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ATCC u 87 mg human brain immortalized cell line
Distribution of acetyl-CoA isotopomers following [U–13C]glucose and [U–13C]glutamine incubation with an isogenic gain-of-function mutation (R132H) in the metabolic enzyme Isocitrate Dehydrogenase 1 <t>(IDH1).</t> <t>U-87</t> MG human brain immortalized cell line, either wild-type or harboring the IDH1-R132H mutation, was incubated with [U– 13 C]glucose or [U– 13 C]glutamine for 20 and 72 h. The x axis represents the different acetyl-CoA isotopomers, showing the number of incorporated 13C atoms, with their origins within the acetyl-CoA structure noted in parentheses (see also ). The y axis indicates the percentage abundance of each isotopomer population, with n = 5 per condition after correction for natural abundance (refer to the Methods section 4.6.3). Statistical significance was assessed using Student’s t-test, with p -values represented as follows: ns: not significant ( p > 0.05); ∗: p ≤ 0.05. Because the M+2 labeling of the acetyl group may arise from either oxidative decarboxylation of pyruvate or reductive carboxylation of citrate, these two indistinguishable sources are jointly annotated as M+2 (Pyr/Cit). Abbreviations: Pyr/Cit, pyruvate- or citrate-derived M+2 (indistinguishable by MRM transitions); Gly, Glycine; For, Formate; R5P, Ribose-5-phosphate. # in x-axis indicates isotopomers with the same number of labeled carbon atoms incorporated, but with different origin and final moiety.
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Distribution of acetyl-CoA isotopomers following [U–13C]glucose and [U–13C]glutamine incubation with an isogenic gain-of-function mutation (R132H) in the metabolic enzyme Isocitrate Dehydrogenase 1 <t>(IDH1).</t> <t>U-87</t> MG human brain immortalized cell line, either wild-type or harboring the IDH1-R132H mutation, was incubated with [U– 13 C]glucose or [U– 13 C]glutamine for 20 and 72 h. The x axis represents the different acetyl-CoA isotopomers, showing the number of incorporated 13C atoms, with their origins within the acetyl-CoA structure noted in parentheses (see also ). The y axis indicates the percentage abundance of each isotopomer population, with n = 5 per condition after correction for natural abundance (refer to the Methods section 4.6.3). Statistical significance was assessed using Student’s t-test, with p -values represented as follows: ns: not significant ( p > 0.05); ∗: p ≤ 0.05. Because the M+2 labeling of the acetyl group may arise from either oxidative decarboxylation of pyruvate or reductive carboxylation of citrate, these two indistinguishable sources are jointly annotated as M+2 (Pyr/Cit). Abbreviations: Pyr/Cit, pyruvate- or citrate-derived M+2 (indistinguishable by MRM transitions); Gly, Glycine; For, Formate; R5P, Ribose-5-phosphate. # in x-axis indicates isotopomers with the same number of labeled carbon atoms incorporated, but with different origin and final moiety.
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Distribution of acetyl-CoA isotopomers following [U–13C]glucose and [U–13C]glutamine incubation with an isogenic gain-of-function mutation (R132H) in the metabolic enzyme Isocitrate Dehydrogenase 1 <t>(IDH1).</t> <t>U-87</t> MG human brain immortalized cell line, either wild-type or harboring the IDH1-R132H mutation, was incubated with [U– 13 C]glucose or [U– 13 C]glutamine for 20 and 72 h. The x axis represents the different acetyl-CoA isotopomers, showing the number of incorporated 13C atoms, with their origins within the acetyl-CoA structure noted in parentheses (see also ). The y axis indicates the percentage abundance of each isotopomer population, with n = 5 per condition after correction for natural abundance (refer to the Methods section 4.6.3). Statistical significance was assessed using Student’s t-test, with p -values represented as follows: ns: not significant ( p > 0.05); ∗: p ≤ 0.05. Because the M+2 labeling of the acetyl group may arise from either oxidative decarboxylation of pyruvate or reductive carboxylation of citrate, these two indistinguishable sources are jointly annotated as M+2 (Pyr/Cit). Abbreviations: Pyr/Cit, pyruvate- or citrate-derived M+2 (indistinguishable by MRM transitions); Gly, Glycine; For, Formate; R5P, Ribose-5-phosphate. # in x-axis indicates isotopomers with the same number of labeled carbon atoms incorporated, but with different origin and final moiety.
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Distribution of acetyl-CoA isotopomers following [U–13C]glucose and [U–13C]glutamine incubation with an isogenic gain-of-function mutation (R132H) in the metabolic enzyme Isocitrate Dehydrogenase 1 <t>(IDH1).</t> <t>U-87</t> MG human brain immortalized cell line, either wild-type or harboring the IDH1-R132H mutation, was incubated with [U– 13 C]glucose or [U– 13 C]glutamine for 20 and 72 h. The x axis represents the different acetyl-CoA isotopomers, showing the number of incorporated 13C atoms, with their origins within the acetyl-CoA structure noted in parentheses (see also ). The y axis indicates the percentage abundance of each isotopomer population, with n = 5 per condition after correction for natural abundance (refer to the Methods section 4.6.3). Statistical significance was assessed using Student’s t-test, with p -values represented as follows: ns: not significant ( p > 0.05); ∗: p ≤ 0.05. Because the M+2 labeling of the acetyl group may arise from either oxidative decarboxylation of pyruvate or reductive carboxylation of citrate, these two indistinguishable sources are jointly annotated as M+2 (Pyr/Cit). Abbreviations: Pyr/Cit, pyruvate- or citrate-derived M+2 (indistinguishable by MRM transitions); Gly, Glycine; For, Formate; R5P, Ribose-5-phosphate. # in x-axis indicates isotopomers with the same number of labeled carbon atoms incorporated, but with different origin and final moiety.
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Elabscience Biotechnology rat bdnf elisa kit
Persistent hyperalgesia in the RPP model (A and B) Paw withdrawal latency (A) and 50% paw withdrawal threshold (B) of each rat ( n = 3–6). (C) Representative histological images of DRG from T10-S4 by H&E staining. Arrow, Schwann cell; ∗, nuclei; #, cytoplasm. Scale bars, 50 μm and 25 μm. (D and E) Representative IHC images (D) and quantification (E) of <t>BDNF</t> in the DRG from T10-S4. Brown DAB staining indicates BDNF immunopositivity. The staining intensity was semi-quantitatively scored as follows: (1) weak, (2) moderate, and (3) intense. Scale bars, 50 μm. ( n = 3 biological replicates per group). (F) Serum BDNF level on days 12 and 24 of RPP modeling ( n = 3). Data are presented as the mean ± SD; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, two-way ANOVA (A and B) or one-way ANOVA (E and F).
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Persistent hyperalgesia in the RPP model (A and B) Paw withdrawal latency (A) and 50% paw withdrawal threshold (B) of each rat ( n = 3–6). (C) Representative histological images of DRG from T10-S4 by H&E staining. Arrow, Schwann cell; ∗, nuclei; #, cytoplasm. Scale bars, 50 μm and 25 μm. (D and E) Representative IHC images (D) and quantification (E) of <t>BDNF</t> in the DRG from T10-S4. Brown DAB staining indicates BDNF immunopositivity. The staining intensity was semi-quantitatively scored as follows: (1) weak, (2) moderate, and (3) intense. Scale bars, 50 μm. ( n = 3 biological replicates per group). (F) Serum BDNF level on days 12 and 24 of RPP modeling ( n = 3). Data are presented as the mean ± SD; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, two-way ANOVA (A and B) or one-way ANOVA (E and F).
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BW of offspring rats from 1-day to 16-week-old (A). Heart damages in offspring at the age of 8 and 16 weeks, including the ratios (B) LVW/BW, (C) HW/BW and (D) NT-proBNP level in serum. Concentration of Ang II in (E) left ventricle and (F) serum. Data are presented as mean ± SD. n=10 in each group (A-C) and n=7 in each group (D-F). *P<0.05, **P<0.01 vs Con. BW, body weight; HW, heart weight; LVW, left ventricular weight; <t>NT-proBNP,</t> <t>N-terminal</t> pro-brain natriuretic peptide; Ang II, angiotensin II; Con, control; LPS, lipopolysaccharide.
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BW of offspring rats from 1-day to 16-week-old (A). Heart damages in offspring at the age of 8 and 16 weeks, including the ratios (B) LVW/BW, (C) HW/BW and (D) NT-proBNP level in serum. Concentration of Ang II in (E) left ventricle and (F) serum. Data are presented as mean ± SD. n=10 in each group (A-C) and n=7 in each group (D-F). *P<0.05, **P<0.01 vs Con. BW, body weight; HW, heart weight; LVW, left ventricular weight; <t>NT-proBNP,</t> <t>N-terminal</t> pro-brain natriuretic peptide; Ang II, angiotensin II; Con, control; LPS, lipopolysaccharide.
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BW of offspring rats from 1-day to 16-week-old (A). Heart damages in offspring at the age of 8 and 16 weeks, including the ratios (B) LVW/BW, (C) HW/BW and (D) NT-proBNP level in serum. Concentration of Ang II in (E) left ventricle and (F) serum. Data are presented as mean ± SD. n=10 in each group (A-C) and n=7 in each group (D-F). *P<0.05, **P<0.01 vs Con. BW, body weight; HW, heart weight; LVW, left ventricular weight; <t>NT-proBNP,</t> <t>N-terminal</t> pro-brain natriuretic peptide; Ang II, angiotensin II; Con, control; LPS, lipopolysaccharide.
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BW of offspring rats from 1-day to 16-week-old (A). Heart damages in offspring at the age of 8 and 16 weeks, including the ratios (B) LVW/BW, (C) HW/BW and (D) NT-proBNP level in serum. Concentration of Ang II in (E) left ventricle and (F) serum. Data are presented as mean ± SD. n=10 in each group (A-C) and n=7 in each group (D-F). *P<0.05, **P<0.01 vs Con. BW, body weight; HW, heart weight; LVW, left ventricular weight; <t>NT-proBNP,</t> <t>N-terminal</t> pro-brain natriuretic peptide; Ang II, angiotensin II; Con, control; LPS, lipopolysaccharide.
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Image Search Results


Distribution of acetyl-CoA isotopomers following [U–13C]glucose and [U–13C]glutamine incubation with an isogenic gain-of-function mutation (R132H) in the metabolic enzyme Isocitrate Dehydrogenase 1 (IDH1). U-87 MG human brain immortalized cell line, either wild-type or harboring the IDH1-R132H mutation, was incubated with [U– 13 C]glucose or [U– 13 C]glutamine for 20 and 72 h. The x axis represents the different acetyl-CoA isotopomers, showing the number of incorporated 13C atoms, with their origins within the acetyl-CoA structure noted in parentheses (see also ). The y axis indicates the percentage abundance of each isotopomer population, with n = 5 per condition after correction for natural abundance (refer to the Methods section 4.6.3). Statistical significance was assessed using Student’s t-test, with p -values represented as follows: ns: not significant ( p > 0.05); ∗: p ≤ 0.05. Because the M+2 labeling of the acetyl group may arise from either oxidative decarboxylation of pyruvate or reductive carboxylation of citrate, these two indistinguishable sources are jointly annotated as M+2 (Pyr/Cit). Abbreviations: Pyr/Cit, pyruvate- or citrate-derived M+2 (indistinguishable by MRM transitions); Gly, Glycine; For, Formate; R5P, Ribose-5-phosphate. # in x-axis indicates isotopomers with the same number of labeled carbon atoms incorporated, but with different origin and final moiety.

Journal: Molecular Metabolism

Article Title: A targeted metabolomic method to detect epigenetically relevant metabolites

doi: 10.1016/j.molmet.2026.102342

Figure Lengend Snippet: Distribution of acetyl-CoA isotopomers following [U–13C]glucose and [U–13C]glutamine incubation with an isogenic gain-of-function mutation (R132H) in the metabolic enzyme Isocitrate Dehydrogenase 1 (IDH1). U-87 MG human brain immortalized cell line, either wild-type or harboring the IDH1-R132H mutation, was incubated with [U– 13 C]glucose or [U– 13 C]glutamine for 20 and 72 h. The x axis represents the different acetyl-CoA isotopomers, showing the number of incorporated 13C atoms, with their origins within the acetyl-CoA structure noted in parentheses (see also ). The y axis indicates the percentage abundance of each isotopomer population, with n = 5 per condition after correction for natural abundance (refer to the Methods section 4.6.3). Statistical significance was assessed using Student’s t-test, with p -values represented as follows: ns: not significant ( p > 0.05); ∗: p ≤ 0.05. Because the M+2 labeling of the acetyl group may arise from either oxidative decarboxylation of pyruvate or reductive carboxylation of citrate, these two indistinguishable sources are jointly annotated as M+2 (Pyr/Cit). Abbreviations: Pyr/Cit, pyruvate- or citrate-derived M+2 (indistinguishable by MRM transitions); Gly, Glycine; For, Formate; R5P, Ribose-5-phosphate. # in x-axis indicates isotopomers with the same number of labeled carbon atoms incorporated, but with different origin and final moiety.

Article Snippet: The U-87 MG human brain immortalized cell line (ATCC® HTB-14TM) (wild type) or the R132H (IDH1 mutant) were plated at a density of 1 million cells per T75 plate in 10 mL complete ATCC Eagle’s Minimum Essential Medium (EMEM) 30-2003 medium, with 5 replicates per condition.

Techniques: Incubation, Mutagenesis, Labeling, Derivative Assay

Persistent hyperalgesia in the RPP model (A and B) Paw withdrawal latency (A) and 50% paw withdrawal threshold (B) of each rat ( n = 3–6). (C) Representative histological images of DRG from T10-S4 by H&E staining. Arrow, Schwann cell; ∗, nuclei; #, cytoplasm. Scale bars, 50 μm and 25 μm. (D and E) Representative IHC images (D) and quantification (E) of BDNF in the DRG from T10-S4. Brown DAB staining indicates BDNF immunopositivity. The staining intensity was semi-quantitatively scored as follows: (1) weak, (2) moderate, and (3) intense. Scale bars, 50 μm. ( n = 3 biological replicates per group). (F) Serum BDNF level on days 12 and 24 of RPP modeling ( n = 3). Data are presented as the mean ± SD; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, two-way ANOVA (A and B) or one-way ANOVA (E and F).

Journal: iScience

Article Title: A pharmacological rat model of recurrent pelvic pain exhibiting hyperalgesia and depression-like behaviors

doi: 10.1016/j.isci.2026.115059

Figure Lengend Snippet: Persistent hyperalgesia in the RPP model (A and B) Paw withdrawal latency (A) and 50% paw withdrawal threshold (B) of each rat ( n = 3–6). (C) Representative histological images of DRG from T10-S4 by H&E staining. Arrow, Schwann cell; ∗, nuclei; #, cytoplasm. Scale bars, 50 μm and 25 μm. (D and E) Representative IHC images (D) and quantification (E) of BDNF in the DRG from T10-S4. Brown DAB staining indicates BDNF immunopositivity. The staining intensity was semi-quantitatively scored as follows: (1) weak, (2) moderate, and (3) intense. Scale bars, 50 μm. ( n = 3 biological replicates per group). (F) Serum BDNF level on days 12 and 24 of RPP modeling ( n = 3). Data are presented as the mean ± SD; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, two-way ANOVA (A and B) or one-way ANOVA (E and F).

Article Snippet: Rat BDNF ELISA Kit , Elabscience , Cat# E-EL-R1235.

Techniques: Staining

Comorbid depression-like behavior in the RPP model (A and B) Serum BDNF (A) and 5-HT (B) levels in the RPP model ( n = 6). (C and D) Sucrose preference ratio (C) and immobility time (D) in the RPP model ( n = 8). Data are presented as the mean ± SD; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, paired t test (A and B) or two-way ANOVA (C and D).

Journal: iScience

Article Title: A pharmacological rat model of recurrent pelvic pain exhibiting hyperalgesia and depression-like behaviors

doi: 10.1016/j.isci.2026.115059

Figure Lengend Snippet: Comorbid depression-like behavior in the RPP model (A and B) Serum BDNF (A) and 5-HT (B) levels in the RPP model ( n = 6). (C and D) Sucrose preference ratio (C) and immobility time (D) in the RPP model ( n = 8). Data are presented as the mean ± SD; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, paired t test (A and B) or two-way ANOVA (C and D).

Article Snippet: Rat BDNF ELISA Kit , Elabscience , Cat# E-EL-R1235.

Techniques:

BW of offspring rats from 1-day to 16-week-old (A). Heart damages in offspring at the age of 8 and 16 weeks, including the ratios (B) LVW/BW, (C) HW/BW and (D) NT-proBNP level in serum. Concentration of Ang II in (E) left ventricle and (F) serum. Data are presented as mean ± SD. n=10 in each group (A-C) and n=7 in each group (D-F). *P<0.05, **P<0.01 vs Con. BW, body weight; HW, heart weight; LVW, left ventricular weight; NT-proBNP, N-terminal pro-brain natriuretic peptide; Ang II, angiotensin II; Con, control; LPS, lipopolysaccharide.

Journal: Molecular Medicine Reports

Article Title: Prenatal lipopolysaccharide exposure programs cardiac fibrosis via dysregulating of connexin 43 in offspring rats

doi: 10.3892/mmr.2026.13830

Figure Lengend Snippet: BW of offspring rats from 1-day to 16-week-old (A). Heart damages in offspring at the age of 8 and 16 weeks, including the ratios (B) LVW/BW, (C) HW/BW and (D) NT-proBNP level in serum. Concentration of Ang II in (E) left ventricle and (F) serum. Data are presented as mean ± SD. n=10 in each group (A-C) and n=7 in each group (D-F). *P<0.05, **P<0.01 vs Con. BW, body weight; HW, heart weight; LVW, left ventricular weight; NT-proBNP, N-terminal pro-brain natriuretic peptide; Ang II, angiotensin II; Con, control; LPS, lipopolysaccharide.

Article Snippet: Serum concentrations of N-terminal pro-BNP (NT-proBNP; cat. no. E-EL-R3023) and Ang II, along with myocardial tissue levels of Ang II (cat. no. E-EL-R1430c), were quantified using commercial ELISA kits (Elabscience Biotechnology Co., Ltd.) following manufacturer protocols.

Techniques: Concentration Assay, Control