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Abstract Sepsis-induced acute respiratory distress syndrome (ARDS) is characterized by uncontrolled pulmonary inflammation and neutrophil-driven pathology. Neutrophil extracellular traps (NETs) have been implicated in ARDS progression, but the role of interleukin-36 (IL-36) in this process remains unclear. This study aimed to investigate the regulatory mechanism of IL-36 via NETs and its impact on NF-κB activation in a murine model of LPS-induced ARDS.
1 Introduction Lung cancer remains a leading cause of cancer-related mortality worldwide, and its metastatic spread represents a significant challenge in clinical management. Despite advancements in early detection and treatment modalities, lung cancer's propensity to metastasize continues to pose formidable challenges for clinicians and researchers [1].
1 Introduction Cervical cancer, as one of the most common gynecologic malignancies, is the fourth leading cause of cancer-related death among women around the world, with over 300,000 deaths worldwide per year (1, 2). In developing countries, the incidence of cervical cancer was approximately 15.7/100,000, and the risk of death due to cervical cancer was nearly 0.9% (3).
1 Introduction It is estimated that in 2019, nearly three million men in the United States were newly diagnosed with prostate cancer (PCa) (1). PCa was the most prevalent of all male cancers. While early-stage diagnosis and treatment have proven successful in managing PCa, reducing long-term mortality and improving quality of life remains a top priority.
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