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Journal: Scientific Reports
Article Title: Association of early VEGF trajectories with bronchopulmonary dysplasia severity in preterm infants
doi: 10.1038/s41598-025-21349-z
Figure Lengend Snippet: Longitudinal Trajectories of Peripheral Blood VEGF Levels in Preterm Infants with No/Mild vs. Moderate/Severe BPD ( a ) This figure illustrates the longitudinal changes in vascular endothelial growth factor (VEGF) concentrations (pg/mL) in peripheral blood over the first four postnatal weeks in preterm infants, stratified by bronchopulmonary dysplasia (BPD) severity. Left Panel (No/Mild BPD Group): VEGF levels exhibit a biphasic trajectory, with an initial progressive increase, peaking around postnatal week 2, followed by a subsequent gradual decline. This pattern suggests transient upregulation of VEGF during early postnatal adaptation. Right Panel (Moderate/Severe BPD Group): VEGF levels display a monotonic decline from birth without an early peak, indicating persistent suppression of VEGF expression in infants with more severe BPD. ( b ) This figure presents the estimated marginal means of vascular endothelial growth factor (VEGF) levels (pg/mL) over time in preterm infants with varying bronchopulmonary dysplasia (BPD) severity, derived from a linear mixed-effects model incorporating the time × group interaction. Group 1 (Red, No/Mild BPD Group): Represents infants with No/Mild BPD, exhibiting a relatively stable VEGF trajectory with only a slight decline over the first four postnatal weeks. Group 2 (Blue, Moderate/Severe BPD Group): Represents infants with Moderate/Severe BPD, showing a significant and continuous decline in VEGF levels over time. Each data point represents the estimated marginal mean VEGF level at a given time point, adjusted for gestational age, birth weight, sex, and oxygenation index (OI). The solid lines depict the fitted regression slopes, while the shaded regions represent 95% confidence intervals (CIs). ( c ) This figure illustrates the predicted vascular endothelial growth factor (VEGF) trajectories over time in preterm infants with different bronchopulmonary dysplasia (BPD) severities, estimated using a linear mixed-effects model incorporating both fixed and random effects. Left Panel (No/Mild BPD Group): Represents infants with No/Mild BPD, suggesting a gradual and modest decline in VEGF levels over the four-week period. Right Panel (Moderate/Severe BPD Group): Represents infants with Moderate/Severe BPD, demonstrating a steep and progressive reduction in VEGF levels. Each line represents the model-derived fitted trajectory for an individual subject, while the solid black lines denote the group-level estimated marginal means. The shaded regions indicate the 95% confidence intervals (CIs) of the predicted values. ( d ) This scatterplot illustrates the estimated participant-specific random intercepts (baseline VEGF levels at birth) and random slopes (rate of VEGF change per week) derived from a linear mixed-effects model, stratified by different groups.
Article Snippet:
Techniques: Expressing, Derivative Assay
Journal: Cell Proliferation
Article Title: Targeting FABP4 to Inhibit AGEs ‐ RAGE / NF ‐ κB Signalling Effectively Ameliorates Nucleus Pulposus Dysfunction and Angiogenesis in Obesity‐Related Intervertebral Disc Degeneration
doi: 10.1111/cpr.70021
Figure Lengend Snippet: FABP4 promoted angiogenesis to exacerbate IVDD under lipotoxic condition. (A) Volcano plot of the DEGs of HFD‐induced IVDD from WT and KO mice. (B) Heart map of the DEGs of HFD‐induced IVDD from WT and KO mic ( n = 5). (C) GO analysis of the DEGs of HFD‐induced IVDD from WT and KO mice. (D) KEGG analysis of the DEGs of HFD‐induced IVDD from WT and KO mice. (E) ELISA result of the VEGF level of the IVD tissue in WT and KO mice ( n = 5). (F) ELISA result of the VEGF level of NPC degeneration model with or without FABP4 silencing or FPS‐ZM1 ( n = 5). (G) IF staining for CD31 and EMCN in WT and KO mice from sham or IVDD groups under HFD condition, respectively. (H and I) Quantitation results of the IF staining for CD31 and EMCN in WT and KO mice from sham or IVDD groups under HFD condition, respectively ( n = 5). (J) Tube formation assay of HUVECs in different groups. (K and L) Branch points and capillary length of HUVECs in different groups ( n = 5). (M and N) Representative images and quantitation results of the scratch wound of HUVECs in different groups ( n = 5). * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.
Article Snippet: FABP4 level (E‐EL‐M2404, Elabscience) and
Techniques: Enzyme-linked Immunosorbent Assay, Staining, Quantitation Assay, Tube Formation Assay
Journal: Cell Proliferation
Article Title: Targeting FABP4 to Inhibit AGEs ‐ RAGE / NF ‐ κB Signalling Effectively Ameliorates Nucleus Pulposus Dysfunction and Angiogenesis in Obesity‐Related Intervertebral Disc Degeneration
doi: 10.1111/cpr.70021
Figure Lengend Snippet: Blocking the interaction of VEGF and VEGFR2 alleviated FABP4‐induced angiogenesis and IVDD (A) Degeneration and angiogenesis evaluated by H&E, SOFG, and IHC staining of IVD tissue from sham, IVDD, IVDD+rFABP4, and IVDD+rFABP4 + Ki8751 groups, respectively. (B) Histological score of IVD tissue from sham, IVDD, IVDD+rFABP4, and IVDD+rFABP4 + Ki8751 groups, respectively ( n = 5). (C and D): Quantitation results of IF staining for CD31 and EMCN of IVD tissue from sham, IVDD, IVDD+rFABP4, and IVDD+rFABP4 + Ki8751 groups, respectively ( n = 5). (E and F) Quantitation results of IHC staining for COL2A1 and MMP3 of IVD tissue from sham, IVDD, IVDD+rFABP4, and IVDD+rFABP4 + Ki8751 groups, respectively ( n = 5). (G) Tube formation assay of HUVECs in different groups. (H and I) Branch points and capillary length of HUVECs in different groups ( n = 5). (J and K) Representative images and quantitation results of the scratch wound of HUVECs in different groups ( n = 5). * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.
Article Snippet: FABP4 level (E‐EL‐M2404, Elabscience) and
Techniques: Blocking Assay, Immunohistochemistry, Quantitation Assay, Staining, Tube Formation Assay
Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Article Title: Vascular Endothelial Growth Factor and the Pathogenesis of Intracranial Aneurysms: A Systematic Review on the Missing Link in a Complex Pathway
doi: 10.1161/JAHA.124.035638
Figure Lengend Snippet: Literature Review Summary of Animal Studies on Vascular Endothelial Growth Factor and Intracranial Aneurysms
Article Snippet: Two other studies measured
Techniques: Animal Model, Comparison, Expressing, Control
Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Article Title: Vascular Endothelial Growth Factor and the Pathogenesis of Intracranial Aneurysms: A Systematic Review on the Missing Link in a Complex Pathway
doi: 10.1161/JAHA.124.035638
Figure Lengend Snippet: Literature Review Summary of Human Studies on Vascular‐Endothelial‐Growth‐Factor and Intracranial Aneurysms
Article Snippet: Two other studies measured
Techniques: Comparison, Control, Expressing, Clinical Proteomics, Software, Inhibition, Over Expression, Migration, RNA Sequencing, Protein-Protein interactions