Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: Evaluation of lung parenchyma, blood vessels, and peripheral blood lymphocytes as a potential source of acute phase reactants in patients with COPD

doi: 10.2147/COPD.S188567

Figure Lengend Snippet: Primers used for reverse transcription quantitative PCR

Article Snippet: Mouse monoclonal antibodies against SAA1 (Novus Biologicals, Cambridge, UK) and CRP (Abcam, Cambridge UK) were used.

Techniques: Reverse Transcription

Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: Evaluation of lung parenchyma, blood vessels, and peripheral blood lymphocytes as a potential source of acute phase reactants in patients with COPD

doi: 10.2147/COPD.S188567

Figure Lengend Snippet: Correlations between expressions of acute phase reactant

Article Snippet: Mouse monoclonal antibodies against SAA1 (Novus Biologicals, Cambridge, UK) and CRP (Abcam, Cambridge UK) were used.

Techniques:

Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: Evaluation of lung parenchyma, blood vessels, and peripheral blood lymphocytes as a potential source of acute phase reactants in patients with COPD

doi: 10.2147/COPD.S188567

Figure Lengend Snippet: Gene expression of acute phase reactants in resistant smokers (controls) and COPD patients in blood cells ( A ). SAA1 (Panel B ) and SAA4 (Panel C ) expression in blood cells according to COPD stage. I, GOLD I COPD; II, GOLD II COPD; III, GOLD III COPD. No statistically significant differences were identified ( P >0.05). Abbreviations: CNT, resistant smokers (controls); SAA, serum amyloid A.

Article Snippet: Mouse monoclonal antibodies against SAA1 (Novus Biologicals, Cambridge, UK) and CRP (Abcam, Cambridge UK) were used.

Techniques: Gene Expression, Expressing

Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: Evaluation of lung parenchyma, blood vessels, and peripheral blood lymphocytes as a potential source of acute phase reactants in patients with COPD

doi: 10.2147/COPD.S188567

Figure Lengend Snippet: Comparison of acute phase reactants gene expression levels in different tissues (blood cells, pulmonary artery, and lung parenchyma) of COPD patients. Panel ( A ): CRP expression; panel ( B ): SAA2 expression; panel ( C ): SAA1 expression and panel ( D ): SAA4 expression. Abbreviations: CRP, C-reactive protein; SAA, serum amyloid A.

Article Snippet: Mouse monoclonal antibodies against SAA1 (Novus Biologicals, Cambridge, UK) and CRP (Abcam, Cambridge UK) were used.

Techniques: Comparison, Gene Expression, Expressing

Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: Evaluation of lung parenchyma, blood vessels, and peripheral blood lymphocytes as a potential source of acute phase reactants in patients with COPD

doi: 10.2147/COPD.S188567

Figure Lengend Snippet: Correlations between different tissues

Article Snippet: Mouse monoclonal antibodies against SAA1 (Novus Biologicals, Cambridge, UK) and CRP (Abcam, Cambridge UK) were used.

Techniques:

Journal: Journal of Translational Medicine

Article Title: Plasma proteomic analysis of autoimmune hepatitis in an improved AIH mouse model

doi: 10.1186/s12967-019-02180-3

Figure Lengend Snippet: The schematic diagram of the experiment design. CYP2D6 cytochrome P450 2D6, AIH autoimmune hepatitis, DEPs differentially expressed proteins, iTRAQ isobaric tags for relative and absolute quantitation, SAA1 serum amyloid A 1, GO gene ontology

Article Snippet: Primary antibody against SAA1 (1:100; 16721-1-AP, Proteintech, Rosemont, IL USA) was incubated overnight at 4 °C.

Techniques: Multiplex sample analysis, Quantitation Assay

Journal: Journal of Translational Medicine

Article Title: Plasma proteomic analysis of autoimmune hepatitis in an improved AIH mouse model

doi: 10.1186/s12967-019-02180-3

Figure Lengend Snippet: Vital DEPs validation in patients with AIH. a Representative H&E staining of liver tissue section from a patient with AIH. b Plasma from patients with AIH, hepatitis B patients, hepatitis C patients, and healthy people were collected and the SAA1 expression levels in the plasma were detected by ELISA (n = 30, ***P < 0.001 vs. Control). c Immunohistochemical staining of human liver tissues for SAA1 detection are shown (n = 3, ×200 magnification). d Box plot of plasma SAA1 level in patients with AIH from different inflammation grades (n = 7 for G0–G1, n = 14 for G2, n = 8 for G3–G4, # Kruskal–Wallis nonparametric test *Mann–Whitney test). The line through the middle of each box represents the median. The length of the box represents the level range. e Box plot of plasma SAA1 level in patients with AIH from different fibrosis stages (n = 14 for S0–S1, n = 8 for S2, n = 7 for S3–S4, # Kruskal–Wallis nonparametric test *Mann–Whitney test)

Article Snippet: Primary antibody against SAA1 (1:100; 16721-1-AP, Proteintech, Rosemont, IL USA) was incubated overnight at 4 °C.

Techniques: Biomarker Discovery, Staining, Clinical Proteomics, Expressing, Enzyme-linked Immunosorbent Assay, Control, Immunohistochemical staining, MANN-WHITNEY

Journal: Frontiers in Immunology

Article Title: De novo Synthesis of SAA1 in the Placenta Participates in Parturition

doi: 10.3389/fimmu.2020.01038

Figure Lengend Snippet: Expression of SAA1 in the human placenta at term. (A) In situ hybridization showed the presence of SAA1 mRNA (red brown) in the nuclei of the syncytial layer of the villous tissue. Scrambled RNA probe was used as the negative control (nc). (B) Immunohistochemical staining showed the presence of SAA1 (red) in the syncytial layer of the villous tissue. Non-immune serum was used as negative control (nc). (C) Immunofluorescence staining showed the colocalization of SAA1 (red) and 11β-HSD2 (green), a marker of syncytiotrophoblast, in the syncytial layer of the villous tissue. Nuclei (blue) were counterstained blue with DAPI.

Article Snippet: After blocking, the section was incubated with a primary antibody against SAA1 (MAB30191; R&D System, Minneapolis, MN, USA) at 1:50 dilution or non-immune serum for negative control overnight at 4°C.

Techniques: Expressing, In Situ Hybridization, Negative Control, Immunohistochemical staining, Staining, Immunofluorescence, Marker

Journal: Frontiers in Immunology

Article Title: De novo Synthesis of SAA1 in the Placenta Participates in Parturition

doi: 10.3389/fimmu.2020.01038

Figure Lengend Snippet: Effect of syncytialization and LPS, TNF-α and cortisol on SAA1 expression in human placental trophoblasts . (A) Hematoxylin-eosin staining of cultured trophoblasts showed cell fusion in vitro . (B) Changes of SAA1 mRNA and secretion before (3 h after cell plating) and after (48 h after cell plating) syncytialization ( n = 3–4). (C–E) LPS (5 ng/mL, 24 h, C ), TNF-α (10 ng/mL, 24 h; D ), and cortisol (1 μM, 24 h; E ) increased SAA1 mRNA and secretion in syncytiotrophoblasts ( n = 4–5). Data are mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: After blocking, the section was incubated with a primary antibody against SAA1 (MAB30191; R&D System, Minneapolis, MN, USA) at 1:50 dilution or non-immune serum for negative control overnight at 4°C.

Techniques: Expressing, Staining, Cell Culture, In Vitro

Journal: Frontiers in Immunology

Article Title: De novo Synthesis of SAA1 in the Placenta Participates in Parturition

doi: 10.3389/fimmu.2020.01038

Figure Lengend Snippet: Increased SAA1 abundance in human placental tissue and maternal blood in labor at term and preterm. (A,B) Abundance of SAA1 mRNA and protein in human placenta tissue collected from elective cesarean section without labor at term (TNL) ( n = 12) and spontaneous labor at term (TL) ( n = 12). (C) Dynamic changes of serum SAA1 in pregnant women before, at the onset of, and 24 h after labor ( n = 5). (D) Changes of SAA1 in maternal blood obtained from iatrogenic preterm birth without histologic chorioamnionitis ( n = 15) and infection-induced preterm birth with histological chorioamnionitis ( n = 12). Data are mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: After blocking, the section was incubated with a primary antibody against SAA1 (MAB30191; R&D System, Minneapolis, MN, USA) at 1:50 dilution or non-immune serum for negative control overnight at 4°C.

Techniques: Infection

Journal: Frontiers in Immunology

Article Title: De novo Synthesis of SAA1 in the Placenta Participates in Parturition

doi: 10.3389/fimmu.2020.01038

Figure Lengend Snippet: Effects of SAA1 on the expression of genes pertinent to parturition in human placental syncytiotrophoblasts. (A,B) Effects of SAA1 (10 ng/mL, 24 h) on IL-8, TNF-α mRNA, and secretion in the presence or absence of a TLR4 antagonist CLI095 (5 μM, 24 h) ( n = 3–4). (C) Effects of SAA1 (10 ng/mL, 24 h) on COX-2 mRNA and protein in the presence or absence of a TLR4 antagonist CLI095 (5 μM, 24 h) ( n = 3). Top panel is a representative immunoblot. (D) Effects of SAA1 (10 ng/mL, 24 h) on PGE2 and PGF2α secretions ( n = 4). Data are mean ± SEM. * P < 0.05 vs. control (0); ** P < 0.01 vs. control (0); # P < 0.05 vs. SAA1.

Article Snippet: After blocking, the section was incubated with a primary antibody against SAA1 (MAB30191; R&D System, Minneapolis, MN, USA) at 1:50 dilution or non-immune serum for negative control overnight at 4°C.

Techniques: Expressing, Western Blot, Control

Journal: Frontiers in Immunology

Article Title: De novo Synthesis of SAA1 in the Placenta Participates in Parturition

doi: 10.3389/fimmu.2020.01038

Figure Lengend Snippet: Expression of SAA1/2 in mouse placenta and fetal membranes. (A–C) Immunohistochemical staining showed the presence of SAA1 (red) in the junctional zone of the placenta (A) and the yolk sac membrane (B) , but not in the amnion (C) at gestational day 18.5. (D) negative control. (E,F) Increased SAA1/A2 abundance in mouse placenta and fetal membranes from gestational days 16.5 to 18.5 ( n = 3). Data are mean ± SEM. * P < 0.05, ** P < 0.01.

Article Snippet: After blocking, the section was incubated with a primary antibody against SAA1 (MAB30191; R&D System, Minneapolis, MN, USA) at 1:50 dilution or non-immune serum for negative control overnight at 4°C.

Techniques: Expressing, Immunohistochemical staining, Staining, Membrane, Negative Control

Journal: Frontiers in Immunology

Article Title: De novo Synthesis of SAA1 in the Placenta Participates in Parturition

doi: 10.3389/fimmu.2020.01038

Figure Lengend Snippet: Induction of proinflammatory factors in placenta and fetal membranes by intraperitoneal administration of LPS or SAA1 in the mouse. (A,B) Induction of SAA1/2 expression in mouse placenta (A) and fetal membranes (B) by intraperitoneal administration of LPS (5 mg/kg BW, 6 h) at gestational day 16.5 ( n = 3). (C–E) Induction of IL-1β (C) , TNF-α (D) and COX-2 (E) in the mouse placenta by intraperitoneal administration of LPS (5 mg/kg BW, 6 h) and SAA1 (8 μg/kg BW, 6 h) at gestational day 16.5 ( n = 4). Data are mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: After blocking, the section was incubated with a primary antibody against SAA1 (MAB30191; R&D System, Minneapolis, MN, USA) at 1:50 dilution or non-immune serum for negative control overnight at 4°C.

Techniques: Expressing

Journal: Frontiers in Immunology

Article Title: De novo Synthesis of SAA1 in the Placenta Participates in Parturition

doi: 10.3389/fimmu.2020.01038

Figure Lengend Snippet: Pregnancy outcome in mice administered with SAA1 and PBS.

Article Snippet: After blocking, the section was incubated with a primary antibody against SAA1 (MAB30191; R&D System, Minneapolis, MN, USA) at 1:50 dilution or non-immune serum for negative control overnight at 4°C.

Techniques: