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    MathWorks Inc boxplot function
    Boxplot Function, supplied by MathWorks 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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    Results of two‐way analysis of variance comparing the relative serum abundance of individual metabolites across four groups, stratified by treatment status and brain atrophy progression as determined from magnetic resonance imaging over the 2 year follow‐up period: placebo progressors (dark red, N = 31), placebo stable (light red, N = 31), B vitamin progressors (non‐responders; dark blue, N = 14), and B vitamin stable (responders; light blue, N = 51). The figure presents follow‐up metabolite levels (adjusted for baseline) to enable interpretation of comparisons across treatment arms (placebo vs. B vitamins), progression status (progressors vs. stable), and within‐group treatment response (responders vs. <t>non‐responders).Tukey</t> post hoc analysis was performed, with results summarized in Table in supporting information. Significant and marginal p values are displayed above the graphs; metabolites without displayed p values were not associated with any significant pairwise comparisons. A, α‐ketoglutaric acid (treatment p = 0.03; atrophy p = 0.32); (B) glutamic acid (treatment p = 0.06; atrophy p = 0.53); (C) succinic acid (treatment p = 0.03; atrophy p = 0.19); (D) glucose (treatment p = 0.12; atrophy p = 0.11); (E) malic acid (treatment p = 0.03; atrophy p = 0.48); (F) N ‐acetylglutamate (treatment p = 0.20; atrophy p = 0.51); (G) glutaric acid (treatment p = 0.10; atrophy p = 0.36); (H) lactic acid (treatment p = 0.06; atrophy p = 0.41); (I) pyruvic acid (treatment p = 0.17; atrophy p = 0.66); (J) α‐ketobutyric (treatment p = 0.03; atrophy p = 0.17); (K) quinolinic acid (treatment p = 0.04; atrophy p = 0.15); (L) glutamine (treatment effect p = 0.19; atrophy effect p = 0.38). One outlier was excluded from the graphical representation to enhance data clarity. This exclusion did not significantly impact the results. VB, vitamin B.
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    Results of two‐way analysis of variance comparing the relative serum abundance of individual metabolites across four groups, stratified by treatment status and brain atrophy progression as determined from magnetic resonance imaging over the 2 year follow‐up period: placebo progressors (dark red, N = 31), placebo stable (light red, N = 31), B vitamin progressors (non‐responders; dark blue, N = 14), and B vitamin stable (responders; light blue, N = 51). The figure presents follow‐up metabolite levels (adjusted for baseline) to enable interpretation of comparisons across treatment arms (placebo vs. B vitamins), progression status (progressors vs. stable), and within‐group treatment response (responders vs. <t>non‐responders).Tukey</t> post hoc analysis was performed, with results summarized in Table in supporting information. Significant and marginal p values are displayed above the graphs; metabolites without displayed p values were not associated with any significant pairwise comparisons. A, α‐ketoglutaric acid (treatment p = 0.03; atrophy p = 0.32); (B) glutamic acid (treatment p = 0.06; atrophy p = 0.53); (C) succinic acid (treatment p = 0.03; atrophy p = 0.19); (D) glucose (treatment p = 0.12; atrophy p = 0.11); (E) malic acid (treatment p = 0.03; atrophy p = 0.48); (F) N ‐acetylglutamate (treatment p = 0.20; atrophy p = 0.51); (G) glutaric acid (treatment p = 0.10; atrophy p = 0.36); (H) lactic acid (treatment p = 0.06; atrophy p = 0.41); (I) pyruvic acid (treatment p = 0.17; atrophy p = 0.66); (J) α‐ketobutyric (treatment p = 0.03; atrophy p = 0.17); (K) quinolinic acid (treatment p = 0.04; atrophy p = 0.15); (L) glutamine (treatment effect p = 0.19; atrophy effect p = 0.38). One outlier was excluded from the graphical representation to enhance data clarity. This exclusion did not significantly impact the results. VB, vitamin B.
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    Results of two‐way analysis of variance comparing the relative serum abundance of individual metabolites across four groups, stratified by treatment status and brain atrophy progression as determined from magnetic resonance imaging over the 2 year follow‐up period: placebo progressors (dark red, N = 31), placebo stable (light red, N = 31), B vitamin progressors (non‐responders; dark blue, N = 14), and B vitamin stable (responders; light blue, N = 51). The figure presents follow‐up metabolite levels (adjusted for baseline) to enable interpretation of comparisons across treatment arms (placebo vs. B vitamins), progression status (progressors vs. stable), and within‐group treatment response (responders vs. <t>non‐responders).Tukey</t> post hoc analysis was performed, with results summarized in Table in supporting information. Significant and marginal p values are displayed above the graphs; metabolites without displayed p values were not associated with any significant pairwise comparisons. A, α‐ketoglutaric acid (treatment p = 0.03; atrophy p = 0.32); (B) glutamic acid (treatment p = 0.06; atrophy p = 0.53); (C) succinic acid (treatment p = 0.03; atrophy p = 0.19); (D) glucose (treatment p = 0.12; atrophy p = 0.11); (E) malic acid (treatment p = 0.03; atrophy p = 0.48); (F) N ‐acetylglutamate (treatment p = 0.20; atrophy p = 0.51); (G) glutaric acid (treatment p = 0.10; atrophy p = 0.36); (H) lactic acid (treatment p = 0.06; atrophy p = 0.41); (I) pyruvic acid (treatment p = 0.17; atrophy p = 0.66); (J) α‐ketobutyric (treatment p = 0.03; atrophy p = 0.17); (K) quinolinic acid (treatment p = 0.04; atrophy p = 0.15); (L) glutamine (treatment effect p = 0.19; atrophy effect p = 0.38). One outlier was excluded from the graphical representation to enhance data clarity. This exclusion did not significantly impact the results. VB, vitamin B.
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    Results of two‐way analysis of variance comparing the relative serum abundance of individual metabolites across four groups, stratified by treatment status and brain atrophy progression as determined from magnetic resonance imaging over the 2 year follow‐up period: placebo progressors (dark red, N = 31), placebo stable (light red, N = 31), B vitamin progressors (non‐responders; dark blue, N = 14), and B vitamin stable (responders; light blue, N = 51). The figure presents follow‐up metabolite levels (adjusted for baseline) to enable interpretation of comparisons across treatment arms (placebo vs. B vitamins), progression status (progressors vs. stable), and within‐group treatment response (responders vs. <t>non‐responders).Tukey</t> post hoc analysis was performed, with results summarized in Table in supporting information. Significant and marginal p values are displayed above the graphs; metabolites without displayed p values were not associated with any significant pairwise comparisons. A, α‐ketoglutaric acid (treatment p = 0.03; atrophy p = 0.32); (B) glutamic acid (treatment p = 0.06; atrophy p = 0.53); (C) succinic acid (treatment p = 0.03; atrophy p = 0.19); (D) glucose (treatment p = 0.12; atrophy p = 0.11); (E) malic acid (treatment p = 0.03; atrophy p = 0.48); (F) N ‐acetylglutamate (treatment p = 0.20; atrophy p = 0.51); (G) glutaric acid (treatment p = 0.10; atrophy p = 0.36); (H) lactic acid (treatment p = 0.06; atrophy p = 0.41); (I) pyruvic acid (treatment p = 0.17; atrophy p = 0.66); (J) α‐ketobutyric (treatment p = 0.03; atrophy p = 0.17); (K) quinolinic acid (treatment p = 0.04; atrophy p = 0.15); (L) glutamine (treatment effect p = 0.19; atrophy effect p = 0.38). One outlier was excluded from the graphical representation to enhance data clarity. This exclusion did not significantly impact the results. VB, vitamin B.
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    MathWorks Inc boxplot function in matlab software r2015a
    ( a ) Droplet-like DPICs were initially formed by mixing 20 μM ATTO565-labeled p53 4M ΔTAD with 0.6 μM ATTO488-labeled Random DNA and incubating for 30 minutes at room temperature. Subsequently, Cy5-labeled p21 DNA was added at varying concentrations and incubated for an additional 120 minutes: (i) 0.15 μM; (ii) 0.225 μM; (iii) 0.3 μM; (iv) 0.45 μM; (v) 0.6 μM; (vi) 0.75 μM; (vii) 0.9 μM. Representative fluorescence images at incubation time t = 4-min and t = 120-min are shown. Independent in vitro droplet experiments were repeated three times (n = 3). ( b ) <t>Boxplot</t> of characteristic time constants τ 1 and τ 2 for p21 DNA concentrations ranging from 0.3 to 0.9 μM. N indicates the number of individual biomolecule-rich condensates analyzed under each condition. In box plots, the black line denotes the median, box edges represent the 25 th and 75 th percentiles, whiskers indicate the range excluding outliers, and outliers are shown as individual dots (•). ( c ) Phase diagram showing normalized fluorescence intensities of ATTO565-labeled p53 4M ΔTAD and ATTO488-labeled Random DNA at the center of condensates under increasing concentrations of p21 DNA (0.3, 0.45, 0.6, and 0.75 μM). Values are shown both before p21 DNA addition and at the end of Stage I. Control experiments in which Random DNA was used in place of p21 DNA are also included. Error bars indicate mean ± s.d. Green dashed lines mark the estimated binodal boundary, and purple dashed lines represent the spinodal boundary, as confirmed by our phase-field model (see – ).
    Boxplot Function In Matlab Software R2015a, supplied by MathWorks 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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    OriginLab corp boxplots generated with
    ( a ) Droplet-like DPICs were initially formed by mixing 20 μM ATTO565-labeled p53 4M ΔTAD with 0.6 μM ATTO488-labeled Random DNA and incubating for 30 minutes at room temperature. Subsequently, Cy5-labeled p21 DNA was added at varying concentrations and incubated for an additional 120 minutes: (i) 0.15 μM; (ii) 0.225 μM; (iii) 0.3 μM; (iv) 0.45 μM; (v) 0.6 μM; (vi) 0.75 μM; (vii) 0.9 μM. Representative fluorescence images at incubation time t = 4-min and t = 120-min are shown. Independent in vitro droplet experiments were repeated three times (n = 3). ( b ) <t>Boxplot</t> of characteristic time constants τ 1 and τ 2 for p21 DNA concentrations ranging from 0.3 to 0.9 μM. N indicates the number of individual biomolecule-rich condensates analyzed under each condition. In box plots, the black line denotes the median, box edges represent the 25 th and 75 th percentiles, whiskers indicate the range excluding outliers, and outliers are shown as individual dots (•). ( c ) Phase diagram showing normalized fluorescence intensities of ATTO565-labeled p53 4M ΔTAD and ATTO488-labeled Random DNA at the center of condensates under increasing concentrations of p21 DNA (0.3, 0.45, 0.6, and 0.75 μM). Values are shown both before p21 DNA addition and at the end of Stage I. Control experiments in which Random DNA was used in place of p21 DNA are also included. Error bars indicate mean ± s.d. Green dashed lines mark the estimated binodal boundary, and purple dashed lines represent the spinodal boundary, as confirmed by our phase-field model (see – ).
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    MathWorks Inc boxplot
    ( a ) Droplet-like DPICs were initially formed by mixing 20 μM ATTO565-labeled p53 4M ΔTAD with 0.6 μM ATTO488-labeled Random DNA and incubating for 30 minutes at room temperature. Subsequently, Cy5-labeled p21 DNA was added at varying concentrations and incubated for an additional 120 minutes: (i) 0.15 μM; (ii) 0.225 μM; (iii) 0.3 μM; (iv) 0.45 μM; (v) 0.6 μM; (vi) 0.75 μM; (vii) 0.9 μM. Representative fluorescence images at incubation time t = 4-min and t = 120-min are shown. Independent in vitro droplet experiments were repeated three times (n = 3). ( b ) <t>Boxplot</t> of characteristic time constants τ 1 and τ 2 for p21 DNA concentrations ranging from 0.3 to 0.9 μM. N indicates the number of individual biomolecule-rich condensates analyzed under each condition. In box plots, the black line denotes the median, box edges represent the 25 th and 75 th percentiles, whiskers indicate the range excluding outliers, and outliers are shown as individual dots (•). ( c ) Phase diagram showing normalized fluorescence intensities of ATTO565-labeled p53 4M ΔTAD and ATTO488-labeled Random DNA at the center of condensates under increasing concentrations of p21 DNA (0.3, 0.45, 0.6, and 0.75 μM). Values are shown both before p21 DNA addition and at the end of Stage I. Control experiments in which Random DNA was used in place of p21 DNA are also included. Error bars indicate mean ± s.d. Green dashed lines mark the estimated binodal boundary, and purple dashed lines represent the spinodal boundary, as confirmed by our phase-field model (see – ).
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    GraphPad Software Inc boxplots generated with graphpad prism 8
    (a) <t>Boxplots</t> of selected DAMFs across all experimental conditions. Accumulation values (3 replicates per experimental condition) were normalised and expressed as a percentage in relation to the sample exhibiting the highest accumulation value (i.e., 100%). Asterisks on the boxplots indicate significance of pairwise t ‐test between MP treatments and the control in the specific condition (i.e., H 2 O as control, CP elicitation and B.cinerea infection). (b) Putative chemical structures and molecular formulas of annotated DAMFs.
    Boxplots Generated With Graphpad Prism 8, 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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    Image Search Results


    Results of two‐way analysis of variance comparing the relative serum abundance of individual metabolites across four groups, stratified by treatment status and brain atrophy progression as determined from magnetic resonance imaging over the 2 year follow‐up period: placebo progressors (dark red, N = 31), placebo stable (light red, N = 31), B vitamin progressors (non‐responders; dark blue, N = 14), and B vitamin stable (responders; light blue, N = 51). The figure presents follow‐up metabolite levels (adjusted for baseline) to enable interpretation of comparisons across treatment arms (placebo vs. B vitamins), progression status (progressors vs. stable), and within‐group treatment response (responders vs. non‐responders).Tukey post hoc analysis was performed, with results summarized in Table in supporting information. Significant and marginal p values are displayed above the graphs; metabolites without displayed p values were not associated with any significant pairwise comparisons. A, α‐ketoglutaric acid (treatment p = 0.03; atrophy p = 0.32); (B) glutamic acid (treatment p = 0.06; atrophy p = 0.53); (C) succinic acid (treatment p = 0.03; atrophy p = 0.19); (D) glucose (treatment p = 0.12; atrophy p = 0.11); (E) malic acid (treatment p = 0.03; atrophy p = 0.48); (F) N ‐acetylglutamate (treatment p = 0.20; atrophy p = 0.51); (G) glutaric acid (treatment p = 0.10; atrophy p = 0.36); (H) lactic acid (treatment p = 0.06; atrophy p = 0.41); (I) pyruvic acid (treatment p = 0.17; atrophy p = 0.66); (J) α‐ketobutyric (treatment p = 0.03; atrophy p = 0.17); (K) quinolinic acid (treatment p = 0.04; atrophy p = 0.15); (L) glutamine (treatment effect p = 0.19; atrophy effect p = 0.38). One outlier was excluded from the graphical representation to enhance data clarity. This exclusion did not significantly impact the results. VB, vitamin B.

    Journal: Alzheimer's & Dementia

    Article Title: Role of B vitamins in modulating homocysteine and metabolic pathways linked to brain atrophy: Metabolomics insights from the VITACOG trial

    doi: 10.1002/alz.70521

    Figure Lengend Snippet: Results of two‐way analysis of variance comparing the relative serum abundance of individual metabolites across four groups, stratified by treatment status and brain atrophy progression as determined from magnetic resonance imaging over the 2 year follow‐up period: placebo progressors (dark red, N = 31), placebo stable (light red, N = 31), B vitamin progressors (non‐responders; dark blue, N = 14), and B vitamin stable (responders; light blue, N = 51). The figure presents follow‐up metabolite levels (adjusted for baseline) to enable interpretation of comparisons across treatment arms (placebo vs. B vitamins), progression status (progressors vs. stable), and within‐group treatment response (responders vs. non‐responders).Tukey post hoc analysis was performed, with results summarized in Table in supporting information. Significant and marginal p values are displayed above the graphs; metabolites without displayed p values were not associated with any significant pairwise comparisons. A, α‐ketoglutaric acid (treatment p = 0.03; atrophy p = 0.32); (B) glutamic acid (treatment p = 0.06; atrophy p = 0.53); (C) succinic acid (treatment p = 0.03; atrophy p = 0.19); (D) glucose (treatment p = 0.12; atrophy p = 0.11); (E) malic acid (treatment p = 0.03; atrophy p = 0.48); (F) N ‐acetylglutamate (treatment p = 0.20; atrophy p = 0.51); (G) glutaric acid (treatment p = 0.10; atrophy p = 0.36); (H) lactic acid (treatment p = 0.06; atrophy p = 0.41); (I) pyruvic acid (treatment p = 0.17; atrophy p = 0.66); (J) α‐ketobutyric (treatment p = 0.03; atrophy p = 0.17); (K) quinolinic acid (treatment p = 0.04; atrophy p = 0.15); (L) glutamine (treatment effect p = 0.19; atrophy effect p = 0.38). One outlier was excluded from the graphical representation to enhance data clarity. This exclusion did not significantly impact the results. VB, vitamin B.

    Article Snippet: Quantitative data are shown as Tukey boxplots (GraphPad Prism 10 software), with whiskers extending to the furthest values within 1.5 times the interquartile range (IQR).

    Techniques: Magnetic Resonance Imaging

    ( a ) Droplet-like DPICs were initially formed by mixing 20 μM ATTO565-labeled p53 4M ΔTAD with 0.6 μM ATTO488-labeled Random DNA and incubating for 30 minutes at room temperature. Subsequently, Cy5-labeled p21 DNA was added at varying concentrations and incubated for an additional 120 minutes: (i) 0.15 μM; (ii) 0.225 μM; (iii) 0.3 μM; (iv) 0.45 μM; (v) 0.6 μM; (vi) 0.75 μM; (vii) 0.9 μM. Representative fluorescence images at incubation time t = 4-min and t = 120-min are shown. Independent in vitro droplet experiments were repeated three times (n = 3). ( b ) Boxplot of characteristic time constants τ 1 and τ 2 for p21 DNA concentrations ranging from 0.3 to 0.9 μM. N indicates the number of individual biomolecule-rich condensates analyzed under each condition. In box plots, the black line denotes the median, box edges represent the 25 th and 75 th percentiles, whiskers indicate the range excluding outliers, and outliers are shown as individual dots (•). ( c ) Phase diagram showing normalized fluorescence intensities of ATTO565-labeled p53 4M ΔTAD and ATTO488-labeled Random DNA at the center of condensates under increasing concentrations of p21 DNA (0.3, 0.45, 0.6, and 0.75 μM). Values are shown both before p21 DNA addition and at the end of Stage I. Control experiments in which Random DNA was used in place of p21 DNA are also included. Error bars indicate mean ± s.d. Green dashed lines mark the estimated binodal boundary, and purple dashed lines represent the spinodal boundary, as confirmed by our phase-field model (see – ).

    Journal: bioRxiv

    Article Title: Hollow condensates emerge from gelation-induced spinodal decomposition

    doi: 10.1101/2025.06.25.661497

    Figure Lengend Snippet: ( a ) Droplet-like DPICs were initially formed by mixing 20 μM ATTO565-labeled p53 4M ΔTAD with 0.6 μM ATTO488-labeled Random DNA and incubating for 30 minutes at room temperature. Subsequently, Cy5-labeled p21 DNA was added at varying concentrations and incubated for an additional 120 minutes: (i) 0.15 μM; (ii) 0.225 μM; (iii) 0.3 μM; (iv) 0.45 μM; (v) 0.6 μM; (vi) 0.75 μM; (vii) 0.9 μM. Representative fluorescence images at incubation time t = 4-min and t = 120-min are shown. Independent in vitro droplet experiments were repeated three times (n = 3). ( b ) Boxplot of characteristic time constants τ 1 and τ 2 for p21 DNA concentrations ranging from 0.3 to 0.9 μM. N indicates the number of individual biomolecule-rich condensates analyzed under each condition. In box plots, the black line denotes the median, box edges represent the 25 th and 75 th percentiles, whiskers indicate the range excluding outliers, and outliers are shown as individual dots (•). ( c ) Phase diagram showing normalized fluorescence intensities of ATTO565-labeled p53 4M ΔTAD and ATTO488-labeled Random DNA at the center of condensates under increasing concentrations of p21 DNA (0.3, 0.45, 0.6, and 0.75 μM). Values are shown both before p21 DNA addition and at the end of Stage I. Control experiments in which Random DNA was used in place of p21 DNA are also included. Error bars indicate mean ± s.d. Green dashed lines mark the estimated binodal boundary, and purple dashed lines represent the spinodal boundary, as confirmed by our phase-field model (see – ).

    Article Snippet: The function of “boxplot” in MATLAB software (R2015a, 64-bit, February 12, 2015) was used to plot the boxplots in , , and Supplementary Fig. 3.

    Techniques: Labeling, Incubation, Fluorescence, In Vitro, Control

    (a) Boxplots of selected DAMFs across all experimental conditions. Accumulation values (3 replicates per experimental condition) were normalised and expressed as a percentage in relation to the sample exhibiting the highest accumulation value (i.e., 100%). Asterisks on the boxplots indicate significance of pairwise t ‐test between MP treatments and the control in the specific condition (i.e., H 2 O as control, CP elicitation and B.cinerea infection). (b) Putative chemical structures and molecular formulas of annotated DAMFs.

    Journal: Physiologia Plantarum

    Article Title: Microplastics in the Soil at Sub‐Toxic Concentrations Cause Metabolic Changes Decreasing Fungal Pathogen Susceptibility in Arabidopsis thaliana

    doi: 10.1111/ppl.70312

    Figure Lengend Snippet: (a) Boxplots of selected DAMFs across all experimental conditions. Accumulation values (3 replicates per experimental condition) were normalised and expressed as a percentage in relation to the sample exhibiting the highest accumulation value (i.e., 100%). Asterisks on the boxplots indicate significance of pairwise t ‐test between MP treatments and the control in the specific condition (i.e., H 2 O as control, CP elicitation and B.cinerea infection). (b) Putative chemical structures and molecular formulas of annotated DAMFs.

    Article Snippet: The shape and size of the MFs within the networks were determined based on the previously calculated log 2 FC from the pairwise comparison of PET 0.5% vs. C. From these networks, a selected set of annotated features from key metabolic categories was identified, and their patterns were illustrated using boxplots generated with GraphPad Prism 8.

    Techniques: Control, Infection