Paul A. Felts

The ventricular layer of the spinal cord is remodelled during embryonic development and ultimately forms the ependymal cell lining of the adult central canal, which retains neural stem cell potential. This anatomical transformation involves the process of dorsal collapse; however, accompanying changes in tissue organisation and cell behaviour as well as the precise origin of cells contributing to the central canal are not well understood. Here, we describe sequential localised cell rearrangements which accompany the gradual attrition of the spinal cord ventricular layer during development. This includes local breakdown of the pseudostratified organisation of the dorsal ventricular layer prefiguring dorsal collapse and evidence for a new phenomenon, ventral dissociation, during which the ventral‐most floor plate cells separate from a subset that are retained around the central canal. Using cell proliferation markers and cell‐cycle reporter mice, we further show that following dorsal collapse, ventricular layer attrition involves an overall reduction in cell proliferation, characterised by an intriguing increase in the percentage of cells in G1/S. In contrast, programmed cell death does not contribute to ventricular layer remodelling. By analysing transcript and protein expression patterns associated with key signalling pathways, we provide evidence for a gradual decline in ventral sonic hedgehog activity and an accompanying ventral expansion of initial dorsal bone morphogenetic protein signalling, which comes to dominate the forming the central canal lining. This study identifies multiple steps that may contribute to spinal cord ventricular layer attrition and adds to increasing evidence for the heterogeneous origin of the spinal cord ependymal cell population, which includes cells from the floor plate and the roof plate as well as ventral progenitor domains.

Cadaver preservation methods impact their utilization in anatomical research and teaching. Thiel‐embalmed cadavers show flexibility, however, the cause remains poorly understood. This study aimed to (1) describe qualitative and quantitative histological differences between Thiel‐embalmed and formalin‐fixed skeletal muscle and tendon tissue; (2) investigate whether boric acid in Thiel solution is solely responsible for modification of tissues; and (3) explore whether the modifications observed could potentially explain the mechanisms underpinning flexibility of Thiel cadavers. Skeletal muscle and tendon samples were harvested from mice preserved using formalin, Thiel solution, or modified‐Thiel solution (without boric acid). Using standard H&E and Gomori's trichrome histological methods, tissues were examined to determine whether differences were apparent between the preservative treatments. Differences were present between the Thiel and formalin‐fixed tissues; formalin‐fixed samples remained substantially more intact while Thiel‐embalmed samples showed fiber fragmentation and lack of nuclei. The mean cell diameter of Thiel‐embalmed muscle (24.4 μm) was significantly smaller (P < 0.005) than formalin‐fixed muscle (40.7 μm). There was significantly greater (P < 0.005) fragmentation in Thiel‐embalmed muscle (631.5 per 1 mm²) compared to formalin‐fixed muscle (75.4 per 1 mm²). Samples embalmed using modified‐Thiel showed a severe lack of integrity within internal tissue structure. This suggests that Thiel solution significantly alters tissue structure at cellular level, with quantitative data demonstrating measurable differences between Thiel and formalin‐fixed specimens. While the precise mechanism for these alterations remains unknown, it is shown that boric acid is not the only component of Thiel responsible for degradation of internal tissue structure. Clin. Anat., 33:696–704, 2020.

The ventricular layer of the spinal cord is remodelled during embryonic development and ultimately forms the adult central canal, which retains neural stem cell potential. This anatomical transformation involves the process of dorsal collapse, however, accompanying changes in tissue organization and cell behaviour as well as the origin of cells contributing to the adult central canal are not well understood. Here we describe sequential localised cell rearrangements which contribute to the gradual attrition of the spinal cord ventricular layer during development. This includes local breakdown of the pseudostratified organisation of the dorsal ventricular layer prefiguring dorsal collapse and evidence for a new phenomenon, ventral dissociation, during which the ventral-most floor plate cells separate from a subset that are retained in the central canal. Using cell proliferation markers and cell-cycle reporter mice, we further show that following dorsal collapse, ventricular layer attrition involves an overall reduction in cell proliferation, characterised by an intriguing increase in the percentage of cells in G1/S. In contrast, programmed cell death does not contribute to ventricular layer remodelling. By analysing transcript and protein expression patterns associated with key signalling pathways, we provide evidence for a gradual decline in ventral sonic hedgehog activity and an accompanying ventral expansion of initial dorsal bone morphogenetic protein signalling, which comes to dominate the forming central canal. This study identifies multiple steps that contribute to spinal cord ventricular layer attrition and adds to increasing evidence for the heterogenous origin of the adult spinal cord central canal, which includes cells from the floor plate and the roof plate as well as ventral progenitor domain.

Background: Although the glenoid labrum has an important role in shoulder stability, little is known about its composition, vascularity and innervation. The aims of this study were therefore to evaluate the histology, vascularity and innervation of the glenoid labrum. Materials and methods: Ten glenoid labrum specimens (three male, two female: mean age 81.2 years, range 76–90 years) were detached at the glenoid neck. Following decalcification, sections were cut through the whole thickness of each specimen perpendicular to the glenoid labrum at 12 radii corresponding to a clock face superimposed on the glenoid fossa. Then they were stained using haematoxylin and eosin, a silver nitrate protocol or subjected to immunohistochemistry using anti-protein gene protein 9.5 to demonstrate neuronal processes. Results: The labrum was fibrocartilaginous, being more fibrous in its free margin. There was a variable distribution of blood vessels, being more vascular in its periphery, with many originating from the fibrous capsule and piercing the glenoid labrum. Immunohistochemistry revealed positive staining of nerve fibres within the glenoid labrum. Conclusion: The glenoid labrum is fibrocartilaginous, being more fibrous in its periphery, and is vascularized, with the anterosuperior aspect having a rich blood supply. Free sensory nerve fibres were also present; no encapsulated mechanoreceptors were observed. The presence of sensory nerve fibres in the glenoid labrum could explain why tears induce pain. It is postulated that these sensory fibres could play a role in glenohumeral joint proprioception.

Background: Tears of the glenoid labrum are common after dislocation of the glenohumeral joint. The outcome for healing or surgical reconstruction of the glenoid labrum relies on the extent of its vascularization. This study aims to evaluate the glenoid labrum blood supply and to determine its regional vascularity. Materials and Methods: A total of 140 shoulders (30 male and 40 female cadavers) were examined: mean age 81.5 years, range 53–101 years. All blood vessels around the glenohumeral joint were dissected and recorded. Ten specimens with the glenoid labrum and fibrous capsule attached were randomly selected and detached at the glenoid neck and subjected to decalcification. Sections (10–20 μm) were cut through the whole thickness of each specimen from the centre of the glenoid fossa perpendicular to the glenoid labrum at 12 radii corresponding to a clock face superimposed on the glenoid. Sections were stained using haematoxylin and eosin and then examined. Results: The blood supply to the glenoid labrum is by direct branches from the second part of the axillary artery, subscapular, circumflex scapular and anterior circumflex humeral and posterior circumflex humeral arteries, as well as branches of muscular arteries supplying the surrounding muscles. Conclusion: This study shows that the glenoid labrum has a rich blood supply suggesting that, regardless of the types of the glenoid labrum lesions or their management, an excellent outcome for glenoid labrum healing and joint stability is possible. The observations also suggest that the blood supply to the glenoid labrum is sufficient, enabling its reattachment.

Summary: Despite widespread use of ultrasound imaging to guide needle placement, the incidence of transient and permanent nerve damage as a complication of regional anaesthesia has not changed over the last decade. In view of the controversy surrounding intraneural injection there is a need to understand the structural changes caused by subepineural and subperineural needle penetration. Clinical ultrasound machines do not provide adequate anatomical resolution, and anaesthetists have difficulty judging the precise location of the needle tip relative to the epineurium. We studied the suitability of micro‐ultrasound imaging (which offers anatomical resolution better than 100 μm) as a tool for viewing neural anatomy and deformation caused by needle insertion. The primary objective was to assess micro‐ultrasound imaging as a method to view fascicles within nerves resected from fresh and soft‐embalmed cadavers. Secondary objectives were to observe any disruption of the neural anatomy caused by anaesthetic needle penetration, and to assess the integrity of fresh and Thiel method soft‐embalmed nerves, after handling and during needle insertion using ultrasound images and histology. We imaged nine nerves from the left and right sides of fresh and soft‐embalmed cadavers. A regional block needle was inserted into three median nerves. We identified fascicles > 0.4 mm in width using micro‐ultrasound. Subepineural needle placement was associated with denting, rotation and elastic deformation of fascicles, whereas subperineural needle insertion split fascicles permanently.

Primary loss and dysfunction of astrocytes may trigger demyelination, as seen in neuromyelitis optica, an inflammatory disease of the central nervous system. In most patients affected by this disease, injury to astrocytes is initiated by the action of autoantibodies targeting aquaporin 4 (AQP-4), a water channel on astrocytes. We show here that damage of astrocytes and subsequent demyelination can also occur in the absence of autoantibody-mediated mechanisms. Following injection of lipopolysaccharide into the white matter initial microglia activation is followed by a functional disturbance of astrocytes, mainly reflected by retraction of astrocytic foot processes at the glia limitans and loss of AQP-4 and connexins, which are involved in the formation of gap junctions between astrocytes and oligodendrocytes. Demyelination and oligodendrocyte degeneration in this model follows astrocyte pathology. Similar structural abnormalities were also seen in a subset of active lesions in multiple sclerosis. Our studies suggest that astrocyte injury may be an important early step in the cascade of lesion formation in brain inflammation.