To explore the new trend of pathogens and antimicrobial resistance in children with urinary tract infection (UTI).Distribution of pathogens and their antimicrobial resistance in 85 culture-positive hospitalized children with UTI from 2008 to 2012 were analyzed.Urine culture was deemed positive with a pure growth 8 10S/ml (single organism).Among 85 strains of bacterium,gram-negative bacilli accounted for 92.9％ (with 64.7％ of E coli.),gram-positive cocci 2.4％ and fungi 4.7％.The resistance rates of Gram-negative bacilli to ampicillin,trimethoprim-sulfamethoxazole and ampicillin/sulbactam were 82.3％,63.3％ and 63.3％ respectively.The resistance rates of E coli.to 3rd and 4th generation cephalosporin were both over 60％.And 0％ and 5.5％ of E coli.UTIs were resistant to imipenem and amikacin respectively.It indicated that E coli.remained a dominant pathogen in childhood UTI.The resistance patterns were grave.Every hospital should monitor the resistance patterns of urinary pathogens on a regular basis and use antibiotics with a low resistance.

OBJECTIVE:To systematically review the clinical efficacy and safety of sirolimus(SRL)versus tacrolimus(Tac) for anti-rejection after renal transplantation,and provide evidence-based reference for clinical treatment. METHODS:Retrieved from PubMed,EMBase,Medline,Science Direct,Cochrane library,CJFD,VIP and Wanfang Database,randomized controlled tri-als(RCT)about SRL(test group)versus Tac(control group)for anti-rejection after renal transplantation were collected. Meta-anal-ysis was performed by using RevMan 5.2 software after data extraction and quality evaluation. RESULTS:Totally 5 RCTs were in-cluded,involving 594 patients. Results of Meta-analysis showed,there was no significant difference in the incidence of acute rejec-tions [RR=1.26,95%CI(0.82,1.93),P=0.30],graft loss rate [RR=0.91,95%CI(0.32,2.55),P=0.85] and mortality rate [RR=0.87,95%CI(0.34,2.22),P=0.77] in 2 groups;while the infection rate in test group was significantly lower than control group, the difference was statistically significant [RR=0.13,95%CI(0.04,0.40),P<0.001]. CONCLUSIONS:Compared with Tac,SRL has the same anti-rejection effect after renal transplantation,not changed graft loss rate and mortality rate,but reduced the infection rate with higher safety.

Objective Based on scientific research grants to explore the feasibility of analyzing the subiect's hot topics. Methotis The CRISP(Computer Retrieval of Information on Scientific Projects)database of National Institutes of Health was used to retrieve the grants related of gene mechanism of essential hypertension in 2006. We obtained concepts from the fields of title and abstract by MetaMap. and then analyzed the key concepts about genes that were found more than 3 times. Results There were 73 related grants about that from CRISP in 2006. After processing the samples by MetaMap, we got 45 high frequency concepts about genes. which were divided into seven groups. Conclusions It iS feasible to analyze and study subject hotspot by scientific research grants. and it can be used to the supplement of normal literature analysis. MetaMap is a better tool for natural language processing, but also has some limitations.

Adolescent ; Adult ; Aged ; Aged, 80 and over ; Child ; Chin ; surgery ; Facial Injuries ; surgery ; Female ; Humans ; Male ; Middle Aged ; Reconstructive Surgical Procedures ; methods ; Surgical Flaps ; Young Adult

Objective To investigate the effect of leucine-rich-repeat-containing G-protein-coupled receptor 5 (LGR5 )on the proliferation and drug resistance of HeLa cells and its possible mechanism.Methods LGR5 expression was interfered using shRNA,and LGR5 knockdown HeLa cells were constructed.The effect of LGR5 on the proliferation and drug resistance of HeLa cell was evaluated by cell count,clone formation and MTT;the expressions of LGR5 and β-catenin in HeLa cells were detected by Western blot method.Results LGR5 knockdown HeLa cell line was successfully constructed;the cell growth rate and clone formation rate in shLGR5 group were markedly decreased compared to those in shCon group (P<0 .01 ).Drug resistance of HeLa to cisplatin differed significantly between shLGR5 group and shCon group (P<0.01 ).Moreover,the LGR5 knockdown inhibited the expression ofβ-catenin in HeLa cells.Conclusion LGR5 plays an important role in cell proliferation and drug resistance of HeLa cells,and its mechanism is related to Wnt/β-catenin signaling pathway.

Objective To analyze the pathogenesis,initially diagnosed symptoms and clinical manifestations of children with chronic kidney disease (CKD) at stage 2 to 5.Methods The data of 108 children who were hospitalized in Children's Hospital Affiliated to Capital Institute of Pediatrics from September 2007 to April 2016 with CKD stage 2 to 5 were retrospectively analyzed.The etiologies,clinical manifestations and examinations were summarized,and the clinical manifestations were compared between the congenital hereditary urinary diseases group and the acquired urinary diseases group.Results (1) In the 108 cases collected,66 cases were male,42 cases were female,aged from 3 months to 15 years and 1 month old.Twenty-four cases were diagnosed at stage 2,26 cases at stage 3,35 cases at stage 4,and 23 cases at stage 5.(2) Twenty-eight kinds of illness were involved in the cause of CKD.Among them,57 cases (52.8％) had congenital anomalies of the kidney and urinary tract,5 cases(4.6％) had hereditary kidney diseases,41 cases (38.0％) had other primary or secondary kidney diseases,and in 5 cases (4.6％) the causes of disease were unknown.(3) For the initially diagnosed symptoms,29 cases(26.9％) were due to complaints associated with kidney disease,36 cases (33.3％) were of other outside kidney symptoms,and 43 cases (39.8 ％) were of negative symptoms.The results of urinary ultrasound were abnormal in 79 cases(73.1％) and 87 cases(80.6％) showed abnormality in urinary analysis.There were 105 cases (97.2％) with abnormal manifestations either in urinary tract ultrasound or in urinary analysis.(4)The ages on diagnosis as CKD in children with congenital hereditary urinary diseases(5.89 years old) were younger than that of children with acquired urinary diseases (9.20 years old),and the difference was significant(Z =-3.434,P =0.001).The frequency of cases with short stature or lower-weight in group of congenital hereditary urinary diseases[66.1％ (41/622 cases),64.5％ (40/62 cases)] were significantly higher than those of the acquired urinary diseases group[43.9％ (18/41cases),43.9％ (18/41 cases)],and the differences were statistically significant(x2 =4.983,4.263,P =0.026,0.039).Conclusions The causes of CKD are complicated,and the congenital anomalies of kidney and urinary tract are the major causes of CKD at stage 2 to 5 in the cases.The initially diagnosed symptoms of CKD are insidious and atypical.The children with congenital hereditary urinary diseases tend to have more serious growth retardation.Urinary analysis and ultrasound may have an important significance for early diagnosis of CKD in children.

Objective To explore the protective effect and underlying mechanism of telmisartan on hyperuricemic nephropathy.Methods (1)High level of uric acid (600 μmol/L) and telmisartan in different concentrations (10nmol/L,100 nmol/L,1000 nmol/L,10000 nmol/L) were added to renal tubule epithelial cells and cultured for 48 h,the expression of UAT,TGF-β1 and α-SMA were detected by Real-time PCR,RT-PCR,Western blotting or cell immunofluorescence.(2) Wister rats were randomly divided into normal control group(Con),high uric acid group (HU),and telmisartan treatment group (Tel).Four weeks later,Scr,BUN and serum uric acid of the rats were detected.The expression of UAT in rat kidney was detected by Western blotting.Results (1)In vitro,compared to control group,high uric acid (600 μmol/L) inhibited the expression of UAT (P ＜ 0.01),and the inhibition could be alleviated by telmisartan; Telmisartan inhibited the upregulation of TGF-β1 and α-SMA induced by high uric acid(all P ＜ 0.05); (2)In vivo,compared to high uric acid group rats,telmisartan group rats had significantly reduced serum uric acid levels (189.9 μmol/L vs 204.5 μmol/L,P＜0.05),upregulated UAT and downregulated TGF-β1 expression in rat kidney (all P＜ 0.05).Conclusion Telmisartan significantly inhibits the upregulation of TGF-β1 and α-SMA induced by uricemia,which may prevent kidney from fibrosis.The protect effect of telmisartan may be related to the upregulation of UAT.

Objective To explore the clinical,laboratory,and pathologic manifestations of the interstitial lung disease(ILD)associated with primary Sj(o)gren's syndrome(pSS,pSS-ILD).Methods Clinical data of 15 patients with pSS-ILD admitted to our hospital from 2006 to 2008 were collected and the different features were compared with 18 patients with pSS without ILD.Eight patients with pSS-ILD were followed up and observed the changes of high-resolution computed tomography (HRCT).Results The age at onset was later in pSS-ILD[(57±11)years]than in pSS without ILD[(43±11)years](P<0.01).The initial symptoms in six of patients with pSS-ILD were cough,expectoration,chest distress or dyspnea upon exertion.The respiratory clinical manifestations,circulationsystem involvement and pulmonary artery hypertension (PAH) were more common in pSS-ILD than in pSS without ILD(P<0.01).Compared with patients with pSS without ILD,patients with pSS-ILD had significantly higher serum IgG level(P<0.01).The common findings of HRCT included reticular changes,irregular linear hyper-attenuating areas,and nodules.Pleural involvement was found in 8 patients,honeycomb change in 5 patients and PAH in 3 patients.After treated for 6 months of 8 patients,radiological findings improved in 4 patients,stable in 2 patients,and worse in 2 patients.The comlnon histological findings included focal fibrosis in alveolar wall and alveolus with and alveolar space inflammatory cell infiltration,interstitial inflammation with mulifocal lymphocyte infiltration.One patient had the pathological changes of nonspecific interstitial pneumonia(NSIP).Conclusion The age at onset of pSS-ILD is late and tends to produce respiratory symptoms and prone to have circulationsystem involvement such as PAH and elevated serum IgG level.Honeycomb change in HRCT can be seen in one third of patients and most patients can improve after treatment,however.NSIP can be observed in histopathologieal

Objective To examine the effects of IL-10 on cardiac fibroblasts ( CFBs) proliferation and phenotype transformation to myofibroblasts (MyoFbs) induced by transforming growth factor-β1 (TGF-β1);and to investigate the regulating pathways .Methods Cardiac fibroblasts were isolated from cardiac ventricles of neonatal SD rats . The passage 2~4 were used and divided into the following groups for treatment:1) control group, 2) IL-10 reac-tion group, 3) TGF-β1 reaction group, and 4) IL-10 plus TGF-β1 reaction group (TGF-β1 treatment followed with IL-10 pretreatment ) .Cells proliferation was assessed by MTT assay and immunocytochemistry staining for prolifera-ting cell nuclear antigen (PCNA);the phenotype transformation into MyoFbs was assessed by immunocytochemistry of α-smooth muscle actin (α-SMA);extracellular signal related kinase ( ERK1/2) and P38 kinase pathways were assessed by western-blot.Results TGF-β1 (10 μg/L) treatment boosted the proliferation and the expression ofα-SMA significantly (P<0.01), while IL-10 (10, 50 or 100 μg/L) plus TGF-β1 co-treatment induced lower cell proliferation and expression of α-SMA than treating with TGF-β1 alone ( P<0.05 ) , with the inhibitory effect of IL-10 being concentration dependent .TGF-β1 could significantly stimulate the ERK 1/2 and P38 kinase phospho-rylation ( P<0.01 ) , however IL-10 (100 μg/L) plus TGF-β1 co-treatment failed to down-regulated the phospho-rylation of ERK1/2 and P38 kinase compared with TGF-β1 alone ( ERK1/2:P<0.05;P38:P<0.01 ) .Conclu-sions IL-10 can attenuate TGF-β1-induced CFBs proliferation and phenotype transformation to MyoFbs .The in-hibitory effects may explained by a mechanism of inhibiting the activation of ERK 1/2 and P38 kinase .

Objective: To prepare and identify recombinant human IL 2/GM CSF(rhIL 2/GM CSF) fusion protein antibodies and to study its specificity and its effect on fusion protein biological activity. Methods: rhIL 2 /GM CSF fusion protein was purified by DEAE Sepharose FF ion exchange chromatography. The purified protein was used to immunize rabbits for the preparation of antisera. The titer and specificity of the antisera were detected by ELISA and Dot ELISA and the biological activity by cell proliferation. Results: The antisera not only reacted with the rhIL 2/GM CSF, IL 2 and GM CSF, but also inhibited the biological activity of the rhIL 2/GM CSF, IL 2 and GM CSF. Conclusion: The obtained antisera can be used to study the structure and function of the rhIL 2/GM CSF.