Noninvasive Fetal Electrocardiography: Models, Technologies, and Algorithms

The fetal electrocardiogram (fECG) was first recorded from the maternal abdominal surface in the early 1900s. During the past fifty years, the most advanced electronics technologies and signal processing algorithms have been used to convert noninvasive fetal electrocardiography into a reliable technology for fetal cardiac monitoring. In this chapter, the major signal processing techniques, which have been developed for the modeling, extraction and analysis of the fECG from noninvasive maternal abdominal recordings are reviewed and compared with one another in detail. The major topics of the chapter include: 1) the electrophysiology of the fECG from the signal processing viewpoint, 2) the mathematical model of the maternal volume conduction media and the waveform models of the fECG acquired from body surface leads, 3) the signal acquisition requirements, 4) model-based techniques for fECG noise and interference cancellation, including adaptive filters and semi-blind source separation techniques, and 5) recent algorithmic advances for fetal motion tracking and online fECG extraction from few number of channels

cMET inhibitor crizotinib impairs angiogenesis and reduces tumor burden in the C3(1)-Tag model of basal-like breast cancer

Epidemiologic studies have associated obesity with increased risk of the aggressive basal-like breast cancer (BBC) subtype. Hepatocyte growth factor (HGF) signaling through its receptor, cMET, is elevated in obesity and is a pro-tumorigenic pathway strongly associated with BBC. We previously reported that high fat diet (HFD) elevated HGF, cMET, and phospho-cMET in normal mammary gland, with accelerated tumor development, compared to low fat diet (LFD)-fed lean controls in a murine model of BBC. We also showed that weight loss resulted in a significant reversal of HFD-induced effects on latency and elevation of HGF/cMET signaling in normal mammary and cMET in normal mammary and tumors. Here, we sought to inhibit BBC tumor progression in LFD- and HFD-fed C3(1)-Tag BBC mice using a small molecule cMET inhibitor, and began crizotinib treatment (50 mg/kg body weight by oral gavage) upon identification of the first palpable tumor. We next investigated if administering crizotinib in a window prior to tumor development would inhibit or delay BBC tumorigenesis. Treatment: Crizotinib significantly reduced mean tumor burden by 27.96 and 37.29 %, and mean tumor vascularity by 35.04 and 33.52 %, in our LFD- and HFD-fed C3(1)-Tag BBC mice, respectively. Prevention: Crizotinib significantly accelerated primary tumor progression in both diet groups but had no effect on total tumor progression or total tumor burden. In sum, cMET inhibition by crizotinib limited tumor development and microvascular density in basal-like tumor-bearing mice but did not appear to be an effective preventive agent for BBC. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s40064-016-1920-3) contains supplementary material, which is available to authorized users