Our understanding of the neural crest, a key vertebrate innovation, is built upon studies of multiple model organisms. Early research on neural crest cells (NCCs) was dominated by analyses of accessible amphibian and avian embryos, with mouse genetics providing complementary insights in more recent years. The zebrafish model is a relative newcomer to the field, yet it offers unparalleled advantages for the study of NCCs. Specifically, zebrafish provide powerful genetic and transgenic tools, coupled with rapidly developing transparent embryos that are ideal for high-resolution real-time imaging of the dynamic process of neural crest development. While the broad principles of neural crest development are largely conserved across vertebrate species, there are critical differences in anatomy, morphogenesis, and genetics that must be considered before information from one model is extrapolated to another. Here, our goal is to provide the reader with a helpful primer specific to neural crest development in the zebrafish model. We focus largely on the earliest events-specification, delamination, and migrationdiscussing what is known about zebrafish NCC development and how it differs from NCC development in non-teleost species, as well as highlighting current gaps in knowledge.

Neural crest cells are multipotent progenitors that dynamically interpret diverse microenvironments to migrate significant distances as a loosely associated collective and contribute to many tissues in the developing vertebrate embryo. Uncovering details of neural crest migration has helped to inform a general understanding of collective cell migration, including that which occurs during cancer metastasis. Here, we discuss several commonalities and differences of neural crest and cancer cell migration and behavior. First, we focus on some of the molecular pathways required for the initial specification and potency of neural crest cells and the roles of many of these pathways in cancer progression. We also describe epithelial-to-mesenchymal transition, which plays a critical role in initiating both neural crest migration and cancer metastasis. Finally, we evaluate studies that demonstrate myriad forms of cell-cell and cell-environment communication during neural crest and cancer collective migration to highlight the remarkable similarities in their molecular and cell biological regulation.

Background and study aims Previous studies have suggested a high prevalence of musculoskeletal injuries (MI) in endoscopists. Little evidence has come from European countries. Our main aim was to evaluate the prevalence, type, and impact of MI among Portuguese endoscopists. We also sought to identify risk factors for the development, severity and number of endoscopy-related MI. Material and methods A 48-question electronic survey was developed by a multidisciplinary group. The electronic survey was sent to all members of Portuguese Society of Gastroenterology (n = 705) during May 2019. Study data were collected and managed using REDCap electronic data capture tools hosted at SPG – CEREGA. Results The survey was completed by 171 endoscopists (response rate of 24.3 %), 55.0 % female with a median age of 36 years (range 26–78). The prevalence of at least one MI related to endoscopy was 69.6 % (n = 119), the most frequent being neck pain (30.4 %) and thumb pain (29.2 %). The median time for MI development was 6 years (range 2 months-30 years). Severe pain was reported by 19.3 %. Change in endoscopic technique was undertaken by 61.3 % and reduction in endoscopic caseload was undertaken by 22.7 %. Missing work was reported by 10.1 %, with the median time off from work being 30 days (range 1–90). Female gender and ≥ 15 years in practice were independently associated with MI and severe pain. Years in practice, weekly-time performing endoscopy, and gender were significant predictors of the number of MI. Conclusions Prevalence of MI was significant among Portuguese endoscopists and had a relevant impact on regular and professional activities.

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The neural crest is regionalized along the anteroposterior axis, as demonstrated by foundational lineage-tracing experiments that showed the restricted developmental potential of neural crest cells originating in the head. Here, we explore how recent studies of experimental embryology, genetic circuits and stem cell differentiation have shaped our understanding of the mechanisms that establish axial-specific populations of neural crest cells. Additionally, we evaluate how comparative, anatomical and genomic approaches have informed our current understanding of the evolution of the neural crest and its contribution to the vertebrate body.

During the larval stages, the visual system of the mosquito Aedes aegypti contains five stemmata, often referred to as larval ocelli, positioned laterally on each side of the larval head. Here we show that stemmata contain two photoreceptor types, distinguished by the expression of different rhodopsins. The rhodopsin Aaop3 (GPROP3) is expressed in the majority of the larval photoreceptors. There are two small clusters of photoreceptors located within the satellite and central stemmata that express the rhodopsin Aaop7 (GPROP7) instead of Aaop3. Electroretinogram analysis of transgenic Aaop7 Drosophila indicates that Aaop3 and Aaop7, both classified as longwavelength rhodopsins, possess similar but not identical spectral properties. Light triggers an extensive translocation of Aaop3 from the photosensitive rhabdoms to the cytoplasmic compartment, whereas light-driven translocation of Aaop7 is limited. The results suggest that these photoreceptor cell types play distinct roles in larval vision. An additional component of the larval visual system is the adult compound eye, which starts to develop at the anterior face of the larval stemmata during the 1st instar stage. The photoreceptors of the developing compound eye show rhodopsin expression during the 4th larval instar stage, consistent with indications from previous reports that the adult compound eye contributes to larval and pupal visual capabilities.

He had previous history of acute myocardial infarction, pulmonary emphysema, type II diabetes mellitus, and arterial hypertension. On physical examination the patient had a fever, was hypotensive and tachycardic, and had left upper abdominal quadrant tenderness. Laboratory investigation revealed neutrophilic leukocytosis (14,000/m 3 white blood cells and 11,500/m 3 neutrophils), an increase of C-reactive protein (180 mg/dL), and a slight elevation of bilirubin levels (total bilirubin 1.8 mg/dL and direct bilirubin 1.0 mg/dL). An abdominal computed tomography scan was obtained revealing the diagnosis (Figure A), which prompted endoscopic evaluation. What is the diagnosis? See the Gastroenterology web site (www. gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI.

Coordination of cell proliferation and migration is fundamental for life, and its dysregulation has catastrophic consequences, such as cancer. How cell cycle progression affects migration, and vice-versa, remains largely unknown. We address these questions by combining in-silico modelling and in vivo experimentation in the zebrafish Trunk Neural Crest (TNC). TNC migrate collectively, forming chains with a leader cell directing the movement of trailing followers. We show that the acquisition of migratory identity is autonomously controlled by Notch signalling in TNC. High Notch activity defines leaders, while low Notch determines followers. Moreover, cell cycle progression is required for TNC migration and is regulated by Notch. Cells with low Notch activity stay longer in G1 and become followers, while leaders with high Notch activity quickly undergo G1/S transition and remain in S-phase longer. In conclusion, TNC migratory identities are defined through the interaction of Notch signalling and cell cycle progression.