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Biotechnological Application of Scanning Electrochemical Microscopy
Published in Allen J. Bard, Michael V. Mirkin, Scanning Electrochemical Microscopy, 2022
Benjamin R. Horrocks, Gunther Wittstock
Immunoassays have also been developed for carcinoembryonic Ag (CEA) [23], human chorionic gonadotropin (HCG) [49] and human placental lactogen (HPL) [49]. CEA is a tumor marker with a molecular weight (MW) of 180,000–200,000; HCG (MW = 38,000) and HPL (MW = 22,000) are peptide hormones that are pregnancy indicators. Yasukawa et al. [130] reported a sandwich immunoassay for pepsinogens (PG) 1 and 2, which are important in the diagnosis of atrophic gastritis and gastric cancer. Anti-PG1 and anti-PG2 Abs were spotted on glass or poly(dimethyl-siloxane) substrates at distinct locations. After capturing the respective Ags, the substrates were exposed to HRP-labeled antibodies forming the sandwich structure. The tip was positioned by recording the hindered diffusion of ferrocene methanol FcCH2OH oxidation at ET = 0.5 V. All assays were performed in the GC mode using an HRP enzyme label after addition of 0.5-mM H2O2 to the working solution and switching the working potential of the tip microelectrode to 0.05 V. At this value FcCH2OH+ formed by HRP can be reduced. Thus, the activity and location of the enzyme label HRP bound in the Ab:Ag:Ab-HRP complex could be detected (Figure 10.24). If the analyte solution contained PG1 or PG2, HRP activity was found only above the active region with the corresponding Ab. When both analytes were present, corresponding levels of activity could be detected over both sensing areas. The assays benefit from structuring the substrates for easy relocation of the spots [49] or using more advanced microfabricated cavities on the substrate to obtain sharper images [130].
Environmental chemicals and adverse pregnancy outcomes: Placenta as a target and possible driver of pre- and postnatal effects
Published in Critical Reviews in Environmental Science and Technology, 2023
Jing Li, Adrian Covaci, Da Chen
PPARs regulate metabolic, anti-inflammatory and development processes (Desvergne & Wahli, 1999). In the placenta, PPARs modulate villous trophoblast differentiation and function, and different isotypes of PPARs (i.e., α, β, γ, and δ) play specific roles (Fournier et al., 2007; Matsuda et al., 2013). PPARγ stimulation of villous trophoblast differentiation is associated with increased human chorionic gonadotropin (hCG) expression and secretion. In cells, PPARγ interacts with retinoid X receptor α (RXRα), and affects the synthesis of human placental lactogen, human placental growth hormone and leptin secretion (Fournier et al., 2007; Matsuda et al., 2013). However, PPARα and PPARβ/δ have no effect on hCG secretion. PPARγ stimulation of the differentiation of trophoblast is also associated with an accumulation of neutral lipids (e.g., cholesterol esters and triglycerides) particularly in the syncytiotrophoblast (Matsuda et al., 2013). In addition, placental transfer of fatty acids from mother to fetus is crucial for adequate fetal growth and development, and is mediated via a complex set of mechanisms involving the regulation of different PPARs (Fournier et al., 2007; Matsuda et al., 2013). Moreover, PPARδ down-regulates at the transcriptional level the 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) in villous trophoblast cells (Julan et al., 2005). In the placenta, 11β-HSD2 activity could protect the fetus from deleterious effects of maternal glucocorticoids, as excessive glucocorticoids in utero may lead to IUGR and predispose to type 2 diabetes and hypertension at the adult age (Dy et al., 2008).