Chronic obstructive pulmonary disease (COPD) is a critical illness with high intensive care unit (ICU) mortality. Traditional glycemic markers like hemoglobin A1c (HbA1c) poorly reflect individual glucose metabolism variability. The hemoglobin glycation index (HGI), derived from the discrepancy between measured HbA1c and values predicted by fasting plasma glucose (FPG), assesses glycometabolic variability but remains unstudied in critically ill COPD patients. This retrospective cohort enrolled 1,125 critically ill COPD patients admitted to the ICU, with data derived from the MIMIC-IV database. HGI was calculated as measured HbA1c minus predicted HbA1c (model: HbA1c = − 0.0095 × FPG + 5.02) and divided into tertiles. Cox regression models, adjusted for demographics, comorbidities, and clinical parameters, evaluated HGI tertile associations with 30-day, 90-day, and 365-day all-cause mortality. Restricted cubic splines (RCS) and threshold analysis explored nonlinear relationships. Among 1,125 patients, higher HGI tertiles were independently associated with lower mortality at all timepoints. In multivariable-adjusted Model II (age, sex, ethnicity, hematocrit, hemoglobin, SOFA score, SAPS II score, corticosteroid use, sepsis, and mechanical ventilation, diabetes), compared to the lowest tertile (T1), T2 and T3 showed significantly reduced mortality. For the 30-day mortality, the hazard ratios (HRs) were 0.54 (95
OBJECTIVE:Disorders related to serum chloride concentration have recently attracted considerable interest. We sought to determine whether initial serum chloride was associated with an increased risk of all-cause mortality among critically ill patients diagnosed with acute kidney injury (AKI). METHODS:We searched the Multiparameter Intelligent Monitoring in the Intensive Care IV database to retrieve clinical data, including demographic factors, clinical variables, lab tests, and scoring systems. Hypothesis testing was conducted using a range of statistical approaches, including the generalized additive model, the Cox proportional hazards model, and subgroup analyses. RESULTS:Our research included 19,107 participants who met the set criteria. We found that the levels of chloride in the patient's serum upon admission had a similar inverted L-shaped relationship with the 30-day all-cause mortality rate in AKI. In multivariate analysis following the adjustment of confounders such as sex, ethnicity, and age, compared with the referent group (100-105 mmol/L), low-chloride (< 100 mmol/L) was a considerable risk predictor for 30-day, 90-day, and 365-day all-cause mortality. In particular, the HRs (95% CIs) for chloride were 1.49 (1.36, 1.63), 1.48 (1.36, 1.61), and 1.59 (1.47, 1.71). After adjusting additional clinical characteristics, low-chloride levels still served independently as a major predictor of all-cause mortality over 30 days, 90 days, and 365 days (HR, 95% CI: 1.24, 1.09-1.41; 1.17, 1.04-1.32; 1.27, 1.14-1.42). CONCLUSIONS:The probability of all-cause mortality was higher in severely ill individuals with AKI who had lower baseline serum chloride levels upon admission to the intensive care unit (ICU).
Glycemic variability is increasingly recognized as a critical factor influencing outcomes in intensive care, yet its prognostic role remains unclear. The Hemoglobin Glycation Index (HGI), which reflects individual glycemic variation, has not been thoroughly studied in critically ill populations. To evaluate the association between HGI and all-cause mortality in critically ill patients using data from a large intensive care unit (ICU) cohort. We conducted a retrospective cohort study using the MIMIC-IV database. The primary outcomes were 30-, 90-, and 365-day all-cause mortality; in-hospital mortality was secondary. Kaplan-Meier analysis, Cox regression, and restricted cubic spline (RCS) modeling were used to assess mortality risk across HGI levels. Propensity score matching (PSM) and subgroup analyses were performed to ensure robustness. Among 9,695 patients, those with low HGI (< − 0.40) had significantly higher mortality (P < 0.001). RCS analysis showed a nonlinear association between HGI and 30-day mortality. Higher HGI values were independently associated with reduced risk of death at all time points, with hazard ratios ranging from 0.43 to 0.76 (P < 0.001). These associations persisted after multivariable adjustment and PSM. Subgroup analyses showed consistent results across patient characteristics. Lower HGI values are associated with increased short- and long-term mortality in critically ill patients. HGI may serve as a valuable prognostic biomarker for risk stratification in ICU settings. This is the first large-scale retrospective cohort study to investigate the prognostic value of the HGI in critically ill patients. A nonlinear association was observed between HGI and short-term and long-term all-cause mortality. Lower HGI values were independently associated with increased 30-, 90-, 365-day, and in-hospital mortality, even after multivariate adjustment and propensity score matching. Subgroup analyses showed consistent associations across various clinical characteristics, supporting the generalizability of HGI as a mortality predictor. HGI may serve as a novel, accessible biomarker for individualized glycemic risk stratification in ICU settings.
Background. There is no evidence suggesting that red blood cell distribution width-to-albumin ratio (RA) predicts outcomes in severely ill older individuals with acute kidney injury (AKI). We hypothesized that RA is associated with all-cause mortality in critically ill older patients with AKI. Methods. We recorded demographics, laboratory tests, comorbidities, vital signs, and other clinical information from the MIMIC-III V1.4 dataset. The primary endpoint was 90-day all-cause mortality, and the secondary endpoints were 30-day mortality, one-year mortality, renal replacement treatment (RRT), duration of stay in the intensive care unit (ICU), sepsis, and septic shock. We generated Cox proportional hazards and logistic regression models to determine RA’s prognostic values and subgroup analyses to determine the subgroups’ mortality. We conducted a Pearson correlation analysis on RA and C-reactive protein (CRP) in the cohort of patients from the Second Affiliated Hospital of Wenzhou Medical University. Results. A total of 6,361 patients were extracted from MIMIC-III based on the inclusion and exclusion criteria. RA levels directly and linearly correlated with 90-day all-cause mortality. After controlling for ethnicity, gender, age, and other confounding variables in multivariate analysis, higher RA was significantly associated with an increased risk of 30-day, 90-day, and one-year all-cause mortality as opposed to the reduced levels of RA (tertile 3 vs. tertile 1: hazard ratios (HRs), 95% confidence intervals (CIs): 1.70, 1.43–2.01; 1.90, 1.64–2.19; and 1.95, 1.72–2.20, respectively). These results suggested that elevated levels of RA were linked to an elevated risk of 30-day, 90-day, and one-year all-cause death. There was a similar trend between RA and the use of RRT, length of stay in ICUs, sepsis, and septic shock. The subgroup analysis did not reveal any considerable interplay among strata. When areas under the curve were compared, RA was a weaker predictor than the SAPS II score but a stronger predictor than red blood cell distribution width (RDW) or albumin alone (P<0.001); RA combined with SAPS II has better predictive power than SAPS II alone (P<0.001). The Second Affiliated Hospital of Wenzhou Medical University cohort showed that CRP positively correlated with RA, with a coefficient of 0.2607 (P<0.001). Conclusions. RA was an independent prognostic predictor in critically ill older patients with AKI, and greater RA was linked to a higher probability of death. The risk of AKI is complicated when RRT occurs; sepsis and septic shock increase with RA levels.
目的:分析影响心原性休克患者短期预后的相关因素,并以列线图形式构建新疆地区心原性休克患者30 d死亡风险的预测模型。方法:回顾性分析新疆医科大学第一附属医院2013—2019年295例心原性休克患者的临床资料。采用单因素和多因素Logistic回归分析影响心原性休克患者30 d死亡的危险因素,并使用列线图构建心原性休克患者死亡风险的预测模型,采用一致性系数和受试者工作特征(ROC)曲线评估模型的优劣性。结果:295例患者中,30 d死亡182例为死亡组,未发生死亡113例为生存组。死亡组与生存组性别构成、年龄、ICU时间、收缩压、白细胞、中性粒细胞计数、红细胞分布宽度(RDW)、凝血酶原时间、血钾、血糖、血肌酐、总胆红素、碳酸氢根、碱剩余、乳酸、脑钠肽前体(NT-proBNP)、心肌肌钙蛋白(cTnI)及呼吸衰竭、肝病、肾病比例比较差异有统计学意义( P<0.01或<0.05)。多因素Logistic回归分析结果显示,NT-proBNP、凝血酶原时间、cTnI、乳酸和收缩压为心原性休克患者死亡的独立危险因素( OR = 1.00、1.10、1.30、1.29和1.04,95% CI 1.00~1.00、1.01~1.18、1.00~1.68、1.01~1.65和1.02~1.07, P<0.01或<0.05)。对多因素分析得到的独立影响因素再结合临床实际,进行赤池信息量准则(AIC)分析选择建模变量,纳入列线图模型的变量为NT-proBNP、凝血酶原时间、cTnI和乳酸。列线图模型在经过500次Bootstrap自抽样内部验证后,得到的C指数为0.805,曲线下面积为0.846,最佳阈值0.486,灵敏度为78.6%,特异度为83.1%。 结论:NT-proBNP、凝血酶原时间、cTnI和乳酸为心原性休克患者短期预后的相关影响因素,并构建了相关列线图预测模型,对心原性休克的早期干预具有指导意义。
Background. Acute kidney injury (AKI) is a common clinical syndrome carrying high morbidity and mortality. Body mass index (BMI) is a common health indicator, and a high BMI value-obesity has been shown to be associated with the outcomes of several diseases. However, the relationship between different BMI categories and mortality in all critically ill patients with AKI is unclear and needs further investigation. Therefore, we evaluated the ability of BMI to predict the severity and all-cause mortality of AKI in critically ill patients. Methods. We extracted clinical data from the MIMIC-III v1.4 database. All adult patients with AKI were initially screened. The baseline data extracted within 24 hours after ICU admission were presented according to WHO BMI categories. Logistic regression models and the Cox proportional hazards models were, respectively, constructed to assess the relationship between BMI and the severity and all-cause mortality of AKI. The generalized additive model (GAM) was used to identify nonlinear relationships as BMI was a continuous variable. The subgroup analyses were performed to further analyze the stability of the association between BMI category and 365-day all-cause mortality of AKI. Result. A total of 15,174 patients were extracted and were divided into four groups according to BMI. Obese patients were more likely to be young and male. In the fully adjusted logistic regression model, we found that overweight and obesity were significant predictors of AKI stage III (OR, 95 CI: 1.17, 1.05-1.30; 1.32, 1.18-1.47). In the fully adjusted Cox proportional hazards model, overweight and obesity were associated with significantly lower 30-day, 90-day, and 365-day all-cause mortality. The corresponding adjusted HRs (95 CIs) for overweight patients were 0.87 (0.77, 0.99), 0.84 (0.76, 0.93), and 0.80 (0.74, 0.88), and for obese patients, they were 0.87 (0.77, 0.98), 0.79 (0.71, 0.88), and 0.73 (0.66, 0.80), respectively. The subgroup analyses further presented a stable relationship between BMI category and 365-day all-cause mortality. Conclusions. BMI was independently associated with the severity and all-cause mortality of AKI in critical illness. Overweight and obesity were associated with increased risk of AKI stage III; however, they were predictive of a relatively lower mortality risk in these patients.
There has been no study exploring the prognostic values of neutrophil percentage-to-albumin ratio (NPAR). We hypothesised that NPAR is a novel marker of inflammation and is associated with all-cause mortality in patients with severe sepsis or septic shock. Patient data were extracted from the MIMIC-III V1.4 database. Only the data for the first intensive care unit (ICU) admission of each patient were used and baseline data were extracted within 24 h after ICU admission. The clinical endpoints were 30-, 90- and 365-day all-cause mortality in critically ill patients with severe sepsis or septic shock. Cox proportional hazards models and subgroup analyses were used to determine the relationship between NPAR and these clinical endpoints. A total of 2166 patients were eligible for this analysis. In multivariate analysis, after adjustments for age, ethnicity and gender, higher NPAR was associated with increased risk of 30-, 90- and 365-day all-cause mortality in critically ill patients with severe sepsis or septic shock. Furthermore, after adjusting for more confounding factors, higher NPAR remained a significant predictor of all-cause mortality (tertile 3 vs. tertile 1: HR, 95% CI: 1.29, 1.04-1.61; 1.41, 1.16-1.72; 1.44, 1.21-1.71). A similar trend was observed in NPAR levels stratified by quartiles. Higher NPAR was associated with increased risk of all-cause mortality in critically ill patients with severe sepsis or septic shock.
目的 观察便携式转运呼吸机在重型颅脑损伤术后患者院内转运中的应用效果.方法 选取2017年6月至2019年5月该院ICU收治符合条件的重型颅脑损伤术后患者150例,随机分为A组与B组各75例.A组采用便携式转运呼吸机转运,B组采用简易呼吸皮囊转运.记录两组转运前后生命体征、血气指标、转运成功率、转运途中并发症发生率.结果 转运后A组HR、R、SpO2及PaO2均低于B组,PaCO2及转运成功率均高于B组,除R外,余差异均有统计学意义(P<0.05).转运途中并发症发生率A组17.3%(13/75),低于B组的66.7%(50/75),差异有统计学意义(P<0.05).结论 重型颅脑损伤术后机械通气患者离开ICU做CT检查时,使用转运呼吸机辅助通气较皮囊辅助通气可使动脉血气分析、生命体征保持稳定提高转运成功率,降低转运并发症发生率.
Background . There is no evidence to suggest the predictive power of neutrophil percentage-to-albumin ratio (NPAR) in patients with acute kidney injury (AKI). We hypothesized that NPAR would correlate with all-cause mortality in critically ill patients with AKI. Methods . From the MIMIC-III V1.4 database, we extracted demographics, vital signs, comorbidities, laboratory tests, and other clinical data. The clinical endpoints were 30-, 90- and 365-day all-cause mortality in critically ill patients with AKI. Cox proportional hazards models were used to evaluate the prognostic values of NPAR, and subgroup analyses were performed to measure mortality across various subgroups. Results . A total of 7,481 eligible subjects were enrolled. In multivariate analysis, after adjustments for age, ethnicity, gender, and other confounding factors, higher NPARs were associated with an increased risk of 30-, 90- and 365-day all-cause mortality in critically ill patients with AKI (tertile 3 versus tertile 1: adjusted HR, 95% CI: 1.48, 1.30–1.69; 1.47, 1.31–1.66; 1.46, 1.32–1.62, respectively; P trend <0.01). A similar trend was observed in the NPAR group division by quintiles. Subgroup analysis revealed no significant interactions in most strata. Conclusions . Increased NPAR correlates with increased risk of all-cause mortality in critically ill patients with AKI.
Background No epidemiological study has investigated the effect of anion gap (AG) on the prognosis of critically ill patients with acute kidney injury (AKI). Therefore, we aimed to determine the association between serum AG and all-cause mortality in these patients. Methods From MIMIC III, we extracted demographics, vital signs, laboratory tests, comorbidities, and scoring systems from the first 24 h after patient ICU admission. A generalized additive model was used to identify a nonlinear association between anion gap and 30-day all-cause mortality. We also used the Cox proportional hazards models to measure the association between AG levels and 30-day, 90-day, and 365-day mortality in patients with AKI. Results A total of 11,573 eligible subjects were extracted from the MIMIC-III. The relationship between AG levels and 30-day all-cause mortality in patients with AKI was nonlinear, with a U-shaped curve. In multivariate analysis, after adjusting for potential confounders, higher AG was a significant predictor of 30-day, 90-day, and 365-day all-cause mortality compared with lower AG (HR, 95% CI: 1.54, 1.33–1.75; 1.55, 1.38–1.73; 1.46, 1.31–1.60). Conclusions The relationship between AG levels and 30-day all-cause mortality described a U-shaped curve. High-AG levels were associated with increased risk 30-day, 90-day, and 365-day all-cause mortality in critically ill patients with AKI.
Background Currently, evidence regarding the predictive significance of red blood cell distribution width (RDW) among patients with acute respiratory distress syndrome (ARDS) remains scarce. The aim of this study was to determine the prognostic value of RDW for critically ill patients with ARDS. Methods We studied all patients with ARDS from the Multiparameter Intelligent Monitoring in Intensive Care Database III (MIMIC-III) for whom RDW was available. The clinical outcomes were 30-day and 90-day mortality. Analyses included logistic multivariate regression model, Receiver Operating Characteristic (ROC) analysis, and subgroup analysis. Results A total of 404 eligible ARDS patients were included. After adjustment for several clinical characteristics related to 30-day mortality, the adjusted OR (95% CIs) for RDW levels ≥14.5% was 1.91 (1.08, 3.39). A similar trend was observed for 90-day mortality. The RDW levels ≥14.5% were also an independent predictor of 90-day mortality (OR, 2.56; 95% CI, 1.50 to 4.37; P = 0.0006) compared with the low RDW levels (<14.5%). In subgroup analyses, RDW showed no significant interactions with other relevant risk factors for 30-day mortality. Conclusions RDW appeared to be a novel, independent predictor of mortality in critically ill patients with ARDS.
Background: There is no previously published epidemiological study exploring the association between red blood cell distribution width (RDW) and mortality in patients with cardiogenic shock (CS). The aim of this study was to examine the association between RDW and the risk of all-cause mortality in these patients. Material/Methods: We analyzed clinical data from the MIMIC-III V1.4 database. We collected data on each patient's demographic parameters, vital signs, laboratory parameters, vital signs, comorbidities, and scoring systems on ICU admission. Cox proportional hazards models were used to assess the association between RDW levels and the 30-day, 90-day, and 365-day mortality in patients with CS. Results: There were 1131 patients meeting inclusion criteria in our study. In multivariate analysis, following adjustment for age, sex, and ethnicity, higher RDW in tertiles and quintiles were all associated with increased risk of 30-day, 90-day, and 365-day all-cause mortality. Furthermore, after adjusting for more relevant confounders, RDW remained a significant predictor of risk of 30-day, 90-day, and 365-day mortality (tertile 3 versus tertile 1: HR, 95% CI: 1.66, 1.19-2.31; 1.73, 1.28-2.33; 1.80, 1.38-2.34). Similarly significant robust associations were found in RDW levels stratified by quintiles. Conclusions: Higher RDW is associated with increased risk of all-cause mortality in critically ill patients with CS.
Background: There have been no epidemiological studies exploring the prognostic ability of serum total and ionized calcium (tCa and iCa) in critically ill patients with acute kidney injury (AKI). We assessed the association of admission tCa and iCa concentrations with all-cause mortality in these patients. Methods: We extracted clinical data from the MIMIC-III V1.4 database. Only the data for the first intensive care unit (ICU) admission of each patient were used and baseline data were extracted within 24 h after ICU admission. Cox proportional hazards models and subgroup analyses were used to determine the relationship between tCa and iCa concentrations and 30, 90 and 365-day all-cause mortality in critically ill patients with AKI. A total of 10,207 eligible patients were studied. In multivariate analysis, adjusted for age, ethnicity and gender, both low-tCa ( < 7.9 mg/dl) and low-iCa ( < 1.06 mmol/l) concentrations were significant predictors of risk of all-cause mortality. Furthermore, after adjusting for more confounding factors, low-iCa concentrations remained a significant predictor of all-cause mortality at 30 days, 90 days, 365 days (HR, 95% CI: 1.19, 1.06-1.33; 1.15, 1.05-1.27; 1.10, 1.01-1.20). Conclusions: Low-iCa concentrations were independent predictors of all-cause mortality in critically ill patients with AKI.
MicroRNA (miR) has been reported to be associated with ischemia and reperfusion (I/R) and cell apoptosis. Suppression of cell apoptosis may reduce the irreversible damage induced by reperfusion. The aims of the current study were to explore the cytoprotective effects of miR-146 against oxygen-glucose deprivation/recovery (OGD/R)-induced injury in H9c2 rat myocardial cells, as well as the underlying mechanisms. Following stimulation with OGD/R, the cells were transfected with miR-146 mimics or negative controls. The levels of miR-146 were analyzed by reverse transcription-quantitative polymerase chain reaction. Thereafter, cell viability and cell apoptosis were analyzed by MTT assay and terminal deoxynucleotidyl-transferase-mediated dUTP nick-end labeling assay, respectively. In addition, the levels of tumor necrosis factor (TNF)-α were determined by ELISA and the levels of B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax), Bcl-2 and phosphorylated (p)-nuclear factor (NF)-κB were measured by western blotting. The results demonstrated that overexpression of miR-146 significantly increased cell viability and decreased apoptosis (P<0.05). It was observed that overexpression of miR-146 statistically reduced the levels of Bax, TNF-α and p-NF-κB but markedly upregulated the levels of Bcl-2 (P<0.05). These results indicate that overexpression of miR-146 may protect against OGD/R-induced cardiomyocyte apoptosis. Overexpression of miR-146 may alleviate the irreversible injury associated with reperfusion and the effects may be achieved by inhibiting the NF-κB/TNF-α signaling pathway.
目的 探讨老年急性心肌梗死患者急诊经皮冠状动脉介入术后在ICU发生医院感染的临床特征及预防措施.方法 收集102例急诊经皮冠状动脉介入治疗的老年急性心肌梗死患者临床资料,观察其术后医院感染的发生率、病原菌的分布,并对医院感染因素进行分析.结果 发生医院感染53例,感染率为51.96%;感染部位以下呼吸道为主,占50.94%.共检出病原菌62株,主要为鲍曼不动杆菌与大肠埃希菌,分别占19.35%与17.74%.Killip分级、使用呼吸机、留置导尿、侵入性操作、预防使用抗菌药物、ICU住院时间是引起老年急性心肌梗死患者急诊经皮冠状动脉介入术后发生医院感染的独立危险因素(均P< 0.05).结论 ICU老年急性心肌梗死患者病情危重,医院感染发生率高,危险因素多,加强医院感染管理,针对危险因素采取相应措施,以预防及控制医院感染的发生.
Background Recent studies suggest that levosimendan does not provide mortality benefit in patients with low cardiac output syndrome undergoing cardiac surgery. These results conflict with previous findings. The aim of the current study is to assess whether levosimendan reduces postoperative mortality in patients with impaired left ventricular function (mean EF ≤ 40%) undergoing cardiac surgery. Methods We conducted a comprehensive search of PubMed, EMBASE, and Cochrane Library Database through November 20, 2017. Inclusion criteria were random allocation to treatment with at least one group receiving levosimendan and another group receiving placebo or other treatments and cardiac surgery patients with a left ventricular ejection fraction of 40% or less. The primary endpoint was postoperative mortality. Secondary outcomes were cardiac index, pulmonary capillary wedge pressure (PCWP), length of intensive care unit (ICU) stay, postoperative atrial fibrillation, and postoperative renal replacement therapy. We performed trial sequential analysis (TSA) to evaluate the reliability of the primary endpoint. Results Data from 2,152 patients in 15 randomized clinical trials were analyzed. Pooled results demonstrated a reduction in postoperative mortality in the levosimendan group [RR = 0.53, 95% CI (0.38–0.73), I2 = 0]. However, the result of TSA showed that the conclusion may be a false positive. Secondary outcomes demonstrated that PCWP, postoperative renal replacement therapy, and length of ICU stay were significantly reduced. Cardiac index was greater in the levosimendan group. No difference was found in the rate of postoperative atrial fibrillation. Conclusions Levosimendan reduces the rate of death and other adverse outcomes in patients with low ejection fraction who were undergoing cardiac surgery, but results remain inconclusive. More large-volume randomized clinical trials (RCTs) are warranted.
Objective To investigate the expression and effect of Slit2/Robo4 signaling pathway in vitro model of transfusion related acute lung injury (TRALI). Methods A two-hit model of polymorphonuclear neutrophils (PMNs)-mediated human pulmonary microvascular endothelial cells (HMVECs) damage was used as TRALI in vitro model. After the HMVECs were incubated for 0, 0.5, 1, 2, 4, and 6 h, the protein expressions of Robo4 and vascular endothelial cadherin (VE-cadherin) were detected by Western-blotting, and the mRNA expressions of Robo4 and Slit2 were analyzed by reverse transcription PCR (RT-PCR). The permeability of HMVECs was detected by in vitro experiment of endothelial cell permeability. Then the HMVECs were incubated with 0, 0.5, 1, 4, 10, and 20 μg/L Slit2-N for 24 h. The integrity and permeability of HMVECs were detected. Results In vitro model of TRALI, the mRNA expressions of Robo4 and Slit2 both showed significant differences at different time points (F=12.880, 11.060; both P<0.001); they were much lower at 2 h (0.72 ± 0.04, 0.78 ± 0.05), 4 h (0.49 ± 0.04, 0.49 ± 0.06), and 6 h (0.34 ± 0.03, 0.43 ± 0.11) than those at 0 h (1.29 ± 0.06, 1.40 ± 0.09; all P<0.05). The protein expression of Robo4 showed significant difference at each time point (F=11.560, P<0.001); it decreased at 2, 4, 6 h (0.99 ± 0.04, 0.66 ± 0.03, 0.45 ± 0.04) in comparing with 0 h (1.44 ± 0.04, all P<0.05). In addition, the protein expression of VE-cadherin at each time point was significantly different (F = 9.667, P < 0.001); its expression decreased significantly at 2, 4, 6 h (0.91 ± 0.08, 0.78 ± 0.05, 0.50 ± 0.04) in comparing with 0 h (1.46 ± 0.09, all P < 0.05). The vitro experiment of endothelial cell permeability revealed that the permeability of HMVECs was significant different at each time point (F=21.940, P<0.001); as comparing with 0 h (1.42 ± 0.16), the permeability of HMVECs was significantly higher at 2, 4, 6 h (4.00 ± 0.35, 5.70 ± 1.71, 10.02 ± 2.24; all P<0.05). After adding the exogenous Slit2-N, the expression of VE-cadherin protein was statistically significantly different (F=13.220, P<0.001); it increased in the 4, 10, 20 μg / L Slit2-N groups (1.19 ± 0.35, 1.49 ± 0.13, 2.12 ± 0.21) as comparing with the 0 μg/L Slit2-N group (0.41 ± 0.08, all P<0.05). The vitro experiment of endothelial cell permeability revealed that the permeability of HMVECs was significant different (F=19.430, P<0.001); the permeability of HMVECs was significantly lower in the 4, 10, 20 μg/L Slit2-N groups (4.2 ± 1.1, 2.1 ± 0.7, 1.8 ± 0.8) as comparing with the 0 μg/L Slit2-N group (10.0 ± 2.2, all P < 0.05). Conclusion The Slit2 / Robo4 signaling pathway may be involved in the pathophysiological process of TRALI. Exogenous Slit2-N may modulate the integrity and permeability of HMVECs in vitro TRALI model, and become a promising candidate for developing novel therapies against TRALI.
Background.Several investigators have sought risk factors for mortality in acute kidney injury (AKI). However, no epidemiological studies have investigated the impact of red blood cell distribution width (RDW) on prognosis for critically ill patients with AKI. The aim of this study was to investigate the association of RDW with mortality in these patients.Methods.We analyzed data from the MIMIC-III. RDW was measured upon ICU admission. The association between RDW and mortality of AKI was determined using a multivariate logistic regression and was expressed as the adjusted odds ratio with associated 95% confidence interval (CI). We also conducted subgroup analyses to determine the consistency of this association.Results.A total of 14,078 critically ill patients with AKI were eligible for this analysis. In multivariate analysis, adjusted for age and gender and compared with the reference group (RDW 11.1-13.4%) related to hospital mortality, the adjusted ORs (95% CIs) for RDW levels 13.5-14.3%, 14.4-15.6%, and 15.7-21.2% were 1.22 (1.05, 1.43), 1.56 (1.35, 1.81), and 2.66 (2.31, 3.06), respectively. After adjusting for confounding factors, with high RDW linked to an increase in mortality (RDW 15.7-21.2% versus 11.1-13.4%: OR, 1.57; 95% CI, 1.22 to 2.01;Ptrend <0.0001). A similar trend was observed for 30-day mortality.Conclusions.RDW appeared to be an independent prognostic marker in critically ill patients with AKI and higher RDW was associated with increased risk of mortality in these patients.
BACKGROUND:Several studies have suggested that serum ionized calcium (iCa) is associated with mortality in critical illness. However, evidence regarding the predictive significance of serum total calcium (tCa) in critical illness remains scarce. The aim of this study was to assess the association of tCa levels with mortality in critical illness.METHODS:We employed the MIMIC-III v1.3 database. tCa was measured upon ICU admission and its relationship with mortality was determined using smooth curve fitting. The association between admission tCa levels and hospital mortality was determined using logistic regression.RESULTS:Inclusion criteria were met by 44,886 critically ill patients. A U-shaped pattern was observed between tCa and hospital mortality. Similar trends were observed for hospital mortality when quintiles were used to group patients according to tCa. In multivariate analysis, adjusted for age and sex, the model indicated that admission tCa levels ⩽7.6mg/dl, 7.7-8.1mg/dl, and ⩾9.0mg/dl were associated with an increase in mortality when compared to the reference level (8.6-9.0mg/dl). However, adjusted for more clinical characteristics, tCa was not associated with hospital mortality.CONCLUSIONS:The relationship between tCa and hospital mortality followed a ''U" shaped curve. tCa had certain prognostic value in critically ill patients, but it had no independent association with hospital mortality.
Objective: To explore the protective effects of Shenfu injection on acute kidney injury of patients with septic shock. Methods: 60 patients with septic shock were randomized to the treatment group and the con-trol group,with 30 in each. All patients were treated with sepsis bundle according to International guidelines for septic shock 2012. The treatment group was treated with Shenfu injection,60 mL,250 mL 0.9%,sodium chloride injection,intravenous drip,while the control group were given an equal amount of 0.9%sodium chloride injection. The course of treatment was 7 days. Before treatment and on 3rd and 7th day after treatment,the levels of serum creatinine (sCr),blood urea nitrogen (BUN),cystatin C, procalcitonin (PCT),C-reactive protein (CRP),tumor necrosis factor-alpha (TNF-α),β2-microglobulin and 24-hour urine protein were measured respectively and A-PACHEⅡ score and SOFA score were recorded before and after treatment. Results: The serum cystatin C in the treatment group was lower than that in the control group on the seventh day(P<0.05);PCT of the treatment group was lower than that of the control group on 3rd and 7th day(P<0.05);the levels of beta 2-MG and UPRO/24 h in the treatment group were lower than those in the control group at seventh days (P<0.05);APACHEⅡ scores in the treatment group were lower than those in the control group on 3rd and 7th day (P<0.05),while SOFA score was lower than that in the control group at seventh days (P<0.05). Conclusion: Shenfu injection has a protec-tive effect on acute kidney injury caused by septic shock.