Journal of anatomy
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The objective of this paper was to collect normative data essential for analyzing the subplate (SP) role in pathogenesis of developmental disorders, characterized by abnormal circuitry, such as hypoxic-ischemic lesions, autism and schizophrenia. The main cytological features of the SP, such as low cell density, early differentiation of neurons and glia, plexiform arrangement of axons and dendrites, presence of synapses and a large amount of extracellular matrix (ECM) distinguish this compartment from the cell-dense cortical plate (CP; towards pia) and large fiber bundles of external axonal strata of fetal white matter (towards ventricle). For SP delineation from these adjacent layers based on combined cytological criteria, we analyzed the sublaminar distribution of different microstructural elements and the associated maturational gradients throughout development, using immunocytochemical and histological techniques on postmortem brain material (Zagreb Neuroembryological Collection). ⋯ The developmental dynamics for the distribution of neuronal, glial and ECM markers comply with sequential ingrowth of afferents in three levels of SP: ECM and synaptic markers shift from deep to superficial SP, with transient forms of glia following this arrangement, and calretinin neurons are concentrated in the SP during the formation phase. These results indicate developmental and morphogenetic roles in the SP cellular (transient glia, neurons and synapses) and ECM framework, enabling the spatial accommodation, navigation and establishment of numerous connections of cortical pathways in the expanded human brain. The original findings of early developmental dynamics of transitional subtypes of astroglia, calretinin neurons, ECM and synaptic markers presented in the SP are interesting in the light of recent concepts concerning its functional and morphogenetic role and an increasing interest in SP as a prospective substrate of abnormalities in cortical circuitry, leading to a cognitive deficit in different neurodevelopmental disorders.
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Decline of tactile sensation associated with ageing depends on modifications in skin and both central and peripheral nervous systems. At present, age-related changes in the periphery of the somatosensory system, particularly concerning the effects on mechanoreceptors, remain unknown. Here we used immunohistochemistry to analyse the age-dependent changes in Meissner's and Pacinian corpuscles as well as in Merkel cell-neurite complexes. ⋯ This study demonstrates that cutaneous Meissner's corpuscles and Merkel cell-neurite complexes (and less evidently Pacinian corpuscles) undergo morphological and size changes during the ageing process, as well as a reduction in terms of density. Furthermore, the mechanoprotein Piezo2 and the neurotrophic TrkB-BDNF system are reduced in aged corpuscles. Taken together, these alterations might explain part of the impairment of the somatosensory system associated with ageing.
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Three-dimensional (3D) printing, or additive manufacturing, is now a widely used tool in pre-operative planning, surgical teaching and simulator training. However, 3D printing technology that produces models with accurate haptic feedback, biomechanics and visuals for the training surgeon is not currently available. Challenges and opportunities in creating such surgical models will be discussed in this review paper. ⋯ This review summarises and evaluates the current biomechanical literature as it relates to human tissues and correlates the impact of this knowledge on developing high fidelity 3D printed surgical training models. We conclude that, currently, a printer technology has not yet been developed which can replicate many of the critical qualities of human tissue. Advances in 3D printing technology will be required to allow the printing of multi-material products to achieve the mechanical properties required.
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The sacroiliac joint (SIJ) is a well-known source of low back and pelvic pain, of increasing interest for both conservative and surgical treatment. Alterations in the kinematics of the pelvis have been hypothesized as a major cause of SIJ-related pain. However, definitions of both the range and the extent of physiological movement are controversial, and there are no clear baseline data for pathological alterations. ⋯ The present study provides evidence of different SIJ motions than reported previously when exerted by physiological loading. Sacroiliac joint kinematics were in the sub-degree and sub-millimeter range, in line with previous in vivo and in vitro findings, largely limited to the sagittal rotation and an inferior translation of the sacrum relative to the ilium. This given physiological loading scenario underlines the relevance of the lumbosacral transition when considering the overall motion of the lumbopelvis, and how relatively little the other segments contribute to overall motion.
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The aim of this study was to analyse the anatomy of the ventricular septal defect (VSD) in heart specimens with interruption of the aortic arch (IAA) in order to explore the hypothesis of different embryologic mechanisms for the different anatomic types of IAA. We examined 42 human heart specimens, 25 with IAA as the main disease with concordant atrioventricular and ventriculo-arterial connections and two distinct great arteries, and 17 hearts with IAA associated with other malformations [six common arterial trunk (CAT), five double-outlet right ventricle (DORV), three transposition of the great arteries (TGA), three atrioventricular septal defect (AVSD)]. The interruption was classified according to Celoria and Patton. ⋯ In addition, IAA type B, when found in the setting of another anomaly, was always associated with neural crest-related anomalies (CAT and DORV), whereas IAA type A was found in association with anomalies not related to the neural crest (TGA and AVSD). These results reinforce the hypothesis that different pathogenic mechanisms are responsible for the two types of IAA, and the inclusion of IAA type B in the group of neural crest defects. Conversely, IAA type A could be due to overlapping mechanisms: flow-related defect (coarctation-like) and neural crest contribution.