Linear cutaneous discoid lupus erythematosus (LCDLE) is a rare presentation of lupus erythematosus, more frequently observed in children and young adults. Clinically, lesions present as unilateral, linear, erythematous plaques, frequently involving the face, but the neck, trunk, or extremities can also be affected. Several reports have documented cutaneous adverse events following both SARS-CoV-2 infection and various types of COVID-19 vaccination. Among these adverse events, autoimmune skin conditions, such as cutaneous lupus erythematosus, have emerged as an area of interest. Here, we present a challenging case of a 15-year-old boy who developed LCDLE on his right upper extremity 1 month after the second dose of COVID-19 vaccination.

Lupus erythematosus (LE) skin lesions are associated with significant dysregulation of the local immune microenvironment. However, the spatial distribution and interactions between stromal and immune cells within affected tissues remain poorly characterized. In this study, we employed Stereo-seq to construct a single-cell resolution spatial transcriptomic atlas of lesional skin from patients with discoid lupus erythematosus (DLE) and systemic lupus erythematosus (SLE). Our analysis revealed that keratinocyte subpopulations in distinct differentiation states presented cell type-specific profiles of inflammatory mediator expression. Notably, a subset of stress keratinocytes located predominantly at the epidermis-dermis interface mediated the recruitment of T cells and plasma cells, potentially through an IFN-γ-JAK-STAT axis driving CXCL9/10/11-CXCR3 signaling, and these effects were more pronounced in active SLE lesions compared to chronic DLE lesions. Spatial profiling revealed immune cell niches resembling tertiary lymphoid structures (TLS), which were particularly prominent in chronic DLE and SLE lesions. These lupus-associated TLS structures were characterized by the coordinated infiltration of multiple cell subsets, including age-associated B cells, precursors of germinal center B cells, naïve B cells, regulatory T cells, T peripheral helper and/or T follicular helper cells, memory T cells, and CCL14+ vascular endothelial cells, which presented the spatial characteristics of the lymphoid follicle-like structures in chronic LE skin lesions. Collectively, our findings provide a comprehensive spatial characterization of the cellular components and molecular features within LE skin lesions.

Discoid lupus erythematosus is a chronic autoimmune inflammatory dermatosis characterized by erythematous, scaly plaques that may progress to permanent atrophy, scarring, and pigmentary alterations. The auricle is a recognized site of involvement in discoid lupus erythematosus; however, isolated lesions confined to the auricular conchae are less frequently described and may pose diagnostic challenges because of their clinical resemblance to other inflammatory, infectious, or neoplastic conditions of the ear. We report the case of a 35-year-old woman with a 15-year history of asymptomatic bilateral lesions involving the auricular conchae. Physical examination revealed violaceous, poorly defined oval plaques with thick, adherent whitish scale, accompanied by multiple whitish filiform papules consistent with the carpet tack sign. Dermoscopic evaluation demonstrated a violaceous-brown plaque with thick adherent scale, multiple whitish punctate projections, and perifollicular whitish halos. Histopathological examination showed epidermal atrophy, prominent follicular plugging, interface dermatitis with apoptotic keratinocytes, dermal melanophages, thickening of the basal membrane, and increased interstitial mucin, findings consistent with discoid lupus erythematosus. This case highlights the diagnostic value of recognizing characteristic clinical and dermoscopic features, particularly the carpet tack sign, in localized auricular disease. Early identification enables timely diagnosis and appropriate management, thereby helping to prevent irreversible scarring and long-term sequelae in this anatomically and aesthetically sensitive area.

Polymer geometry is a primary determinant of physical behavior and biological performance. Beyond conventional spherical and bulk morphologies, unconventional three-dimensional (3D) architectures - ranging from anisotropic particles and fibers to complex membrane-based systems - have emerged as powerful tools for biomedicine. Advances in fabrication methods, including microfluidics, lithography, and physical deformation techniques, now enable precise control of particle shape, anisotropy, and compartmentalization at the nano- and microscale. These geometrical cues strongly influence critical biological processes such as cellular adhesion, phagocytosis, biodistribution, and immune activation, while also modulating drug release, tissue targeting, and responsiveness to external stimuli. Bioinspired designs, including red-blood-cell-like discoids, microneedles, and helical fibers, exemplify how shape engineering can enhance circulation time, mechanical adaptability, and improve integration with biological systems. Moreover, membrane-based polymersomes and multicompartment capsules extend this paradigm by introducing hierarchical organization and dynamic shape transformation. This Review focuses on the most recent advances in the design, fabrication, and biomedical translation of polymeric structures with unconventional geometries, highlighting the interplay between form and function as a central principle in next-generation biomaterials. Ultimately, controlling shape across scales offers unprecedented opportunities to develop responsive, multifunctional, and clinically relevant polymeric systems.

The placenta is essential for fetal development, yet its molecular evolution across mammals remains elusive. Here, we present a comprehensive single-cell transcriptomic atlas of ~300,000 cells from ten species representing the four primary placental types: discoid, cotyledonary, diffuse, and zonary. Our cross-species analysis identifies trophoblast lineages as the primary drivers of placental diversification. By reconstructing differentiation trajectories, we elucidate the regulatory networks shaping trophoblast development across diverse architectures. We propose that the unique gene expression profile of human trophoblasts underlies the susceptibility to preeclampsia and miscarriage. Functional experiments demonstrate that TGIF1 acts as a key upstream regulator of extravillous trophoblast growth and migration. TGIF1 and its targets, including ADAM12, WNT3A, and ZNF831, are associated with preeclampsia and pregnancy loss. Collectively, this high-resolution framework provides fundamental insights into the molecular evolution of the placenta and its contribution to reproductive success and diseases.

Eastern Asia has long been viewed as exhibiting biocultural stasis and technological conservatism during the late Middle Pleistocene (ca. 300-120 ka BP). However, recent fossil, genetic, and archaeological findings reveal a more complex evolutionary and behavioral landscape. This study further challenges this narrative by examining lithic technology at Lingjing (ca. 146-90 ka BP), northern China, a critical site for understanding human evolution in eastern Asia. Integrating three-dimensional morphometrics with the logical analytical system, we investigate discoid core reduction at the site, reconstructing volumetric exploitation, raw material management, and technical design. New [230]Th dates are presented that place Lingjing's initial occupation 20,000 years older than previously estimated. Our study demonstrates the earliest use of sophisticated, systematic centripetal flaking systems in eastern Asia. Hierarchical cores exhibit advanced predetermination, standardized reduction sequence, and sustained platform and surface maintenance, demanding refined cognitive planning and technical skill. Coupled with formal tool production, curated lithic provisioning, and bone tool manufacture, they suggest intentionality beyond strategic opportunism. Such technological complexity coincides with archaic human fossils displaying morphological mosaicism, linking technological sophistication to human evolution or hybridization in eastern Asia. A comparative analysis across 100 Chinese Paleolithic sites indicates discoid technology became a strategic adaptation to late Middle Pleistocene ecological and demographic shifts.

Discoid meniscus is the most common congenital meniscal abnormality encountered in pediatric patients and frequently involves the lateral meniscus. While some discoid menisci remain asymptomatic, many children and adolescents develop pain, mechanical symptoms, or instability requiring surgical treatment. Historically, subtotal or total meniscectomy was commonly performed to address pain, mechanical symptoms, and functional limitation associated with symptomatic discoid meniscus. However, growing evidence regarding the biomechanical and long-term consequences of meniscal loss has led to a significant shift in treatment philosophy. Contemporary surgical management therefore emphasizes preservation of meniscal tissue whenever possible. Arthroscopic reshaping of the discoid meniscus combined with repair of associated tears or peripheral instability allows restoration of meniscal morphology while maintaining its biomechanical function. Given the long life expectancy and activity demands of pediatric patients, meniscal preservation should be considered the primary objective when surgically treating symptomatic discoid meniscus in children.

Skin diseases frequently coexist with other disorders, such as metabolic syndrome, diabetes mellitus, depression, psoriatic arthritis, and cardiovascular disease. Altered levels of distinct chemokines, like CCL5/RANTES, CXCL12/SDF-1a, CCL7/MCP-3, CCL2/MCP-1, CXCL1/GROa, and the eotaxin family, contribute to the development and/or exacerbation of inflammation, which is a common feature of numerous skin diseases as well as metabolic syndrome. The pathological and molecular connections between chronic inflammatory skin diseases and metabolic syndrome are increasingly recognized as being driven by shared inflammatory pathways, oxidative stress, and adipokine dysregulation. While systemic inflammation acts as a common thread, the precise mechanisms for some conditions remain partially understood. Nevertheless, the exact pathological and molecular connections between skin diseases (i.e., psoriasis, atopic dermatitis, pemphigus vulgaris, acute and chronic spontaneous urticaria, bullous pemphigoid, squamous cell carcinoma, alopecia areata, systemic sclerosis, discoid lupus erythematosus, diffuse large B-cell lymphoma) and metabolic syndrome are not yet fully understood. This narrative review summarizes the robust association between various chronic inflammatory skin diseases and metabolic syndrome in the context of pro-inflammatory chemokines.

Cutaneous lupus erythematosus (CLE) is a well-known autoimmune disorder within dermatology. However, findings of lipid-laden macrophages and xanthomas in a subset of these cases are less understood and usually labeled as a rare, incidental finding. For this reason, a very limited amount of literature has been published regarding the phenomenon. We reviewed 84 cases diagnosed as CLE from 2022 to 2024 from our dermatopathology laboratory. Of the 84 cases of CLE, 9 (11%) demonstrated xanthomatous changes, with 67% sub-classified as discoid lupus and 33% as lupus panniculitis. CLE with xanthomatous reactions may be more common than once thought, as our sampling revealed a prevalence of 11%. Further studies are needed to investigate prevalence as well as possible clinical correlations, as these could influence diagnosis, prognosis, and treatment for this subset of cases.