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p1np  (Novus Biologicals)


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    Novus Biologicals p1np
    P1np, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 93/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p1np/product/Novus Biologicals
    Average 93 stars, based on 8 article reviews
    p1np - by Bioz Stars, 2026-05
    93/100 stars

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    Effects of neonatally administered zingerone (40 mg/kg/day) and adolescent alcohol (1 g/kg) on plasma concentrations of (A) BALP, (B) OC, and (C) <t>P1NP</t> as bone health markers. Data were presented as mean ± standard deviation. BALP, OC, and P1NP levels were elevated in the alcohol‐treated groups with or without zingerone. Statistically significant if ∗ p ≤ 0.05, ∗∗ p ≤ 0.01, ∗∗∗ p ≤ 0.001, ∗∗∗∗ p ≤ 0.0001 between treatment groups. Group 1 ( C ) received no treatment in the neonatal phase and during adolescence; Group 2 ( Z + W ) was treated with zingerone (40 mg/kg) in the neonatal phase and water during adolescence; Group 3 ( A + A ) treated with alcohol during both the neonatal and adolescent phase (1 g/kg ethanol); Group 4 ( Z + A ) treated with zingerone in the neonatal phase and alcohol in adolescence; Group 5 (ZA + A ) treated with a combination of zingerone–alcohol in the neonatal phase, followed by alcohol in adolescence. A —alcohol; C —control; W —water; Z —zingerone; ZA—zingerone‐alcohol; BALP—bone‐specific alkaline phosphatase, OC—osteocalcin, P1NP—procollagen Type 1 N‐terminal propeptide.
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    CIH induces bone loss and growth retardation in young mice. Three‐week‐old male or female wild‐type (WT) mice were subjected to CIH or normoxia condition for four weeks. A–E) Representative micro‐CT images of both male and female mice were shown in (A) with quantitative analysis of BV/TV (B), Tb. N (C), Tb. Th (D) and Tb. Sp (E). F,G) The serum concentrations of <t>P1NP</t> and CTX of both male and female mice were measured by ELISA. General view of the femurs was shown in H), and the length of the femurs were measured in I). J,K) H&E staining was performed to show the general morphology of the femoral bone and growth plate. RZ, resting zone; PZ, proliferating zone; HZ, hypertrophic zone; GP, growth plate. The fold change of GP length, RZ length, PZ length, and HZ length was quantified in L–O). n = 5‐6 mice Data were represented as mean ± SD. p values were determined by one‐way ANOVA.
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    CIH induces bone loss and growth retardation in young mice. Three‐week‐old male or female wild‐type (WT) mice were subjected to CIH or normoxia condition for four weeks. A–E) Representative micro‐CT images of both male and female mice were shown in (A) with quantitative analysis of BV/TV (B), Tb. N (C), Tb. Th (D) and Tb. Sp (E). F,G) The serum concentrations of <t>P1NP</t> and CTX of both male and female mice were measured by ELISA. General view of the femurs was shown in H), and the length of the femurs were measured in I). J,K) H&E staining was performed to show the general morphology of the femoral bone and growth plate. RZ, resting zone; PZ, proliferating zone; HZ, hypertrophic zone; GP, growth plate. The fold change of GP length, RZ length, PZ length, and HZ length was quantified in L–O). n = 5‐6 mice Data were represented as mean ± SD. p values were determined by one‐way ANOVA.
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    CIH induces bone loss and growth retardation in young mice. Three‐week‐old male or female wild‐type (WT) mice were subjected to CIH or normoxia condition for four weeks. A–E) Representative micro‐CT images of both male and female mice were shown in (A) with quantitative analysis of BV/TV (B), Tb. N (C), Tb. Th (D) and Tb. Sp (E). F,G) The serum concentrations of <t>P1NP</t> and CTX of both male and female mice were measured by ELISA. General view of the femurs was shown in H), and the length of the femurs were measured in I). J,K) H&E staining was performed to show the general morphology of the femoral bone and growth plate. RZ, resting zone; PZ, proliferating zone; HZ, hypertrophic zone; GP, growth plate. The fold change of GP length, RZ length, PZ length, and HZ length was quantified in L–O). n = 5‐6 mice Data were represented as mean ± SD. p values were determined by one‐way ANOVA.
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    Immunodiagnostic Systems p1np (bone formation)
    CIH induces bone loss and growth retardation in young mice. Three‐week‐old male or female wild‐type (WT) mice were subjected to CIH or normoxia condition for four weeks. A–E) Representative micro‐CT images of both male and female mice were shown in (A) with quantitative analysis of BV/TV (B), Tb. N (C), Tb. Th (D) and Tb. Sp (E). F,G) The serum concentrations of <t>P1NP</t> and CTX of both male and female mice were measured by ELISA. General view of the femurs was shown in H), and the length of the femurs were measured in I). J,K) H&E staining was performed to show the general morphology of the femoral bone and growth plate. RZ, resting zone; PZ, proliferating zone; HZ, hypertrophic zone; GP, growth plate. The fold change of GP length, RZ length, PZ length, and HZ length was quantified in L–O). n = 5‐6 mice Data were represented as mean ± SD. p values were determined by one‐way ANOVA.
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    Image Search Results


    Effects of neonatally administered zingerone (40 mg/kg/day) and adolescent alcohol (1 g/kg) on plasma concentrations of (A) BALP, (B) OC, and (C) P1NP as bone health markers. Data were presented as mean ± standard deviation. BALP, OC, and P1NP levels were elevated in the alcohol‐treated groups with or without zingerone. Statistically significant if ∗ p ≤ 0.05, ∗∗ p ≤ 0.01, ∗∗∗ p ≤ 0.001, ∗∗∗∗ p ≤ 0.0001 between treatment groups. Group 1 ( C ) received no treatment in the neonatal phase and during adolescence; Group 2 ( Z + W ) was treated with zingerone (40 mg/kg) in the neonatal phase and water during adolescence; Group 3 ( A + A ) treated with alcohol during both the neonatal and adolescent phase (1 g/kg ethanol); Group 4 ( Z + A ) treated with zingerone in the neonatal phase and alcohol in adolescence; Group 5 (ZA + A ) treated with a combination of zingerone–alcohol in the neonatal phase, followed by alcohol in adolescence. A —alcohol; C —control; W —water; Z —zingerone; ZA—zingerone‐alcohol; BALP—bone‐specific alkaline phosphatase, OC—osteocalcin, P1NP—procollagen Type 1 N‐terminal propeptide.

    Journal: BioMed Research International

    Article Title: The Effects of Neonatal Zingerone Administration and Adolescent Alcohol Exposure on Bone Health Markers and Morphometry in Male Sprague–Dawley Rats

    doi: 10.1155/bmri/7060593

    Figure Lengend Snippet: Effects of neonatally administered zingerone (40 mg/kg/day) and adolescent alcohol (1 g/kg) on plasma concentrations of (A) BALP, (B) OC, and (C) P1NP as bone health markers. Data were presented as mean ± standard deviation. BALP, OC, and P1NP levels were elevated in the alcohol‐treated groups with or without zingerone. Statistically significant if ∗ p ≤ 0.05, ∗∗ p ≤ 0.01, ∗∗∗ p ≤ 0.001, ∗∗∗∗ p ≤ 0.0001 between treatment groups. Group 1 ( C ) received no treatment in the neonatal phase and during adolescence; Group 2 ( Z + W ) was treated with zingerone (40 mg/kg) in the neonatal phase and water during adolescence; Group 3 ( A + A ) treated with alcohol during both the neonatal and adolescent phase (1 g/kg ethanol); Group 4 ( Z + A ) treated with zingerone in the neonatal phase and alcohol in adolescence; Group 5 (ZA + A ) treated with a combination of zingerone–alcohol in the neonatal phase, followed by alcohol in adolescence. A —alcohol; C —control; W —water; Z —zingerone; ZA—zingerone‐alcohol; BALP—bone‐specific alkaline phosphatase, OC—osteocalcin, P1NP—procollagen Type 1 N‐terminal propeptide.

    Article Snippet: The plasma activity of BALP (Catalog No. ER0761, FineTest, Wuhan, China), OC (Catalog No. ER1205, FineTest, Wuhan, China), and P1NP (Catalog No. E‐EL‐R1414, Elabscience, Houston, Texas, United States) were determined in rat plasma as described by the manufacturer′s instructions.

    Techniques: Clinical Proteomics, Standard Deviation, Control

    CIH induces bone loss and growth retardation in young mice. Three‐week‐old male or female wild‐type (WT) mice were subjected to CIH or normoxia condition for four weeks. A–E) Representative micro‐CT images of both male and female mice were shown in (A) with quantitative analysis of BV/TV (B), Tb. N (C), Tb. Th (D) and Tb. Sp (E). F,G) The serum concentrations of P1NP and CTX of both male and female mice were measured by ELISA. General view of the femurs was shown in H), and the length of the femurs were measured in I). J,K) H&E staining was performed to show the general morphology of the femoral bone and growth plate. RZ, resting zone; PZ, proliferating zone; HZ, hypertrophic zone; GP, growth plate. The fold change of GP length, RZ length, PZ length, and HZ length was quantified in L–O). n = 5‐6 mice Data were represented as mean ± SD. p values were determined by one‐way ANOVA.

    Journal: Advanced Science

    Article Title: Epigenetic Targeting of Senescent Cells Prevents the Deleterious Effects of Obstructive Sleep Apnea on Growing Skeleton

    doi: 10.1002/advs.202502697

    Figure Lengend Snippet: CIH induces bone loss and growth retardation in young mice. Three‐week‐old male or female wild‐type (WT) mice were subjected to CIH or normoxia condition for four weeks. A–E) Representative micro‐CT images of both male and female mice were shown in (A) with quantitative analysis of BV/TV (B), Tb. N (C), Tb. Th (D) and Tb. Sp (E). F,G) The serum concentrations of P1NP and CTX of both male and female mice were measured by ELISA. General view of the femurs was shown in H), and the length of the femurs were measured in I). J,K) H&E staining was performed to show the general morphology of the femoral bone and growth plate. RZ, resting zone; PZ, proliferating zone; HZ, hypertrophic zone; GP, growth plate. The fold change of GP length, RZ length, PZ length, and HZ length was quantified in L–O). n = 5‐6 mice Data were represented as mean ± SD. p values were determined by one‐way ANOVA.

    Article Snippet: N‐terminal propeptide of type I procollagen (P1NP) was measured using P1NP ELISA kit (E‐EL‐M0233, Elabscience) and β‐CTx ELISA kit (E‐EL‐M0372, Elabscience) as described by the company.

    Techniques: Micro-CT, Enzyme-linked Immunosorbent Assay, Staining

    Elevated H3K27me3 alleviates CIH‐induced osteoprogenitor senescence and bone loss. Three‐week‐old female UTX iKO mice and WT (UTX floxed) mice were subjected to CIH or normoxia condition for four weeks. A,B) Representative co‐immunofluorescence staining of OSX and H3K27me3 in distal femur section in (A) and analysis of cell number per mm 2 tissue area (N. OSX + H3K27me3 + cells/ Ar) in (B). C,D) Representative images of SA‐βGal staining in the distal femur section in (C) and analysis of cell number per mm 2 tissue area (N. SA‐βGal + cells/ Ar) in (D). E,F) Representative co‐immunofluorescence staining of OSX and γ H2A.X in the distal femur section in (E) and analysis of cell number per mm 2 tissue area (N. OSX + γ H2A.X + cells/ Ar) in (F). G,H) Representative immunofluorescence staining of OCN in distal femur section in (G) and analysis of cell number per mm 2 tissue area (N. OCN + cells/ Ar) in (H). Representative micro‐CT images were shown in I) with quantitative analysis of BV/TV J), Tb. N K), Tb. Th L) and Tb. Sp M). N,O) The concentrations of P1NP and CTX were measured by ELISA. n = 5‐6 mice. Data were represented as mean ± SD. p ‐values were determined by one‐way ANOVA.

    Journal: Advanced Science

    Article Title: Epigenetic Targeting of Senescent Cells Prevents the Deleterious Effects of Obstructive Sleep Apnea on Growing Skeleton

    doi: 10.1002/advs.202502697

    Figure Lengend Snippet: Elevated H3K27me3 alleviates CIH‐induced osteoprogenitor senescence and bone loss. Three‐week‐old female UTX iKO mice and WT (UTX floxed) mice were subjected to CIH or normoxia condition for four weeks. A,B) Representative co‐immunofluorescence staining of OSX and H3K27me3 in distal femur section in (A) and analysis of cell number per mm 2 tissue area (N. OSX + H3K27me3 + cells/ Ar) in (B). C,D) Representative images of SA‐βGal staining in the distal femur section in (C) and analysis of cell number per mm 2 tissue area (N. SA‐βGal + cells/ Ar) in (D). E,F) Representative co‐immunofluorescence staining of OSX and γ H2A.X in the distal femur section in (E) and analysis of cell number per mm 2 tissue area (N. OSX + γ H2A.X + cells/ Ar) in (F). G,H) Representative immunofluorescence staining of OCN in distal femur section in (G) and analysis of cell number per mm 2 tissue area (N. OCN + cells/ Ar) in (H). Representative micro‐CT images were shown in I) with quantitative analysis of BV/TV J), Tb. N K), Tb. Th L) and Tb. Sp M). N,O) The concentrations of P1NP and CTX were measured by ELISA. n = 5‐6 mice. Data were represented as mean ± SD. p ‐values were determined by one‐way ANOVA.

    Article Snippet: N‐terminal propeptide of type I procollagen (P1NP) was measured using P1NP ELISA kit (E‐EL‐M0233, Elabscience) and β‐CTx ELISA kit (E‐EL‐M0372, Elabscience) as described by the company.

    Techniques: Immunofluorescence, Staining, Micro-CT, Enzyme-linked Immunosorbent Assay

    GSK‐J4 rescues CIH‐impaired bone growth and mineral acquisition. Three‐week‐old female WT mice were subjected to CIH or normoxia condition for four weeks, and at the same time, treated with GSK‐J4 at 10 mg kg −1 per day or vehicle. Representative micro‐CT images were shown in A) with quantitative analysis of BV/TV B), Tb. N C), Tb. Th D) and Tb. Sp E). F,G) The concentrations of P1NP and CTX were measured by ELISA. General view of the femurs was shown in H), and the length of the femurs were measured in I). J,K) H&E staining was performed to show tissue morphology. RZ, resting zone; PZ, proliferating zone; HZ, hypertrophic zone; GP, growth plate. The fold change of GP length, RZ length, PZ length, and HZ length were quantified in L–O). n = 5–6 mice. Data were represented as mean ± SD. p ‐values were determined by one‐way ANOVA.

    Journal: Advanced Science

    Article Title: Epigenetic Targeting of Senescent Cells Prevents the Deleterious Effects of Obstructive Sleep Apnea on Growing Skeleton

    doi: 10.1002/advs.202502697

    Figure Lengend Snippet: GSK‐J4 rescues CIH‐impaired bone growth and mineral acquisition. Three‐week‐old female WT mice were subjected to CIH or normoxia condition for four weeks, and at the same time, treated with GSK‐J4 at 10 mg kg −1 per day or vehicle. Representative micro‐CT images were shown in A) with quantitative analysis of BV/TV B), Tb. N C), Tb. Th D) and Tb. Sp E). F,G) The concentrations of P1NP and CTX were measured by ELISA. General view of the femurs was shown in H), and the length of the femurs were measured in I). J,K) H&E staining was performed to show tissue morphology. RZ, resting zone; PZ, proliferating zone; HZ, hypertrophic zone; GP, growth plate. The fold change of GP length, RZ length, PZ length, and HZ length were quantified in L–O). n = 5–6 mice. Data were represented as mean ± SD. p ‐values were determined by one‐way ANOVA.

    Article Snippet: N‐terminal propeptide of type I procollagen (P1NP) was measured using P1NP ELISA kit (E‐EL‐M0233, Elabscience) and β‐CTx ELISA kit (E‐EL‐M0372, Elabscience) as described by the company.

    Techniques: Micro-CT, Enzyme-linked Immunosorbent Assay, Staining