Sepsis-associated acute lung injury (ALI) is a life-threatening condition with limited targeted therapies. Ferroptosis, an iron-dependent form of regulated cell death, has been implicated in the pathogenesis of ALI. Forsythiaside A (FTA), a natural compound derived from Forsythia suspensa, exhibits anti-inflammatory and antioxidant properties, yet its role in regulating ferroptosis during sepsis-induced ALI remains unclear. Here, we investigated whether FTA protects against ALI by suppressing the early growth response protein 1/glutaminase 2 (EGR1/GLS2) axis, a pathway that contributes to ferroptosis. In a cecal ligation and puncture (CLP)-induced septic mouse model, FTA treatment significantly improved survival, attenuated lung histopathological injury, reduced pulmonary edema, and suppressed inflammatory cytokine levels. RNA sequencing and gene set enrichment analysis (GSEA) revealed ferroptosis as a major pathway affected by FTA. Mechanistically, FTA inhibited the upregulation of EGR1 and its downstream target GLS2, leading to decreased glutamate/α-ketoglutarate flux, reduced lipid peroxidation, and enhanced glutathione peroxidase 4 (GPX4) activity. In LPS-stimulated MLE-12 lung epithelial cells, FTA similarly suppressed the EGR1/GLS2 axis, mitigated lipid reactive oxygen species (ROS) accumulation, and preserved mitochondrial membrane potential. Overexpression of EGR1 reversed the protective effects of FTA in vitro, while the ferroptosis inducer Erastin partially abolished FTA-mediated lung protection in vivo. Collectively, our findings suggest that FTA alleviates sepsis-associated ALI, an effect that may involve inhibition of ferroptosis and suppression of the EGR1/GLS2 axis. FTA thus merits further investigation as a potential therapeutic agent for septic lung injury.

Paraquat, a highly toxic herbicide, frequently causes acute poisoning, predominantly inducing pulmonary injury and fibrosis with high mortality, and no specific antidote is available. This study aimed to explore its pathogenesis using a paraquat-induced mouse model. Results showed that paraquat caused dose-dependent body weight changes, pulmonary edema, and pathological damage (alveolar structure destruction, inflammatory cell infiltration), with elevated levels of inflammatory factors (IL-6, TNF-α, IL-1β) in BALF and lung tissues. It also induced pulmonary early pro-fibrotic responses, evidenced by increased collagen deposition and upregulated mesenchymal markers (α-SMA, Vimentin, Collagen I). RNA sequencing revealed KLF4 was significantly downregulated, and differentially expressed genes (DEGs) were enriched in inflammatory pathways. KLF4 negatively correlated with core genes (GSK3B, MLH1, PRKACA, VDAC1, WNT7B) in pathways like Wnt signaling pathway. These findings indicated that paraquat-induced pulmonary injury and early pro-fibrotic responses are associated with KLF4 downregulation and inflammatory pathway activation, identifying KLF4 as a potential therapeutic target for clinical intervention.

Vascular and interventional radiology (VIR) has expanded to include the periprocedural and inpatient management of critically ill patients. Acute respiratory failure and airway compromise in VIR settings may arise from a range of causes, including oversedation, pneumothorax, massive hemoptysis, pulmonary edema, anaphylaxis, or exacerbations of pre-existing respiratory conditions. The ability to promptly assess and treat acutely decompensating patients is essential for interventional radiologists. The management of acute respiratory failure begins with a rapid assessment of airway, breathing, and circulation, in conjunction with evaluation of vital signs, pulse oximetry, end-tidal CO2, arterial or venous blood gases, all while determining the underlying etiology. This review provides a concise overview of the mechanisms underlying respiratory failure, the devices used for monitoring and management, and a focused approach to treating patients with acute respiratory failure.

Cytoreductive surgery (CRS) with heated intraperitoneal chemotherapy (HIPEC) is a treatment for peritonitis carcinomatosa. These procedures often involve significant blood and fluid loss, leading to hyperdynamic circulation and vasodilation, necessitating intraoperative fluids and vasoconstrictors such as catecholamines. Excessive fluid administration to counteract vasodilation can cause intraoperative fluid overload, which is linked to increased postoperative complications. Vasopressin has emerged as a potential alternative to catecholamines, restoring vascular tone via non-adrenergic pathways and supporting perfusion pressure, potentially reducing the need for compensatory fluids solely administered to compensate for vasodilation. We hypothesise that compared with norepinephrine, vasopressin reduces cumulative intraoperative fluid administration during CRS-HIPEC within a goal-directed fluid therapy (GDFT) protocol, ultimately leading to a lowering of postoperative complications.

Acute lung injury (ALI) is characterized by a severe inflammatory response that triggers pulmonary edema, reduced lung compliance, and hypoxemic respiratory failure. To date, there is no effective standard pharmacotherapy for this condition. Recent studies have demonstrated that the Morita-Baylis-Hillman adduct (CISACN) exhibits anti-inflammatory activities in models of asthma and allergic rhinitis, alongside antitumor and antimalarial properties. It also presents low toxicity, low cytotoxicity, and good oral availability. Therefore, this study aimed to investigate the anti-inflammatory activity of the CISACN adduct in a lipopolysaccharide (LPS)-induced ALI model. BALB/c mice were challenged by nasal instillation with LPS and orally treated with CISACN (6.25, 12.5, or 25 mg/kg). Twenty-four hours later, bronchoalveolar lavage fluid (BALF), serum, and lung tissue were collected. Treatment with CISACN, primarily at a dose of 12.5 mg/kg, significantly reduced lung inflammation, as evidenced by decreased cell migration, levels of TNF-α, IL-1β, and IL-6, as well as reduced protein exudate in BALF. Additionally, it decreased serum TNF-α levels and attenuated histopathological alterations in the lung, such as edema, inflammatory cell infiltration, and hemorrhage. The anti-inflammatory effect of CISACN was related to its high energy and affinity with TLR4/p38 MAPK molecules, as evidenced by an in silico approach and confirmed by in vitro analysis, which showed inhibition of p38 MAPK activity. Therefore, this study highlights the anti-inflammatory potential of CISACN by inhibiting a key inflammatory pathway, identifying it as a promising agent for treating inflammatory processes.

We report the case of a previously healthy 27-year-old man who developed acute pulmonary edema shortly after receiving neostigmine-atropine for neuromuscular blockade reversal during appendectomy under general anesthesia. Before extubation, he developed severe hypoxemia, increased airway pressures, pink frothy tracheal secretions, and bilateral diffuse pulmonary infiltrates on chest radiography. Cardiogenic pulmonary edema, fluid overload, negative-pressure pulmonary edema, and perioperative hypersensitivity were considered unlikely based on the clinical findings, bedside cardiac ultrasound, limited intraoperative fluids, normal histamine and tryptase levels, and negative skin testing. The event was therefore considered a diagnosis of exclusion temporally associated with neostigmine administration. This case highlights the importance of careful differential diagnosis and cautious causal attribution when respiratory compromise occurs after reversal.

Streptococcus canis (S. canis) is an underrecognized zoonotic pathogen capable of causing invasive human infection. We report a case of sepsis with acute hypoxic respiratory failure due to S. canis bacteremia in a 73-year-old woman with multiple comorbidities, including breast cancer complicated by chronic lymphedema and cardiovascular disease. She presented with fever, progressive dyspnea, hypoxemia, leukocytosis, acute kidney injury, and rising cardiac troponin levels. Imaging demonstrated bilateral interstitial opacities consistent with pulmonary edema, and her clinical course required intensive care management. Two sets of blood cultures grew S. canis, a group G β-hemolytic streptococcus most commonly associated with dogs and cats. Species-level identification was achieved using polymerase chain reaction-based blood culture testing followed by automated biochemical confirmation. The patient was initially treated with broad-spectrum antibiotics and subsequently transitioned to intravenous penicillin G after susceptibility testing demonstrated β-lactam sensitivity. Further history revealed frequent exposure to a household dog without history of bites or scratches, supporting probable non-traumatic zoonotic transmission. The patient improved with targeted therapy and completed a 13-day course of intravenous antibiotics. This case demonstrates that S. canis can cause severe cardiopulmonary compromise in elderly patients and highlights the epidemiologic value of species-level identification in recognizing zoonotic transmission and prompting targeted assessment of animal exposure in patients with group G streptococcal sepsis.

Acute lung injury (ALI) is characterized by dysregulated pulmonary inflammation, in which alveolar macrophages (AMs) play a crucial role. The m[6]A reader protein YTHDF2, known to facilitate mRNA degradation, is implicated in inflammation; however, its specific function in ALI pathogenesis remains unclear. Using myeloid-specific Ythdf2 knockout mice subjected to cecal ligation and puncture (CLP)-induced ALI, we demonstrate that Ythdf2 deficiency significantly attenuates lung injury, as evidenced by reduced histopathological damage, pulmonary edema, and inflammatory cell infiltration, along with lower levels of pro-inflammatory cytokines (IL-6, TNF-α) in both bronchoalveolar lavage fluid and serum. Moreover, Ythdf2 deletion was accompanied by a substantial upregulation of Hmox1 protein expression in both lung tissues and AMs, an observation consistent with the known role of Ythdf2 in pulmonary hypertension. Furthermore, global m[6]A methylation levels and the expression of key methyltransferases (Mettl3, Mettl14) were elevated during ALI, coinciding with increased Ythdf2 expression. This upregulation of m[6]A regulators (YTHDF2, METTL3, METTL14) was also confirmed in pulmonary macrophages from human septic lungs. In conclusion, our findings support the concept that the myeloid-specific deletion of Ythdf2 ameliorates lung injury, an effect closely associated with the upregulation of Hmox1, highlighting Ythdf2 as a potential therapeutic target for ALI.

Background Accurate volume assessment during immediate post-kidney transplantation period reduces morbidity and mortality. Lung ultrasound (LUS), VExUS score, and bioimpedance (BIA) are emerging methods for volume evaluation. We hypothesize LUS+VExUS may provide accurate means of congestion assessment in renal transplant patients, allowing more precise care. Method Exploratory, prospective, single-centre pilot study. A prospective cohort (Group 1, n = 31) underwent volume assessment using a combined VExUS + LUS protocol on days +1 and +7 post-transplantation, alongside physical examination (PhE) and bioimpedance analysis (BIA). Findings were compared with a historical reference cohort (Group 2, n = 40) managed with standard clinical assessment alone. Results Groups differed significantly in delayed graft function (45.2% vs. 15.0%, p = 0.008) and cold ischaemia time (p = 0.027). Acute pulmonary oedema occurred in 2/31 patients (6.5%) in Group 1 and 6/40 (15.0%) in Group 2, though this difference was not statistically significant (Fisher exact p = 0.452). VExUS showed no correlation with BIA (Spearman ρ = 0.127, p = 0.545), BNP (ρ = 0.187, p = 0.349), or CA-125 (ρ = 0.241, p = 0.226). VExUS detected venous congestion (grade ≥ 1) in 2/14 patients (14.3%) with normal PhE on Day +1. Physical examination showed poor agreement with VExUS (κ = 0.043) and moderate agreement with LUS (κ = 0.469). Combined ultrasound identified subclinical congestion in 28.6% of patients with normal PhE. Ultrasound findings prompted therapeutic modifications in 74.2% of cases on Day +1 (primarily IV fluid reduction) and 16.1% on Day +7. Conclusion In this exploratory pilot study, VExUS and LUS provided additional diagnostic information beyond physical examination and influenced clinical decision-making in the majority of cases. These hypothesis-generating findings warrant confirmation in larger, multicentre, prospective studies with standardised protocols.