Clinical Anatomy最新文献

Mast cells are present in all classes of Vertebrates and have emerged > 500 million years ago, long before the development of adaptive immunity. Mast cells were first identified by the Nobel Prize winner Paul Ehrlich in 1878, when he was still a medical student. Mast cells are localized at the junction point of the host and external environment at places of entry of antigens (gastrointestinal tract, skin, and respiratory epithelium). Mast cells have been recognized as crucial effectors in both innate and adaptive immune responses. Mast cells protect against bacteria, fungi, protozoa, and viruses through the release of proinflammatory and chemotactic mediators. There is evidence that mast cells exert relevant functions in tissue homeostasis, remodeling, repair, and fibrosis. Moreover, mast cells accumulate at sites of tumor growth in response to numerous chemoattractants and release a vast array of mediators, some of which have promoting and others inhibitory effects on malignancies.

The Calvarial Blooming Model (CBM) describes cranial vault growth as a Class III lever system in which patterned brain expansion supplies the effort, dural tethers act as fulcra, and sutures serve as load-transfer zones. In contrast to models emphasizing muscular loading or genetic determinism, CBM frames the cranium as a compliant, tension-sensitive structure shaped by cerebral growth, cerebrospinal fluid (CSF) buoyancy, and intracranial pulsations. Evidence from multiple sources was used to illustrate the framework. Bolton Standards cephalometric superimpositions (ages 6-18) provided conservative estimates of sutural displacement and vault surface area expansion. Cases from the AAOF Legacy Collection demonstrated late-phase remodeling often absent in standard datasets. Published finite-element analyses of sutural strain and dural tension pathways, together with clinical and histological observations, further supported the model. Perturbations of genetic and environmental regulators-including RUNX2, FGFRs, and BMPs-disrupt these strain pathways and produce craniofacial anomalies consistent with CBM predictions. Recognizing cranial vault expansion as the action of a tensioned dural hammock operating under Class III lever mechanics clarifies how patterned brain growth directs vault remodeling and suggests new approaches to craniosynostosis correction and growth modification.

The uterine tubes and uterus develop from the paramesonephric (Müllerian) ducts. Most experimental data are obtained in rodents. Since the (micro-)anatomy of the murine urogenital tract differs from that in humans, evaluation of the translatability of mouse data to human development is relevant. We studied the Müllerian ducts in serially sectioned female human embryos and fetuses between 5 and 15 weeks of development and prepared 3D-reconstructions to establish topographic relations. At 5 weeks of development, the dorsocranial peritoneal epithelium thickens locally to form a placode-like structure, which remodels into the tubal orifice at 6 weeks. The subsequent caudal extension of the Müllerian ducts requires its temporary stay with the mesonephric (Wolffian) duct inside a common basement membrane. The site where the Müllerian segment expands passes as a wave along the Wolffian duct. This wave breaks when the tubes reach the lesser pelvis in the 8th week. There, both Müllerian ducts fuse to form the single uterovaginal canal. No fusion occurs most caudally, where the Müllerian ducts elicit the Müllerian tubercle in the dorsal wall of the urogenital sinus. The uterovaginal canal becomes encased in a mesenchymal cuff, the genital cord. The gubernaculum, which appears at 6.5 weeks as a tissue bridge between the mesonephros and the lateral body wall, eventually becomes the round ligament in females. At 12 weeks, it is still an intraperitoneal structure in an evagination of the abdominal cavity. Unexpectedly, the early development of the uterovaginal canal was similar in human and mouse embryos.

Xenotransplantation (specifically, genetically modified pig-to-human transplant of organs, tissues, or cells) clinical trials are set to begin in the United States after decades of pre-clinical studies and recent decedent and compassionate use investigations. This article provides a primer on the key ethical issues attendant with this emerging therapy. We explore four central areas of concern: (i) the use of animals to meet human transplant needs, as well as their welfare since they are housed in non-natural conditions, (ii) the risk of infectious disease transfer from the porcine graft to the human recipient, known as xenozoonosis, (iii) patient selection criteria for initial clinical trials when an unknown risk/benefit ratio exists, and (iv) the necessity of public engagement in order to increase acceptance and trust of this novel potential therapy. The article argues that the long-term success and social acceptance of xenotransplantation are contingent not only on overcoming immunological hurdles but also on thoughtfully considering the ethical issues.

The structural and functional adaptation of soft tissues to mechanical load controls their ability to withstand injury and influences their capacity for healing. Similar to the knee meniscus, the acetabular labrum exhibits zonal differences in mechanical load distribution, resulting in distinct regions with unique structural and functional properties. However, little is known about the effect of these zonal adaptations on the severity and distribution of labral degenerative changes. This study aims to assess the impact of labral zonal adaptations on the severity and distribution of histopathologic features. Human tissue was obtained from 9 embalmed cadavers, comprising a total of 16 hemipelves (10 males and 6 females) with an average age of 80 years (age range 66-99). Each hip was divided into 8 distinct regions, resulting in 128 regional segments. Slides were stained using Hematoxylin and Eosin (H&E) and Safranin-O (Saf O), with the incorporation of fluorescent scanning of eosin (F-Eosin). Labral histopathologic features were assessed using established modified grading criteria for the knee meniscus. These features were evaluated both globally across the anatomical quadrants of the hip joint and zonally across the inner and outer zones. The global analysis of the labrum revealed a similar distribution of histopathologic features across the superior, anterior, inferior, and posterior quadrants of the hip joint. Conversely, across 128 labral segments, pairwise zonal assessments revealed a significant increase (p < 0.05) in the severity of degenerative features, which were predominantly concentrated in the inner labral zone near the articular surface. These degenerative changes encompassed alterations in matrix proteoglycan content, cellularity, collagen organization, and labral articular surface, including the lamellar layer. The increased compactness of labral fibers in the inner zone, minimal vascular penetration, and significant degenerative changes imply that it is a vulnerable area for injury with a potentially limited capacity for healing. The delineation of these distinct zonal frameworks highlights the labrum's functional adaptation to its mechanical environment. The zonal analysis of the labrum provided a considerably more detailed perspective on the distribution dynamics of histopathologic features compared to previous global analyses, offering a more precise understanding of the anatomical factors that may explain zone-specific vulnerability to injury and degeneration.

Neurogenic thoracic outlet syndrome (TOS) occurs in three major anatomical locations, including the interscalene triangle. Because symptoms of TOS are reproduced on upper limb abduction, this study aimed to examine the impact of glenohumeral abduction on the triangle's dimensions and whether this may contribute to compression of the structures which traverse it. Ten interscalene triangles were dissected from five body donor specimens bilaterally to measure the length of the anterior and middle scalene muscles, and inferior border of the scalene triangle when the upper limb was abducted to 0°, 90°, and at maximal abduction. Both the anterior and middle scalene lengths decreased as the angle of abduction increased, with the greatest decrease being between 0° and 90° (p = 0.0003). No significant decrease in length was shown between 90° and > 90° abduction (p = 0.48) nor was there a significant change in the overall area of the triangle throughout abduction (p = 0.58). This suggests that TOS symptoms may not correlate with the degree of upper limb abduction as previously thought. Additionally, there were significant differences between parameters of the superficial triangle measured by most previous studies, and a deeper triangle within the same space at all levels of abduction. This study therefore recommends further exploration into the dynamic nature of the interscalene triangle.