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The current study aimed to investigate whether prognostic nutritional index (PNI) is an independent predictor of acute kidney injury (AKI) and mortality of patients in the coronary care unit (CCU). In the present two-stage observational study of patients in the CCU, 6,444 patients from the Medical Information Mart for Intensive Care (MIMIC) III database were first enrolled (test cohort), after which 412 patients from Zhongnan Hospital of Wuhan University were recruited in the validation cohort. AKI was defined based on the Kidney Disease Improving Global Outcomes AKI criteria. The primary endpoint was the incidence of AKI stratified by severity, while the second endpoint included in-hospital mortality and 2-year mortality. In the test cohort, 4,457 (69.2%) patients developed AKI during hospitalization. Following multivariable adjustment, the highest quartile of the PNI value was associated with a 1.8-fold increased risk of AKI compared with the lowest quartile. For the prediction of AKI, the area under the receiver operating characteristic curve outperformed the acute physiology score III score and clinical model in patients with or without preexisting chronic kidney disease, and this was further validated in the hospital cohort used in the present study. A total of 2,219 patients suffered mortality during the 2-year follow-up, and PNI was indicated to independently predict the risk of in-hospital mortality and 2-year mortality in the test cohort and in the validation cohort. Decision curve analysis indicated that the PNI values were clinically useful; Therefore, the current study demonstrated that the PNI value is an independent predictor of AKI and mortality in patients within the CCU. [ABSTRACT FROM AUTHOR]

The present study aimed to construct targeted cationic microbubbles (TCMBs) by synthesizing cationic microbubbles conjugated to an intercellular adhesion molecule-1 (ICAM-1) antibody, and then to use the TCMBs to deliver the angiopoietin-1 (Ang-1) gene into infarcted heart tissue using ultrasound-mediated microbubble destruction. It was hypothesized that the TCMBs would accumulate in higher numbers than non-targeted cationic microbubbles (CMBs) in the infarcted heart, and would therefore increase the efficiency of targeted Ang-1 gene transfection and promote angiogenesis. The results of the study demonstrated that the ability of TCMBs to target inflammatory endothelial cells was 18.4-fold higher than that of the CMBs in vitro. The accumulation of TCMBs was greater than that of CMBs in TNF-α-stimulated human umbilical cord veins, indicated by a 212% higher acoustic intensity. In vivo, the TCMBs specifically accumulated in the myocardial infarct area in a rabbit model. Three days after ultrasound microbubble-mediated gene transfection, Ang-1 protein expression in the TCMB group was 2.7-fold higher than that of the CMB group. Angiogenesis, the thickness of the infarct region and the heart function of the TCMB group were all significantly improved compared with those in the CMB and control groups at 4 weeks following gene transfection (all P<0.01). Therefore, the results of the current study demonstrate that ultrasound-mediated TCMB destruction effectively delivered the Ang-1 gene to the infarcted myocardium, resulting in improved cardiac morphology and function in the animal model. Ultrasound-mediated TCMB destruction is a promising strategy for improving gene therapy in the future. [ABSTRACT FROM AUTHOR]