Type 1 diabetes mellitus (T1DM) is a chronic condition primarily managed with insulin replacement, leading to significant treatment costs. Complications include vasculopathy, cardiovascular diseases, nephropathy, neuropathy, and reticulopathy. Pancreatic islet transplantation is an option but its success does not depend solely on adequate vascularization. The main limitations to clinical islet transplantation are the scarcity of human pancreas, the need for immunosuppression, and the inadequacy of the islet isolation process. Despite extensive research, T1DM remains a major global health issue. In 2015, diabetes affected approximately 415 million people, with projected expenditures of USD 1.7 trillion by 2030. Pancreas transplantation faces challenges due to limited organ availability and complex vascularization. T1DM is caused by the autoimmune destruction of insulin-producing pancreatic cells. Advances in biomaterials, particularly the extracellular matrix (ECM), show promise in tissue reconstruction and transplantation, offering structural and regulatory functions critical for cell migration, differentiation, and adhesion. Tissue engineering aims to create bioartificial pancreases integrating insulin-producing cells and suitable frameworks. This involves decellularization and recellularization techniques to develop biological scaffolds. The challenges include replicating the pancreas’s intricate architecture and maintaining cell viability and functionality. Emerging technologies, such as 3D printing and advanced biomaterials, have shown potential in constructing bioartificial organs. ECM components, including collagens and glycoproteins, play essential roles in cell adhesion, migration, and differentiation. Clinical applications focus on developing functional scaffolds for transplantation, with ongoing research addressing immunological responses and long-term efficacy. Pancreatic bioengineering represents a promising avenue for T1DM treatment, requiring further research to ensure successful implementation.

Type 1 diabetes mellitus (T1DM) involves the destruction of pancreatic β-cells, requiring ongoing insulin therapy. A promising alternative for management is pancreatic islet transplantation, or the bioartificial pancreas. Here, we examine the primary implantation sites for the bioartificial pancreas, highlighting their anatomical, physical, and immunological characteristics in the context of T1DM treatment. Traditionally used for islet transplantation, the liver promotes metabolic efficiency due to portal drainage; however, it presents issues such as hypoxia and inflammatory responses. The omentum offers excellent vascularization but has limited capacity for subsequent transplants. The renal subcapsular space is advantageous when combined with kidney transplants; however, its use is limited due to low vascularization. The subcutaneous space is notable for its accessibility and lower invasiveness, although its poor vascularization poses significant challenges. These challenges can be mitigated with bioengineering strategies. The gastrointestinal submucosa provides easy access and good vascularization, which makes it a promising option for endoscopic approaches. Additionally, the intrapleural space, which remains underexplored, offers benefits such as increased oxygenation and reduced inflammatory response. Selecting the ideal site for bioartificial pancreas implantation should balance graft support, complication reduction, and surgical accessibility. Bioengineered devices and scaffolds can address the limitations of traditional sites and enhance T1DM management.

O fêmur é um dos ossos longos mais frequentemente acometidos por fraturas em cães, sendo uma ocorrência comum na rotina de atendimento na clínica de pequenos animais. Dentre as diversas lesões que podem afetá-lo, destacam-se principalmente as fraturas transversas, oblíquas e cominutivas, que figuram entre as mais observadas em casos clínicos. A alta incidência de fraturas femorais reforça a importância do desenvolvimento de recursos didáticos e tecnológicos que auxiliem no estudo das conformações ósseas e dos diferentes tipos de lesões, permitindo maior familiaridade dos estudantes e profissionais com essas alterações ortopédicas. Frente a esse cenário, o presente estudo desenvolveu quatro modelos impressos 3D, de fêmur esquerdo canino, contendo fraturas dos tipos transversa, oblíqua, espiralada e cominutiva. Este trabalho tem como objetivo desenvolver através da impressão 3D modelos de fratura em ossos artificias, como método complementar ao progresso de ensino e aprendizagem medicina veterinária, desenvolvendo um material prático para o auxílio do estudo teórico. Os modelos foram elaborados a partir de exames de tomografia computadorizada de um fêmur íntegro, associados a imagens radiográficas de casos clínicos reais, passando por processamento em softwares específicos até a impressão 3D. A tecnologia 3D se mostra, portanto, como uma ferramenta complementar no ensino, capaz de proporcionar experiências práticas, acessíveis e eticamente responsáveis, alinhando-se aos avanços tecnológicos na educação veterinária.

Bovine spongiform encephalopathy (BSE) is a fatal transmissible spongiform encephalopathy caused by the misfolding of the host prion protein (PrP), representing a unique intersection between molecular pathology, neuroanatomy, and public health regulation. Although historically framed as a single feedborne epizootic, BSE is now recognized as a spectrum of strain-defined prion disorders encompassing classical and atypical forms with distinct origins, neuroanatomical trajectories, and surveillance implications. This review integrates advances in prion biology, neurodegenerative mechanisms, and anatomical pathways of neuroinvasion to reframe BSE as a heterogeneous disease entity. We synthesize evidence on PrP^C structure, trafficking, and proteolytic processing to explain how normal cellular physiology enables strain-specific conversion to pathogenic PrP^Sc and subsequent neurotoxicity. Distinct patterns of neuroinvasion and regional vulnerability are discussed for classical versus atypical (H- and L-type) BSE, highlighting differences in lymphoid involvement, brainstem targeting, and cortical or cerebellar tropism. We further examine how these biological differences translate into diagnostic sensitivity, surveillance design, and zoonotic risk assessment. By integrating molecular strain diversity with neuroanatomical connectivity, this review underscores the limitations of obex-centered surveillance for atypical BSE and emphasizes the need for proportionate yet precautionary monitoring strategies. These considerations should be interpreted in light of surveillance-dependent detection biases, which influence the apparent distribution of BSE forms. Ultimately, BSE emerges as a critical model for understanding how protein misfolding disorders bridge cellular mechanisms, animal health, and human public health policy.

The extracellular matrix (ECM) is increasingly recognized as an active regulator of breast cancer progression rather than a passive structural scaffold. This narrative review examines how ECM remodeling contributes to tumor aggressiveness through changes in matrix composition, collagen architecture, tissue stiffness, mechanotransduction, stromal permissiveness, immune and metabolic programs, invasion, metastasis and therapeutic response. A structured narrative search of literature published from 1981 to June 2026 was used to support this synthesis. Evidence from breast cancer studies indicates that collagens, fibronectin, laminins, proteoglycans, matricellular proteins, ECM-remodeling enzymes, and matrix-crosslinking pathways regulate integrin–FAK/Src, RhoA–ROCK, PI3K–AKT, MAPK, TGF-β/SMAD, Wnt/β-catenin, and YAP/TAZ signaling. Spontaneous canine mammary tumors are discussed as complementary comparative models that may preserve selected tumor–stroma–ECM interactions under naturally occurring disease conditions while requiring cautious interpretation due to species-specific biological and clinical differences. Proteomics, lipidomics, metabolomics, spatial omics, digital pathology, and artificial intelligence may support ECM-informed biomarker discovery and response prediction. However, translational application requires standardized pathology, reproducible assays, harmonized metadata, external validation, model interpretability, and clinically meaningful endpoints. Overall, ECM-informed comparative oncology is best viewed as a framework grounded in rigorous validation for identifying matrix-defined tumor phenotypes and prioritizing future biomarker and therapeutic strategies.

South American camelids inhabit high-altitude environments characterized by hypoxia, influencing embryonic, fetal, and placental development. This study examined the term placenta morphology of alpacas (Vicugna pacos, N = 12) and the immunoexpression of antioxidant selenoproteins (SP). We hypothesize that the placenta of alpacas, adapted to high altitudes, has characteristics with other species also adapted to altitude. Placentas were paraffin-embedded, sectioned (3–5 µm), stained with hematoxylin–eosin (H&E), Masson’s trichrome, and picrosirius red, and analyzed via light and polarized light microscopy. The chorion showed simple cuboidal epithelium with binucleated cells, a subepithelial mesenchyme rich in blood capillaries (area: 124.90 ± 9.82 µm²), and type III collagen fibers. The chorionic villi measured 2740.22 ± 132.75 µm. The allantois contained a simple columnar epithelium and mesenchyme with type I collagen fibers. Immunohistochemistry localized SP-N, SP-P, Dio-3, and GPx-3 in the blood capillaries and mesenchymal tissue of the chorion but not in the allantois. These findings were compared to human and sheep placentas from different altitudes due to a lack of camelid data at low levels. The morphological features resembled adaptations to hypoxia observed in other species. This preliminary study suggests a potential role for selenoproteins in hypoxia adaptation, providing a basis for future functional studies.