Biologics can improve disease control in patients with psoriasis vulgaris (PsO) and psoriatic arthritis (PsA); however, refractory regions may persist despite biologic therapy. This study aimed to evaluate refractory anatomical regions in patients with PsO and PsA who underwent biologic switching. We retrospectively analyzed 71 biologic-switching episodes from 50 patients treated at Jichi Medical University Hospital between January 1, 2010 and December 31, 2019. Patients who underwent more than one biologic switch contributed multiple switching episodes. Refractory regions were assessed across 13 anatomical regions at the time of biological switching and at the end of the observation period. The lower extremities were the most frequently affected refractory region in both PsO and PsA, followed by the upper extremities in PsO and the scalp in PsA. Overall, the distribution of refractory regions was broadly similar before and after biologic switching. Improvement was defined as complete disappearance of a lesion that had been explicitly documented as present before biologic switching. Regions explicitly documented as lesion-free before switching were classified as non-improved, whereas regions without documentation regarding the presence or absence of a lesion before switching were excluded from the analysis. A logistic generalized linear mixed-effects model with a random intercept for switching episode was used to account for within-episode correlation among anatomical regions. The oral-to-biologic group had higher odds of documented lesion improvement than the biologic-to-biologic group (odds ratio, 2.12; p < 0.001), whereas disease subtype was not significantly associated with documented lesion improvement (PsO vs. PsA: odds ratio, 1.03; p = 0.876). These findings suggest that patients requiring biologic-to-biologic switching may represent a more treatment-refractory population. The lower extremities remained a particularly challenging anatomical region after biologic switching. Further prospective studies are warranted to clarify the factors associated with site-specific treatment response.

Genomic testing has become an essential adjunct to conventional histomorphology and immunohistochemistry in modern diagnostic surgical pathology, enabling more precise tumour classification, particularly in diagnostically challenging cases. This review focuses on the diagnostic applications of genomic techniques across multiple subspecialties, including bone and soft tissue pathology, dermatopathology, neuropathology, paediatric pathology, uropathology, and lymphoma pathology. A range of methodologies, such as fluorescence in situ hybridisation, polymerase chain reaction-based assays, and next-generation sequencing approaches (targeting DNA and RNA), are employed depending on the clinical question and the type of genomic alteration being investigated. In bone and soft tissue pathology, recurrent gene fusions, amplifications, and mutations serve as key diagnostic markers, especially in morphologically ambiguous lesions. In dermatopathology, genomic profiling plays a critical role in classifying melanocytic neoplasms, distinguishing histological mimics, and providing prognostic information. Neuropathology has pioneered integrated molecular-histological classification systems, with genomic alterations now central to the definition and grading of many central nervous system tumours. In paediatric pathology, tumours are frequently driven by structural chromosomal rearrangements and gene fusions, making RNA-based sequencing particularly valuable for diagnosis and therapeutic stratification. Similarly, molecular testing has refined the classification of renal tumours and improved the diagnostic accuracy of rare entities in uropathology. In lymphoma pathology, genomic alterations aid in distinguishing overlapping entities, confirming diagnoses, and identifying clinically significant subgroups. Emerging applications such as mutational signature analysis further enhance diagnostic precision by linking tumours to specific aetiological exposures or biological processes, which may assist in determining tumour origin in challenging cases. Despite its expanding role, genomic testing must be used judiciously and interpreted in the context of morphology, as many genetic alterations are not entirely disease-specific and assay limitations exist. Overall, the integration of genomic data with traditional pathology remains critical for accurate diagnosis, prognostication, and the advancement of precision medicine.

Due to increased understanding of the importance of high-throughput sequencing, the available literature on the microbiome of humans, non-human animals, and plants has increased in recent years. Unfortunately, research investigating fungi, as part of the microbiome, lags far behind bacterial research, and significant data gaps persist. However, the emergence of significant fungal diseases over the past few decades underscores the importance of understanding the mycobiota and their roles in host health and disease. Filling these knowledge gaps is critical for understanding and preventing diseases caused by fungi, especially for threatened and imperiled species. Here we focus on the imperiled leatherback sea turtle (Dermochelys coriacea). Recent work revealed that eggs and neonatal leatherbacks appear to be especially susceptible to fungal infections such as sea turtle egg fusariosis and mycotic dermatitis, respectively. As such, understanding of their mycobiota will add to our understanding of the pathogenesis of these diseases. Here, we characterize the mycobiota of leatherback sea turtles across three distinct life-stage classes (i.e., nesting females, neonates at nest emergence, and neonates at 3-4 weeks of age). We identified large shifts in the most predominant families and genera of fungi between life-stage classes and anatomic locations. Additionally, we found significant differences in beta diversity, suggesting that the fungal communities on leatherback skin differ between life-stage classes and anatomical locations. These data not only provide novel baseline mycobiota data for leatherback sea turtles but may also help elucidate the source of fungal infections in this species.

Magnesium (Mg)-based implants are promising for lamina defect reconstruction because of their biodegradability, mechanical compatibility, and bioactivity. However, in vivo degradation is usually assessed at the whole-implant level, and it remains unclear whether distinct regions of the same implant experience different degradation-repair couplings. In this study, a ZE21C Mg alloy artificial lamina was implanted in a New Zealand rabbit lumbar lamina defect reconstruction model to evaluate region-dependent degradation and local repair responses. Finite element analysis showed higher equivalent stress and strain on the residual-bone side. SEM/EDS and micro-CT analyses demonstrated the asymmetric degradation of the same implant in vivo. The residual-bone side exhibited faster Mg degradation, more severe surface and interfacial degradation, and higher TRAP-related remodeling activity, whereas the opposite side degraded more slowly, maintained a denser interface, and exhibited better bone formation and tissue integration. At 12 weeks, the remaining implant volume was 20.2 ± 2.0% on the residual-bone side, compared with 41.9 ± 5.3% on the opposite side, demonstrating pronounced region-dependent degradation within the same implant. Transcriptomic analysis indicated that rapid degradation was accompanied by stronger bone resorption and inflammatory interface reactions. The slow degradation area is associated with a more vascularized repair microenvironment that supports the matrix. These findings indicate that accelerated regional degradation does not necessarily promote bone regeneration. Therefore, region-specific degradation control may be critical for designing biodegradable Mg implants in complex anatomical environments. STATEMENT OF SIGNIFICANCE: Biodegradable magnesium implants are generally evaluated by their average degradation rate, despite regional differences in mechanical and biological environments. In a rabbit lamina reconstruction model, we directly compared two regions of the same ZE21C magnesium artificial lamina, limiting implant- and animal-level variability. The residual-bone side experienced higher stress, faster degradation, a less stable interface, stronger osteoclast-related activity, and poorer bone formation; the opposite side degraded more slowly and supported better tissue integration. Transcriptomic analysis linked these outcomes to distinct inflammatory, bone-resorptive, vascular, and matrix-remodeling responses. Thus, faster magnesium degradation does not necessarily improve repair. This work identifies region-specific degradation control as a key design principle for biodegradable orthopedic implants in complex anatomical environments.