Cardiac tumors are rare and linked to high mortality rates in both human and veterinary medicine. Despite their clinical significance, the effects of these tumors on coagulation and cardiac function remain poorly understood. This retrospective study assessed coagulation profiles and echocardiographic parameters in 14 dogs with cardiac tumors compared to 10 healthy controls. Tumors were identified through echocardiography, with further confirmation by computed tomography/magnetic resonance imaging. Coagulation was evaluated using conventional tests (prothrombin time (PT) and activated partial thromboplastin time (aPTT)) and thromboelastography (TEG). The employed conventional coagulation tests and echocardiographic parameters showed no significant differences between the groups. However, TEG revealed a hypercoagulable state in the majority of tumor-bearing dogs (8 out of 14), characterized by shortened reaction and clot formation times, as well as an increased α-angle and coagulation index (p < 0.05–0.001). No significant correlations were found between TEG parameters and echocardiographic indices. This study is the first to demonstrate subclinical hemostatic alterations using TEG in dogs with cardiac neoplasia. The results support the utility of TEG as a more sensitive tool than conventional tests for detecting hypercoagulability, potentially guiding individualized anticoagulant strategies in affected dogs.

Background and Objectives: Tendon healing is a multifactorial process influenced by inflammation and oxidative stress. Avocado–soybean unsaponifiables (ASU), recognized for their anti-inflammatory and antioxidant properties in osteoarthritis, have not yet been evaluated in tendon repair. This study aimed to investigate the effects of systemic ASU administration on histological, biomechanical, and biochemical parameters of tendon healing in a rat Achilles tendon injury model. Materials and Methods: Twenty male Wistar rats underwent bilateral Achilles tendon transection and repair. The ASU group received intraperitoneal ASU (300 mg/kg/day) for four weeks; controls received saline. Right tendons were analyzed histologically using a semiquantitative scoring system adapted from Curtis–DeLee, Bonar, and Modified Soslowsky criteria. Left tendons were tested biomechanically for maximum force, displacement, stress, stiffness, and energy parameters. Serum interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) were measured by ELISA. Results: ASU markedly improved histological healing with better collagen alignment, reduced inflammation, and normalized tenocyte morphology (p < 0.001). Biomechanical strength increased, with higher maximum force (p = 0.002), displacement (p = 0.004), stress (p = 0.001), and total energy to failure (p = 0.001). Serum IL-1β, IL-6, and TNF-α levels were lower (p < 0.001), while TAS increased and TOS/OSI decreased (p < 0.001). Conclusions: Systemic ASU administration enhances tendon healing by improving tissue organization, increasing mechanical strength, and modulating systemic inflammation and oxidative stress. These findings suggest that ASU may serve as a safe, clinically relevant adjunct therapy to promote tendon regeneration.

Background: Anaphylaxis is classically framed around IgE‐FcεRI, yet a subset of severe reactions engages an IgG–FcγR‐mediated arm whose consequences for mucosal barrier integrity and epithelial repair remain undefined under recurrence. We propose that mucosal surfaces sustain function during severe anaphylaxis through coordinated operation of immunological composition, structural integrity and reparative capacity—which we term mucosal allostasis—and asked whether the two pathways diverge along this framework. Methods: BALB/c mice were resolved into IgE‐ and IgG‐mediated arms using a hybrid active/passive (ASA‐PSA) sensitisation model and subjected to acute or recurrent severe anaphylaxis, with pharmacological reversal enabling matched rechallenge. Lung, small intestine, colon and serum were profiled across cytokine, mediator, junctional, repair and bacterial 16S rDNA panels; ILC subsets and junctional integrity were resolved by flow cytometry and immunohistochemistry. Results: Despite comparable systemic clinical severity, the two pathways diverged sharply at the mucosal level. IgE‐mediated recurrence preserved junctional expression and mounted a coordinated AREG/EGF/periostin/TFF3/MUC2 repair programme, whereas IgG‐mediated recurrence dismantled both: Claudin‐1, Occludin, ZO‐1 and E‐cadherin declined in tissue and rose reciprocally in serum, repair mediators failed to engage where junctional injury was greatest, and bacterial DNA translocation rose 48‐fold, alongside a type 2/regulatory to inflammatory shift and an ILC2 to ILC1/NCR ⁺ ILC3 reorganisation. Conclusion: Recurrent IgE‐ and IgG‐mediated severe anaphylaxis diverge into two mechanistically opposite allostatic phenotypes. IgG‐mediated recurrence produces an allostatic collapse in which structural failure proceeds uncoupled from reparative engagement, identifying barrier–repair coupling as a candidate axis for intervention in refractory anaphylaxis.