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Pooled data of stress (A) and [Ca2+]i transients (B) at varied [Ca2+]o (1-5 mM) from WT and gravin-t/t muscles. Both stress and [Ca2+]i transient increased as [Ca2+]o was raised. Stress was similar in both groups of muscles but [Ca2+]i transients remained significantly lower in gravin-t/t muscles (P<0.001; repeated <t>MANOVA,</t> n=8 in each group).
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Pooled data of stress (A) and [Ca2+]i transients (B) at varied [Ca2+]o (1-5 mM) from WT and gravin-t/t muscles. Both stress and [Ca2+]i transient increased as [Ca2+]o was raised. Stress was similar in both groups of muscles but [Ca2+]i transients remained significantly lower in gravin-t/t muscles (P<0.001; repeated <t>MANOVA,</t> n=8 in each group).
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Pooled data of stress (A) and [Ca2+]i transients (B) at varied [Ca2+]o (1-5 mM) from WT and gravin-t/t muscles. Both stress and [Ca2+]i transient increased as [Ca2+]o was raised. Stress was similar in both groups of muscles but [Ca2+]i transients remained significantly lower in gravin-t/t muscles (P<0.001; repeated <t>MANOVA,</t> n=8 in each group).
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(A) Qualitative analysis of infection at 3 dpi is summarized in the schematic (n = 15). Each row represents an embryo injected with ZIKV at stage (s) 11 or 12. (B) Alternate sections from a 3 dpi ZIKV-infected embryo (embryo 1 in A) stained for PAX6 (brown), SHH (purple), and dsRNA; this example is representative of n = 10 embryos. Some ZIKV infection hotspots are labeled with arrowheads. Relative dorsal-ventral position is indicated by the percentile. Red bracket at 39% shows a peculiar crenellation defect of the neuroepithelium (40% occurrence). Red circle at 69% marks a hemorrhage reflecting diaminobenzidine (DAB) pigment oxidation by endogenous peroxidase in red blood cells. (C and D) At the MB midline, SHH expression is weaker where ZIKV infection is heavy qualitatively (C) and quantitatively (D). PTCH1 , a gene downstream of SHH, is also weaker in expression (C). Magnified views are shown in the flanking red panels. (E) PAX6+ pixel count was not changed by ZIKV infection. (F) The Pax6+ population develops closer to the midline in ZIKV-infected embryos, possibly due to reduced SHH signal ( SHH pixels) (one-tailed mixed effects SAS model). Left and right sides of each embryo are plotted independently. (G) Convex hull plot of PAX6 lateral edge against number of SHH pixels show ZIKV data in the lower left quadrant of the plot <t>(MANOVA).</t> (H and I) Although the NKX2.2 population does not show a statistically significant difference in the position of the domain, the convex hull plot shows the cloud of ZIKV data in the lower left quadrant. ***p < 0.001; **p < 0.01; *p < 0.05; n.s., not significant. Error bars represent mean ± SEM. AP, alar plate; A, anterior; BP, basal plate; D, dorsal; FP, floor plate; Hypo, hypothalamus; L, lateral; MHB, MB-HB boundary; PreT, pretectum; Pth, prethalamus; P, posterior; RP, roof plate; Th, thalamus. See also , and .
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(A) Qualitative analysis of infection at 3 dpi is summarized in the schematic (n = 15). Each row represents an embryo injected with ZIKV at stage (s) 11 or 12. (B) Alternate sections from a 3 dpi ZIKV-infected embryo (embryo 1 in A) stained for PAX6 (brown), SHH (purple), and dsRNA; this example is representative of n = 10 embryos. Some ZIKV infection hotspots are labeled with arrowheads. Relative dorsal-ventral position is indicated by the percentile. Red bracket at 39% shows a peculiar crenellation defect of the neuroepithelium (40% occurrence). Red circle at 69% marks a hemorrhage reflecting diaminobenzidine (DAB) pigment oxidation by endogenous peroxidase in red blood cells. (C and D) At the MB midline, SHH expression is weaker where ZIKV infection is heavy qualitatively (C) and quantitatively (D). PTCH1 , a gene downstream of SHH, is also weaker in expression (C). Magnified views are shown in the flanking red panels. (E) PAX6+ pixel count was not changed by ZIKV infection. (F) The Pax6+ population develops closer to the midline in ZIKV-infected embryos, possibly due to reduced SHH signal ( SHH pixels) (one-tailed mixed effects SAS model). Left and right sides of each embryo are plotted independently. (G) Convex hull plot of PAX6 lateral edge against number of SHH pixels show ZIKV data in the lower left quadrant of the plot <t>(MANOVA).</t> (H and I) Although the NKX2.2 population does not show a statistically significant difference in the position of the domain, the convex hull plot shows the cloud of ZIKV data in the lower left quadrant. ***p < 0.001; **p < 0.01; *p < 0.05; n.s., not significant. Error bars represent mean ± SEM. AP, alar plate; A, anterior; BP, basal plate; D, dorsal; FP, floor plate; Hypo, hypothalamus; L, lateral; MHB, MB-HB boundary; PreT, pretectum; Pth, prethalamus; P, posterior; RP, roof plate; Th, thalamus. See also , and .
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(A) Qualitative analysis of infection at 3 dpi is summarized in the schematic (n = 15). Each row represents an embryo injected with ZIKV at stage (s) 11 or 12. (B) Alternate sections from a 3 dpi ZIKV-infected embryo (embryo 1 in A) stained for PAX6 (brown), SHH (purple), and dsRNA; this example is representative of n = 10 embryos. Some ZIKV infection hotspots are labeled with arrowheads. Relative dorsal-ventral position is indicated by the percentile. Red bracket at 39% shows a peculiar crenellation defect of the neuroepithelium (40% occurrence). Red circle at 69% marks a hemorrhage reflecting diaminobenzidine (DAB) pigment oxidation by endogenous peroxidase in red blood cells. (C and D) At the MB midline, SHH expression is weaker where ZIKV infection is heavy qualitatively (C) and quantitatively (D). PTCH1 , a gene downstream of SHH, is also weaker in expression (C). Magnified views are shown in the flanking red panels. (E) PAX6+ pixel count was not changed by ZIKV infection. (F) The Pax6+ population develops closer to the midline in ZIKV-infected embryos, possibly due to reduced SHH signal ( SHH pixels) (one-tailed mixed effects SAS model). Left and right sides of each embryo are plotted independently. (G) Convex hull plot of PAX6 lateral edge against number of SHH pixels show ZIKV data in the lower left quadrant of the plot <t>(MANOVA).</t> (H and I) Although the NKX2.2 population does not show a statistically significant difference in the position of the domain, the convex hull plot shows the cloud of ZIKV data in the lower left quadrant. ***p < 0.001; **p < 0.01; *p < 0.05; n.s., not significant. Error bars represent mean ± SEM. AP, alar plate; A, anterior; BP, basal plate; D, dorsal; FP, floor plate; Hypo, hypothalamus; L, lateral; MHB, MB-HB boundary; PreT, pretectum; Pth, prethalamus; P, posterior; RP, roof plate; Th, thalamus. See also , and .
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(A) Qualitative analysis of infection at 3 dpi is summarized in the schematic (n = 15). Each row represents an embryo injected with ZIKV at stage (s) 11 or 12. (B) Alternate sections from a 3 dpi ZIKV-infected embryo (embryo 1 in A) stained for PAX6 (brown), SHH (purple), and dsRNA; this example is representative of n = 10 embryos. Some ZIKV infection hotspots are labeled with arrowheads. Relative dorsal-ventral position is indicated by the percentile. Red bracket at 39% shows a peculiar crenellation defect of the neuroepithelium (40% occurrence). Red circle at 69% marks a hemorrhage reflecting diaminobenzidine (DAB) pigment oxidation by endogenous peroxidase in red blood cells. (C and D) At the MB midline, SHH expression is weaker where ZIKV infection is heavy qualitatively (C) and quantitatively (D). PTCH1 , a gene downstream of SHH, is also weaker in expression (C). Magnified views are shown in the flanking red panels. (E) PAX6+ pixel count was not changed by ZIKV infection. (F) The Pax6+ population develops closer to the midline in ZIKV-infected embryos, possibly due to reduced SHH signal ( SHH pixels) (one-tailed mixed effects SAS model). Left and right sides of each embryo are plotted independently. (G) Convex hull plot of PAX6 lateral edge against number of SHH pixels show ZIKV data in the lower left quadrant of the plot <t>(MANOVA).</t> (H and I) Although the NKX2.2 population does not show a statistically significant difference in the position of the domain, the convex hull plot shows the cloud of ZIKV data in the lower left quadrant. ***p < 0.001; **p < 0.01; *p < 0.05; n.s., not significant. Error bars represent mean ± SEM. AP, alar plate; A, anterior; BP, basal plate; D, dorsal; FP, floor plate; Hypo, hypothalamus; L, lateral; MHB, MB-HB boundary; PreT, pretectum; Pth, prethalamus; P, posterior; RP, roof plate; Th, thalamus. See also , and .
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(A) Qualitative analysis of infection at 3 dpi is summarized in the schematic (n = 15). Each row represents an embryo injected with ZIKV at stage (s) 11 or 12. (B) Alternate sections from a 3 dpi ZIKV-infected embryo (embryo 1 in A) stained for PAX6 (brown), SHH (purple), and dsRNA; this example is representative of n = 10 embryos. Some ZIKV infection hotspots are labeled with arrowheads. Relative dorsal-ventral position is indicated by the percentile. Red bracket at 39% shows a peculiar crenellation defect of the neuroepithelium (40% occurrence). Red circle at 69% marks a hemorrhage reflecting diaminobenzidine (DAB) pigment oxidation by endogenous peroxidase in red blood cells. (C and D) At the MB midline, SHH expression is weaker where ZIKV infection is heavy qualitatively (C) and quantitatively (D). PTCH1 , a gene downstream of SHH, is also weaker in expression (C). Magnified views are shown in the flanking red panels. (E) PAX6+ pixel count was not changed by ZIKV infection. (F) The Pax6+ population develops closer to the midline in ZIKV-infected embryos, possibly due to reduced SHH signal ( SHH pixels) (one-tailed mixed effects SAS model). Left and right sides of each embryo are plotted independently. (G) Convex hull plot of PAX6 lateral edge against number of SHH pixels show ZIKV data in the lower left quadrant of the plot <t>(MANOVA).</t> (H and I) Although the NKX2.2 population does not show a statistically significant difference in the position of the domain, the convex hull plot shows the cloud of ZIKV data in the lower left quadrant. ***p < 0.001; **p < 0.01; *p < 0.05; n.s., not significant. Error bars represent mean ± SEM. AP, alar plate; A, anterior; BP, basal plate; D, dorsal; FP, floor plate; Hypo, hypothalamus; L, lateral; MHB, MB-HB boundary; PreT, pretectum; Pth, prethalamus; P, posterior; RP, roof plate; Th, thalamus. See also , and .
Multivariate Anova (Manova), supplied by Minitab 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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Pooled data of stress (A) and [Ca2+]i transients (B) at varied [Ca2+]o (1-5 mM) from WT and gravin-t/t muscles. Both stress and [Ca2+]i transient increased as [Ca2+]o was raised. Stress was similar in both groups of muscles but [Ca2+]i transients remained significantly lower in gravin-t/t muscles (P<0.001; repeated MANOVA, n=8 in each group).

Journal: European journal of pharmacology

Article Title: Force development and intracellular Ca 2+ in intact Cardiac Muscles from Gravin Mutant Mice

doi: 10.1016/j.ejphar.2017.04.020

Figure Lengend Snippet: Pooled data of stress (A) and [Ca2+]i transients (B) at varied [Ca2+]o (1-5 mM) from WT and gravin-t/t muscles. Both stress and [Ca2+]i transient increased as [Ca2+]o was raised. Stress was similar in both groups of muscles but [Ca2+]i transients remained significantly lower in gravin-t/t muscles (P<0.001; repeated MANOVA, n=8 in each group).

Article Snippet: 2.5 Statistical Analysis These data were analyzed by Student's t-test, one-way ANOVA and repeated two-way multivariate ANOVA (MANOVA) (Systat 10.2 or GraphPad Prism 5).

Techniques: Muscles

Dynamics of stress and [Ca2+]i transient of trabecular muscles from WT and gravin-t/t mice. The time to peak stress (A) and [Ca2+]i (B) was prolonged in gravin-t/t muscles (as determined by MANOVA) whereas the time to 50% relaxation of stress (C) and [Ca2+]i (D) was not different between WT and gravin-t/t muscles. However, the initial relaxation time (time to 75% of peak) in twitch (E) was significantly slowed in gravin-t/t muscles (P<0.01 repeated MANOVA) whereas the initial relaxation time (time to 75% of peak) in [Ca2+]i (F) was not different between WT and gravin-t/t muscle. (n=8 in each group)

Journal: European journal of pharmacology

Article Title: Force development and intracellular Ca 2+ in intact Cardiac Muscles from Gravin Mutant Mice

doi: 10.1016/j.ejphar.2017.04.020

Figure Lengend Snippet: Dynamics of stress and [Ca2+]i transient of trabecular muscles from WT and gravin-t/t mice. The time to peak stress (A) and [Ca2+]i (B) was prolonged in gravin-t/t muscles (as determined by MANOVA) whereas the time to 50% relaxation of stress (C) and [Ca2+]i (D) was not different between WT and gravin-t/t muscles. However, the initial relaxation time (time to 75% of peak) in twitch (E) was significantly slowed in gravin-t/t muscles (P<0.01 repeated MANOVA) whereas the initial relaxation time (time to 75% of peak) in [Ca2+]i (F) was not different between WT and gravin-t/t muscle. (n=8 in each group)

Article Snippet: 2.5 Statistical Analysis These data were analyzed by Student's t-test, one-way ANOVA and repeated two-way multivariate ANOVA (MANOVA) (Systat 10.2 or GraphPad Prism 5).

Techniques: Muscles

(A) Peak stress and peak [Ca2+]i transient relationships of trabecular muscles from WT and gravin-t/t mice (pooled data, n=8 in each group). In WT, force = 41 [Ca2+]i – 8.22; in gravin-t/t, force = 67 [Ca2+]i – 7.08. The relationship is also shifted leftward in gravin-t/t muscles. These two relationships are significantly different (P<0.001; MANOVA). (B) Representative phase-plane plots for stress vs. [Ca2+]i transient from WT and gravin-t/t muscles. The phase-plane plot is stress vs. [Ca2+]i transient point-to-point over the entire trajectory of the twitch. Note the phase-plane plot of gravin-t/t muscle is shifted to the left. (C) Comparison of [Ca2+]i at which stress relaxed to 50%. *P<0.05 vs. WT; n=6, [Ca2+]o = 1.0 mM.

Journal: European journal of pharmacology

Article Title: Force development and intracellular Ca 2+ in intact Cardiac Muscles from Gravin Mutant Mice

doi: 10.1016/j.ejphar.2017.04.020

Figure Lengend Snippet: (A) Peak stress and peak [Ca2+]i transient relationships of trabecular muscles from WT and gravin-t/t mice (pooled data, n=8 in each group). In WT, force = 41 [Ca2+]i – 8.22; in gravin-t/t, force = 67 [Ca2+]i – 7.08. The relationship is also shifted leftward in gravin-t/t muscles. These two relationships are significantly different (P<0.001; MANOVA). (B) Representative phase-plane plots for stress vs. [Ca2+]i transient from WT and gravin-t/t muscles. The phase-plane plot is stress vs. [Ca2+]i transient point-to-point over the entire trajectory of the twitch. Note the phase-plane plot of gravin-t/t muscle is shifted to the left. (C) Comparison of [Ca2+]i at which stress relaxed to 50%. *P<0.05 vs. WT; n=6, [Ca2+]o = 1.0 mM.

Article Snippet: 2.5 Statistical Analysis These data were analyzed by Student's t-test, one-way ANOVA and repeated two-way multivariate ANOVA (MANOVA) (Systat 10.2 or GraphPad Prism 5).

Techniques: Muscles, Comparison

Pooled data of stress (A) and [Ca2+]i transients (B) at varied [Ca2+]o (1-5 mM) from WT and gravin-t/t muscles. Both stress and [Ca2+]i transient increased as [Ca2+]o was raised. Stress was similar in both groups of muscles but [Ca2+]i transients remained significantly lower in gravin-t/t muscles (P<0.001; repeated MANOVA, n=8 in each group).

Journal: European journal of pharmacology

Article Title: Force development and intracellular Ca 2+ in intact Cardiac Muscles from Gravin Mutant Mice

doi: 10.1016/j.ejphar.2017.04.020

Figure Lengend Snippet: Pooled data of stress (A) and [Ca2+]i transients (B) at varied [Ca2+]o (1-5 mM) from WT and gravin-t/t muscles. Both stress and [Ca2+]i transient increased as [Ca2+]o was raised. Stress was similar in both groups of muscles but [Ca2+]i transients remained significantly lower in gravin-t/t muscles (P<0.001; repeated MANOVA, n=8 in each group).

Article Snippet: These data were analyzed by Student's t-test, one-way ANOVA and repeated two-way multivariate ANOVA (MANOVA) (Systat 10.2 or GraphPad Prism 5).

Techniques: Muscles

Dynamics of stress and [Ca2+]i transient of trabecular muscles from WT and gravin-t/t mice. The time to peak stress (A) and [Ca2+]i (B) was prolonged in gravin-t/t muscles (as determined by MANOVA) whereas the time to 50% relaxation of stress (C) and [Ca2+]i (D) was not different between WT and gravin-t/t muscles. However, the initial relaxation time (time to 75% of peak) in twitch (E) was significantly slowed in gravin-t/t muscles (P<0.01 repeated MANOVA) whereas the initial relaxation time (time to 75% of peak) in [Ca2+]i (F) was not different between WT and gravin-t/t muscle. (n=8 in each group)

Journal: European journal of pharmacology

Article Title: Force development and intracellular Ca 2+ in intact Cardiac Muscles from Gravin Mutant Mice

doi: 10.1016/j.ejphar.2017.04.020

Figure Lengend Snippet: Dynamics of stress and [Ca2+]i transient of trabecular muscles from WT and gravin-t/t mice. The time to peak stress (A) and [Ca2+]i (B) was prolonged in gravin-t/t muscles (as determined by MANOVA) whereas the time to 50% relaxation of stress (C) and [Ca2+]i (D) was not different between WT and gravin-t/t muscles. However, the initial relaxation time (time to 75% of peak) in twitch (E) was significantly slowed in gravin-t/t muscles (P<0.01 repeated MANOVA) whereas the initial relaxation time (time to 75% of peak) in [Ca2+]i (F) was not different between WT and gravin-t/t muscle. (n=8 in each group)

Article Snippet: These data were analyzed by Student's t-test, one-way ANOVA and repeated two-way multivariate ANOVA (MANOVA) (Systat 10.2 or GraphPad Prism 5).

Techniques: Muscles

(A) Peak stress and peak [Ca2+]i transient relationships of trabecular muscles from WT and gravin-t/t mice (pooled data, n=8 in each group). In WT, force = 41 [Ca2+]i – 8.22; in gravin-t/t, force = 67 [Ca2+]i – 7.08. The relationship is also shifted leftward in gravin-t/t muscles. These two relationships are significantly different (P<0.001; MANOVA). (B) Representative phase-plane plots for stress vs. [Ca2+]i transient from WT and gravin-t/t muscles. The phase-plane plot is stress vs. [Ca2+]i transient point-to-point over the entire trajectory of the twitch. Note the phase-plane plot of gravin-t/t muscle is shifted to the left. (C) Comparison of [Ca2+]i at which stress relaxed to 50%. *P<0.05 vs. WT; n=6, [Ca2+]o = 1.0 mM.

Journal: European journal of pharmacology

Article Title: Force development and intracellular Ca 2+ in intact Cardiac Muscles from Gravin Mutant Mice

doi: 10.1016/j.ejphar.2017.04.020

Figure Lengend Snippet: (A) Peak stress and peak [Ca2+]i transient relationships of trabecular muscles from WT and gravin-t/t mice (pooled data, n=8 in each group). In WT, force = 41 [Ca2+]i – 8.22; in gravin-t/t, force = 67 [Ca2+]i – 7.08. The relationship is also shifted leftward in gravin-t/t muscles. These two relationships are significantly different (P<0.001; MANOVA). (B) Representative phase-plane plots for stress vs. [Ca2+]i transient from WT and gravin-t/t muscles. The phase-plane plot is stress vs. [Ca2+]i transient point-to-point over the entire trajectory of the twitch. Note the phase-plane plot of gravin-t/t muscle is shifted to the left. (C) Comparison of [Ca2+]i at which stress relaxed to 50%. *P<0.05 vs. WT; n=6, [Ca2+]o = 1.0 mM.

Article Snippet: These data were analyzed by Student's t-test, one-way ANOVA and repeated two-way multivariate ANOVA (MANOVA) (Systat 10.2 or GraphPad Prism 5).

Techniques: Muscles, Comparison

(A) Qualitative analysis of infection at 3 dpi is summarized in the schematic (n = 15). Each row represents an embryo injected with ZIKV at stage (s) 11 or 12. (B) Alternate sections from a 3 dpi ZIKV-infected embryo (embryo 1 in A) stained for PAX6 (brown), SHH (purple), and dsRNA; this example is representative of n = 10 embryos. Some ZIKV infection hotspots are labeled with arrowheads. Relative dorsal-ventral position is indicated by the percentile. Red bracket at 39% shows a peculiar crenellation defect of the neuroepithelium (40% occurrence). Red circle at 69% marks a hemorrhage reflecting diaminobenzidine (DAB) pigment oxidation by endogenous peroxidase in red blood cells. (C and D) At the MB midline, SHH expression is weaker where ZIKV infection is heavy qualitatively (C) and quantitatively (D). PTCH1 , a gene downstream of SHH, is also weaker in expression (C). Magnified views are shown in the flanking red panels. (E) PAX6+ pixel count was not changed by ZIKV infection. (F) The Pax6+ population develops closer to the midline in ZIKV-infected embryos, possibly due to reduced SHH signal ( SHH pixels) (one-tailed mixed effects SAS model). Left and right sides of each embryo are plotted independently. (G) Convex hull plot of PAX6 lateral edge against number of SHH pixels show ZIKV data in the lower left quadrant of the plot (MANOVA). (H and I) Although the NKX2.2 population does not show a statistically significant difference in the position of the domain, the convex hull plot shows the cloud of ZIKV data in the lower left quadrant. ***p < 0.001; **p < 0.01; *p < 0.05; n.s., not significant. Error bars represent mean ± SEM. AP, alar plate; A, anterior; BP, basal plate; D, dorsal; FP, floor plate; Hypo, hypothalamus; L, lateral; MHB, MB-HB boundary; PreT, pretectum; Pth, prethalamus; P, posterior; RP, roof plate; Th, thalamus. See also , and .

Journal: Cell reports

Article Title: Zika Virus Can Strongly Infect and Disrupt Secondary Organizers in the Ventricular Zone of the Embryonic Chicken Brain

doi: 10.1016/j.celrep.2018.03.080

Figure Lengend Snippet: (A) Qualitative analysis of infection at 3 dpi is summarized in the schematic (n = 15). Each row represents an embryo injected with ZIKV at stage (s) 11 or 12. (B) Alternate sections from a 3 dpi ZIKV-infected embryo (embryo 1 in A) stained for PAX6 (brown), SHH (purple), and dsRNA; this example is representative of n = 10 embryos. Some ZIKV infection hotspots are labeled with arrowheads. Relative dorsal-ventral position is indicated by the percentile. Red bracket at 39% shows a peculiar crenellation defect of the neuroepithelium (40% occurrence). Red circle at 69% marks a hemorrhage reflecting diaminobenzidine (DAB) pigment oxidation by endogenous peroxidase in red blood cells. (C and D) At the MB midline, SHH expression is weaker where ZIKV infection is heavy qualitatively (C) and quantitatively (D). PTCH1 , a gene downstream of SHH, is also weaker in expression (C). Magnified views are shown in the flanking red panels. (E) PAX6+ pixel count was not changed by ZIKV infection. (F) The Pax6+ population develops closer to the midline in ZIKV-infected embryos, possibly due to reduced SHH signal ( SHH pixels) (one-tailed mixed effects SAS model). Left and right sides of each embryo are plotted independently. (G) Convex hull plot of PAX6 lateral edge against number of SHH pixels show ZIKV data in the lower left quadrant of the plot (MANOVA). (H and I) Although the NKX2.2 population does not show a statistically significant difference in the position of the domain, the convex hull plot shows the cloud of ZIKV data in the lower left quadrant. ***p < 0.001; **p < 0.01; *p < 0.05; n.s., not significant. Error bars represent mean ± SEM. AP, alar plate; A, anterior; BP, basal plate; D, dorsal; FP, floor plate; Hypo, hypothalamus; L, lateral; MHB, MB-HB boundary; PreT, pretectum; Pth, prethalamus; P, posterior; RP, roof plate; Th, thalamus. See also , and .

Article Snippet: A multivariate ANOVA (MANOVA) test was used in SAS for SHH -PAX6 and SHH -NKX2.2 convex hull plot quantification.

Techniques: Infection, Injection, Staining, Labeling, Expressing, One-tailed Test