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Objective. The hemoglobin-to-red cell distribution width ratio (HRR) is associated with the prognosis of sepsis-associated encephalopathy (SAE). This study aimed to determine the relationship between HRR and SAE and to clarify the possible mechanism of HRR as a prognostic factor for SAE. Methods. A multivariate Cox proportional-hazards regression model was used to assess the correlation between HRR and all-cause mortality. Piecewise linear regression and smooth-curve Cox proportional-hazards regression models were used to observe whether there was a nonlinear relationship between HRR and all-cause mortality in SAE. Results. This study included 8853 patients with SAE. A nonlinear relationship between HRR and SAE was observed through a two-segment regression model. The left inflection point for the HRR threshold was calculated to be 15.54, which was negatively correlated with all-cause mortality (HR = 0.83, 95% CI = 0.76–0.91, p < 0.001 ). Subgroup analyses revealed significant interactions between white blood cell count, glucose, and patients who received dialysis and HRR. The inverse correlation between HRR and SAE was more pronounced in patients who did not receive vasopressin (HR = 0.91, 95% CI = 0.87–0.96, p < 0.001 ) than in those who did receive vasopressin (HR = 0.94, 95% CI = 0.88–1.02, p = 0.152 ) and was significantly more pronounced in patients without myocardial infarction (HR = 0.91, 95% CI = 0.88–0.96, p < 0.001 ) than in those with myocardial infarction (HR = 0.94, 95% CI = 0.87–1.02, p < 0.114 ). Conclusion. This large retrospective study found a nonlinear relationship between all-cause mortality and HRR in patients with SAE in intensive care units, with low HRR being inversely associated with increased all-cause mortality in patients with SAE.

ObjectiveTo prospectively assess whether air pollution, including PM2.5, PM10, and NOx, is associated with the risk of all-cause dementia, Alzheimer’s disease (AD), and vascular dementia, and to investigate the potential relationship between air pollution and genetic susceptibility in the development of AD.Methods and resultsOur study included 437,932 participants from the UK Biobank with a median follow-up period of over 10 years. Using a Cox proportional hazards model, we found that participants exposed to PM2.5 levels of ≥10 μg/m3 had a higher risk of developing all-cause dementia (HR = 1.1; 95% CI: 1.05–1.28; p &lt; 0.05) compared to the group exposed to PM2.5 levels of &lt;10 μg/m3. However, there was no significant association between PM10 levels of ≥15 μg/m3 and the risk of all-cause dementia, AD, or vascular dementia when compared to the group exposed to PM10 levels of &lt;15 μg/m3. On the other hand, participants exposed to NOx levels of ≥50 μg/m3 had a significantly higher risk of all-cause dementia (HR = 1.14; 95% CI: 1.02–1.26; p &lt; 0.05) and AD (HR = 1.26; 95% CI: 1.08–1.48; p &lt; 0.05) compared to the group exposed to NOx levels of &lt;50 μg/m3. Furthermore, we examined the combined effect of air pollution (PM2.5, PM10, and NOx) and Alzheimer’s disease genetic risk score (AD-GRS) on the development of AD using a Cox proportional hazards model. Among participants with a high AD-GRS, those exposed to NOx levels of ≥50 μg/m3 had a significantly higher risk of AD compared to those in the group exposed to NOx levels of &lt;50 μg/m3 (HR = 1.36; 95% CI: 1.03–1.18; p &lt; 0.05). Regardless of air pollutant levels (PM2.5, PM10, or NOx), participants with a high AD-GRS had a significantly increased risk of developing AD. Similar results were obtained when assessing multiple variables using inverse probability of treatment weighting (IPTW).ConclusionOur findings indicate that individuals living in areas with PM2.5 levels of ≥10 μg/m3 or NOx levels of ≥50 μg/m3 are at a higher risk of developing all-cause dementia. Moreover, individuals with a high AD-GRS demonstrated an increased risk of developing AD, particularly in the presence of NOx ≥ 50 μg/m3.