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anova analysis followed by post hoc tukey–kramer test  (GraphPad Software Inc)


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    Structured Review

    GraphPad Software Inc anova analysis followed by post hoc tukey–kramer test
    Bone loss and cortical porosity in Sp7 R342C knock-in mice. a R342C mutation does not affect femur length of 8-week-old mice. b H&E-stained paraffin-embedded sections from the tibia show no growth plate morphological differences between Sp7 R342C/R342C mice and wild-type littermates. Scale bars are shown in the images. c μCT images from the femoral metaphysis and diaphysis of 8-week-old mice show bone loss and increased cortical porosity in Sp7 R342C/R342C mice compared to wild-type littermates. Scale bars are shown in the images. d Quantification of metaphysis parameters. e Quantification of midshaft diaphysis. BMD: bone mineral density, BV/TV: bone volume fraction, Ct. TMD: cortical bone tissue mineral density, Ct. porosity: cortical porosity. Two-way <t>ANOVA</t> analysis followed by post <t>hoc</t> <t>Tukey–Kramer</t> test was performed (* P < 0.05; ** P < 0.01, *** P < 0.001, **** P < 0.000 1)
    Anova Analysis Followed By Post Hoc Tukey–Kramer 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
    https://www.bioz.com/result/anova analysis followed by post hoc tukey–kramer test/product/GraphPad Software Inc
    Average 90 stars, based on 1 article reviews
    anova analysis followed by post hoc tukey–kramer test - by Bioz Stars, 2026-06
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    Images

    1) Product Images from "Osteoclast-independent osteocyte dendrite defects in mice bearing the osteogenesis imperfecta-causing Sp7 R342C mutation"

    Article Title: Osteoclast-independent osteocyte dendrite defects in mice bearing the osteogenesis imperfecta-causing Sp7 R342C mutation

    Journal: Bone Research

    doi: 10.1038/s41413-025-00440-1

    Bone loss and cortical porosity in Sp7 R342C knock-in mice. a R342C mutation does not affect femur length of 8-week-old mice. b H&E-stained paraffin-embedded sections from the tibia show no growth plate morphological differences between Sp7 R342C/R342C mice and wild-type littermates. Scale bars are shown in the images. c μCT images from the femoral metaphysis and diaphysis of 8-week-old mice show bone loss and increased cortical porosity in Sp7 R342C/R342C mice compared to wild-type littermates. Scale bars are shown in the images. d Quantification of metaphysis parameters. e Quantification of midshaft diaphysis. BMD: bone mineral density, BV/TV: bone volume fraction, Ct. TMD: cortical bone tissue mineral density, Ct. porosity: cortical porosity. Two-way ANOVA analysis followed by post hoc Tukey–Kramer test was performed (* P < 0.05; ** P < 0.01, *** P < 0.001, **** P < 0.000 1)
    Figure Legend Snippet: Bone loss and cortical porosity in Sp7 R342C knock-in mice. a R342C mutation does not affect femur length of 8-week-old mice. b H&E-stained paraffin-embedded sections from the tibia show no growth plate morphological differences between Sp7 R342C/R342C mice and wild-type littermates. Scale bars are shown in the images. c μCT images from the femoral metaphysis and diaphysis of 8-week-old mice show bone loss and increased cortical porosity in Sp7 R342C/R342C mice compared to wild-type littermates. Scale bars are shown in the images. d Quantification of metaphysis parameters. e Quantification of midshaft diaphysis. BMD: bone mineral density, BV/TV: bone volume fraction, Ct. TMD: cortical bone tissue mineral density, Ct. porosity: cortical porosity. Two-way ANOVA analysis followed by post hoc Tukey–Kramer test was performed (* P < 0.05; ** P < 0.01, *** P < 0.001, **** P < 0.000 1)

    Techniques Used: Knock-In, Mutagenesis, Staining

    Osteocyte dendrite defects caused by R342C mutation are independent of osteoclast activity. a Schematic illustration of OPG-Fc injection. b Serum CTX-1 level is significantly reduced in OPG-Fc injected wild-type and R342C mutant mice. c TRAP staining of decalcified, paraffin-embedded tibia sections reveals decreased osteoclasts in both wild-type and Sp7 R342C mice following OPG-Fc treatment. Bottom left: low magnification image showing the staining of the whole section. The region with red dashed lines is zoomed in. Right: Quantification of TRAP + multinucleated osteoclasts per bone area (N.Oc/BA) in the cortical bone with Image J. d Silver nitrate staining shows no difference in the canaliculi number per cell between OPG-Fc and vehicle-treated Sp7 R342C mice. Bottom right: low magnification image showing the staining of the whole section. The region with red dashed lines is zoomed in. e Phalloidin staining shows no difference in the dendrite filament density between OPG-Fc and vehicle-treated Sp7 R342C mice. Two-way ANOVA analysis followed by post hoc Tukey–Kramer test was performed (* P < 0.05; ** P < 0.01, *** P < 0.001, **** P < 0.000 1). Scale bars are shown in the images
    Figure Legend Snippet: Osteocyte dendrite defects caused by R342C mutation are independent of osteoclast activity. a Schematic illustration of OPG-Fc injection. b Serum CTX-1 level is significantly reduced in OPG-Fc injected wild-type and R342C mutant mice. c TRAP staining of decalcified, paraffin-embedded tibia sections reveals decreased osteoclasts in both wild-type and Sp7 R342C mice following OPG-Fc treatment. Bottom left: low magnification image showing the staining of the whole section. The region with red dashed lines is zoomed in. Right: Quantification of TRAP + multinucleated osteoclasts per bone area (N.Oc/BA) in the cortical bone with Image J. d Silver nitrate staining shows no difference in the canaliculi number per cell between OPG-Fc and vehicle-treated Sp7 R342C mice. Bottom right: low magnification image showing the staining of the whole section. The region with red dashed lines is zoomed in. e Phalloidin staining shows no difference in the dendrite filament density between OPG-Fc and vehicle-treated Sp7 R342C mice. Two-way ANOVA analysis followed by post hoc Tukey–Kramer test was performed (* P < 0.05; ** P < 0.01, *** P < 0.001, **** P < 0.000 1). Scale bars are shown in the images

    Techniques Used: Mutagenesis, Activity Assay, Injection, Staining



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    Bone loss and cortical porosity in Sp7 R342C knock-in mice. a R342C mutation does not affect femur length of 8-week-old mice. b H&E-stained paraffin-embedded sections from the tibia show no growth plate morphological differences between Sp7 R342C/R342C mice and wild-type littermates. Scale bars are shown in the images. c μCT images from the femoral metaphysis and diaphysis of 8-week-old mice show bone loss and increased cortical porosity in Sp7 R342C/R342C mice compared to wild-type littermates. Scale bars are shown in the images. d Quantification of metaphysis parameters. e Quantification of midshaft diaphysis. BMD: bone mineral density, BV/TV: bone volume fraction, Ct. TMD: cortical bone tissue mineral density, Ct. porosity: cortical porosity. Two-way <t>ANOVA</t> analysis followed by post <t>hoc</t> <t>Tukey–Kramer</t> test was performed (* P < 0.05; ** P < 0.01, *** P < 0.001, **** P < 0.000 1)
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    Image Search Results


    Bone loss and cortical porosity in Sp7 R342C knock-in mice. a R342C mutation does not affect femur length of 8-week-old mice. b H&E-stained paraffin-embedded sections from the tibia show no growth plate morphological differences between Sp7 R342C/R342C mice and wild-type littermates. Scale bars are shown in the images. c μCT images from the femoral metaphysis and diaphysis of 8-week-old mice show bone loss and increased cortical porosity in Sp7 R342C/R342C mice compared to wild-type littermates. Scale bars are shown in the images. d Quantification of metaphysis parameters. e Quantification of midshaft diaphysis. BMD: bone mineral density, BV/TV: bone volume fraction, Ct. TMD: cortical bone tissue mineral density, Ct. porosity: cortical porosity. Two-way ANOVA analysis followed by post hoc Tukey–Kramer test was performed (* P < 0.05; ** P < 0.01, *** P < 0.001, **** P < 0.000 1)

    Journal: Bone Research

    Article Title: Osteoclast-independent osteocyte dendrite defects in mice bearing the osteogenesis imperfecta-causing Sp7 R342C mutation

    doi: 10.1038/s41413-025-00440-1

    Figure Lengend Snippet: Bone loss and cortical porosity in Sp7 R342C knock-in mice. a R342C mutation does not affect femur length of 8-week-old mice. b H&E-stained paraffin-embedded sections from the tibia show no growth plate morphological differences between Sp7 R342C/R342C mice and wild-type littermates. Scale bars are shown in the images. c μCT images from the femoral metaphysis and diaphysis of 8-week-old mice show bone loss and increased cortical porosity in Sp7 R342C/R342C mice compared to wild-type littermates. Scale bars are shown in the images. d Quantification of metaphysis parameters. e Quantification of midshaft diaphysis. BMD: bone mineral density, BV/TV: bone volume fraction, Ct. TMD: cortical bone tissue mineral density, Ct. porosity: cortical porosity. Two-way ANOVA analysis followed by post hoc Tukey–Kramer test was performed (* P < 0.05; ** P < 0.01, *** P < 0.001, **** P < 0.000 1)

    Article Snippet: When more than two experimental groups were present, ANOVA analysis followed by post hoc Tukey–Kramer test was performed (GraphPad Prism 9).

    Techniques: Knock-In, Mutagenesis, Staining

    Osteocyte dendrite defects caused by R342C mutation are independent of osteoclast activity. a Schematic illustration of OPG-Fc injection. b Serum CTX-1 level is significantly reduced in OPG-Fc injected wild-type and R342C mutant mice. c TRAP staining of decalcified, paraffin-embedded tibia sections reveals decreased osteoclasts in both wild-type and Sp7 R342C mice following OPG-Fc treatment. Bottom left: low magnification image showing the staining of the whole section. The region with red dashed lines is zoomed in. Right: Quantification of TRAP + multinucleated osteoclasts per bone area (N.Oc/BA) in the cortical bone with Image J. d Silver nitrate staining shows no difference in the canaliculi number per cell between OPG-Fc and vehicle-treated Sp7 R342C mice. Bottom right: low magnification image showing the staining of the whole section. The region with red dashed lines is zoomed in. e Phalloidin staining shows no difference in the dendrite filament density between OPG-Fc and vehicle-treated Sp7 R342C mice. Two-way ANOVA analysis followed by post hoc Tukey–Kramer test was performed (* P < 0.05; ** P < 0.01, *** P < 0.001, **** P < 0.000 1). Scale bars are shown in the images

    Journal: Bone Research

    Article Title: Osteoclast-independent osteocyte dendrite defects in mice bearing the osteogenesis imperfecta-causing Sp7 R342C mutation

    doi: 10.1038/s41413-025-00440-1

    Figure Lengend Snippet: Osteocyte dendrite defects caused by R342C mutation are independent of osteoclast activity. a Schematic illustration of OPG-Fc injection. b Serum CTX-1 level is significantly reduced in OPG-Fc injected wild-type and R342C mutant mice. c TRAP staining of decalcified, paraffin-embedded tibia sections reveals decreased osteoclasts in both wild-type and Sp7 R342C mice following OPG-Fc treatment. Bottom left: low magnification image showing the staining of the whole section. The region with red dashed lines is zoomed in. Right: Quantification of TRAP + multinucleated osteoclasts per bone area (N.Oc/BA) in the cortical bone with Image J. d Silver nitrate staining shows no difference in the canaliculi number per cell between OPG-Fc and vehicle-treated Sp7 R342C mice. Bottom right: low magnification image showing the staining of the whole section. The region with red dashed lines is zoomed in. e Phalloidin staining shows no difference in the dendrite filament density between OPG-Fc and vehicle-treated Sp7 R342C mice. Two-way ANOVA analysis followed by post hoc Tukey–Kramer test was performed (* P < 0.05; ** P < 0.01, *** P < 0.001, **** P < 0.000 1). Scale bars are shown in the images

    Article Snippet: When more than two experimental groups were present, ANOVA analysis followed by post hoc Tukey–Kramer test was performed (GraphPad Prism 9).

    Techniques: Mutagenesis, Activity Assay, Injection, Staining