Abstract Background Research on articular cartilage development provides a foundation for the repair and regeneration of cartilage following injury. Methods In this study, eight embryonic time points were selected: embryonic days 30 (E30), E35, E45, E55, E75, E85, E90, and E100, along with knee joints from newborn (P0) and 30 day old (P30) piglets. The dynamic developmental characteristics of knee cartilage were systematically analyzed by Safranin O‐Fast Green, Toluidine blue, and Masson staining. Results The results indicate that the mesenchymal condensation (interzone) of the knee joint has formed by embryonic day 30 (E30), marking the initiation of joint development. Chondrification commences in the diaphyses of the femur and tibia, establishing the foundation for primary ossification in femur and tibia regions at E35. By E45, the epiphyseal cartilage cells have distinctly differentiated into two morphologically distinct populations, round epiphyseal chondrocytes and spindle‐shaped growth plate chondrocytes. At E55, cartilage canals begin to emerge in the cartilage zone. The number of cartilage canal and chondrocytes progressively increase from E75 to E90. Growth plate chondrocytes progressively differentiate from a disorganized, undifferentiated state into a highly organized, spindle‐shaped, columnar array. The secondary ossification center of the knee joint appears at E100, concomitant with hypertrophy of adjacent chondrocytes and resorption of cartilage canals. From postnatal day 0 (P0) to P30, the secondary ossification center undergoes progressive peripherally expansion. By P30, partial chondrocytes display reduced Safranin O staining intensity, indicative of diminished extracellular matrix secretion. By P30, secondary ossification has progressed sufficiently to replace the cartilaginous zone proximal to the growth plate with mineralized tissue. The growth plate becomes completely separated from the epiphyseal cartilage zone, marking the completion development of growth plate. Conclusions This study dynamically charts the developmental process of the knee joint cartilage from the embryonic stage to postnatal life, revealing key developmental events including the origin of knee joint development, chondrification, primary ossification, secondary ossification, formation of the cartilage canals and growth plate. The results provide foundational material for research in cartilage tissue engineering and regenerative medicine.
Abstract Post‐stroke cognitive impairment (PSCI) is a major cause of long‐term disability after ischemic stroke, yet its mechanisms remain incompletely explained by infarct volume, lesion location, or conventional vascular risk factors alone. Animal models are indispensable for clarifying how ischemic injury evolves into delayed cognitive dysfunction and for determining which mechanisms are experimentally tractable, reproducible, and translationally relevant. This review examines PSCI from a neurovascular trafficking perspective, focusing on how laboratory animal models can be used to investigate secretory pathway stress, endolysosomal dysfunction, autophagy‐lysosomal flux, extracellular vesicle signaling, blood–brain barrier disruption, glial reactivity, myelin debris clearance, white matter injury, and cognition‐relevant behavioral phenotypes. Rodent models of transient or permanent middle cerebral artery occlusion, photothrombotic stroke, embolic stroke, chronic cerebral hypoperfusion, bilateral carotid artery stenosis, and subcortical white‐matter injury each reproduce selected components of the human PSCI spectrum. No single model fully captures the temporal, vascular, cellular, and cognitive complexity of human PSCI; therefore, model selection should be driven by the mechanistic question, disease phase, vascular pathology, cellular compartment, cognitive domain, and welfare burden under investigation. The central argument is not that neurovascular trafficking failure is already a proven causal pathway, but that well‐designed animal studies can test, refine, or falsify this hypothesis. Future studies should integrate model validity, translational rigor, and welfare refinement through longitudinal cognitive testing, multimodal imaging, cell‐specific molecular profiling, extracellular vesicle phenotyping, intervention‐based validation, randomization, blinding, sample‐size justification, humane endpoints, perioperative care, and transparent reporting.
Abstract Background ATP‐binding cassette transporter A1 (ABCA1) mediates cellular cholesterol efflux, yet its role in inflammatory bowel disease (IBD) remains incompletely understood. This study investigated the consequences of intestinal epithelial cholesterol accumulation—primarily driven by ABCA1 deficiency—on colonic inflammation and the underlying molecular mechanisms. Methods ABCA1 knockout (KO) and wild‐type (WT) Syrian golden hamsters were fed a high‐cholesterol high‐fat diet for 12 weeks. Colon specimens were analyzed for pathological changes, inflammatory markers, cholesterol accumulation, and gene expression profiles. Furthermore, in vitro experiments were performed using the human colon epithelial cell line Caco‐2. Results ABCA1 deficiency, in the context of a high‐cholesterol high‐fat diet, triggered significant colonic inflammation in KO hamsters, characterized by epithelial damage, inflammatory cell infiltration, and elevated pro‐inflammatory cytokine levels. These pathological changes were associated with impaired mucosal barrier integrity, a four‐fold increase in epithelial cholesterol accumulation, and reduced E‐cadherin, ZO‐1 and occludin expression. Furthermore, ABCA1 deficiency promoted oxidative stress and induced marked remodeling of the gut microbiota. Conclusions Our findings establish a pathogenic role for ABCA1 deficiency in driving colonic epithelial injury and inflammation, suggesting that ABCA1 may play an important role in the pathogenesis of IBD.
Abstract Anemia of inflammation (AI) represents one of the most prevalent secondary anemias in clinical practice, frequently complicating a wide spectrum of chronic inflammatory diseases. Given its highly heterogeneous etiology and complex pathophysiological mechanisms, the establishment of rational and high‐fidelity animal models is vital for elucidating the core mechanisms of AI and optimizing clinical diagnostic and therapeutic strategies. This narrative review provides a structured categorization of current AI animal models into three major paradigms: sterile inflammation models, disease‐specific models, and genetically engineered models. We provide an in‐depth comparative analysis of their underlying modeling principles, methodological protocols, and characteristic phenotypic profiles, while comprehensively evaluating their respective translational advantages and intrinsic limitations. Furthermore, we discuss the prospective applications of these models in deciphering pathomechanisms, validating therapeutic targets, and developing interventional strategies. To enhance reproducibility and translational relevance, we propose a streamlined phenotyping panel and a model selection framework. The precise selection and rational application of these tailored models will contribute to improved reliability of fundamental AI research and accelerate its translational progression from bench to bedside.
Abstract Background Rodent models are widely used in oral health research; however, maintaining stable and effective intraoral retraction in the small oral cavity is challenging. Manual retraction methods often lead to procedural instability, operator fatigue, and increased tissue trauma during rodent oral surgery. Methods A stainless‐steel wire mouth prop incorporating helices for self‐retention and auxiliary lateral soft tissue displacement prongs was fabricated. 32 adult Wistar albino rats were randomly allocated to two groups ( n = 16 each). In the experimental group, procedures were performed using a custom mouth prop, and the control group underwent conventional manual retraction. Outcomes included time to achieve adequate retraction, slippage events per procedure, operator fatigue scores, and complication rates. Student's t ‐test was used for statistical analysis of retraction time, and the Mann–Whitney U test was used for slippage frequency, and fatigue scores. Statistical significance was determined using a Bonferroni‐adjusted threshold of p < 0.017. Results Retraction time was significantly shorter in the experimental group (2.5 ± 0.6 min) than in control group (6.3 ± 1.2 min, p < 0.001). Slippage events per procedure were markedly lower with mouth prop (0.1 vs . 3.4 ± 1.1, p < 0.001). Operator fatigue scores were also reduced (2.4 ± 0.8 vs . 7.2 ± 1.4, p < 0.001). Complication rates were significantly lower in the experimental group ( p = 0.024). Conclusion The proposed custom‐made mouth prop demonstrated favorable procedural handling characteristics during rat intraoral surgery and may serve as a practical, low‐cost refinement tool for improving intraoral access and procedural stabilization in experimental oral research settings.
