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Fetal arrhythmias
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Júlia Hajdú, Valéria Váradi, Zoltán Papp
In avian embryos, a pacemaker is first established in the inflow tract at the straight heart tube stage. When the embryonic heart first begins to contract, it has no specialized conduction system. It is thought that the cardiac conduction system is derived from independent parent cells linked together to establish the integrated conduction system of the heart. Terminal differentiation of conduction tissue occurs late in development (1,2). By 6 weeks postconception, atrioventricular (AV) synchrony can be demonstrated using standard Doppler techniques. The heart rate is 150 bpm by 14 weeks; by 20 weeks it is 140 bpm with a gradual decrease to 130 bpm by term (3).
HER-2 as a Prognostic and Predictive Biomarker in Cancer
Published in Sherry X. Yang, Janet E. Dancey, Handbook of Therapeutic Biomarkers in Cancer, 2021
Alexandra S. Zimmer, Suparna B. Wedamb, Stanley Lipkowitza
Homozygous deletion of HER-2 in mice results in embryonic lethality due to defective development ofcardiac trabeculae [22]. Also, HER-2 null mice have abnormal development of the nervous system and the neuromuscular junction [22–25]. Homozygous deletion of neuregulin, which binds to HER-3 and HER-4 and stimulates heterodimerization of these receptors with HER-2 and activation of the HER-2 kinase activity, causes similar developmental defects in the heart and nervous system [26]. In the developing heart, HER-2 is expressed in embryonic myocytes while the ligand neuregulin is expressed in the adjacent endocardium, consistent with a paracrine developmental signal (reviewed in [27]). Thus, HER-2 is essential for cardiac and neural development. Also, HER-2 serves important functions in the adult heart. Mice with conditional deletion of HER-2 targeted to cardiomyocytes have normal embryonic heart development but develop dilated cardiomyopathy at 3 months of age [28]. Doxorubicin treatment of mice with a heterozygous deletion of neuregulin-1 results in increased cardiac damage and mortality and induces less phosphorylation of HER-2, HER-4, ERK 1 and 2, AKT, and 70S6K in the heterozygous neuregulin deficient mice compared to wild type mice [29]. Together these data demonstrate a role for HER-2 in normal homeostasis and response to damage in the adult heart. This is likely to explain the cardiac toxicity observed in breast cancer patients treated with the anti-HER-2 antibody trastuzumab (reviewed in [30]).
Ultrasound Follow-Up in Early Pregnancy
Published in Howard J.A. Carp, Recurrent Pregnancy Loss, 2020
Fetal heart activity is the earliest proof of a viable pregnancy and it has been documented in utero by TVS as early as 36 days’ menstrual age. From 5−9 weeks of gestation there is a rapid increase in the mean heart rate from 110−175 bpm. The heart rate then gradually decreases to around 160–170 bpm. An abnormal developmental pattern of fetal heart rate (FHR) and/or bradycardia has been associated with subsequent miscarriage. In particular, a slow FHR at 6–8 weeks appears to be associated with subsequent fetal demise. A single observation of an abnormally slow heart rate does not necessarily indicate subsequent embryonic death, but a continuous decline of embryonic heart activity is inevitably associated with miscarriage [6].
Different cellular mechanisms from low- and high-dose zinc oxide nanoparticles-induced heart tube malformation during embryogenesis
Published in Nanotoxicology, 2022
Mengwei Wang, Ping Zhang, Zeyu Li, Yu Yan, Xin Cheng, Guang Wang, Xuesong Yang
The immunofluorescent staining was implemented in whole-mount chicken embryos or embryonic heart sections as previously described (Nikolopoulou et al. 2017). Briefly, the chicken or mouse embryos were fixed in 4% PFA at 4 °C overnight, and then incubated with the following primary antibodies: MF20 (1:1000, MF20-S, Developmental Studies Hybridoma Bank, USA), E-cadherin (1:200, 610181, BD Biosciences, USA), C-caspase3 (1:200, 9664S, Cell Signaling Technology, USA), GPX4 (1:200, ab125066, Abcam, UK) at 4 °C on a shaker. After extensive rinsing in PBST (0.1% Tween-20), the whole-mount embryos or sections were incubated overnight with the corresponding Alexa Fluor secondary antibodies (1:1000, Invitrogen, USA) at 4 °C on a shaker. All embryos or sections were counterstained with DAPI (1:1000, Invitrogen, USA) at room temperature for 1 hour. Subsequently, the chicken embryos were cut into 10 μm sections using a cryostat apparatus (Leica CM1900) and the cells were imaged using an Olympus IX51epifluorescent microscope.
Precision medicine in cardiac electrophysiology: where we are and where we need to go
Published in Expert Review of Precision Medicine and Drug Development, 2020
Ashish Correa, Syed Waqas Haider, Wilbert S. Aronow
Genomic studies have now started to unravel putative genetic modulators of AF. GWAS have shown that variants in a region on chromosome 4q25 are associated with familial AF [74,75]. This region is near the PITX2 gene which suppresses sino-atrial node (SAN) gene-expression in the left atrium and thus plays an essential role in left-right differentiation in the embryonic heart. Presumably, defects in this gene permit the SAN-specific gene program in the left atrium, thereby promoting aberrant pacemaker tissue development in the left atrium and encouraging atrial arrhythmogenesis. Studies in mice models have shown precisely this, whereby PITX2 suppression resulted in AF and atrial tachycardias [76]. Interestingly, PITX2 is responsible for forming the tissue of the pulmonary vein myocardial sleeve, which has been shown to be the origin of AF in electrophysiologic mapping studies. A recent study showed that a common SNP on chromosome 4q25 significantly influenced the response to anti-arrhythmic drugs in AF patients [77]. This points to a modulatory role of genes not just in the susceptibility to AF but also the response to therapy.
Correlation between HCN4 gene polymorphisms and lone atrial fibrillation risk
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Xiao-Hong Li, Ya-Min Hu, Guang-Li Yin, Ping Wu
Hyperpolarization activated cyclic nucleotide gated potassium channel 4 (HCN4) is one subtype of HCN family. HCN family could code the funny current (If) pathway which is the necessary element for cardiac pacemaking process [14,15]. Besides, HCNs are also involved in the spontaneous membrane depolarization process of SA node cells during diastole [16]. Stieber et al. found that HCN4 was overexpressed in embryonic heart, especially in SA node [17]. Mutations in this gene have been proved to be associated with AF [18]. A meta-analysis based on multiple GWAS samples of European population identified that rs7164883 SNP of HCN4 gene was a susceptibility loci for AF [19]. Furthermore, the single nucleotide polymorphisms (SNPs) in HCN4 gene (rs498005 and rs7164883) were with the minor allele frequencies more than 0.05 in CHB (Chinese Han in Beijing) population. Thus, we hypothesize that the two SNPs might be associated with AF in Chinese Han population.