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Background: Adults with congenital heart disease (ACHD) experience a high prevalence of atrial arrhythmia (AA) and thromboembolic cerebrovascular complications. However, data on AA and associated long-term outcomes are limited in ACHD patients with coarctation of the aorta (CoA)., Objectives: This study aimed to characterize the prevalence and risk factors for AA and thromboembolic complications in adults with CoA., Methods: We conducted a retrospective cohort study in a tertiary ACHD care center and included consecutive CoA patients older than 18 years old with more than one year of follow-up., Results: Two hundred seventy patients with CoA were followed for 7.2 ± 3.95 years. The mean age was 35.3 ± 11.1 and 55.2% were male. Patients had a mean of 2.1 ± 1.8 cardiovascular surgical or transcatheter procedures. Thirty-five patients (13%) had AA. Ten subjects (3.8%) had a thromboembolic cerebrovascular event, of which four (1.4%) had AA. In univariate analysis, age (p = 0.005) and total intracardiac interventions (p = 0.007) were associated with the presence of AA. Age (p = 0.021), history of heart failure (p = 0.022), and dyslipidemia (p = 0.019) were associated with thromboembolism. In multivariate analysis, age (p < 0.001) and intracardiac interventions (p = 0.007) were associated with AA., Conclusions: The rate of AA is higher in adults with CoA than in the general population but lower than in other ACHD. Increasing age and intracardiac interventions were associated with AA. The rate of thromboembolic events was low. Some traditional risk factors for stroke may apply. Larger studies are needed to validate predictors for stroke in this population., Competing Interests: Conflicts of interest The authors report no relationships that could be construed as a conflict of interest., (Copyright © 2023 Elsevier B.V. All rights reserved.)

The cochleovestibular (CV) nerve, which connects the inner ear to the brain, is the nerve that enables the senses of hearing and balance. The aim of this study was to document the morphological development of the mouse CV nerve with respect to the two embryonic cells types that produce it, specifically, the otic vesicle-derived progenitors that give rise to neurons, and the neural crest cell (NCC) progenitors that give rise to glia. Otic tissues of mouse embryos carrying NCC lineage reporter transgenes were whole mount immunostained to identify neurons and NCC. Serial optical sections were collected by confocal microscopy and were compiled to render the three dimensional (3D) structure of the developing CV nerve. Spatial organization of the NCC and developing neurons suggest that neuronal and glial populations of the CV nerve develop in tandem from early stages of nerve formation. NCC form a sheath surrounding the CV ganglia and central axons. NCC are also closely associated with neurites projecting peripherally during formation of the vestibular and cochlear nerves. Physical ablation of NCC in chick embryos demonstrates that survival or regeneration of even a few individual NCC from ectopic positions in the hindbrain results in central projection of axons precisely following ectopic pathways made by regenerating NCC., (© 2013 Published by Elsevier Inc.)

The enteric nervous system (ENS) is formed from vagal and sacral neural crest cells (NCC). Vagal NCC give rise to most of the ENS along the entire gut, whereas the contribution of sacral NCC is mainly limited to the hindgut. This, and data from heterotopic quail-chick grafting studies, suggests that vagal and sacral NCC have intrinsic differences in their ability to colonize the gut, and/or to respond to signalling cues within the gut environment. To better understand the molecular basis of these differences, we studied the expression of genes known to be essential for ENS formation, in sacral NCC within the chick hindgut. Our results demonstrate that, as in vagal NCC, Sox10, EdnrB, and Ret are expressed in sacral NCC within the gut. Since we did not detect a qualitative difference in expression of these ENS genes we performed DNA microarray analysis of vagal and sacral NCC. Of 11 key ENS genes examined from the total data set, Ret was the only gene identified as being highly differentially expressed, with a fourfold increase in expression in vagal versus sacral NCC. We also found that over-expression of RET in sacral NCC increased their ENS developmental potential such that larger numbers of cells entered the gut earlier in development, thus promoting the fate of sacral NCC towards that of vagal NCC.

Background/aims: Hepatic stellate cells (HSC) have been hypothesised to derive from the neural crest, based on their expression of multiple neural/neuroendocrine features and their contacts with autonomic nerve endings., Methods: We studied the emergence of HSC in the liver during embryonic development in a transgenic mouse line expressing yellow fluorescent protein (YFP) in all neural crest cells and their derivatives. Cellular YFP expression in these mice was compared with desmin expression between embryonic day (E) 11.5 and adulthood., Results: YFP was abundantly expressed in neural crest cells delaminating from the neural tube and in all known neural crest-derived structures and cell populations. In particular, YFP expressing cells perfectly mimicked the spatial and temporal pattern of enteric nervous system development from neural crest cells migrating from the postotic region. Cells within the adrenal medulla were also YFP positive. Analysis of the liver showed that desmin-expressing, stellate-shaped, perisinusoidally located HSC were evident from E11.5 onwards. However, no detectable YFP expression was seen in the developing liver or in HSC, from E11.5 until adulthood., Conclusions: These findings suggest HSC do not descend from the neural crest, and therefore may derive from the septum transversum mesenchyme, from endoderm or from the mesothelial liver capsule.