Objective:To compare the early diagnostic value of the indicators of endothelial injury, renal injury, inflammation and coagulation in patients with sepsis-induced acute kidney injury (AKI).Methods:A retrospective study was performed on 119 patients with sepsis from February 2017 to March 2018. Lab tests were performed on patients at admission, which included:ing soluble thrombomodulin (sTM), tissue plasminogen activators and inhibitors (t-PAI-C), antithrombin III (AT-III), thrombin-antithrombin (TAT) complex, plasmin-alpha 2, plasmin inhibitor complex (PIC), fibrin degradation product (FDP), fibrinogen (FIB), D-Dimer, prothrombin time (PT), prothrombin time international normalized ratio (PT-INR), procalcitoni (PCT), white blood cell (WBC), neutrophil (Neu), and platelet count (PLT). The receiver-operating characteristic curve was used to analyze the predictive value of the above indicators, and logistic regression analysis was used to analyze the risk factors of sepsis-induced AKI. A prospective study was conducted from April 2018 to September 2018 and 46 patients were enrolled. The lab tests results retrieved including sTM, t-PAI-C, FDP, AT-III, TAT, PIC, FIB, D-Dimer, PT, PCT, serum cystatin C (Cys C), urine albumin (microalbumin) and albumin to creatinine ratio (ACR), urinary neutrophil gelatinase-associated lipocalin (uNGAL), urinary N-acetyl-beta-glucosaminidase (uNAG), and urinary retinol-binding protein (uRBP). As same with the previous group, the receiver-operating characteristic curve was used to analyze the diagnostic value of the above indicators, and logistic regression Was used to analyze the risk factors of sepsis-induced AKI.Results:(1) In the retrospective study: sTM, D-Dimer, PCT, PT, and PT-INR were statistically different. sTM, D-Dimer, PCT, PT, and PT-INR had a good diagnostic value for septis-induced AKI, among which, sTM had a highest diagnostic value (AUC: 0.857; 95% CI: 0.790, 0.924), better sensitivity (64.4%) and specificity (91.8%). The high expression of sTM and history of chronic kidney disease were independent risk factors for septis-induced AKI.(2) In the prospective study: PCT, sTM , Cys C, and uNGAL were statistically different. PCT, sTM, Cys C, uNGAL showed good predictive features for septis-induced AKI. sTM had the highest sensitivity (>0.999) while uNGAL had the highest specificity (0.800). The high expression of sTM was an independent risk factor for septis-induced AKI. Conclusions:sTM and uNGAL represent endothelial injury and renal tubular injury respectively. sTM is an independent risk factor of sepsis-induced AKI.

Objective:To investigate the association between exposure to major air pollutants (including PM 2.5, PM 10, NO 2, SO 2, O 3 and CO) and 28-day all-cause mortality in patients admitted to the intensive care unit (ICU). Methods:The electronic medical records of critically ill patients admitted to the ICU in Hubei Province General Hospital and Jingzhou Central Hospital were collected from August 2018 to August 2019 and from May 2021 to May 2022. Patients' exposure to air pollutants was assessed based on the average concentrations at their place of residence during the previous two months. A generalized linear regression model was used to estimate the association between air pollutant exposure and 28-day all-cause mortality in critically ill patients. Subgroup analysis was then conducted to examine the impact of individual air pollutant exposure on 28-day mortality, which served as the primary outcome in this study. The effect size and confidence interval were adjusted for patient characteristics including age, gender, smoking or drinking habits, length of hospital stay, and SOFA score. Additionally, mediation analysis was conducted using the mediation package (Bruce R) in R software. The direct effect represented the association between exposure to air pollutants and risk of mortality, while the indirect effect aimed to assess whether neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR), and monocyte- lymphocyte ratio (MLR) served as mediating variables in the correlation between exposure to air pollutants and mortality risk.Results:The study included a total of 3 772 critically ill patients admitted to the ICU, with a 28-day all-cause mortality rate of 40.0% (1 509/3 772). A significant positive correlation was observed between an incremental increase of 1 μg/m 3 in air pollutants (specifically PM 2.5, NO 2 and CO) and an elevated risk of mortality within 28 days among critically ill patients. Conversely, there is an inverse relationship between O 3 levels and mortality risk. Additionally, male gender and SOFA rating >3 scores were identified as independent risk factors for all-cause mortality in ICU patients exposed to NO 2 or CO. The Neutrophil/lymphocyte ratio (NLR) played a mediating role in the correlation between PM 2.5 or CO exposure and mortality risk, accounting for 9.09% or 4.71% of the correlations, respectively. Conclusions:The exposure to air pollutants (PM 2.5, NO 2, CO) significantly associate with a high risk of 28-day all-cause mortality in ICU patients. Even at low levels of air pollution, NO 2, CO remains positively correlate with the mortality risk in critically ill patients, who belong to a vulnerable population.

Objective:To investigate the differential expression of cyclooxygenase (COX) gene between familial aggregated atherosclerotic large-artery atherosclerosis(LAA) cerebral infarction patients and sporadic LAA cerebral infarction patients.Methods:Twenty-five patients with familial aggregation LAA cerebral infarction (familial aggregation LAA group) and 25 sporadic LAA cerebral infarction patients (sporadic LAA group) were collected.Another 25 patients with non-cardiovascular and cerebrovascular diseases were selected as control group.Real-time quantitative PCR and ELISA were used to detect COX-1 and COX-2 protein in the supernatant of samples.Results:The expression level of COX-1 gene was 0.5436±0.2737, 0.2400±0.1656 and 0.8340±0.3799 in the familial aggregation, sporadic LAA cerebral infarction and control groups.Compared with control group, COX-1 gene expression in sporadic LAA cerebral infarction group and familial aggregation LAA cerebral infarction group was significantly down-regulated, the differences were significant( P<0.05). The expression level of COX-2 gene was 1.3672±0.8249, 1.3932±0.7158 and 0.7212±0.9623 in the familial aggregation, sporadic LAA cerebral infarction and control groups.Compared with the normal control group, the expression of COX-2 gene in familial aggregation LAA cerebral infarction group and sporadic LAA cerebral infarction group increased significantly( P<0.05). The expression of COX-1 protein was 2.9956±0.5672, 2.5572±1.0289 and 2.6721±0.7944 in the familial aggregation, sporadic cerebral infarction and control groups.The expression of COX-2 protein was 16.63±4.06, 16.86±7.93 and 15.94±5.94 in the familial aggregation, sporadic cerebral infarction and control groups.There was no significant difference in the relative expression of COX-1 and COX-2 proteins among familial aggregation LAA cerebral infarction group, sporadic LAA cerebral infarction group and control group(all P>0.05). Conclusion:There is significant difference in COX-1 gene expression between patients with familial LAA and sporadic LAA cerebral infarction.