Mechanical ventilation is a widely used short-term life support technique, but an accompanying adverse consequence can be pulmonary damage which is called ventilator-induced lung injury (VILI). Mechanical ventilation can potentially affect the central nervous system and lead to long-term cognitive impairment. In recent years, many studies revealed that VILI, as a common lung injury, may be involved in the central pathogenesis of cognitive impairment by inducing hypoxia, inflammation, and changes in neural pathways. In addition, VILI has received attention in affecting the treatment of cognitive impairment and provides new insights into individualized therapy. The combination of lung protective ventilation and drug therapy can overcome the inevitable problems of poor prognosis from a new perspective. In this review, we summarized VILI and non-VILI factors as risk factors for cognitive impairment and concluded the latest mechanisms. Moreover, we retrospectively explored the role of improving VILI in cognitive impairment treatment. This work contributes to a better understanding of the pathogenesis of VILI-induced cognitive impairment and may provide future direction for the treatment and prognosis of cognitive impairment.

Background: The High Mobility Group Box 1 (HMGB1) protein, a member of the HMG family, plays a crucial role in both cancer progression and inflammatory responses. HMGB1 can act as a damage‐associated molecular pattern (DAMP) to activate immune responses and modulate inflammation. Its dualistic roles in promoting and inhibiting tumor growth, as well as its involvement in DNA repair and drug resistance, make it a key target for understanding and treating cancer and inflammatory diseases. Objective: This review aims to explore the dualistic roles of HMGB1 in cancer and inflammation, focusing on its pro‐inflammatory and anti‐inflammatory functions in the tumor microenvironment, its impact on DNA damage repair and tumor drug resistance, and its potential as a therapeutic target for cancer and inflammatory diseases. Methods: We conducted a comprehensive review of the literature on HMGB1, analyzing its structural features, biological functions, and mechanisms of action in various pathological contexts. We also examined the impact of HMGB1 on tumor progression, immune responses, and metabolic reprogramming in cancer cells, as well as its role in inflammatory signaling pathways. Results: HMGB1 exhibits both oncogenic and tumor‐suppressive effects in cancer. It promotes tumor growth, metastasis, and immune evasion through mechanisms such as shaping the tumor microenvironment, driving metabolic reprogramming, and inducing drug resistance. Conversely, HMGB1 can enhance anti‐tumor immunity by activating dendritic cells and T cells. In inflammation, HMGB1 acts as a DAMP, activating immune responses via receptors like RAGE and TLR4. Its redox state and subcellular localization determine its proinflammatory or anti‐inflammatory functions. Targeting HMGB1 has shown promise in preclinical and clinical studies, with potential applications in anti‐cancer and anti‐inflammatory therapies. Conclusion: The dualistic roles of HMGB1 in cancer and inflammation highlight its complexity and potential as a therapeutic target. Future research should focus on elucidating the context‐specific mechanisms of HMGB1, developing precision‐targeted therapies to modulate its multifunctional activities, and translating these findings into clinical practice to improve patient outcomes.

Background: At present, the role of uric acid in mental disorders is receiving increasing attention, but its relationship with depression is controversial, and previous studies have corresponding limitations. The relationship between them has not been fully elucidated.Objective: The purpose of this study is to explore the relationship between uric acid and depression in American adults using data from the National Health and Nutrition Examination Survey (NHANES).Methods: This cross-sectional study included participants from the National Health and Nutrition Examination Survey 2011-2020. Use logistic regression and restricted cubic spline analysis to investigate the relationship between uric acid and depression. The interactions between variables were determined using subgroup analysis and described in a forest plot.Results: 37033 participants were included in this study, with depression patients accounting for 8.95%. The uric acid levels in the depression group and nondepression group were 317.69 μ mol/L and 323.34 μ mol/L, respectively, with the former having significantly lower uric acid levels than the latter. In the fully adjusted model, participants in the third tertile of uric acid showed a significant correlation (P=0.002, OR; 0.85 (0.76 ~ 0.94)) with a higher risk of depression compared to participants in the first tertile. There is an approximately linear negative correlation between uric acid and depression (P for nonlinear=0.360), and the OR value of uric acid is 1 when the uric acid value is 312.20 μ mol/L.Conclusions: Current research suggests that serum uric acid is associated with depression in American adults. More discoveries and causal relationships require further investigation.