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The fetal magnetoencephalogram (fMEG) is measured in the presence of large interference from the maternal and fetal magnetocardiograms. This interference can be efficiently attenuated by orthogonal projection of the corresponding spatial vectors. However, the projection operators redistribute the fMEG signal among sensors. Although redistribution can be readily accounted for in the forward solution, visual interpretation of the fMEG signal topography is made difficult. We have devised a general, model-independent method for correction of the redistribution effect that utilizes the assumption that we know in which channels the fMEG should be negligible (such channels are distant from the known fetal head position). In a simplified case where the fMEG can be explained by equivalent current dipoles, the correction can also be obtained from fitting the dipoles to the fMEG signal. The corrected fMEG signal topography then corresponds to the dipole forward solution, but without orthogonal projection. We illustrate the redistribution correction on an example of experimentally measured flash evoked fMEG.

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Serotonin (5-HT) transporter (SERT) regulates the level of 5-HT in placenta. Initially, we found that in gestational diabetes mellitus (GDM), whereas free plasma 5-HT levels were elevated, the 5-HT uptake rates of trophoblast were significantly down-regulated, due to impairment in the translocation of SERT molecules to the cell surface. We sought to determine the factors mediating the down-regulation of SERT in GDM trophoblast. We previously reported that an endoplasmic reticulum chaperone, ERp44, binds to Cys200 and Cys209 residues of SERT to build a disulfide bond. Following this posttranslational modification, before trafficking to the plasma membrane, SERT must be dissociated from ERp44; and this process is facilitated by insulin signaling and reversed by the insulin receptor blocker AGL2263. However, the GDM-associated defect in insulin signaling hampers the dissociation of ERp44 from SERT. Furthermore, whereas ERp44 constitutively occupies Cys200/ Cys209 residues, one of the SERT glycosylation sites, Asp208 located between the two Cys residues, cannot undergo proper glycosylation, which plays an important role in the uptake efficiency of SERT. Herein, we show that the decrease in 5-HT uptake rates of GDM trophoblast is the consequence of defective insulin signaling, which entraps SERT with ERp44 and impairs its glycosylation. In this regard, restoring the normal expression of SERT on the trophoblast surface may represent a novel approach to alleviating some GDM-associated complications.serotonin | ERp44 | insulin | serotonin transporter | gestational diabetes mellitus

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