BackgroundRed blood cell distribution width (RDW) to albumin ratio (RAR) is associated with poor prognosis in diabetic comorbidities and cancer. However, the association between RAR and prognosis in patients with sepsis remains unclear, which was investigated in this study.MethodsWe conducted a retrospective cohort study based on the Medical Information Mart for Intensive Care (MIMIC) IV version 2.0 database. The primary outcome of this study was 28-day mortality. Secondary outcomes included 90-day mortality, in-hospital mortality, length of hospital stay, and length of intensive care unit (ICU) stay. Multivariate regression analysis and subgroup analysis were performed to investigate the association between RAR and prognosis in patients with sepsis.ResultsA total of 14,639 participants were included in this study. The mean age of the participants was 65.2 ± 16.3 years and the mean RAR was 5.5 ± 1.9 % /g/dl. For 28-day mortality, after adjusting for covariates, HRs [95% confidence intervals (CIs)] for tertiles 2 (4.4–5.8) and 3 (RAR > 5.8) were 1.33 (1.20, 1.46) and 1.98 (1.79, 2.19), respectively. Similar results were observed for 90-day mortality and in-hospital mortality. According to Kaplan-Meier curve analysis, the higher RAR group had higher 28-day mortality and 90-day mortality.ConclusionOur study shows that RAR is significantly associated with poor clinical prognosis in sepsis. The higher the RAR, the higher the 28-day, 90-day, and in-hospital mortality.

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Background: Human serum albumin (HSA) is a commonly used medication for the treatment of sepsis. However, there is no conclusive evidence as to whether different concentrations of HSA are associated with patient prognosis. This study aimed to evaluate the association between different concentrations of HSA and 28-day mortality in patients with sepsis.Methods: The data for this retrospective study were collected from the Medical Information Mart for Intensive Care IV database. Patients with sepsis were divided into two groups according to the concentration of HSA received: 25% and 5% HSA. The primary outcome of this study was the 28-day mortality in patients with sepsis. To ensure the robustness of our findings, we used multivariate Cox regression, propensity score matching, double-robust estimation, and inverse probability weighting models.Results: A total of 76,943 patients were screened, of whom 5,009 were enrolled. 1,258 and 3,751 patients received 25% and 5% HSA, respectively. The 28-day mortality rate was 38.2% (481/1,258) for patients in the 25% HSA group and 8.7% (325/3,751) for patients in the 5% HSA group. After propensity score matching, 1,648 patients were identified. The inverse probability weighting model suggested that 5% HSA received was associated with lower 28-day mortality (hazard ratio [HR]: 0.63, 95% confidence interval [CI]: 0.54–0.73, p < 0.001). Subgroup and sensitivity analysis confirmed the robustness of the results.Conclusion: In patients with sepsis, 5% HSA received may be associated with a lower risk of 28-day mortality than 25% HSA. Further randomized controlled trials are required to confirm this association.

Objective: Paraquat (N,N0-dimethyl-4,40-bipyridinium dichloride;PQ) is a highly toxic pesticide, which usually leads to acute lung injury and subsequent development of pulmonary fibrosis. The exact mechanism underlying PQ-induced lung fibrosis remain largely unclear and as yet, no specific treatment drugs have been approved. Our study aimed to identify its potential mechanisms of PQ-induced fibrosis through a modeling study in vitro studies and bioinformatics analysis. Methods: Gene expression datasets associated with PQ-induced lung fibrosis were obtained from the Gene Expression Omnibus, wherefrom differentially expressed genes (DEGs) were identified using GEO2R. Functional enrichment analyses were performed using the Database for Annotation Visualization and Integrated Discovery. The DEGs analyzed by a protein–protein interaction network was constructed with the Search Tool for the Retrieval of Interacting Genes database. MCODE, a Cytoscape plugin, was subsequently used to identify the most significant modules. The expression of the key genes in PQ-induced pulmonary fibrotic tissues was verified by reverse transcription-quantitative PCR (RT-qPCR). Results: Two datasets were analyzed and revealed 92 overlapping DEGs. Functional analysis demonstrated that these 92 DEGs were enriched in the ‘TNF signaling pathway’, ‘CXCR chemokine receptor binding’, and ‘core promoter binding’. Moreover, nine hub genes were identified from the protein–protein interaction network formed from the DEGs. These results suggested that the TNF signaling pathway and nine hub genes are possibly involved in PQ-induced lung fibrosis progression. Conclusions: This integrative analysis identified candidate genes and pathways potentially involved in PQ-induced lung fibrosis, and could benefit future development of novel approaches for controlling and treating this disease.

The brain ischemia/reperfusion (I/R) injury have a great impact on human life and property safety, as far as we know, mild hypothermia (MH) is an effective measure which reduces neuronal injury. However, the precise mechanism is not extremely clear. The purpose of this study was to explore whether mild therapeutic hypothermia can play a protective role in nerve cells dealing with brain I/R injury and its specific mechanism in vitro. A flow cytometer, cell counting kit-8 (CCK-8) assay, lactate dehydrogenase (LDH) release assay were performed to detect apoptotic rate of cells, cell viability and cytotoxicity respectively, while reactive oxygen species (ROS) assay kit, JC-1 fluorescent methods, immunofluorescence, western blot were used to explore ROS, mitochondrial transmembrane potential (Δψm), mitochondrial permeability transition pore (MPTP), expression of proteins respectively. The result indicated that the activity was decreased, while the cytotoxicity and apoptosis rate were increased after treating with OGD/R in PC12, however, MH could antagonize this phenomenon. Strangely, treating with OGD/R increased the release of ROS and the transfer of Cytochrome C (Cyt-C) from mitochondria to cytoplasm, besides, it also upregulated the expression of γH2AX, Bax and Clv-caspase3 but downregulated the expression of PCNA, Rad51, Bcl-2 and inhibited the function of mitochondria in PC12, the opposite trend was observed after MH treatment. Therefore, our results suggest that MH alleviates PC12 against oxygen-glucose deprivation/ reoxygenation-induced injury with the mechanism of inhibiting cell apoptosis by reducing ROS production, improving mitochondrial function, reducing DNA damage, and enhancing DNA repair.