RESUMEN
BACKGROUND: Optimal oxygen supply is the cornerstone of the management of critically ill patients after extubation. High flow oxygen system is an alternative to standard oxygen therapy. This research explored the efficacy of high-flow nasal cannula (HFNC) oxygen therapy in patients after extubation in the intensive care unit (ICU). METHOD: We retrospectively analyzed critically ill patients admitted to the ICU and subjected to HFNC or conventional oxygen therapy from January 2018 to June 2022 at the Suzhou Hospital of Integrated Traditional Chinese and Western Medicine. Blood gas analysis, a cough and sputum assessment, and cardiovascular function examinations were performed to evaluate the effect of HFNC oxygen therapy on patients. Also, the 28-d mortality rate, reintubation rate and incidence of respiratory failure were analyzed to evaluate whether HFNC oxygen therapy could improve patients' outcome. RESULTS: In patients who received HFNC oxygen therapy, the partial pressure of oxygen and oxygenation index increased, and the respiratory rate decreased. HFNC oxygen therapy improved the patients' ability to cough up sputum and promoted the expulsion of sputum. In terms of cardiovascular function, patients who received HFNC oxygen therapy had a significant improvement in heart rate, but there was no real effect on patients' arterial pressure. There was no significant difference in the rates of reintubation (P = 0.202), 28-d mortality (P = 0.558) or respiratory failure (P = 0.677) between patients who received different oxygen therapies including HFNC oxygen therapy. CONCLUSION: HFNC oxygen therapy improves the respiratory function of patients after extubation in their ICU and improves their coughing ability.
RESUMEN
BACKGROUNDS: To date, there are no specific drugs approved for the treatment of sepsis associated acute kidney injury (AKI). Shionone is a natural component with anti-inflammatory activity. In this study, we sought to determine the functional role of Shionone in sepsis-induced AKI. METHODS: Animal models of AKI were constructed by cecum ligation and puncture (CLP) surgery. C57BL/6 mice were randomly assigned to the Sham, CLP, 10 mg/kg DXM, 50 mg/kg Shionone and 100 mg/kg Shionone groups. RAW264.7 treated with lipopolysaccharides (LPS) was used as an in vitro sepsis model and cells were divided into control, LPS, 1 µg/mL Shionone and 2 µg/mL Shionone groups. The pathological status was assessed by Hematoxylin-Eosin (HE) staining assay, protein expressions were detected by immunofluorescence staining and Western blot, macrophage typing was detected by flow, and the levels of pro-inflammatory factors (IL-6, IL-12, IL-1ß, TNF-α) and anti-inflammatory factors (IL-10 and TGF-ß) were measured using the corresponding kits. RESULTS: ECM1 is highly expressed in tissue-infiltrating macrophages under inflammatory conditions. It has been observed that Shionone inhibits the expression of ECM1 and attenuates sepsis-induced injury in kidney and inflammatory factor levels in serum. In addition, Shionone may reduce inflammatory factor levels through the promotion of M2 macrophages by GM-CSF/STAT5/Arg1 pathway to alleviate sepsis induced inflammation in vitro. CONCLUSION: These findings demonstrate that Shionone can alleviate sepsis-induced AKI by promoting M2 macrophage polarization through regulating the ECM1/STAT5 pathway.
RESUMEN
Purpose: The purpose of the present study was to estimate the effect of shionone (SHI) on sepsis-induced acute lung injury (ALI). Methods: The cecal ligation and puncture (CLP) surgery was performed to induce sepsis in mice. Pulmonary hematoxylin and eosin staining, the wet/dry ratio, myeloperoxidase (MPO) activity, and the survival rate were detected. The RAW264.7 cells were treated with SHI and stimulated with lipopolysaccharide (LPS). The cells were also overexpressed by extracellular mechanism protein 1 (ECM1) adenovirus. The relative levels of granulocyte-macrophage colony-stimulating factor, IL-6, IL-1ß, TNF-α, IL-10, and TGF-ß in the serum and supernatant were measured by ELISA. The protein expressions of ECM1, p-STAT5, signal transducer and activator of transcription 5 (STAT5), p-NF-κB, nuclear factor kappa-B (NF-κB), Arg1, CD206, CD16/32, and iNOS in the CLP-induced lung tissues and LPS-induced cells were detected by western blot. The cell counts of Ly6G, F4/80, CD16/32, and CD206 were evaluated by flow cytometry. The ECM1 expression was also observed by immunohistochemistry and immunofluorescence staining. Results: As a result, the histopathological change, pulmonary edema, and the MPO activity were relieved by SHI. SHI treatment increased the percentage of neutrophil and macrophage in the bronchoalveolar lavage fluid. Besides, SHI administration inhibited pro-inflammatory cytokines and M1 phenotype indices, as well as augmented the anti-inflammatory cytokines and M2 phenotype indices. SHI also attenuated the ECM1/STAT5/NF-κB pathway both in vivo and in vitro. The overexpression of ECM1 confirmed that the regulated effect of SHI was due to ECM1 signaling. Conclusion: In conclusion, the present study suggests that SHI ameliorated sepsis-induced ALI by screwing M1 phenotype to M2 phenotype macrophage via the ECM1/STAT5/NF-κB pathway.
RESUMEN
BACKGROUND: This study examines the clinical utility of the level of increased platelet distribution width (PDW) as a predictor of outcome in patients with traumatic brain injury. METHODS: In this retrospective study, 120 patients with traumatic brain injury (TBI) were recruited. Age, gender, PDW, and Glasgow Coma Scale (GCS) scores were measured. These patients were divided into two groups based on their 30-day outcomes. Receiver operating curves (ROCs) were generated to identify predictors of 30-day mortality. RESULTS: One hundred twenty patients with traumatic brain injury were enrolled in this study, 89 males (74.2%) and 31 females (25.8%) with a median age of 49.5 (19 - 89) years. The in-hospital mortality rate was 10.8% (n = 13). PDW levels in non-surviving patients were higher than in surviving patients. The higher the PDW, the lower the GSC score. The area under the curve (AUC) for PDW levels with regard to predicting 30-day mortality was 0.88 (95% confidence interval (CI), 0.78 to 0.97; p < 0.001). There was correlation between PDW level and GCS score (r = -0.30, 95% confidence interval (CI), - 0.46 to - 0.13; p < 0.001). CONCLUSIONS: PDW levels were associated with injury severity and mortality in patients with severe TBI.
