human c4 elisa kit  (Elabscience Biotechnology)

Journal: Brain : a journal of neurology

Article Title: Extracellular vesicle biomarkers for complement dysfunction in schizophrenia.

doi: 10.1093/brain/awad341

Figure Lengend Snippet: Figure 2 Characteristics of EV-derived complement DEPs in patients with schizophrenia. (A) Comparison of C3 expression between patients with schizophrenia (SZ) and healthy controls (HC). *P = 0.039, Cohen's d = 0.78. (B) Comparison of C4A expression. ***P < 0.001, Cohen's d = 1.57. (C) Comparison of C4B expression. ***P < 0.001, Cohen's d = 1.24. (D) Comparison of C4BPA expression. **P = 0.0029, Cohen's d = 1.17. (E) Comparison of C4BPB expression. *P = 0.0129, Cohen's d = 0.88. (F) Comparison of PROS1 expression. ***P < 0.001, Cohen's d = 1.20. Although the levels of body mass index (BMI) and diastolic blood pressure (DBP) were significantly different between patients and controls, they did not demonstrate significant correlations with the levels of extracellular vesicle (EV)-derived complement associated components within each independent group. Hence, they were not adjusted as covariates. (G and H) The heat map of correlation analysis between EV-derived non-differentially expressed proteins (DEPs) and DEPs in the complement network and the disease course. Significant correlation was defined as absolute R values ≥0.4 and P-value <0.05 [−log10 (P) > 1.3]. Pearson or Spearman correlation was used as appropriate. (I) Box plot of the absolute R value of correlation analysis. **P = 0.0015, Cohen's d = 1.67. (J–L) Expression levels of NOE1, KIRR3 and LMO4 mRNA in different tissues; their mRNA expression were mostly enriched in brain. Data were extracted from the Human Protein Atlas. (M) Heat map of linear correlation results between the EV-derived complement DEPs and brain enriched proteins of NOE1, KIRR3 and LMO4 in patients and healthy controls. The number in each box and the legend represent the R-value. *P < 0.05; **P < 0.01; ***P < 0.001.

Article Snippet: Complement C3 (C3, Cloud-Clone, SEA861Hu), Complement C4 (C4, Elabscience, E-EL-H6027), C4b-binding protein alpha chain (C4BPA, Cloud-Clone, SEB620Hu) and vitamin K-dependent protein S (PROS1, Cloud-Clone, SEB971Hu) were analysed.

Techniques: Derivative Assay, Comparison, Expressing

Journal: Brain : a journal of neurology

Article Title: Extracellular vesicle biomarkers for complement dysfunction in schizophrenia.

doi: 10.1093/brain/awad341

Figure Lengend Snippet: Figure 3 Potential biomarkers validated in EVs in patients with schizophrenia and healthy controls. The concentration of extracellular vesicle (EV)-derived complement differentially expressed proteins were detected by proteomics (Set 1) and Mesoscale Discovery technology (Set 2). (A and B) C3 amount in EVs. Set 1: *P = 0.039, Cohen's d = 0.78. Set 2: **P < 0.001, Cohen's d = 1.13. (C and D) C4 amount in EVs. Set 1: ***P < 0.001, Cohen's d = 1.36. C4 intensity was the combination of C4A and C4B intensity. Set 2: *P = 0.019, Cohen's d = 0.67. (E and F) C4BPA amount in EVs. Set 1: **P = 0.003, Cohen's d = 1.17. Set 2: ***P < 0.001, Cohen's d = 2.04. (G and H) PROS1 amount in EVs. Set 1: ***P < 0.001, Cohen's d = 1.20. Set 2: **P = 0.0023, Cohen's d = 0.90. Although the levels of body mass index or diastolic blood pressure were significantly different between patients (SZ) and controls (HC), they did not demonstrate significant correlations with the levels of complement-associated components within each independent group. Hence, they were not adjusted as covariates. (I–L) Western blot analysis of the activation of EV-derived Complement C3 and C4. Neoepitope-specific antibodies of C3a and C4a were used. Human serum purified proteins of C3a des Arg and C4a des Arg were used as the positive controls. The last lane of each membrane was the positive control. n = 11 for each group. SZ = schizophrenia; HC = healthy controls.

Article Snippet: Complement C3 (C3, Cloud-Clone, SEA861Hu), Complement C4 (C4, Elabscience, E-EL-H6027), C4b-binding protein alpha chain (C4BPA, Cloud-Clone, SEB620Hu) and vitamin K-dependent protein S (PROS1, Cloud-Clone, SEB971Hu) were analysed.

Techniques: Concentration Assay, Derivative Assay, Western Blot, Activation Assay, Purification, Membrane, Positive Control

Journal: Brain : a journal of neurology

Article Title: Extracellular vesicle biomarkers for complement dysfunction in schizophrenia.

doi: 10.1093/brain/awad341

Figure Lengend Snippet: Figure 4 Potential biomarkers validated in plasma in patients with schizophrenia and healthy controls. The concentration of complement differen tially expressed proteins in plasma were detected by ELISA. (A and B) Plasma concentration of C3. Set 1: P = 0.16, Cohen's d = 0.43. Set 2: P = 0.22, Cohen's d = 0.35. (C and D) Plasma concentration of C4. Set 1: P = 0.76, Cohen's d = 0.0005. Set 2: P = 0.72, Cohen's d = 0.098. (E and F) Plasma concentration of C4BPA. Set 1: P = 0.25, Cohen's d = 0.35. Set 2: *P = 0.03, Cohen's d = 0.27. (G and H) Plasma concentration of PROS1. Set 1: **P = 0.001, Cohen's d = 1.11. Set 2: P = 0.87, Cohen's d = 0.02. Although the levels of body mass index or diastolic blood pressure were significantly different between patients and controls, they did not demonstrate significant correlations with the levels of complement associated components within each independent group. Consequently, they were not adjusted as covariates. SZ = schizophrenia; HC = healthy controls; n.s. = not significant.

Article Snippet: Complement C3 (C3, Cloud-Clone, SEA861Hu), Complement C4 (C4, Elabscience, E-EL-H6027), C4b-binding protein alpha chain (C4BPA, Cloud-Clone, SEB620Hu) and vitamin K-dependent protein S (PROS1, Cloud-Clone, SEB971Hu) were analysed.

Techniques: Clinical Proteomics, Concentration Assay, Enzyme-linked Immunosorbent Assay