郭素萍
阜外华中心血管病医院 重症医学科
OBJECTIVE:The study aimed to investigate whether lymphopenia and red blood cell distribution width (RDW) elevation are associated with an increased risk of mortality in acute aortic dissection (AAD).METHODS:This multicenter retrospective cohort study enrolled patients diagnosed with AAD by aortic computed tomographic angiography (CTA) from 2010 to 2021 in five teaching hospitals in central-western China. Cox proportional hazards regression and Kaplan-Meier curves were used in univariable and multivariable models. Clinical outcomes were defined as all-cause in-hospital mortality, while associations were evaluated between lymphopenia, accompanied by an elevated RDW, and risk of mortality.RESULTS:Of 1903 participants, the median age was 53 (interquartile range [IQR], 46-62) years, and females accounted for 21.9%. Adjusted increased risk of mortality was linearly related to the decreasing lymphocyte percentage (P-non-linearity = 0.942) and increasing RDW (P-non-linearity = 0.612), and per standard deviation (SD) of increment lymphocyte percentage and RDW was associated with the 26% (0.74, 0.64-0.84) decrement and 5% (1.05, 0.95-1.15) increment in hazard ratios (HRs) and 95% confidence intervals (CIs) of mortality, respectively. Importantly, lymphopenia and elevation of RDW exhibited a significant interaction with increasing the risk of AAD mortality (P-value for interaction = 0.037).CONCLUSIONS:Lymphopenia accompanied by the elevation of RDW, which may reflect the immune dysregulation of AAD patients, is associated with an increased risk of mortality. Assessment of immunological biomarkers derived from routine tests may provide novel perspectives for identifying the risk of mortality.
PloS one 2023
Background:Polymyxins have become an important treatment option for carbapenem-resistant organisms (CRO) infections. However, there is a rare of clinical studies on colistin sulfate. This study sought to investigate the rate of clinical improvement and adverse reactions of colistin sulfate in the treatment of severe infections caused by CRO in critically ill patients and assess the factors associated with 28-day all-cause mortality.Methods:This multicenter retrospective cohort study included intensive care unit (ICU) patients who received colistin sulfate due to CRO infections during July 2021 and May 2022. The primary endpoint was clinical improvement at end of therapy. Secondary endpoints included adverse reactions bacterial clearance rate and 28-day all-cause mortality.Results:A total of 122 patients, who were included between July 2021 and May 2022, were included in this study, of whom 86 (70.5%) showed clinical improvement and 36 (29.5%) showed clinical failure. The comparison of the clinical data of the patients showed that the median sequential organ failure assessment (SOFA) score was higher in the failure group than the improvement group {9.5 [7, 11] vs. 7 [4, 9], P=0.002}, the proportion of patients receiving extracorporeal membrane oxygenation (ECMO) was higher in the failure group than the improvement group (27.8% vs. 12.8%, P=0.046), and the median duration of treatment was longer in the improvement group than the failure group {12 [8, 15] vs. 5.5 [4, 9.75], P<0.001}. A total of 5 (4.1%) patients suffered from acute kidney injury due to increases in creatinine during colistin sulfate treatment. The Cox regression survival analysis showed that the SOFA score [hazards ratio (HR) =1.198, P=0.001], ECMO treatment (HR =2.373, P=0.029), and duration of treatment (HR =0.736, P<0.001) were independently associated with 28-day all-cause mortality.Conclusions:Colistin sulfate is a reasonable choice for the treatment of CRO infections in the current treatment options are limited. The possible kidney injury caused by the colistin sulfate requires intensive monitoring.
Journal of thoracic disease 2023
AIMS:Myocardial infarction is the leading cause of death worldwide. The aim of this study was to investigate the function and mechanism of lncRNA RMST in myocardial infarction.MATERIALS AND METHODS:H/R and H2O2 models were established to assess the function of lncRNA RMST in vitro. Mouse myocardial infarction was used to analyze the function of lncRNA RMST in vivo. Bioinformatics analysis was performed to predict the potential binding target of lncRNA RMST. Rescue experiments were performed to verify the relationship between RMST and its target.RESULTS:The expression of lncRNA RMST was significantly increased with H/R or H2O2 treatment. Knockdown of lncRNA RMST improved cell death and protected mitochondria from H/R injury in vitro. In vivo, cardiac function was significantly attenuated by knockdown of lncRNA RMST. We also provided evidence that miR-5692 was a direct target of lncRNA RMST. Rescue experiments showed that knockdown of miR-5692 could restore the function of RMST.CONCLUSION:Our study is the first to prove the function and mechanism of lncRNA RMST in myocardial infarction. Thus, a deeper understanding of the role of lncRNA RMST in myocardial infarction may provide new insights for the clinical intervention of MI.
American journal of translational research 2021
Studies have shown that matrine showed cardiovascular protective effects; however, its role and mechanism in myocardial ischemia/reperfusion (I/R) injury remain unknown. The Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway activation and elevated heat shock protein (HSP) 70 are closely related to the prevention of myocardial I/R injury. The cardioprotective effects of matrine were determined in hypoxia/reoxygenation (H/R)-treated primary rat cardiomyocytes and left anterior descending coronary artery ligation and reperfusion animal models. The molecular mechanisms of matrine in myocardial I/R injury were focused on JAK2/STAT3 pathway activation and HSP70 expression. We found that matrine significantly increased H/R-induced the suppression of cell viability, decreased lactate dehydrogenase release, creatine kinase activity, and cardiomyocytes apoptosis in vitro. Moreover, matrine notably reduced the serum levels of creatine kinase-myocardial band (CK-MB) and cardiac troponin I, lessened the infarcted area of the heart, and decreased the apoptotic index of cardiomyocytes induced by I/R in vivo. Matrine activated the JAK2/STAT3 signaling, upregulated HSP70 expression both in vitro and in vivo. The cardioprotective effects of matrine were abrogated by AG490, a JAK2 inhibitor, and HSP70 siRNA. In addition, AG490 reduced HSP70 expression increased by matrine. In conclusion, matrine attenuates myocardial I/R injury by upregulating HSP70 expression via the activation of the JAK2/STAT3 pathway.
Shock (Augusta, Ga.) 2018
