Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft最新文献

Background: For ventricular arrhythmias originating from the left ventricular summit (LVS), the anatomical characteristics of ablation sites may influence lesion formation and ablation outcome.

Methods: Dissection was performed on 12 swine hearts to investigate anatomical characteristics of the LVS. Radiofrequency ablation was conducted in 17 swine hearts at 6 distinct sites, including the great cardiac vein (GCV), accessible area of the LVS, inaccessible area of the LVS, left coronary cusp (LCC), left ventricular outflow tract (LVOT) and right ventricular outflow tract (RVOT), for the purpose of evaluating ablation lesions.

Results: Anatomically, the LVS apex carried a thicker epicardial-fat pad and a thinner myocardial wall than its base. The great cardiac vein/anterior interventricular vein (GCV/AIV) was separated from underlying myocardium by 2.54 mm (1.43, 3.86mm) of epicardial fat. Between the LCC and myocardium, a 1.51±0.82 mm layer of fibrous tissue was consistently found. Among 263 radiofrequency applications, 29 (11.0%) produced steam pops; 17 of these (58.6%) occurred in the accessible area. Seventy lesions (26.6%) left no discernible myocardial necrosis; the vast majority of these ineffective applications were delivered to the inaccessible area, the accessible area, within the GCV, or on the LCC. Mean lesion depth in the inaccessible area (1.52±0.28 mm), accessible area (1.64±0.99 mm), GCV (2.16±0.70 mm) and LCC (2.60±0.72 mm) was significantly shallower than in the LVOT (4.43±0.57 mm) or RVOT (4.15±0.52 mm) (P<0.05).

Conclusions: At the apex of the LVS, epicardial fat is thickest and the underlying myocardium thinnest. Consequently, epicardial ablation produces markedly shallower lesion and a significantly higher incidence of steam pop than endocardial ablation.

Background: Accurate determination of sheep age is essential for optimizing meat quality, reproductive efficiency, feeding strategies, and market value. Conventional age estimation methods rely on subjective visual inspection of dental structures and are prone to inconsistency and human error. Therefore, automated solutions capable of providing objective and reproducible assessments are needed.

Methods: This study proposes a fully automated deep learning and image processing framework for sheep age estimation using dental images. Class imbalance in the dataset was addressed through systematic data augmentation. The images were then segmented using the You Only Look Once version 8 (YOLOv8) algorithm to isolate anatomically relevant tooth regions. Several Convolutional Neural Network (CNN) architectures were evaluated and compared, including VGG16, ResNet50, EfficientNetB0, MobileNetV2, and Xception, fine-tuned via transfer learning, as well as a custom BasicCNN model. A graphical user interface (GUI) was also developed and deployed as a publicly accessible, containerized application to provide a practical and user-friendly implementation of the prediction system.

Results: Among the evaluated models, EfficientNetB0 achieved the highest performance, attaining an overall accuracy of 95%, with 97% for the 3-12-month and 2-3-year groups, 92% for the 1-1.5-year group, and 93% for the 1.5-2-year group. These results demonstrate that combining automatic segmentation with transfer learning substantially improves model generalization and classification accuracy.

Conclusions: The proposed framework offers a robust, automated, and scalable solution for sheep age estimation. By eliminating manual assessment, the system contributes to precision livestock farming and supports informed decision-making in agricultural practice. The integration of deep learning, automatic segmentation, and a user-friendly interface highlights its potential for broader adoption in real-world field applications.

Background: Contemporary anatomical education exhibits significant systemic representational biases, which undermine clinical preparedness and health equity. This study assesses the current state of racial, sex, and skin tone diversity across key anatomical education resources, including literature, textbooks, and digital platforms.

Methods: A multi-modal content analysis was conducted. A systematic search of PubMed/MEDLINE (1800-2025) identified 8,635 articles for sex analysis and 2,291 for racial analysis. All 5,712 illustrations from four major anatomy textbooks (Grant's, Netter's, Gray's, Sobotta) were screened, with 1,954 meeting inclusion criteria. Six commercial digital anatomy platforms were evaluated for their default and adjustable sex and skin tone settings. Data on sex, race/ethnicity, and skin tone were extracted using standardized coding protocols with high inter-rater reliability (Cohen's κ > 0.85).

Results: Textbook illustrations were overwhelmingly male (86.13%) and depicted light skin tones (over 95%). Literature analysis revealed a historical predominance of male-only studies, which has decreased over time, while female-only studies remain chronically underrepresented (<26%). Racial reporting showed a dramatic decline in mentions of African/Black populations (32.78% to 10.86%) and a surge in Asian mentions (15.23% to 46.96%). Most digital platforms (83.3%) defaulted to light skin and lacked skin tone adjustability.

Conclusions: Anatomical education resources persistently reflect a Eurocentric, male-centric norm. These representational biases risk perpetuating clinical disparities. Urgent, systemic reforms-including redesigning curricular resources, enhancing technological customization, and implementing educator bias training-are imperative to align anatomical pedagogy with global human diversity and advance equitable healthcare.

Background: The intra- and inter-lobular configuration of pulmonary lymph vessels and nodules remains obscure. CD169-positive macrophages and dendritic cells (DCs) cross-present cancer antigens to T lymphocytes.

Methods: We examined 40 tissue blocks from 20 surgically obtained lung lobes immunohistochemically and morphometrically. All 20 patients with lung cancer survived more than five years without metastasis.

Results: Podoplanin-positive lymph vessels (LVs) with or without concomitant arteriole arose from interalveolar septa, where lymph vessel endothelia adjoined alveolar epithelia. In contrast, we did not find LVs along the terminal bronchiole within 0.5mm from the end at alveoli. Lymph nodules were rare in alveolar tissue 60-80mm from the cancer lesion; if present, they were 0.1-0.3mm across, attached to a lymph vessel, and largely composed of T lymphocytes. By contrast, alveolar tissue near the cancer (5-10mm) often contained larger nodules 0.2-1.0mm thick. These nodules had no polarization in architecture and consistently accompanied LVs. Arteriole-associated nodules and subpleural nodules were predominant, while bronchiole-associated nodules were fewer in all specimens. The subpleural nodule, receiving LVs along interlobular veins, was sometimes large. The nodule near the cancer always contained DC-SIGN-positive DCs, CD169-positive macrophages, and B cell-dominant lymphocytes; CD1a- or CD83-positive DCs were occasionally present. Nodules from smokers contained significantly more DCs and CD169-positive macrophages.

Conclusion: Lymph nodules seemed to obtain cancer antigens from "afferent LVs" along intralobular arterioles and interlobular veins and they might play a critical role for providing activated or suppressed DCs and macrophages to the regional node. 250.

Introduction: According to the current concept the joint is an organ composed of multiple tissues forming manifold communicating interfaces. Moreover, cartilage itself presents typical intrinsic zonal interfaces. Since the healthy joint cartilage is not vascularized, soluble mediators are distributed by the synovia fluid flow in the cartilage extracellular matrix (ECM) of the joint compartments. This distribution is dependent on intermittent mechanical loading and water flow in the joint. Hence, soluble factors play a pivotal role in articular cartilage interfacial communication. These mediators must traverse the cartilage ECM, whose permeability and binding capacity for growth factors and signaling molecules vary according to its structural integrity (e.g. pathology) and homeostasis.

Main part: Cartilage lesions, e.g., due to osteoarthritis (OA), substantially alter the interfacial communication. Chondrocyte phenotype, subpopulations and cartilage ECM density changes in OA. Superficial zones, and during disease progression, deep zones, are lost over time. OA is closely linked to metabolic disorders like type 2 diabetes mellitus (T2DM), characterized by hyperglycemia. Elevated glucose levels promote aberrant glycosylation of cellular and ECM glycoproteins, formation of advanced glycation end products (AGEs), excessive ECM cross-linking, reduced elasticity, and chondrocyte aging associated with the senescence-associated secretory phenotype (SASP). Cartilage immunobiology comprises a dysregulation of complement split fragments and pro-/anti-inflammatory mediators: their release influences chondrocyte phenotype.

Conclusions: Intrinsic cartilage interface communication changes in joint cartilage disorders such as OA and associated systemic diseases. The role of immunobiological complement factors and pleiotrophic cytokines is still to be elucidated in articular cartilage in vivo and in OA patients.

The osteochondral unit is formed by the articular cartilage, calcified cartilage and subchondral bone. They structurally and functionally communicate with each other in a mechano-adapted fashion, in joint homeostasis and osteoarthritis (OA). The tibial plateau is in the focus of many anatomical and translational studies because it enables knee stability and function and is frequently affected by OA. The normal human tibial plateau has a thin and porous subchondral bone plate, covered by a considerably thicker articular cartilage. Fundamental topographical relationships exist between many components of a normal ovine osteochondral unit in the central region. The absence of such correlations in the submeniscal (peripheral) region highlights the clinical importance of the meniscus within this osteochondral-meniscal unit. In OA, pathological remodeling of the subchondral bone is associated with enhanced articular cartilage degradation in a location-dependent fashion. Early OA established in sheep following a defined meniscus injury reflects the important clinical fact that human knee OA is spatially heterogeneous. Many previously normal correlations within an osteochondral unit are reduced in OA. Varus alignment of the leg in the frontal plane is characterized by site-specific effects of OA on the osteochondral unit of the lesser loaded lateral compartment. Therapeutic surgical unloading has shown its value both in translational models and clinical studies to be capable of shifting the osteochondral phenotype towards normal, restoring several disturbed osteochondral correlations. This concept of spatial osteochondral patterning emphasizes the importance of understanding how its individual parts are interconnected at different levels in joint homeostasis and OA.

Introduction: The Leopoldina Symposium on "Skeletal Interfaces in Health and Disease" at Paracelsus Medical University (Salzburg, Austria) gathered an interdisciplinary community of young and experienced scientists, to explore how crossing disciplinary boundaries can generate new insights and methodologies. While research traditionally focuses on organ- or disease-specific questions, this symposium aimed to connect seemingly distant scientific fields by exploring interfaces, pivotal zones of separation and integration. It intended to foster broader understanding of musculoskeletal biology and diseases, including domains of skeletal development, anthropology, research, and technology.

Main part: The symposium opened with the Young Investigator poster (pitch) session showcasing new topics in musculoskeletal research. The first invited session focused on developmental, anthropologic, structure/outcome, academia/industry, and artificial/natural intelligence interfaces. The public evening lecture discussed how bones "learn to listen", highlighting vibration therapy and bone-interface biomechanics. The next session featured cartilage-cartilage, cartilage-tissue, and cartilage-meniscus interfaces. Bone-cartilage interfaces were then explored from a molecular, imaging, translational and immunological perspectives. The final session dealt with tendon-tissue, tendon-bone (enthesis), synovial tissue and epiphyseal interfaces, followed by a podium discussion that integrated insights across disciplines.

Conclusions: By creating a platform for cross-disciplinary exchange, the symposium illustrated how musculoskeletal research benefits from conceptual bridges between different scientific fields. Such interfaces may not only inspire novel research questions, but also hold potential to redefine clinical applications and public health strategies. This perspective article reflects the transdisciplinary spirit of the symposium, aiming to capture and communicate the enthusiasm, scientific breadth, and collaborative energy that emerged during the meeting.

The bone-immune interface is increasingly recognized as a central regulator of skeletal regeneration. In addition to its structural and metabolic functions, bone contains specialized immunological niches that shape the composition and behavior of adaptive and innate immune cells. Recent advances in osteoimmunology demonstrate that the dynamics of immune cells - particularly the balance between pro-inflammatory effector responses and their regulatory mechanisms - critically influence the course of fracture healing. Dysregulated adaptive immunity can prolong early inflammation and impair the function of osteogenic progenitors, thereby disrupting the coordinated progression of the repair process. This Perspective synthesizes emerging evidence on how immunological memory, inflammatory kinetics and adaptive immune heterogeneity interact to shape skeletal repair. It highlights the growing potential of immune profiling for early risk stratification, alongside preclinical and early clinical data supporting targeted immunomodulatory strategies aimed at restoring a pro-regenerative inflammatory environment. Together, these developments support a conceptual shift from purely mechanical models of fracture healing toward biologically informed, precision‑guided approaches with the potential to improve outcomes in patients at increased risk of regenerative failure.

Musculoskeletal tissue interfaces (TIs), including osteotendinous, myotendinous, and osteochondral junctions, are specialized regions that enable effective force transmission, mechanical stability, and long-term tissue integration. These interfaces are defined by gradients in cellular composition, extracellular matrix (ECM) organization, and mechanical properties, and their maintenance relies in part on tightly regulated cell-matrix interactions. Beyond structural ECM components, matricellular proteins such as Secreted Protein Acidic and Rich in Cysteine (SPARC), thrombospondins, osteopontin, periostin, and tenascins have emerged as critical modulators of interface biology by shaping ECM assembly, mechanotransduction, and adaptive cellular responses to load. SPARC has been shown to impact on collagen fibrillogenesis, ECM organization, and cell-matrix signaling across multiple musculoskeletal tissues. It is increasingly recognized as a regulator of load-bearing musculoskeletal tissue interfaces, where its dysregulation drives maladaptive remodeling marked by fibrosis, ectopic mineralization, and reduced regenerative capacity across pathologies such as tendinopathy, intervertebral disc disease, and osteoarthritis. This mini-review summarizes current knowledge on matricellular regulation at musculoskeletal tissue interfaces, with a focus on SPARC, integrating evidence from genetic models to investigate its role in interface homeostasis, mechanical adaptation, and pathological remodeling.