0.05).(3) The ratio of meticillin-resistant staphylococci was 91.5%.The ratio of resistance of staphylococci to(gentamicin),(erythromycin),ciprofloxacin and tetracycline was all above 50%,but was low to(nitrofurantoin) and rifampin.In 12 strains of Enterococcus faecalis,3 strains were VRE;8 resisted to high-level gentamicin;6 resisted to high-level streptomycin;the resistance rate to tetracycline,ciprofloxacin,rifampin and(erythromycin) ranged from 58.3% to 100.0%.In E.coli,8 of 14 isolates were positive for ESBLs.The resistance was high to usual antibiotics except imipenem,amikacin and Tazocillin.CONCLUSIONS Bacteria are the main pathogens of chronic prostatitis and terribly resist to clinical usual antibiotics.Infection with Uu,Mh and Ct should not be(ignored).It is necessary to diagnose and treat chronic prostatitis according to the results of pathogen(isolation) and drug sensitivity test.

Twenty healthy subjects in each of 3 groups were fed with monounsaturated fatty-acid diet,polyunsaturated fatty-acid diet, or saturated fatty-acid diet separately for 3 days. It suggested that monounsaturated fatty-acids may ameliorate the oxidative stress and improve insulin sensitivity.

Following extensive bowel resection， the intestinal tract undergoes a variety of adaptive responses to enhance bowel function． The purpose of this study was to determine the effect of glutamine-supplemented parenteral nutrition on mucosal cellularity and gut function． In addition， enterocyte gene expression of two relevant systems was also characterized and related to the structural and functional changes that occurred．Male Wistar rats underwent a 60％ small bowel resection and jugular vein catheterization and were randomized into two groups． The control group （n＝10） received a standard intravenous nutritional solution and the study group （n＝10） received a similar solution but enriched with alanylglutamine dipeptide． After 7 days blood was taken for amino acid analysis， and bowel was harvested to determine mucosal morphology and expression of mucosal cell glutaminase and IGF-I mRNA． Mesentery lymphnodes were cultured to determine the presence of bacteria and thus access bacteria translocation． Serum glutamine concentration and mucosal architecture were maintained in the study group compared to the controls． Seventy percent of lymphnodes were cultured positive in control vs． only 20％ in the study group （P＜0．05）． Jejunal mucosal glutaminase and ileum mucosal IGF-I mRNA increased twofold and threefold respectively compared to control animals．Parenteral nutrition supplemented with alanyl-glutamine dipeptide supports mucosal cellularity and regional immune function in rodents following intestinal resection， These alterations are associated with enhanced enterocyte expression of glutaminase and IGF-I． These changes may facilitate the structural and functional alterations which were observed in the glutamine treated animals．

Objective To explore the molecular mechanisms and cell-cell interactions in the injury process of pancreatic islet transplantation.Methods Single-cell transcriptome data from mouse islets treated with inflammatory factors were used,and data processing was performed using the Seurat package,with integrated data to remove batch effects.Cell subpopulations were annotated based on known markers.Cell-cell interactions in the inflammatory factor-treated group were analyzed using the CellChat package,and inferred based on the expression of cell surface receptors and ligands.Gene set enrichment analysis was used to clarify the biological processes enriched in β-cells after treatment with inflammatory factors.Finally,differentially expressed transcription factors were identified and verified using microarray datasets of donor islet ischemic injury and Western blotting.Results A total of 7 different cell subpopulations were found in mouse islets,with β-cells being the most abundant.Cell-cell interaction network analysis showed that the number and strength of interactions between ductal cells and other cells were the highest.Gene set enrichment analysis showed that after treatment with inflammatory factors,the immune response was positively enriched in β-cells,while peptide hormone metabolism,bile acid metabolism,and ion homeostasis were downregulated.The common differential transcription factors identified in the mouse single-cell transcriptome and the microarray dataset of donor islet ischemic injury were early growth response 1(EGR1),nuclear factor-κB inhibitor α(NFKBIA),and activating transcription factor 3(ATF3).Among them,NFKBIA and ATF3 were upregulated,while EGR1 was downregulated.The expression of EGR1 protein was downregulated after 24 h,48 h,and 72 h of cold ischemia.Conclusions EGR1 is a transcription factor closely related to islet cold ischemia,and future research should focus on the specific mechanisms of EGR1 and its downstream target genes,in order to provide more effective strategies for clinical treatment of islet transplantation.