Table 2.
MeSH Terms | Other Search Terms |
---|---|
Infant, Small for Gestational Age | Amino acids |
Infant, Small for Gestational Age/growth and development | Nutrients |
Infant, Small for Gestational Age/blood | Glucose |
Infant, Small for Gestational Age/metabolism | Fatty acids |
Infant, Small for Gestational Age/physiology | Fetal growth restriction |
Premature Birth | Intrauterine growth retardation |
Pre-Eclampsia | Intrauterine growth restriction |
Receptor, Fibroblast Growth Factor, Type 1 | Placenta malperfusion |
Placenta Diseases | Vascular endothelial growth factor |
Placenta Growth Factor | Flt-1 |
Placenta Growth Factor, PLGF-1 Isoform | Thiol adduct |
Receptors, Vascular Endothelial Growth Factor | Thio/seleno-protein |
Receptors, Androgen | Oxidative stress |
Receptors, Estrogen | DNA polymerase gamma |
Small for Gestational Age | |
Small for Gestational Age/growth and development | |
Small for Gestational Age/blood | |
Small for Gestational Age/metabolism | |
Small for Gestational Age/physiology | |
Fetal growth restriction | |
Intrauterine growth retardation | |
Intrauterine growth restriction | |
IUGR | |
Inhibition Cytochrome P450 enzyme activity | |
Inhibition CYP17A1 activity | |
Decreased Aromatase mRNA | |
Decreased Cyp19a1 mRNA | |
Fetal growth | |
AO | Increase, Growth inhibition |
AO | Growth, reduction |
AO | Decrease, Growth |
MIE | Inhibition, VegfR2 |
KE | Decreased, angiogenesis |
KE | Defect of Embryogenesis |
KE | Decrease, Growth |
KE | Reduction, Progesterone synthesis |
Oxidative stress | |
MIE | Activation, NRF2 |
KE | ROS formation |
KE | Increase, Oxidative Stress |
KE | Activation, PMK-1 P38 MAPK |
KE | Down Regulation, GSS and GSTs gene |
KE | Glutathione synthesis |
KE | Glutathione homeostasis |
MIE | Thiol group of chemicals interact with sulfhydryl groups of proteins to form thiol adducts |
MIE | Inhibition of mitochondrial DNA polymerase gamma |
KE | Dysfunction, Mitochondria |
MIE | Binding, Thiol/seleno-proteins involved in protection against oxidative stress |
Signaling pathways | |
KE | Activation, AKT2 |
KE | Activation, HIF-1 |
KE | Activation, JAK/STAT pathway |
KE | Activation, TGF-beta pathway |
KE | Activation, JNK |
MIE | Wnt ligand stimulation |
KE | Inhibition, Wnt pathway |
KE | Frizzled activation |
KE | Alteration, Wnt pathway |
Endocrine related pathways | |
MIE | Activation, Androgen receptor |
MIE | Decreased, Androgen receptor activity |
MIE | Activation, Estrogen receptor |
KE | Increased, Estrogen receptor activity |
KE | Increased, ER activity |
KE | Decrease, testosterone synthesis |
KE | Decrease, testosterone level |
KE | Decrease, dihydrotestosterone level |
KE | Decrease, DHT level |
KE | Decrease, androgen receptors (AR) activation |
KE | Decrease, AR activation |
KE | Reduction, 17-OH-pregnenolone conversion in DHEA |
KE | Reduction, 17-OH-progesterone conversion in androstenedione |
KE | Thyroid hormone disruption |
Others | |
MIE | Inhibition, Cytochrome P450 enzyme (CYP17A1) activity |
MIE | Binding of substrate, endocytic receptor |
MIE | Inhibition, Aromatase |
KE | Decreased, Aromatase (Cyp19a1) mRNA |
KE | Perturbation of cholesterol |
KE | GSK3beta inactivation |
KE | β-catenin activation |
Abbreviations: AO, adverse outcome; MIE, molecular initiating event; KE, key event.