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boxplots tukey  (GraphPad Software Inc)


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    GraphPad Software Inc boxplots tukey
    Boxplots Tukey, 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
    https://www.bioz.com/product/tukey+boxplot/tukey+box+and+whisker+plots/pmc04746072-145-0-6
    Average 90 stars, based on 1 article reviews
    boxplots tukey - by Bioz Stars, 2026-11
    90/100 stars

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    Whisker Assay:

    Article Title: Reversal of insulin resistance in people with obesity by lifestyle-induced weight loss does not impact the proportion of circulating 12α-hydroxylated bile acids.
    Article Snippet: Plasma levels of total cholesterol were determined using commercially available diagnostic system solutions (DiaSys Diagnostic Systems). .. Data are presented as Tukey box and whisker plots, produced using GraphPad Prism 8 (GraphPad Software). ..

    Article Title: Fungal microtubule organizing centers are evolutionarily unstable structures.
    Article Snippet: For most Eukaryotic species the requirements of cilia formation dictate the structure of microtubule organizing centers (MTOCs).. In this study we find that loss of cilia corresponds to loss of evolutionary stability for fungal MTOCs.. We used iterative search algorithms to identify proteins homologous to those found in Saccharomyces cerevisiae, and Schizosaccharomyces pombe MTOCs, and calculated site-specific rates of change for those proteins that were broadly phylogenetically distributed.

    Produced:

    Article Title: Reversal of insulin resistance in people with obesity by lifestyle-induced weight loss does not impact the proportion of circulating 12α-hydroxylated bile acids.
    Article Snippet: Plasma levels of total cholesterol were determined using commercially available diagnostic system solutions (DiaSys Diagnostic Systems). .. Data are presented as Tukey box and whisker plots, produced using GraphPad Prism 8 (GraphPad Software). ..

    other:

    Article Title: Testing of rapid evaporative mass spectrometry for histological tissue classification and molecular diagnostics in a multi-site study
    Article Snippet: The relative abundance of selected ions-of-interest is presented as box-and-whisker plots using the method of Tukey (Graphpad PRISM).

    Article Title: Imaging with [89Zr]Zr-DFO-SC16.56 anti-DLL3 antibody in patients with high-grade neuroendocrine tumours of the lung and prostate: a phase 1/2, first-in-human trial
    Article Snippet: Department of Medicine (S Tendler MD, N J Choudhury MD, Prof M J Morris MD, Prof C M Rudin MD, J T Poirier PhD), Department of Radiology (M P Dunphy DO, M Agee MD, Prof H Schoder MD, Prof S K Lyashchenko PhD, Prof L Bodei MD, Prof J S Lewis PhD), Department of Medical Physics (J O’Donoghue PhD, A Kesner PhD, Prof A Kirov PhD), Department of Pathology (R G Aly MD, M K Baine MD, Prof N Rekhtman MD), Department of Epidemiology and Biostatistics (A Mauguen PhD), and Molecular Pharmacology Program (Prof J S Lewis, J T Poirier), Memorial Sloan Kettering Cancer Center, New York, NY, USA; Department of Radiology (M Agee), Department of Medicine (Prof M J Morris, Prof C M Rudin), and Department of Pharmacology (Prof J S Lewis, Prof C M Rudin), Weill Cornell Medicine, New York, NY, USA; Department of Nuclear Medicine, School of Medicine and Health, Technical University of Munich, Munich, Germany (Prof W A Weber MD); Perlmutter Cancer Center, New York University Langone Health, New York, NY, USA (J T Poirier) Imaging with [89Zr]Zr-DFO-SC16.56 anti-DLL3 antibody in patients with high-grade neuroendocrine tumours of the lung and prostate: a phase 1/2, first-in-human trial

    Article Title: Testing of rapid evaporative mass spectrometry for histological tissue classification and molecular diagnostics in a multi-site study.
    Article Snippet: The relative abundance of selected ions-of-interest is presented as box-andwhisker plots using the method of Tukey (Graphpad PRISM).

    Generated:

    Article Title: Fungal microtubule organizing centers are evolutionarily unstable structures.
    Article Snippet: For most Eukaryotic species the requirements of cilia formation dictate the structure of microtubule organizing centers (MTOCs).. In this study we find that loss of cilia corresponds to loss of evolutionary stability for fungal MTOCs.. We used iterative search algorithms to identify proteins homologous to those found in Saccharomyces cerevisiae, and Schizosaccharomyces pombe MTOCs, and calculated site-specific rates of change for those proteins that were broadly phylogenetically distributed.



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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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    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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    boxplots tukey  (GraphPad Software Inc)
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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.
    Boxplots Tukey, 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