primary DKO mouse skin fibroblasts (right). The signal in the dermis around hair follicles, in growth plate chondrocytes, and in fibroblasts and their ECM originating from the monoclonal ADAMTS17 antibody was strongly reduced in KO and DKO tissues and cells, indicating lack of ADAMTS17 protein in Adamts17 KO mice. D) Pie chart showing Mendelian distribution of genotypes recovered from Adamts17 Het intercrosses at the time of genotyping (P7-P10) (n=94 mice). E) Breeding scheme to generate WT, Adamts10 KO (10KO), Adamts17 KO (17KO), and DKO mice. F) Pie chart showing distribution of genotypes recovered from Adamts10 Het;Adamts17 Het intercrosses at P7-P10 (n=180 mice). Statistical analysis was performed using Chi square calculation. <t>G)</t> <t>Kaplan-Meier</t> survival analysis of DKO mice. The numbers of observed dead/total mice for the individual genotypes are indicated in brackets. Statistical significance was determined using a log-rank test. H) Whole mount images of WT, 10KO, 10KO;17Het mice at 4 weeks of age shows progressive reduction in body size. I) Bar graphs showing body weights of 4-week-old mice of the indicated genotypes. The number of mice is indicated below the genotypes. J) Bar graphs showing body weight normalized to average femur length for the genotypes that were significantly different in I. In I, J floating bars indicate the 25 th – 75 th percentile range, lines the mean value, and whiskers the standard deviation. Statistical differences in I, J were determined using a one-way ANOVA with post-hoc Tukey test. a, p<0.05 compared to WT.
Log Rank (Mantel Cox) Test That Compares Kaplan–Meier Survival Curves Graphpad Prism Windows Version 6.01, supplied by GraphPad Software Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mantel-haenszel logrank test  (GraphPad Software Inc)
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GraphPad Software Inc mantel-haenszel logrank test
A) Domain organization of ADAMTS17 shows location and targeting of exon 3 by CRISPR/Cas9 gRNA to induce non-homologous end joining. The nucleotide and amino acid sequence of the ADAMTS17 WT allele (green) and after AT insertion (red) are indicated. The dinucleotide insertion induced a frameshift, which resulted in a premature stop codon after 12 amino acids. B) Sanger sequencing traces of a PCR product generated with primers flanking exon 3 showing the AT insertion (underlined) in the Adamts17 KO. C) Micrographs of ADAMTS17 immunostaining of sections through WT and Adamts17 KO skin (left), <t>DKO</t> growth plates (middle), and of primary DKO mouse skin fibroblasts (right). The signal in the dermis around hair follicles, in growth plate chondrocytes, and in fibroblasts and their ECM originating from the monoclonal ADAMTS17 antibody was strongly reduced in KO and DKO tissues and cells, indicating lack of ADAMTS17 protein in Adamts17 KO mice. D) Pie chart showing Mendelian distribution of genotypes recovered from Adamts17 Het intercrosses at the time of genotyping (P7-P10) (n=94 mice). E) Breeding scheme to generate WT, Adamts10 KO (10KO), Adamts17 KO (17KO), and DKO mice. F) Pie chart showing distribution of genotypes recovered from Adamts10 Het;Adamts17 Het intercrosses at P7-P10 (n=180 mice). Statistical analysis was performed using Chi square calculation. <t>G)</t> <t>Kaplan-Meier</t> survival analysis of DKO mice. The numbers of observed dead/total mice for the individual genotypes are indicated in brackets. Statistical significance was determined using a log-rank test. H) Whole mount images of WT, 10KO, 10KO;17Het mice at 4 weeks of age shows progressive reduction in body size. I) Bar graphs showing body weights of 4-week-old mice of the indicated genotypes. The number of mice is indicated below the genotypes. J) Bar graphs showing body weight normalized to average femur length for the genotypes that were significantly different in I. In I, J floating bars indicate the 25 th – 75 th percentile range, lines the mean value, and whiskers the standard deviation. Statistical differences in I, J were determined using a one-way ANOVA with post-hoc Tukey test. a, p<0.05 compared to WT.
Mantel Haenszel Logrank Test, supplied by GraphPad Software Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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log-rank mantel-cox  (GraphPad Software Inc)
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GraphPad Software Inc log-rank mantel-cox
A) Domain organization of ADAMTS17 shows location and targeting of exon 3 by CRISPR/Cas9 gRNA to induce non-homologous end joining. The nucleotide and amino acid sequence of the ADAMTS17 WT allele (green) and after AT insertion (red) are indicated. The dinucleotide insertion induced a frameshift, which resulted in a premature stop codon after 12 amino acids. B) Sanger sequencing traces of a PCR product generated with primers flanking exon 3 showing the AT insertion (underlined) in the Adamts17 KO. C) Micrographs of ADAMTS17 immunostaining of sections through WT and Adamts17 KO skin (left), <t>DKO</t> growth plates (middle), and of primary DKO mouse skin fibroblasts (right). The signal in the dermis around hair follicles, in growth plate chondrocytes, and in fibroblasts and their ECM originating from the monoclonal ADAMTS17 antibody was strongly reduced in KO and DKO tissues and cells, indicating lack of ADAMTS17 protein in Adamts17 KO mice. D) Pie chart showing Mendelian distribution of genotypes recovered from Adamts17 Het intercrosses at the time of genotyping (P7-P10) (n=94 mice). E) Breeding scheme to generate WT, Adamts10 KO (10KO), Adamts17 KO (17KO), and DKO mice. F) Pie chart showing distribution of genotypes recovered from Adamts10 Het;Adamts17 Het intercrosses at P7-P10 (n=180 mice). Statistical analysis was performed using Chi square calculation. <t>G)</t> <t>Kaplan-Meier</t> survival analysis of DKO mice. The numbers of observed dead/total mice for the individual genotypes are indicated in brackets. Statistical significance was determined using a log-rank test. H) Whole mount images of WT, 10KO, 10KO;17Het mice at 4 weeks of age shows progressive reduction in body size. I) Bar graphs showing body weights of 4-week-old mice of the indicated genotypes. The number of mice is indicated below the genotypes. J) Bar graphs showing body weight normalized to average femur length for the genotypes that were significantly different in I. In I, J floating bars indicate the 25 th – 75 th percentile range, lines the mean value, and whiskers the standard deviation. Statistical differences in I, J were determined using a one-way ANOVA with post-hoc Tukey test. a, p<0.05 compared to WT.
Log Rank Mantel Cox, supplied by GraphPad Software Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anova and tukey-kramer multiple comparison tests, kruskal-wallis and dunn’s post-test, log-rank tests  (GraphPad Software Inc)
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GraphPad Software Inc anova and tukey-kramer multiple comparison tests, kruskal-wallis and dunn’s post-test, log-rank tests
Tumor growth assessment: data for each time-point in mm 3 are mean ± SEM. ( A ) M-234p, N = 6/group; Day 21: Control (600.96 ± 93) vs Cy+Los (20.96 ± 9.01) ( P < 0.05); ( B ) M-406, N = 6–7/group; Day 17: Control (1397.00 ± 328.32) vs Cy (372.00 ± 55.25) ( P < 0.01), vs Los (451.07 ± 143.94) ( P < 0.05), vs Cy+Los (123.43 ± 45.71) ( P < <t>0.001).</t> <t>Kruskal-Wallis</t> multiple comparison test and <t>Dunn’s</t> post-test. Overall survival (Kaplan-Meier), Median Survival (MS): ( C ) M-234p, N = 5–6/group; Control (MS: 34 days); Cy (MS: 47 days); Los (MS: 32 days); Cy+Los (MS: undefined, Day 32: 60% [3/5] complete tumor regressions). Cy+Los vs Control, vs Los, vs Cy ( P < 0.01); ( D ) M-406, N = 6–7/group); Control (MS: 24 days); Cy (MS: 36.5 days); Los (MS: 33 days); Cy+Los (MS: 47 days). Control vs Cy ( P < 0.01), vs Los ( P < 0.01), vs Cy+Los ( P < 0.001); Cy+Los vs Cy ( P < 0.05), vs Los ( P < 0,001). Log-rank Test.
Anova And Tukey Kramer Multiple Comparison Tests, Kruskal Wallis And Dunn’s Post Test, Log Rank Tests, supplied by GraphPad Software Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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log-rank tests  (CAREpath Inc)
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CAREpath Inc log-rank tests
Tumor growth assessment: data for each time-point in mm 3 are mean ± SEM. ( A ) M-234p, N = 6/group; Day 21: Control (600.96 ± 93) vs Cy+Los (20.96 ± 9.01) ( P < 0.05); ( B ) M-406, N = 6–7/group; Day 17: Control (1397.00 ± 328.32) vs Cy (372.00 ± 55.25) ( P < 0.01), vs Los (451.07 ± 143.94) ( P < 0.05), vs Cy+Los (123.43 ± 45.71) ( P < <t>0.001).</t> <t>Kruskal-Wallis</t> multiple comparison test and <t>Dunn’s</t> post-test. Overall survival (Kaplan-Meier), Median Survival (MS): ( C ) M-234p, N = 5–6/group; Control (MS: 34 days); Cy (MS: 47 days); Los (MS: 32 days); Cy+Los (MS: undefined, Day 32: 60% [3/5] complete tumor regressions). Cy+Los vs Control, vs Los, vs Cy ( P < 0.01); ( D ) M-406, N = 6–7/group); Control (MS: 24 days); Cy (MS: 36.5 days); Los (MS: 33 days); Cy+Los (MS: 47 days). Control vs Cy ( P < 0.01), vs Los ( P < 0.01), vs Cy+Los ( P < 0.001); Cy+Los vs Cy ( P < 0.05), vs Los ( P < 0,001). Log-rank Test.
Log Rank Tests, supplied by CAREpath Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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log-rank test and cox regression analyses  (RStudio)
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RStudio log-rank test and cox regression analyses
Tumor growth assessment: data for each time-point in mm 3 are mean ± SEM. ( A ) M-234p, N = 6/group; Day 21: Control (600.96 ± 93) vs Cy+Los (20.96 ± 9.01) ( P < 0.05); ( B ) M-406, N = 6–7/group; Day 17: Control (1397.00 ± 328.32) vs Cy (372.00 ± 55.25) ( P < 0.01), vs Los (451.07 ± 143.94) ( P < 0.05), vs Cy+Los (123.43 ± 45.71) ( P < <t>0.001).</t> <t>Kruskal-Wallis</t> multiple comparison test and <t>Dunn’s</t> post-test. Overall survival (Kaplan-Meier), Median Survival (MS): ( C ) M-234p, N = 5–6/group; Control (MS: 34 days); Cy (MS: 47 days); Los (MS: 32 days); Cy+Los (MS: undefined, Day 32: 60% [3/5] complete tumor regressions). Cy+Los vs Control, vs Los, vs Cy ( P < 0.01); ( D ) M-406, N = 6–7/group); Control (MS: 24 days); Cy (MS: 36.5 days); Los (MS: 33 days); Cy+Los (MS: 47 days). Control vs Cy ( P < 0.01), vs Los ( P < 0.01), vs Cy+Los ( P < 0.001); Cy+Los vs Cy ( P < 0.05), vs Los ( P < 0,001). Log-rank Test.
Log Rank Test And Cox Regression Analyses, supplied by RStudio, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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log-rank (mantel–cox) test medcalc software version 8.0.2.0  (MedCalc Software Ltd)
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MedCalc Software Ltd log-rank (mantel–cox) test medcalc software version 8.0.2.0
Tumor growth assessment: data for each time-point in mm 3 are mean ± SEM. ( A ) M-234p, N = 6/group; Day 21: Control (600.96 ± 93) vs Cy+Los (20.96 ± 9.01) ( P < 0.05); ( B ) M-406, N = 6–7/group; Day 17: Control (1397.00 ± 328.32) vs Cy (372.00 ± 55.25) ( P < 0.01), vs Los (451.07 ± 143.94) ( P < 0.05), vs Cy+Los (123.43 ± 45.71) ( P < <t>0.001).</t> <t>Kruskal-Wallis</t> multiple comparison test and <t>Dunn’s</t> post-test. Overall survival (Kaplan-Meier), Median Survival (MS): ( C ) M-234p, N = 5–6/group; Control (MS: 34 days); Cy (MS: 47 days); Los (MS: 32 days); Cy+Los (MS: undefined, Day 32: 60% [3/5] complete tumor regressions). Cy+Los vs Control, vs Los, vs Cy ( P < 0.01); ( D ) M-406, N = 6–7/group); Control (MS: 24 days); Cy (MS: 36.5 days); Los (MS: 33 days); Cy+Los (MS: 47 days). Control vs Cy ( P < 0.01), vs Los ( P < 0.01), vs Cy+Los ( P < 0.001); Cy+Los vs Cy ( P < 0.05), vs Los ( P < 0,001). Log-rank Test.
Log Rank (Mantel–Cox) Test Medcalc Software Version 8.0.2.0, supplied by MedCalc Software Ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


A) Domain organization of ADAMTS17 shows location and targeting of exon 3 by CRISPR/Cas9 gRNA to induce non-homologous end joining. The nucleotide and amino acid sequence of the ADAMTS17 WT allele (green) and after AT insertion (red) are indicated. The dinucleotide insertion induced a frameshift, which resulted in a premature stop codon after 12 amino acids. B) Sanger sequencing traces of a PCR product generated with primers flanking exon 3 showing the AT insertion (underlined) in the Adamts17 KO. C) Micrographs of ADAMTS17 immunostaining of sections through WT and Adamts17 KO skin (left), DKO growth plates (middle), and of primary DKO mouse skin fibroblasts (right). The signal in the dermis around hair follicles, in growth plate chondrocytes, and in fibroblasts and their ECM originating from the monoclonal ADAMTS17 antibody was strongly reduced in KO and DKO tissues and cells, indicating lack of ADAMTS17 protein in Adamts17 KO mice. D) Pie chart showing Mendelian distribution of genotypes recovered from Adamts17 Het intercrosses at the time of genotyping (P7-P10) (n=94 mice). E) Breeding scheme to generate WT, Adamts10 KO (10KO), Adamts17 KO (17KO), and DKO mice. F) Pie chart showing distribution of genotypes recovered from Adamts10 Het;Adamts17 Het intercrosses at P7-P10 (n=180 mice). Statistical analysis was performed using Chi square calculation. G) Kaplan-Meier survival analysis of DKO mice. The numbers of observed dead/total mice for the individual genotypes are indicated in brackets. Statistical significance was determined using a log-rank test. H) Whole mount images of WT, 10KO, 10KO;17Het mice at 4 weeks of age shows progressive reduction in body size. I) Bar graphs showing body weights of 4-week-old mice of the indicated genotypes. The number of mice is indicated below the genotypes. J) Bar graphs showing body weight normalized to average femur length for the genotypes that were significantly different in I. In I, J floating bars indicate the 25 th – 75 th percentile range, lines the mean value, and whiskers the standard deviation. Statistical differences in I, J were determined using a one-way ANOVA with post-hoc Tukey test. a, p<0.05 compared to WT.

Journal: bioRxiv

Article Title: Combined ADAMTS10 and ADAMTS17 inactivation exacerbates bone shortening and compromises extracellular matrix formation

doi: 10.1101/2025.01.23.634616

Figure Lengend Snippet: A) Domain organization of ADAMTS17 shows location and targeting of exon 3 by CRISPR/Cas9 gRNA to induce non-homologous end joining. The nucleotide and amino acid sequence of the ADAMTS17 WT allele (green) and after AT insertion (red) are indicated. The dinucleotide insertion induced a frameshift, which resulted in a premature stop codon after 12 amino acids. B) Sanger sequencing traces of a PCR product generated with primers flanking exon 3 showing the AT insertion (underlined) in the Adamts17 KO. C) Micrographs of ADAMTS17 immunostaining of sections through WT and Adamts17 KO skin (left), DKO growth plates (middle), and of primary DKO mouse skin fibroblasts (right). The signal in the dermis around hair follicles, in growth plate chondrocytes, and in fibroblasts and their ECM originating from the monoclonal ADAMTS17 antibody was strongly reduced in KO and DKO tissues and cells, indicating lack of ADAMTS17 protein in Adamts17 KO mice. D) Pie chart showing Mendelian distribution of genotypes recovered from Adamts17 Het intercrosses at the time of genotyping (P7-P10) (n=94 mice). E) Breeding scheme to generate WT, Adamts10 KO (10KO), Adamts17 KO (17KO), and DKO mice. F) Pie chart showing distribution of genotypes recovered from Adamts10 Het;Adamts17 Het intercrosses at P7-P10 (n=180 mice). Statistical analysis was performed using Chi square calculation. G) Kaplan-Meier survival analysis of DKO mice. The numbers of observed dead/total mice for the individual genotypes are indicated in brackets. Statistical significance was determined using a log-rank test. H) Whole mount images of WT, 10KO, 10KO;17Het mice at 4 weeks of age shows progressive reduction in body size. I) Bar graphs showing body weights of 4-week-old mice of the indicated genotypes. The number of mice is indicated below the genotypes. J) Bar graphs showing body weight normalized to average femur length for the genotypes that were significantly different in I. In I, J floating bars indicate the 25 th – 75 th percentile range, lines the mean value, and whiskers the standard deviation. Statistical differences in I, J were determined using a one-way ANOVA with post-hoc Tukey test. a, p<0.05 compared to WT.

Article Snippet: Since we observed early postnatal lethality of Adamts10 ; Adamts17 DKO mice, we quantified postnatal survival with Kaplan-Meier survival analysis, where we observed significant postnatal mortality of DKO mice with 50% survival at 23 d (+/-7.1 d) after birth (probe > Chi = 0.00029, log-rank test) ( ).

Techniques: CRISPR, Non-Homologous End Joining, Sequencing, Generated, Immunostaining, Standard Deviation

A) Images of sections through growth plates of 4 week-old WT and Adamts10;Adamts17 DKO mice. Proliferative (PZ) and hypertrophic (HZ) zones are outlined with dashed lines. B) Bar graphs showing widths of PZ and HZ from WT and DKO growth plates. Data points represent the average of multiple measurements across the growth plate zone from n=3 mice. C) Higher magnification of growth plate from images in A showing disorganized proliferative zone in DKO growth plates. D) Micrograph of ADAMTS17 immunostaining of hypertrophic chondrocytes at the cartilage-bone interface. The boxed area is magnified in the right-hand panel. E) Schematic representation of experimental design for pellet culture to induce chondrocyte-like differentiation of C3H/10T1/2 cells. F) Bar graphs showing relative Adamts10, Adamts17, and Col2a1 mRNAs levels during differentiation of C3H/10T1/2 cell pellets normalized to Gapdh (n=3 replicates). G) Schematic representation of the mechanism of action of okadaic acid in de-repressing chondrocyte hypertrophy genes. H) Bar graphs showing relative changes of Adamts10 (TS10), Adamts17 (TS17), Fbn1, Fn1, and Col10a1 mRNA levels 24 h after treatment of primary chondrocytes with 50 nM okadaic acid or DMSO (n=3 replicates). I) Micrographs of immunostaining of fibrillin-1 (FBN1) and fibronectin (FN) deposition in the ECM of primary chondrocytes 3 days after treatment with okadaic acid or DMSO only. J) Quantification of mean fluorescence intensity from I (n=3 fields-of-view). K) Schematic representation of osteogenic differentiation of P5 primary rib chondrocytes isolated from Adamts10 KO or Adamts17 KO mice. The bottom panels show brightfield micrographs of freshly isolated primary chondrocytes (-3 d, left) and confluent chondrocytes (0 d, right). L) Micrographs of two individual wells/genotype of primary WT or Adamts10 KO (10KO) chondrocytes stained with alizarin red after 21 d of culture in osteogenic medium. M) Bar graph showing quantification of mean signal intensity of alizarin red deposits (isolates from n=4-5 biological replicates/genotype). N) Micrographs of two individual wells/genotype of primary WT or Adamts17 KO chondrocytes stained with alizarin red after 21 d of culture in osteogenic medium. O) Bar graph showing quantification of mean signal intensity of alizarin red deposits (isolates from n=5 biological replicates/genotype). In B, F, H, J, M, O, bars indicate mean values and whiskers the standard deviation. Statistical significance in B, H, J, M, O was calculated with a 2-sided Student t-test and in F with one-way ANOVA followed by post-hoc Tukey test.

Journal: bioRxiv

Article Title: Combined ADAMTS10 and ADAMTS17 inactivation exacerbates bone shortening and compromises extracellular matrix formation

doi: 10.1101/2025.01.23.634616

Figure Lengend Snippet: A) Images of sections through growth plates of 4 week-old WT and Adamts10;Adamts17 DKO mice. Proliferative (PZ) and hypertrophic (HZ) zones are outlined with dashed lines. B) Bar graphs showing widths of PZ and HZ from WT and DKO growth plates. Data points represent the average of multiple measurements across the growth plate zone from n=3 mice. C) Higher magnification of growth plate from images in A showing disorganized proliferative zone in DKO growth plates. D) Micrograph of ADAMTS17 immunostaining of hypertrophic chondrocytes at the cartilage-bone interface. The boxed area is magnified in the right-hand panel. E) Schematic representation of experimental design for pellet culture to induce chondrocyte-like differentiation of C3H/10T1/2 cells. F) Bar graphs showing relative Adamts10, Adamts17, and Col2a1 mRNAs levels during differentiation of C3H/10T1/2 cell pellets normalized to Gapdh (n=3 replicates). G) Schematic representation of the mechanism of action of okadaic acid in de-repressing chondrocyte hypertrophy genes. H) Bar graphs showing relative changes of Adamts10 (TS10), Adamts17 (TS17), Fbn1, Fn1, and Col10a1 mRNA levels 24 h after treatment of primary chondrocytes with 50 nM okadaic acid or DMSO (n=3 replicates). I) Micrographs of immunostaining of fibrillin-1 (FBN1) and fibronectin (FN) deposition in the ECM of primary chondrocytes 3 days after treatment with okadaic acid or DMSO only. J) Quantification of mean fluorescence intensity from I (n=3 fields-of-view). K) Schematic representation of osteogenic differentiation of P5 primary rib chondrocytes isolated from Adamts10 KO or Adamts17 KO mice. The bottom panels show brightfield micrographs of freshly isolated primary chondrocytes (-3 d, left) and confluent chondrocytes (0 d, right). L) Micrographs of two individual wells/genotype of primary WT or Adamts10 KO (10KO) chondrocytes stained with alizarin red after 21 d of culture in osteogenic medium. M) Bar graph showing quantification of mean signal intensity of alizarin red deposits (isolates from n=4-5 biological replicates/genotype). N) Micrographs of two individual wells/genotype of primary WT or Adamts17 KO chondrocytes stained with alizarin red after 21 d of culture in osteogenic medium. O) Bar graph showing quantification of mean signal intensity of alizarin red deposits (isolates from n=5 biological replicates/genotype). In B, F, H, J, M, O, bars indicate mean values and whiskers the standard deviation. Statistical significance in B, H, J, M, O was calculated with a 2-sided Student t-test and in F with one-way ANOVA followed by post-hoc Tukey test.

Article Snippet: Since we observed early postnatal lethality of Adamts10 ; Adamts17 DKO mice, we quantified postnatal survival with Kaplan-Meier survival analysis, where we observed significant postnatal mortality of DKO mice with 50% survival at 23 d (+/-7.1 d) after birth (probe > Chi = 0.00029, log-rank test) ( ).

Techniques: Immunostaining, Fluorescence, Isolation, Staining, Standard Deviation

A) Micrographs of Masson’s trichrome-stained cross-sections through dorsal skin from 4-week-old WT, Adamts10 KO (10KO), Adamts17 KO (17KO), and DKO mice. ED, epidermis; D, dermis; HD, hypodermis; PC, panniculus carnosus. B-D) Bar graphs showing quantification of overall skin thickness (B) and the thicknesses of the epidermis, dermis, hypodermis (C), and panniculus carnosus (p. carnosus, D). Individual data points represent multiple measurements along the different skin layers from n=3 mice/genotype. E) Stacked bar graphs showing the relative proportions of individual skin layers. The percentage values are indicated. F) Bar graphs showing the quantification of hair follicle numbers in the skin for each genotype. G, H) Bar graphs showing normalized gene expression in fragments per kilobase of transcript per million mapped reads (FPKM) for Adamts10 and Adamts17 in individual skin cell types at E14.5 (G) and P5 (H). Data were extracted from the Hair-GEL database , . I-K) Micrographs showing the localization of Adamts17 mRNA (red/dark purple) in WT skin cross-sections at E13.5 (I), E16.5 (J), and P0 (K) detected by RNAscope in-situ hybridization with a probe specific for Adamts17. Sections were counterstained with hematoxylin. L) Micrograph of ADAMTS17 immunostaining (green) of cross-sections through WT skin. Nuclei were stained with DAPI (blue). M) Micrographs of primary mouse skin fibroblasts after immunostaining for fibrillin-1 (red) and fibronectin (green). Nuclei were counterstained with DAPI (blue). N) Quantification of mean fluorescence intensity from M (n=4 biological replicates). In B, C, D, F, floating bars indicate 25 th – 75 th percentile range, lines the mean value and whiskers the standard deviation. In N, the bars represent the mean value and the whiskers the standard deviation. Statistical differences in B, C, D, F, N were determined using a one-way ANOVA with post-hoc Tukey test. a, p<0.05 compared to WT; b, p<0.05 compared to Adamts10 KO; p<0.05 compared to Adamts17 KO.

Journal: bioRxiv

Article Title: Combined ADAMTS10 and ADAMTS17 inactivation exacerbates bone shortening and compromises extracellular matrix formation

doi: 10.1101/2025.01.23.634616

Figure Lengend Snippet: A) Micrographs of Masson’s trichrome-stained cross-sections through dorsal skin from 4-week-old WT, Adamts10 KO (10KO), Adamts17 KO (17KO), and DKO mice. ED, epidermis; D, dermis; HD, hypodermis; PC, panniculus carnosus. B-D) Bar graphs showing quantification of overall skin thickness (B) and the thicknesses of the epidermis, dermis, hypodermis (C), and panniculus carnosus (p. carnosus, D). Individual data points represent multiple measurements along the different skin layers from n=3 mice/genotype. E) Stacked bar graphs showing the relative proportions of individual skin layers. The percentage values are indicated. F) Bar graphs showing the quantification of hair follicle numbers in the skin for each genotype. G, H) Bar graphs showing normalized gene expression in fragments per kilobase of transcript per million mapped reads (FPKM) for Adamts10 and Adamts17 in individual skin cell types at E14.5 (G) and P5 (H). Data were extracted from the Hair-GEL database , . I-K) Micrographs showing the localization of Adamts17 mRNA (red/dark purple) in WT skin cross-sections at E13.5 (I), E16.5 (J), and P0 (K) detected by RNAscope in-situ hybridization with a probe specific for Adamts17. Sections were counterstained with hematoxylin. L) Micrograph of ADAMTS17 immunostaining (green) of cross-sections through WT skin. Nuclei were stained with DAPI (blue). M) Micrographs of primary mouse skin fibroblasts after immunostaining for fibrillin-1 (red) and fibronectin (green). Nuclei were counterstained with DAPI (blue). N) Quantification of mean fluorescence intensity from M (n=4 biological replicates). In B, C, D, F, floating bars indicate 25 th – 75 th percentile range, lines the mean value and whiskers the standard deviation. In N, the bars represent the mean value and the whiskers the standard deviation. Statistical differences in B, C, D, F, N were determined using a one-way ANOVA with post-hoc Tukey test. a, p<0.05 compared to WT; b, p<0.05 compared to Adamts10 KO; p<0.05 compared to Adamts17 KO.

Article Snippet: Since we observed early postnatal lethality of Adamts10 ; Adamts17 DKO mice, we quantified postnatal survival with Kaplan-Meier survival analysis, where we observed significant postnatal mortality of DKO mice with 50% survival at 23 d (+/-7.1 d) after birth (probe > Chi = 0.00029, log-rank test) ( ).

Techniques: Staining, Gene Expression, RNAscope, In Situ Hybridization, Immunostaining, Fluorescence, Standard Deviation

Tumor growth assessment: data for each time-point in mm 3 are mean ± SEM. ( A ) M-234p, N = 6/group; Day 21: Control (600.96 ± 93) vs Cy+Los (20.96 ± 9.01) ( P < 0.05); ( B ) M-406, N = 6–7/group; Day 17: Control (1397.00 ± 328.32) vs Cy (372.00 ± 55.25) ( P < 0.01), vs Los (451.07 ± 143.94) ( P < 0.05), vs Cy+Los (123.43 ± 45.71) ( P < 0.001). Kruskal-Wallis multiple comparison test and Dunn’s post-test. Overall survival (Kaplan-Meier), Median Survival (MS): ( C ) M-234p, N = 5–6/group; Control (MS: 34 days); Cy (MS: 47 days); Los (MS: 32 days); Cy+Los (MS: undefined, Day 32: 60% [3/5] complete tumor regressions). Cy+Los vs Control, vs Los, vs Cy ( P < 0.01); ( D ) M-406, N = 6–7/group); Control (MS: 24 days); Cy (MS: 36.5 days); Los (MS: 33 days); Cy+Los (MS: 47 days). Control vs Cy ( P < 0.01), vs Los ( P < 0.01), vs Cy+Los ( P < 0.001); Cy+Los vs Cy ( P < 0.05), vs Los ( P < 0,001). Log-rank Test.

Journal: Oncotarget

Article Title: Losartan improves the therapeutic effect of metronomic cyclophosphamide in triple negative mammary cancer models

doi: 10.18632/oncotarget.27694

Figure Lengend Snippet: Tumor growth assessment: data for each time-point in mm 3 are mean ± SEM. ( A ) M-234p, N = 6/group; Day 21: Control (600.96 ± 93) vs Cy+Los (20.96 ± 9.01) ( P < 0.05); ( B ) M-406, N = 6–7/group; Day 17: Control (1397.00 ± 328.32) vs Cy (372.00 ± 55.25) ( P < 0.01), vs Los (451.07 ± 143.94) ( P < 0.05), vs Cy+Los (123.43 ± 45.71) ( P < 0.001). Kruskal-Wallis multiple comparison test and Dunn’s post-test. Overall survival (Kaplan-Meier), Median Survival (MS): ( C ) M-234p, N = 5–6/group; Control (MS: 34 days); Cy (MS: 47 days); Los (MS: 32 days); Cy+Los (MS: undefined, Day 32: 60% [3/5] complete tumor regressions). Cy+Los vs Control, vs Los, vs Cy ( P < 0.01); ( D ) M-406, N = 6–7/group); Control (MS: 24 days); Cy (MS: 36.5 days); Los (MS: 33 days); Cy+Los (MS: 47 days). Control vs Cy ( P < 0.01), vs Los ( P < 0.01), vs Cy+Los ( P < 0.001); Cy+Los vs Cy ( P < 0.05), vs Los ( P < 0,001). Log-rank Test.

Article Snippet: Data obtained was analyzed using ANOVA and Tukey-Kramer Multiple Comparison tests, Kruskal-Wallis and Dunn’s post-test, and Log-rank tests were used to examine the differences between groups with GraphPad Prism version 3.0 (GraphPad Software, San Diego, CA).

Techniques: Control, Comparison

Proliferation: Ki67 + cells/field (median, range). ( A ) M-234p Control vs Cy+Los ( P < 0.01); ( B ) M-406 Control vs Cy+Los ( P < 0.05; ( C ) M-234p and ( D ) M-406, representative images of Control and Cy+Los treated tumors, 1000× magnification. Apoptosis: TUNEL + cells/field (median, range). ( E ) M-234p Control vs Cy+Los ( P < 0.05): ( F ) M-406 N. S; Kruskal-Wallis multiple comparison test and Dunn’s post-test; ( G ) M-234p and ( H ) M-406 representative images of Control and Cy+Los treated tumors, 1000× magnification.

Journal: Oncotarget

Article Title: Losartan improves the therapeutic effect of metronomic cyclophosphamide in triple negative mammary cancer models

doi: 10.18632/oncotarget.27694

Figure Lengend Snippet: Proliferation: Ki67 + cells/field (median, range). ( A ) M-234p Control vs Cy+Los ( P < 0.01); ( B ) M-406 Control vs Cy+Los ( P < 0.05; ( C ) M-234p and ( D ) M-406, representative images of Control and Cy+Los treated tumors, 1000× magnification. Apoptosis: TUNEL + cells/field (median, range). ( E ) M-234p Control vs Cy+Los ( P < 0.05): ( F ) M-406 N. S; Kruskal-Wallis multiple comparison test and Dunn’s post-test; ( G ) M-234p and ( H ) M-406 representative images of Control and Cy+Los treated tumors, 1000× magnification.

Article Snippet: Data obtained was analyzed using ANOVA and Tukey-Kramer Multiple Comparison tests, Kruskal-Wallis and Dunn’s post-test, and Log-rank tests were used to examine the differences between groups with GraphPad Prism version 3.0 (GraphPad Software, San Diego, CA).

Techniques: Control, TUNEL Assay, Comparison

Hematoxylin and eosin (H&E) representative tumor sections from M-234p and M-406, 400×. In both models the behavior was similar. Control group: ( A ) M-234p and ( C ) M-406: capillaries with small endothelial cells with barely stained nuclei and intercellular gaps (yellow arrow), lack of pericytes or cells with structure and staining compatible with pericytes. Cy+Los group: ( B ) M-234p and ( D ) M-406: intra- and peritumoral capillaries with structure and morphology similar to normal tissues. Endothelial cells with defined nuclei provide a continuous uninterrupted lining (yellow arrow), and well defined basal membrane covered with pericytes (red arrow). M-406 magnified section (1000×): vessel with normal vascular morphology. HIF1α expression: HIF1α + cells/field (median, range). ( E ) Control vs Cy ( P < 0.05), ( F ) Control vs Cy ( P < 0.05), vs Cy+Los ( P < 0.05), ( G ) and H ), representative images of Control and Cy+Los treated tumors, 100× magnification. Kruskal-Wallis multiple comparison test and Dunn’s post-test.

Journal: Oncotarget

Article Title: Losartan improves the therapeutic effect of metronomic cyclophosphamide in triple negative mammary cancer models

doi: 10.18632/oncotarget.27694

Figure Lengend Snippet: Hematoxylin and eosin (H&E) representative tumor sections from M-234p and M-406, 400×. In both models the behavior was similar. Control group: ( A ) M-234p and ( C ) M-406: capillaries with small endothelial cells with barely stained nuclei and intercellular gaps (yellow arrow), lack of pericytes or cells with structure and staining compatible with pericytes. Cy+Los group: ( B ) M-234p and ( D ) M-406: intra- and peritumoral capillaries with structure and morphology similar to normal tissues. Endothelial cells with defined nuclei provide a continuous uninterrupted lining (yellow arrow), and well defined basal membrane covered with pericytes (red arrow). M-406 magnified section (1000×): vessel with normal vascular morphology. HIF1α expression: HIF1α + cells/field (median, range). ( E ) Control vs Cy ( P < 0.05), ( F ) Control vs Cy ( P < 0.05), vs Cy+Los ( P < 0.05), ( G ) and H ), representative images of Control and Cy+Los treated tumors, 100× magnification. Kruskal-Wallis multiple comparison test and Dunn’s post-test.

Article Snippet: Data obtained was analyzed using ANOVA and Tukey-Kramer Multiple Comparison tests, Kruskal-Wallis and Dunn’s post-test, and Log-rank tests were used to examine the differences between groups with GraphPad Prism version 3.0 (GraphPad Software, San Diego, CA).

Techniques: Control, Staining, Membrane, Expressing, Comparison

M-234p: ( A ) CD4 cells, N. S. ( B ) CD8 cells, N. S. ( C ) Treg cells, N. S. ( D ) Th17 cells, N. S. M-406: ( E ) CD4 cells, N. S. ( F ) CD8 cells, N. S. ( G ) Treg cells, ( P = 0.064). ( H ) Th17 cells: Control vs Cy+Los, ( P = 0.0580). Kruskal-Wallis multiple comparison test and Dunn’s post-test.

Journal: Oncotarget

Article Title: Losartan improves the therapeutic effect of metronomic cyclophosphamide in triple negative mammary cancer models

doi: 10.18632/oncotarget.27694

Figure Lengend Snippet: M-234p: ( A ) CD4 cells, N. S. ( B ) CD8 cells, N. S. ( C ) Treg cells, N. S. ( D ) Th17 cells, N. S. M-406: ( E ) CD4 cells, N. S. ( F ) CD8 cells, N. S. ( G ) Treg cells, ( P = 0.064). ( H ) Th17 cells: Control vs Cy+Los, ( P = 0.0580). Kruskal-Wallis multiple comparison test and Dunn’s post-test.

Article Snippet: Data obtained was analyzed using ANOVA and Tukey-Kramer Multiple Comparison tests, Kruskal-Wallis and Dunn’s post-test, and Log-rank tests were used to examine the differences between groups with GraphPad Prism version 3.0 (GraphPad Software, San Diego, CA).

Techniques: Control, Comparison

Lymphocytes/field (median, range). M-234p: ( A ) CD4 + cells, N. S. ( B ) CD8 + cells, N. S. ( C ) Foxp3 + cells: Control vs Los, P < 0.05, vs Cy+Los, ( P < 0.05); ( D – F ) representative images of Control and Cy+Los treated tumors, 100× magnification; M-406: ( G ) CD4 + cells, N. S. ( H ) CD8 + cells, N. S. ( I ) Foxp3 + cells: Control vs Cy+Los, ( P < 0.05); ( J – L ) representative images of Control and Cy+Los treated tumors, 100× magnification. Kruskal-Wallis multiple comparison test and Dunn’s post-test.

Journal: Oncotarget

Article Title: Losartan improves the therapeutic effect of metronomic cyclophosphamide in triple negative mammary cancer models

doi: 10.18632/oncotarget.27694

Figure Lengend Snippet: Lymphocytes/field (median, range). M-234p: ( A ) CD4 + cells, N. S. ( B ) CD8 + cells, N. S. ( C ) Foxp3 + cells: Control vs Los, P < 0.05, vs Cy+Los, ( P < 0.05); ( D – F ) representative images of Control and Cy+Los treated tumors, 100× magnification; M-406: ( G ) CD4 + cells, N. S. ( H ) CD8 + cells, N. S. ( I ) Foxp3 + cells: Control vs Cy+Los, ( P < 0.05); ( J – L ) representative images of Control and Cy+Los treated tumors, 100× magnification. Kruskal-Wallis multiple comparison test and Dunn’s post-test.

Article Snippet: Data obtained was analyzed using ANOVA and Tukey-Kramer Multiple Comparison tests, Kruskal-Wallis and Dunn’s post-test, and Log-rank tests were used to examine the differences between groups with GraphPad Prism version 3.0 (GraphPad Software, San Diego, CA).

Techniques: Control, Comparison

Quantification of tumor infiltrating lymphocytes by flow cytometry: M-234p, day 42, Cy vs Cy+Los: ( A ) CD4 cells, N. S. ( B ) CD8 cells, N. S. ( C ) Treg cells, ( P < 0.001). ( D ) Th17 cells, ( P < 0.05). Kruskal-Wallis multiple comparison test and Dunn’s post -test.

Journal: Oncotarget

Article Title: Losartan improves the therapeutic effect of metronomic cyclophosphamide in triple negative mammary cancer models

doi: 10.18632/oncotarget.27694

Figure Lengend Snippet: Quantification of tumor infiltrating lymphocytes by flow cytometry: M-234p, day 42, Cy vs Cy+Los: ( A ) CD4 cells, N. S. ( B ) CD8 cells, N. S. ( C ) Treg cells, ( P < 0.001). ( D ) Th17 cells, ( P < 0.05). Kruskal-Wallis multiple comparison test and Dunn’s post -test.

Article Snippet: Data obtained was analyzed using ANOVA and Tukey-Kramer Multiple Comparison tests, Kruskal-Wallis and Dunn’s post-test, and Log-rank tests were used to examine the differences between groups with GraphPad Prism version 3.0 (GraphPad Software, San Diego, CA).

Techniques: Flow Cytometry, Comparison

αSMA : % of αSMA + area/field (median, range). ( A ) M-234p Control vs Los, ( P < 0.05), vs Cy+Los, ( P < 0.01). ( B ) M-406 Control vs Cy, ( P < 0.01), vs Los ( P < 0.01), vs Cy+Los ( P < 0.001). ( C ) M-234p and ( D ) M-406 representative images of Control and Cy+Los treated tumors, 100× magnification. Kruskal-Wallis multiple comparison test and Dunn’s post-test. Collagen : % of collagen area/field (median, range). ( E ) M-234p Control vs Cy+Los ( P < 0.01). ( F ) M-406 N. S. ( G ) M-234p and ( H ) M-406 representative images of Control and Cy+Los treated tumors, 100× magnification.

Journal: Oncotarget

Article Title: Losartan improves the therapeutic effect of metronomic cyclophosphamide in triple negative mammary cancer models

doi: 10.18632/oncotarget.27694

Figure Lengend Snippet: αSMA : % of αSMA + area/field (median, range). ( A ) M-234p Control vs Los, ( P < 0.05), vs Cy+Los, ( P < 0.01). ( B ) M-406 Control vs Cy, ( P < 0.01), vs Los ( P < 0.01), vs Cy+Los ( P < 0.001). ( C ) M-234p and ( D ) M-406 representative images of Control and Cy+Los treated tumors, 100× magnification. Kruskal-Wallis multiple comparison test and Dunn’s post-test. Collagen : % of collagen area/field (median, range). ( E ) M-234p Control vs Cy+Los ( P < 0.01). ( F ) M-406 N. S. ( G ) M-234p and ( H ) M-406 representative images of Control and Cy+Los treated tumors, 100× magnification.

Article Snippet: Data obtained was analyzed using ANOVA and Tukey-Kramer Multiple Comparison tests, Kruskal-Wallis and Dunn’s post-test, and Log-rank tests were used to examine the differences between groups with GraphPad Prism version 3.0 (GraphPad Software, San Diego, CA).

Techniques: Control, Comparison