OBJECTIVE To study the cause of bacterial infection of ventilator-associated pneumonia(VAP) in intensive care unit(ICU) and summarize effective methods to prevent and control the infection.METHODS Epidemiologic study on 300 patients with VAP in ICU from Dec 1,2003 to Jul 13,2006.Preventing and controlling strategy was as follows.RESULTS Pathogenic bacteria of VAP in ICU mostly were multidrug-resistant ones,of which the G-were 56.3%,G+ were 23% and fungi were 13.7%.CONCLUSIONS To control VAP in ICU proper technique and method are important.Management of hospital infection and related training of staff in ICU are the basic way.

Small ubiquitin-related modifier(SUMOylation)is a dynamic post-translational modification that maintains cardiac function and can protect against a hypertrophic response to cardiac pressure overload.However,the function of SUMOylation after myocardial infarction(MI)and the molecular details of heart cell responses to SUMO1 deficiency have not been determined.In this study,we demonstrated that SUMO1 protein was inconsistently abundant in different cell types and heart regions after MI.However,SUMO1 knockout significantly exacerbated systolic dysfunction and infarct size after myocardial injury.Single-nucleus RNA sequencing revealed the differential role of SUMO1 in regulating heart cells.Among cardiomyocytes,SUMO1 deletion increased the Nppa+Nppb+Ankrd1+cardiomyocyte subcluster pro-portion after MI.In addition,the conversion of fibroblasts to myofibroblasts subclusters was inhibited in SUMO1 knockout mice.Importantly,SUMO1 loss promoted proliferation of endothelial cell subsets with the ability to reconstitute neovascularization and expressed angiogenesis-related genes.Computational analysis of ligand/receptor interactions suggested putative pathways that mediate cardiomyocytes to endothelial cell communication in the myocardium.Mice preinjected with cardiomyocyte-specific AAV-SUMO1,but not the endothelial cell-specific form,and exhibited ameliorated cardiac remodeling following MI.Collectively,our results identified the role of SUMO1 in cardiomyocytes,fibroblasts,and endothelial cells after Ml.These findings provide new insights into SUMO1 involvement in the patho-genesis of MI and reveal novel therapeutic targets.

Animals ; Blood-Brain Barrier ; metabolism ; Ferritins ; metabolism ; Horses ; Mice ; Receptors, Transferrin ; metabolism ; Spleen ; chemistry