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Objective: This study reviews the palaeopathological literature discussing maxillary sinusitis to examine current trends and issues within the study of this condition, and to make recommendations for future research in this area., Materials: Seventy-five studies were identified through a literature search of digital and physical sources., Methods: Information regarding study metadata, the populations investigated, sinusitis diagnostic criteria, and sinusitis prevalence was examined., Results: Populations from the UK and Europe were the most studied, reflecting both palaeopathology's systemic colonialism and academic legacies. Most studies used diagnostic criteria published in the mid-1990s, with some subsequent studies modifying these criteria., Conclusions: The diagnostic criteria from 1995 are widely used but do not include all possible bone changes seen within sinusitis. There is also a need for researchers to engage in issues of data reductionism when using descriptive categories for archaeological sites and populations., Significance: This paper provides considerations as to how the 1995 diagnostic criteria may be revised by future researchers and synthesises much of the published sinusitis prevalence data to assist researchers interested in the palaeopathology of respiratory disease., Limitations: More general osteological research, which includes palaeopathological information, was likely missed from this review due to the choice of key terms and languages used in the literature search., Suggestions for Further Research: Additional research into sinusitis in archaeological populations outside of Western Europe is required. Further work examining the ability to compare pathological data from macroscopic observation and medical imaging would be advantageous to palaeopathology as a whole., Competing Interests: Declaration of Competing Interest The authors declare no competing interests or sources of funding in the production of this work., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Use of percutaneous mechanical circulatory support has grown exponentially. Vascular complications remain a growing concern and best practices for device removal do not exist. We describe a novel post-closure technique for the next generation Impella CP removal and immediate hemostasis., Methods: This study is a single center, retrospective, exploratory analysis of 11 consecutive patients receiving an Impella CP for either high-risk PCI or cardiogenic shock and then referred for post-closure compared to 20 patients receiving manual compression for Impella CP removal between 2017 and 2019., Results: Mean age range was 62.7-65.4 years and 50-65% male between groups. Average duration of Impella CP treatment ranged from 3.4 to 5.2 days. Patients referred for post-closure had significantly lower rates of all-cause adverse vascular events (0% versus 40%; n = 0/11 versus n = 8/20; p = 0.01). There was no significant difference in BARC 3 or greater bleeding, transfusion requirement, hospitalization duration or intensive care duration between removal strategies., Conclusion: The novel post-closure technique may significantly reduce vascular complications associated with device removal and may improve clinical outcomes for these critically ill patients., Competing Interests: Declaration of competing interest CSH, KLT report no conflicts of interest. NKK is currently funded by the National Institutes of Health (RO1HL139785, RO1H133215) and has received research funding from Abiomed Inc., Abbott Inc., Boston Scientific Inc., MD Start Inc. and Maquet Cardiovascular Inc., (Copyright © 2021. Published by Elsevier Inc.)

Objective: To evaluate through differential diagnosis whether hypertrophic osteoarthropathy was present on an adult macaque skeleton., Materials: Skeletal remains of a well-preserved adult macaque (Macaca) of unknown species curated by the archaeology department at University College London., Methods: Macroscopic and radiographic evaluation of pathological lesions., Results: Widespread bilateral and symmetrical periosteal new bone growth primarily affecting the limbs was observed., Conclusion: A careful differential diagnosis of the lesions and comparison with previously published cases of hypertrophic osteoarthropathy among humans and non-humans suggests this animal displays a case of Hypertrophic osteoarthropathy., Significance: Only been three reported cases of HOA in non-human primates have been reported, and all were apes. This study serves as the first reported case of HOA among non-hominoid simians, providing a detailed description of the skeletal lesions to aid future with paleopathological analyses., Limitations: Small sample sizes for comparison and lack of context for this specimen limits discussion of the scope of this disease among non-human primates., Suggestions for Further Research: Re-evaluate skeletal collections which have not been subject to recent osteological and pathological analysis., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Failure of neural tube closure leads to neural tube defects (NTDs), common congenital abnormalities in humans. Among the genes whose loss of function causes NTDs in mice, Grainyhead-like3 (Grhl3) is essential for spinal neural tube closure, with null mutants exhibiting fully penetrant spina bifida. During spinal neurulation Grhl3 is initially expressed in the surface (non-neural) ectoderm, subsequently in the neuroepithelial component of the neural folds and at the node-streak border, and finally in the hindgut endoderm. Here, we show that endoderm-specific knockout of Grhl3 causes late-arising spinal NTDs, preceded by increased ventral curvature of the caudal region which was shown previously to suppress closure of the spinal neural folds. This finding supports the hypothesis that diminished Grhl3 expression in the hindgut is the cause of spinal NTDs in the curly tail, carrying a hypomorphic Grhl3 allele. Complete loss of Grhl3 function produces a more severe phenotype in which closure fails earlier in neurulation, before the stage of onset of expression in the hindgut of wild-type embryos. This implicates additional tissues and NTD mechanisms in Grhl3 null embryos. Conditional knockout of Grhl3 in the neural plate and node-streak border has minimal effect on closure, suggesting that abnormal function of surface ectoderm, where Grhl3 transcripts are first detected, is primarily responsible for early failure of spinal neurulation in Grhl3 null embryos., (Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.)

The enteric nervous system (ENS) is an extensive network of neurons in the gut wall that arises from neural crest-derived cells. Like other populations of neural crest cells, it is known that enteric neural crest-derived cells (ENCCs) influence the behaviour of each other and therefore must communicate. However, little is known about how ENCCs communicate with each other. In this study, we used Ca 2+ imaging to examine communication between ENCCs in the embryonic gut, using mice where ENCCs express a genetically-encoded calcium indicator. Spontaneous propagating calcium waves were observed between neighbouring ENCCs, through both neuronal and non-neuronal ENCCs. Pharmacological experiments showed wave propagation was not mediated by gap junctions, but by purinergic signalling via P2 receptors. The expression of several P2X and P2Y receptors was confirmed using RT-PCR. Furthermore, inhibition of P2 receptors altered the morphology of the ENCC network, without affecting neuronal differentiation or ENCC proliferation. It is well established that purines participate in synaptic transmission in the mature ENS. Our results describe, for the first time, purinergic signalling between ENCCs during pre-natal development, which plays roles in the propagation of Ca 2+ waves between ENCCs and in ENCC network formation. One previous study has shown that calcium signalling plays a role in sympathetic ganglia formation; our results suggest that calcium waves are likely to be important for enteric ganglia development., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Little is known of the first transcriptional events that regulate neural fate in response to extracellular signals such as Bmps and Fgfs. Sox3 is one of the earliest transcription factors to be expressed in the developing CNS and has been shown to be regulated by these signalling pathways. We have used both gain- and loss-of-function experiments in zebrafish to elucidate the role of Sox3 in determining neural fate. Ectopic Sox3 caused induction of neural tissue from a very early stage of cell specification in the ectoderm and this effect was maintained such that large domains of additional CNS were apparent, including almost complete duplications of the CNS. Knock-down of Sox3 using morpholinos resulted in a reduction in the size of the CNS, ears and eyes and subsequent inhibition of some aspects of neurogenesis. Our data also suggest that the pro-neural effects of Sox3 can compensate for inhibition of Fgf signalling in inducing neural tissue but it is not sufficient to maintain neural fate, suggesting the presence of Sox3-independent roles of Fgf at later stages.

The epibranchial placodes are cranial, ectodermal thickenings that give rise to sensory neurons of the peripheral nervous system. Despite their importance in the developing animal, the signals responsible for their induction remain unknown. Using the placodal marker, sox3, we have shown that the same Fgf signaling required for otic vesicle development is required for the development of the epibranchial placodes. Loss of both Fgf3 and Fgf8 is sufficient to block placode development. We further show that epibranchial sox3 expression is unaffected in mutants in which no otic placode forms, where dlx3b and dlx4b are knocked down, or deleted along with sox9a. However, the forkhead factor, Foxi1, is required for both otic and epibranchial placode development. Thus, both the otic and epibranchial placodes form in a common region of ectoderm under the influence of Fgfs, but these two structures subsequently develop independently. Although previous studies have investigated the signals that trigger neurogenesis from the epibranchial placodes, this represents the first demonstration of the signaling events that underlie the formation of the placodes themselves, and therefore, the process that determines which ectodermal cells will adopt a neural fate.