Spinal cord infarction (SCI) is a rare but severe cause of acute myelopathy, and evidence supporting reperfusion therapies remains limited.

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are pathologically characterized by disruption of the alveolar-capillary barrier, excessive inflammatory responses, and dysregulated intra-pulmonary coagulation. Although inflammatory and thrombotic cascades have been extensively studied, endogenous epithelial-derived signaling mechanisms coordinating barrier stabilization with immunothrombotic restraint remain undefined. Here, we identify fibroblast growth factor 20 (FGF20) as a constitutive epithelial regulator suppressed in alveolar barrier-associated cells during sepsis-induced ALI. In a CLP rat model, both prophylactic and therapeutic administration of recombinant human FGF20 (rhFGF20) improved 7-day survival, attenuated pulmonary edema and inflammation, restored gas exchange, and preserved alveolar-capillary integrity. rhFGF20 restrained procoagulant and antifibrinolytic mediators tissue factor (TF) and plasminogen activator inhibitor-1 (PAI-1) while suppressing NF-κB activation. Mechanistically, FGF20 acted through fibroblast growth factor receptor 1 (FGFR1) to engage the FGFR1-PI3K-AKT cascade. AKT activation bifurcated into two axes: (i) inhibition of NF-κB phosphorylation and nuclear translocation, restraining TF/PAI-1 transcription; and (ii) inhibitory phosphorylation of glycogen synthase kinase 3β (GSK3β) at Ser9, stabilizing epithelial and endothelial junctional proteins (E-cadherin, VE-cadherin, ZO-1). Pharmacological inhibition of FGFR1 or AKT abolished both barrier-protective and anticoagulant effects, confirming pathway dependency. Clinically, serum and bronchoalveolar lavage fluid FGF20 levels were reduced in ARDS patients and positively correlated with PaO₂/FiO₂ ratios, linking reduced FGF20 to disease severity. Collectively, these findings position FGF20 as an upstream integrator of structural and immunothrombotic homeostasis within the alveolar-capillary unit. Restoration of the FGF20-FGFR1 axis reconstitutes a proximal checkpoint stabilizing barrier architecture and constraining NF-κB-dependent procoagulant activation, highlighting FGF20 as a mechanistically grounded therapeutic target in sepsis-induced ALI/ARDS. CLINICAL SIGNIFICANCE.

BACKGROUND Pulmonary embolism is associated with increased morbidity and mortality, yet the patient can sometimes look deceptively calm at the bedside. A normal blood pressure reading does not rule out a struggling right ventricle, and patients classified as intermediate-high-risk can deteriorate quickly. A mobile right-heart thrombus (clot-in-transit) adds another layer of urgency because embolization can be sudden and unpredictable. CASE REPORT A 45-year-old woman with a previous pulmonary embolism presented with abrupt dyspnea, tachycardia, and hypoxemia shortly after stopping apixaban. Bedside transthoracic echocardiography showed marked right ventricular dilation and a mobile right atrial thrombus consistent with clot-in-transit. Computed tomography pulmonary angiography confirmed bilateral segmental/subsegmental pulmonary embolism. Although she remained normotensive, biomarker positivity and a lactate rise suggested early hypoperfusion. After immediate anticoagulation with unfractionated heparin, the Pulmonary Embolism Response Team was activated, and, after multidisciplinary discussion, we decided to treat the patient with reduced-dose systemic alteplase (50 mg over 2 hours). The patient improved rapidly without bleeding complications and was discharged on long-term anticoagulation. She remained in excellent clinical condition at her 2-month follow-up. CONCLUSIONS This case demonstrates that in pulmonary embolism, stability is more than a blood pressure reading. The presence of right ventricular strain together with a clot-in-transit can justify immediate treatment escalation. Reduced-dose systemic thrombolysis can be a reasonable option in carefully selected patients, but decisions should remain individualized.

Membrane oxygenator exchange can be a frequent requirement during extracorporeal membrane oxygenation (ECMO). In low-income health systems, the scarcity and cost of disposables pose significant challenges to timely exchanges. We describe a 48-year-old woman placed on veno-venous ECMO for refractory hypoxemic respiratory failure secondary to pneumonia. Within 30 min, the oxygenator developed thrombosis, characterized by a transmembrane pressure gradient of 229 mmHg. A total of 10 mg of recombinant tissue plasminogen activator (rt-PA) was administered through the premembrane port. Sixty minutes after infusion, the gradient decreased to 116 mmHg, with subsequent improvement in oxygenation. No bleeding occurred. The patient was successfully weaned from ECMO and discharged from the ICU without complications. Low-dose rtPA instillation into a failing oxygenator can postpone exchange and represents a viable salvage strategy for resource-limited ECMO programs.