Objective To explore the main sites,pathogen distribution and risk factors of healthcare-associated in-fections (HAI)in children with acute leukemia,and provide scientific evidence for prevention and treatment. Methods Data of 828 children with acute leukemia admitted to a hospital in 2011 -2012 were collected,infection site,pathogen distribution and risk factors of infection were analyzed.Results Of 828 patients,184 cases and 196 times of HAI occurred with the incidence of 22.22% and 23.67%,respectively.HAI occurred mostly in respiratory tract (52.56%).A total of 96 pathogenic strains were isolated,among which gram-negative and gram-positive bac-teria accounted for 58.33%(n=56)and 29.17%(n=28)respectively.Univariate analysis revealed that risk factors for HAI were leukemia remission induction chemotherapy,hospital stay ≥ 30 days,peripheral leukocyte count (WBC)≤3×109/L,granulocyte count ≤0.5 ×109/L,and acute nonlymphocytic leukemia.Multivariate analysis revealed that hospital stay ≥30 days was independent risk factors for HAI.Conclusion Children with acute leuke-mia have a high incidence of HAI,infection mainly occurs in respiratory system,and gram-negative bacteria are ma-jor pathogens.The incidence of HAI is correlated with remission induction chemotherapy,long length of hospital stay,low WBC,low number of neutrophils,and acute myeloid leukemia.

Children with hematological diseases usually accompanied by low autoimmune function,and repeated chemotherapy exacerbated the damage to their immune system and hematopoietic function.Those lead to high incidence of nosocomial infection,most of infection were caused by multi-drug resistant bacteria and fungi.The major infections in hematological children are the following:multi-drug resistant Escherichia coli/Klebsiella pneumonia bacteria;multi-drug resistance Pseudomonas and Acinetobacte;Methicillin-resistant coagulase negative Staphylococcus and aureus;multi-drug resistance Enterococcus faecium.This review presents updated treatment strategies from the published clinical literature and provides recommendations for clinical treatment of multi-drug resistant bacteria in children with hematonosis.

AIM:To study whether albumin overload in proximal tubular epithelial cells(PTCs)induces epithelial to myofibroblast transdifferentiation(EMT).METHODS:Rat renal proximal tubular cell line NRK52E was cultured on 6 well plates.When the cells reached 70% confluens or complete confluens,cells were serum starved for 24 h.Different concentrations of delipidated bovine serum albumin(dBSA),ranging from 0-30 g/L,were then added to the cells.The media was changed every 48 h until the end of 144 h.Cell shapes were monitored by light microscope during experiment.Cell structures were detected by electron microscopy.Epithelial cell markers:E-cadherin,?-catenin,and myofibroblast marker:?-smooth muscle actin(?-SMA)were detected by immunofluorescent microscopy and Western blotting.RESULTS:dBSA overload induced the expression of ?-SMA in sub-confluent NRK52E,and a few cells elongated,but the induced expression of ?-SMA was not in a dose dependent manner.dBSA overload did not induce the expression of ?-SMA in complete confluent NRK52E,cell shape did not change either.dBSA overload did not inhibit expression of E-cadherin or ?-catenin both in sub-confluent and complete confluent NRK52E.The electron microscope showed that these cells retained epithelial phenotype,with microvilli and tight junction.CONCLUSION:Albumin overload induces PTCs expressing myofibroblast marker ?-SMA and promotes EMT.However,complete EMT does not achieve.Complete confluens(cell-cell contacts)inhibits albumin induced ?-SMA expression in PTCs.

Objective To study the occurrence of asymptomatic coronary artery endothelial lesions,and its relationship with coronary heart disease(CHD).Methods From June 2003 to September 2004,120 patients with old myocardial infarction(OMI)and stable angina pectoris(SAP)were enrolled in this study.The angioscopy of non-culprit vessels was successfully performed to detect the endothelial lesions including yellow plaque,plaque rupture and/or thrombosis.Meanwhile,the relationships between coronary artery endothelial lesions and hypertension,diabetes mellitus(DM)and low-density lipoprotein cholesterol(LDL-C)were examined.Results Detailed angioscopic findings were obtained in 80 of the 120 patients(66.67%)(in 155 non-culprit vessels).These lesions demonstrated a significantly higher occurrence in patients with hypertension,in patients with high level of LDL-C and in patients with DM than in patients without endothelial lesions(P

Objective To examine the effects of intracerebroventricular administration of adrenomedullin (AM) on the expression of Fos and spontaneous electric activity of area postrema (AP) neurons in sino-aortic denervated rats. Methods To determine the expression of Fos and the spontaneous electrical activity of AP neurons in male Sprague-Dawley rats by immunohistochemistry. Results Following Intracerebroventricular administration of AM (1 nmol/kg, 3 nmol/kg), Fos-like immunoreactive (Fos-LI) neurons and the discharge rate of AP neurons markedly increased. Pretreatment with calcitonin gene-related peptide(CGRP) receptor antagonist CGRP8-37 (30 nmol/kg) significantly inhibited the effects of AM (3 nmol/kg). Conclusion AM may activate the neurons in AP via CGRP receptors.

OBJECTIVE:To systematically review the efficacy,safety and economy of acarbose versus metformin in the treat-ment of type 2 diabetes,and provide evidence-based reference for the clinical treatment. METHODS:Retrieved from PubMed, Medline,CJFD,Wanfang database,VIP database,randomized controlled trails (RCT) about acarbose (test group) versus metfor-min(control group)in the treatment of type 2 diabetes were collected. Meta-analysis was performed by using Rev Man 5.2 statis-tics software,and the decision tree model was used to do the cost-effectiveness analysis by using TreeAge Pro 2011.1.0.12.1 soft-ware. RESULTS:A total of 8 RCT,involving 418 patients. Results of Meta-analysis showed 2 h postprandial blood glucose (2 h PG)in test group [MD=-2.21,95%CI(-2.92,-1.51),P<0.001] was lower than that of control group,there was no signifi-cant diffcrencc in the glycated hemoglobin levels[MD=0.02,95%CI(-0.38,0.34),P=0.91],fasting blood glucose level[MD=0.05,95%CI(0.91,1.01),P=0.92] and incidence of adverse reactions [OR=1.84,95%CI(0.80,4.24),P=0.92] between 2 groups. Results of decision tree analysis showed the cost-effectiveness ratio in test group and control group was 847.15 and 272.53,respec-tively;and incremental cost-effectiveness ratio was 13 776. CONCLUSIONS:Acarbose shows an obvious advantage on decreasing the 2 h PG of type 2 diabetes,however,pharmacoeconomics shows metformin has higher economic effects. Due to the limit of methodological quality,large-scale and high quality RCT are required for further validation of the conclusions.

Objective:To prepare fenofibrate PEG2000-DSPE micelles in order to improve the solubility of fenofibrate, and study the oral pharmacokinetics of the micelles in SD rats. Methods:Fenofibrate PEG2000-DSPE micelles were prepared and characterized. The rats were administrated with fenofibrate PEG2000-DSPE micelles and fenofibrate suspension, respectively. The blood samples were collected from eye socket and determined by HPLC. The compartmental pharmacokinetics was analyzed by DAS software. Results:Fenofibrate PEG2000-DSPE micelles were prepared successfully. The mean particle size was (23. 40 ± 3. 62) nm, the drug loading and the entrapment efficiency was (97. 65 ± 3. 32) % and (1. 33 ± 0. 32) %, respectively. The mean plasma concentration-time curves of fenofibric acid were both in accordance with two-compartment mode after oral administration of fenofibrate PEG2000-DSPE micelles and fenofibrate suspension in rats. After the oral administration, AUC(0-24) and Cmax of fenofibrate PEG2000-DSPE micelles was respectively 7-fold and 14-fold higher than that of fenofibrate suspension [(61. 41 ± 5. 71)μg·h·ml-1 vs (8. 49 ± 0. 66)μg·h·ml-1, and (9.67±1.65) μg·ml-1 vs (0.71 ±0.09) μg·ml-1]. The relative bioavailability of fenofibrate PEG2000-DSPE micelles was 723. 3%. Conclusion:The bioavailability and absorption rate of fenofibrate are both increased by the micelles remarkably when com-pared with those of fenofibrate suspension after oral administration. The PEG2000-DSPE micelles served as drug carrier for oral delivery present promising application perspectives.

Objective To investigate the correlations between HLAⅡgene polymorphism and the development of Mycoplasma pneumoniae pneumonia ( MPP ) in children and to identify the susceptibility genes and protective genes for MPP for further elucidating the pathogenesis of MPP and providing the guid-ance for researches on gene therapy for MPP. Methods Genotypes of HLAⅡgene ( HLA-DQA1 and HLA-DRB1) in 60 children with MPP and 30 healthy children were detected by using sequence specific primer polymerase chain reaction ( SSP-PCR) . The haplotype frequencies, linkage disequilibrium and correlations with MPP were analyzed by using Arlequin software and Chi-square test. Results The frequencies of HLA-DQA1*0201/*0301 in children with MPP (35. 83%/30. 00%) were higher than those in healthy children (16. 67%/8. 33%) (χ2=12. 139, P<0. 05, OR=5. 059;χ2=15. 142, P<0. 05, OR=7. 500). However, the frequency of HLA-DQA1*0401 in children with MPP decreased to 12. 50% as compared with 40. 00%in healthy children (χ2=24. 638, P<0. 05, OR=0. 083). The frequencies of HLA-DRB1*07/*15 in children with MPP increased to 38. 33%/30. 00% as compared with 20. 00%/16. 67% in healthy children (χ2=11. 735, P<0. 05, OR=4. 929; χ2=5. 692, P<0. 05, OR=3. 000). But the frequency of HLA-DRB1*11 dropped to 15. 00% as compared with 43. 33% in healthy children (χ2=19. 448, P<0. 05, OR=0. 087). Conclusion HLA-DQA1*0201, HLA-DQA1*0301, HLA-DRB1*07 and HLA-DRB1*15 might be the susceptibility genes for MPP in children, while HLA-DQA1*0401 and HLA-DRB1*11 were probably associated with the resistance to MPP. No extensive linkage disequilibrium was found between HLA-DQA1 and HLA-DRB1.

Objective To investigate the activation of β-sheet breaker peptide H102 on ERK signal transduction pathway in brain of PAP double transgenic mice. Methods PAP double transgenic mice were randomly divided into model group and H102 treatment group (n=10 for each group). A group of C57BL/6J mice with the same genetic background was served as controls. H102 (5.8 mg/kg) 5 μL was infused by intranasal administration to mice in H102 treatment group, and equal volume of blank solution of H102 (chitosan, BSA) was given to mice in control group and model group. The ability of spatial reference memory was tested by Morris water maze after 30 days of treatment. Then immunohistochemistry tests and Western blot technique were used to detect the content of RAS, P-MEK and P-ERK proteins in mouse brain. Results (1) The ability of learning and memory was significantly lower in model group than that of control group. The ability of learning and memory was significantly improved in treatment group than that in model group (P<0.05). (2) The contents of RAS, P-MEK and P-ERK in mouse brain were significantly lower in model group than those of control group, and these protein ex-pressions were significantly increased in treatment group than those in model group (P<0.01). Conclusion β-sheet break-er peptide H102 can activate ERK signal transduction pathway in brain of PAP double transgenic mice, increase PAS, P-MEK and P-ERK levels in nerve cells, and improve the ability of learning and memory in PAP mice.

Objective To establish an infection model using Caenorhabditis elegans (C.elegans)-extensively drug-resistant Klebsiella pneumoniae (XDRKP)system.Methods Clinically isolated XDRKP strains were used to infect C.elegans in the liquid killing assay,the nematode survival and the number of bacteria in C.elegans digestive tract was observed.Results C.elegans was significantly retarded after being infected by XDRKP,different concentra-tions of XDRKP led to different patterns of the worm death.Log-rank test showed that survival curves of C. elegans infected with 1 .5×106 CFU/mL of XDRKP and E.coli OP50 (control)were not significantly different (χ2 =0.08,P >0.05);survival curves of C.elegans infected with 1 .5 ×107 CFU/mL,1 .5 ×108 CFU/mL of XDRKP and E.coli OP50 were significantly different(χ2 =229.37,275.98,respectively,both P <0.001).The survival rates of 1 .5×108 and 1 .5 ×107 CFU/mL XDRKP groups were both lower than that of the control group.Supernatant suspension obtained from test was performed bacterial culture,identification and antimicrobial susceptibility testing, XDRKP was determined.After being infected with XDRKP 4,6,12,and 24 hours,the total number of bacteria in C.elegans were(0.28±0.02)×105 CFU/mL,(0.50 ±0.38)×105 CFU/mL,(1 .73 ±0.56)×105 CFU/mL,and (2.62±0.53)×105 CFU/mL,respectively,the number of bacteria in C.elegans digestive tract was significantly different at different time points (F =1 363.39,P <0.001).Conclusion The infection model of C.elegans-XDRKP is established successfully.