Growing stronger: Nine decades of physical disability representation in children's media and implications for pediatric rehabilitation.

The coronavirus disease 2019 (COVID-19) pandemic has resulted in a substantial global health burden, not only from acute infection but also from long-term sequelae affecting a subset of patients. Post-COVID-19 syndrome (PCS), also known as long COVID, is characterized by the persistence of symptoms such as fatigue, dyspnea, and cognitive disturbances for weeks or months after the resolution of acute SARS-CoV-2 infection []. The pathophysiology of PCS is complex and remains incompletely understood; however, accumulating evidence supports a central role for persistent thromboinflammatory processes, endothelial dysfunction, and dysregulated angiogenic signaling []. Endothelial dysfunction is a hallmark of acute COVID-19, driven by direct viral injury and an exaggerated inflammatory response []. It manifests as impaired vasodilation, increased vascular permeability, and a prothrombotic state, contributing to the high incidence of thromboembolic complications observed in severe disease []. In parallel, SARS-CoV-2 infection has been associated with alterations in angiogenic pathways, including imbalances in pro- and anti-angiogenic mediators, which may promote aberrant vascular remodeling and microvascular injury. While some studies suggest partial resolution of these abnormalities, others indicate that endothelial and angiogenic disturbances may persist for months or years, potentially contributing to the chronic manifestations of PCS []. Hemostatic abnormalities are also well documented in acute COVID-19, including elevated D-dimer levels, platelet hyperreactivity, and alterations in coagulation parameters such as prothrombin time (PT) and activated partial thromboplastin time (aPTT) []. These findings reflect a hypercoagulable and thromboinflammatory state closely linked to endothelial activation and immune dysregulation, and are associated with an increased risk of thrombotic events []. However, the long-term trajectory of these thromboinflammatory alterations in PCS remains poorly defined, with some studies reporting normalization and others demonstrating persistent abnormalities, particularly in patients with severe acute disease or underlying comorbidities [].