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boxplots tukey method graphpad prism  (GraphPad Software Inc)


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    GraphPad Software Inc boxplots tukey method graphpad prism
    Boxplots Tukey Method Graphpad Prism, 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/boxplots/pm31665348-112-1-4
    Average 90 stars, based on 1 article reviews
    boxplots tukey method graphpad prism - by Bioz Stars, 2026-11
    90/100 stars

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    Article Title: Sex differences in the diagnosis latency of Parkinson's disease in Latin America.
    Article Snippet: All analyses were performed using R v4.0.0 and boxplots were created in GraphPad Prism v9.4.0 (GraphPad Software, Inc., San Diego, CA).

    Article Title: Teixobactin: A Resistance-Evading Antibiotic for Treating Anthrax.
    Article Snippet: The antimicrobial resistance (AMR) crisis has been associated with millions of deaths.. Of particular concern is the threat of bioweapons, exemplified by anthrax.. Introduction of novel antibiotics helps mitigate AMR, but does not address the threat of bioweapons with engineered resistance.

    Article Title: Downregulation of Aging-Associated Gene SUCLG1 Marks the Aggressiveness of Liver Disease
    Article Snippet: Boxplots were created using GraphPad Prism (version 10.2.3).

    Generated:

    Article Title: Targeting ACAT1 for Precision Chemo‐Immunoprevention in Lung Cancer
    Article Snippet: Lung cancer (LC) is a leading cause of cancer-related deathworldwide, and altered cholesterol metabolism is a hallmark of cancer cells.. Acyl-CoA:cholesterol acyltransferase 1(ACAT1), or Sterol O-acyltransferase 1 (SOAT1), isa key cholesterol esterification enzyme.. Its overexpression promotes tumorprogression by accumulating cholesterol esters.

    Article Title: Diffusion-Weighted MRI and Human Papillomavirus (HPV) Status in Oropharyngeal Cancer
    Article Snippet: Analyses have been performed using SAS software (version 9.4 of the SAS System for Windows). .. Boxplots were generated using Graphpad (version 10). ..

    Article Title: Multiomic analysis of lactylation and mitochondria-related genes in hepatocellular carcinoma identified MRPL3 as a new prognostic biomarker
    Article Snippet: .. Visualizations, including scatter plots, boxplots, and Kaplan-Meier survival curves, were generated using GraphPad Prism version 9 (GraphPad Software, San Diego, CA, USA) to enhance the clarity and reproducibility of the results. ..

    Article Title: Alleviation of sepsis-induced lung and liver injury by polysaccharides from Tetrastigma hemsleyanum Diels et Gilg via suppression of TLR4/NF-κB/COX-2 pathway and modulation of immune checkpoint molecules.
    Article Snippet: Sepsis, a common clinical complication, leads to multi-organ damage due to systemic infection and currently lacks effective therapeutic drugs.. Polysaccharide derived from Tetrastigma hemsleyanum Diels et Gilg (TH), abbreviated as THP, is a water-soluble component extracted from TH, exhibiting anti-inflammatory and immunomodulatory properties.. This study aims to investigate the effects and mechanisms of THP in sepsis.



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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.
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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. 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