Osteoarthritis (OA) is a chronic degenerative joint disease accompanied by an inflammatory milieu that results in painful joints. The pathogenesis of OA is multifactorial, with genetic predisposition, environmental factors, and traumatic injury resulting in the direct or indirect loss of cartilage. The articular cartilage can also be damaged by direct focal traumatic injury. Articular cartilage provides a smooth, deformable bearing surface with a low coefficient of friction, increased contact area, and reduced contact stress. Articular type II hyaline cartilage lines the synovial joints and, when injured, has a limited ability for repair, except for the most superficial layers via diffusion from the synovial fluid, secondary to no blood supply, a complex structure, and a low metabolic rate. Restoring the articular surface can relieve pain and restore function. Although many strategies have been developed to regenerate type II collagen based on the extent of the lesion, surgical treatments are still evolving. The peroxisome proliferator-activated receptor delta (PPARδ) agonist and collagen treatment of mesenchymal stem cells (MSCs) enhance the chondrogenic capacity in vitro. We present a novel technique for cartilage restoration in a rabbit cartilage osteochondral defect model using a PPARδ agonist (GW0742)-infused 3D collagen scaffold to induce type II cartilage from MSCs.

Pasteurella species commonly cause soft tissue infections following direct animal bites or scratches. However, transmission through indirect contact with contaminated materials remains underrecognized. We report an unusual, suspected case of Pasteurella multocida infection acquired through contact with catnip contaminated by feline saliva, resulting in progressive soft tissue infection and extensor tendon rupture in the hand of an otherwise healthy individual. Operative debridement, tendon repair, culture‐directed antibiotic therapy, and structured occupational therapy resulted in functional recovery with grip strength equal to the uninjured hand, a residual 37° total extension deficit, and a Quick Disabilities of the Arm, Shoulder, and Hand (QuickDASH) score of 4.55% at four months postinjury. This case emphasizes the importance of recognizing atypical transmission routes and implementing timely interventions to prevent severe complications.

Glioblastoma (GBM) is the most common and aggressive primary central nervous system malignancy. Significant resistance to therapeutic intervention is a core feature of GBM that drives tumor recurrence and underlies the remarkably poor clinical outcomes associated with this disease. This review explores the therapeutic strategies and molecular pathways involved in GBM. Therapy resistance in GBM depends on multiple interconnected macrostructural and biomolecular mechanisms, including aggressive and diffuse invasion, tumor microtube network formation, stem-like cell enrichment, selective neurovascular permeability, an immunosuppressive microenvironment, and a high degree of inter- and intra-tumoral heterogeneity. Collectively, these pathobiological features insulate specific tumor compartments and maintain GBM viability despite significant treatment-induced cellular stress. While there is enthusiasm for addressing GBM therapeutic resistance, the scale of the challenge remains immense. The identified resistance mechanisms extensively interact and can compensate for single-target assaults. Emerging overlaps between neuro-oncology and developmental neurobiology additionally suggest that GBM may exploit therapeutic resistance mechanisms yet to be identified, functioning beyond the current scientific understanding. Thus, the scope and diversity of this problem demand a comprehensive therapeutic approach capable of targeting multiple interacting mechanisms of therapeutic resistance.