Objective To study the isolation and antimicrobial resistance of pathogens isolated from patients with brain damage in hyperbaric oxygenation department,so as to provide reference for clinical anti-infective treatment.Methods Bacterial culture and antimicrobial susceptibility testing results of pathogens isolated from blood,sputum,and urine specimens of 975 patients with brain damage in the hyperbaric oxygenation department of a hospital between January 2013 and December 2014 were analyzed retrospectively.Results A total of 1 328 strains of pathogens were detected,877(66.04%)of which were gram-negative bacteria,213(16.04%)were gram-positive bacteria,and 238(17.92%)were fungi.The top five isolated pathogens were Pseudomonas aeruginosa,Klebsiella pneumoniae,Escherichia coli,Acinetobacter baumannii,and Candida albicans.Specimens mainly isolated from sputum and urine,accounting for 58.59%and 35.24%respectively,resistance rates of Klebsiella pneumoniae,Pseudomonas aeruginosa,Acinetobacter baumannii,and Escherichia coli to imipenem were 16.67%,81.82%,82.44%,and 4.65%respectively.Vancomycin-resistant strains was not found among gram-positive bacteria,resistance rates of Enterococcus faecalis to most antimicrobial agents were lower than those of Enterococcus faecium.Conclusion Respiratory and urinary tract infection account for most of the infection in patients with brain damage in hyperbaric oxygenation department,gram-negative bacteria are the predominant pathogens causing infection.

Objective To explore the factors related to the outcome of idiopathic facial palsy. Methods 308 patients with idiopathic fa-cial palsy were included. The data of clinic and follow-up were collected from January, 2010 to December, 2014. The data were analyzed by Logistic regression analysis. Results 210 cases (68.2%) were cured (good group) and 98 cases (31.8%) appeared sequelae of different de-grees (poor group). The age, onset of disease, type of disease, damaged section, impaired glucose control, high neutrophil-to-lymphocyte ra-tio (NLR), high blood glucose, high blood triglyceride, time and methods of invention were significant factors related to the outcome (P<0.05). Conclusion Old, servious facial nerve injury, Hunt's palsy, high damaged section, poor glucose control in the patients with diabetes, high NLR, high blood triglyceride, delay and simple invention are independent risk factors for the poor outcome of idiopathic facial palsy.

Objective:To investigate the effect of dimethyl amiloride (DMA) on invasive activity of PGCL3 cells from a human highly-metastatic lung carcinoma cell line in vitro and elucidate its possible mechanism. Methods:The invasion and migration capacities of PGCL3 cells were measured by using Transwell chamber assay after pretreatment with DMA. The effects of DMA on the activity of urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1) secreted by PGCL3 cells were measured by chromogenic substrate assay. The effects of DMA on uPA, urokinase-type plasminogen activator receptor (uPAR), and PAI-1 mRNAs transcription were determined by RT-PCR. The expression levels of extracellular regulated protein kinases 2 (ERK2) and ras protein were assessed by Western blot. Results:DMA inhibited invasion and migration capabilities of PGCL3 cells in vitro, down-regulated the mRNA transcription of uPA, uPAR and PAI-1, as well as up-regulated the expression of ras protein. After 24-hour treatment, DMA reduced the activity of uPA at higher concentration, but DMA had no effects on the activity of secreted PAI-1 protein and expression of ERK2 protein. Conclusion:DMA inhibits the invasion and migration of highly-metastatic lung cancer PGCL3 cells. The mechanism might be associated with down-regulation of the expression of uPA system.

Objective: To investigate the effect of amiloride on in vitro invasive activity and uPA (urokinase-type plasminogen activator)system of human highly metastatic lung carcinoma cell line PGCL3. Methods: At 6 hours after treatment with amiloride at the concentrations of 25μmol/L，50μmol/L and 100μmol/L for PGCL3 cells，Transwell Chamber assay was performed to detect the effect of amiloride on the invasive and migratory capacity of PGCL3 cells.Effect of amiloride on the activity of uPA and PAI-1(plasminogen activator inhibitor-1)secreted by PGCL3 cells were measured by chromogenic substrate assay after PGCL3 cells were incubated with amiloride for 24 hours.RT-PCR was used to analyze the effect of amilorede on mRNA levels of uPA，uPAR(urokinase-type plasminogen activator receptor)and PAI-1.The expression levels of uPA，ERK2(extracellular regulated protein kinases 2)and ras protein were assessed by Western blot. Results: The number of cells through membrane was significantly decreased in invasion and migration test in vitro.The inhibitory rates of invasion and migration after treatment with amiloride of 100μmol/L were 37.7%±4.1%and 64.9%±4.9%.respectively,with a significant difference from those in the control group(P<0.01).At 24 hours after amiloride treatment，the chromogenic substrate assay showed direct inhibition of the activity of uPA and PAI-1 secreted by PGCL3 cells.No effect on the expression of uPAR in mRNA level was observed,but the expression of PAI-1 in mRNA level was significantly inhibited.Amiloride of 100μmol/L dramatically inhibited the expression of uPA mRNA.The expression level of uPA protein was decreased with the increase of the concentration of amiloride,but no effect was observed on the expression of ERK2 and ras in protein level.Conclusion: Amiloride can inhibit the invasion and migration of PGCL3 cells,through inhibiting the expression and activity of uPA and PAI-1.Amiloride is a potential agent to inhibit cancer invasion and metastasis.

MicroRNAs (miRNA) are a newly discovered class of endogenous,evolutionarily conserved small noncoding RNAs involved in posttranscriptional gene regulation. Functionally speaking,miRNAs act as key regulators in a wide variety of biological processes,including cell proliferation,cell differentiation,apoptosis,metabolism,developmental timing,signal transduction and tumor. Recent publications have provided compelling evidence that a range of miRNAs are involved in the regulation of immunity,including the innate immunity,proliferation of monocytes and neutrophils,the development and differentiation of B and T cells,infection and immunity,and the release of inflammatory mediators. In this review,we examine what is presently known of the function and mechanism of these miRNAs in the regulation of the innate and acquired immune response.

Adult ; Altitude ; Arteries ; metabolism ; Calcitonin Gene-Related Peptide ; blood ; Humans ; beta-Endorphin ; blood

Objective To evaluate the effects of B7-H3 gene transfection on 18F-FDG uptake and 18F-FLT uptake in prostate cancer cells.Methods The absorption (A) values of untransfected prostate cancer(RM1) cells and B7-H3 gene-transfected RM1 (RM1-B7-H3) cells were detected at different culturing time points (0.5,1,2,3,4 and 5 d) with cell counting kit-8 (CCK-8) test.Cell cycle phase distribution of RM1 and RM1-B7-H3 cells was measured with flow cytometry.18F-FDG uptake of RM1 and RM1-B7-H3 cells was measured with γcounter and calculated under different conditions:5× 104-5× 106 cells; 0-11.0 mmol/L glucose; 20-120 min incubation in 37 ℃.18F-FLT uptake of RM1 and RM1-B7-H3 cells was measured in 1×106 cells under incubation for 100 min at 37 ℃.After administering anti-B7-H3 monoclonal antibody 4H7,18F-FDG uptake of RM1-B7-H3 cells was measured.The data were analyzed using one-way analysis of variance and two-sample t test.Results The A values of RM1-B7-H3 cells after being incubated for 1,2 and 3 d were higher than those of RM1 cells(1.59±0.23,2.26±0.15 and 2.01±0.60 vs 1.22±0.14,1.10± 0.09 and 1.04±0.15,t=3.923,19.228,4.467,all P＜0.01).There was no statistical significance between the 2 groups at other time points (t=-0.094,0.858,2.000,all P＞0.05).The ratios of RM1-B7-H3 cells in G1,S and G2/M phases were(32.96±2.56) ％,(39.11 ±2.57) ％ and (27.94±0.21) ％,respectively.The ratio of S phase in RM1-B7-H3 cells was higher than that in RM1 cells ((32.76±1.90)％,t=3.442,P＜ 0.05).18F-FDG uptake of the both cell lines decreased with the increase of glucose concentrations,while the uptake went up with the increase of cell number and incubation time.With the cell number of 1.0× 106,incubation time of 100 min and temperature of 37 ℃,the 18F-FDG uptake of RM1-B7-H3 and RM1 cells was (55.07±3.99)％ vs (44.16±3.60)％ (t=4.977,P＜0.01) ; and 18F-FLT uptake of RM1-B7-H3 and RM1 cells was (5.25±0.81)％ vs (3.33±0.64)％ (t=4.567,P＜0.01).After treated with antibody 4H7,18F-FDG uptake of RM1-B7-H3 cells ((45.36±2.92) ％) was lower than that of untreated group (F=10.001,P＜ 0.01).Conclusion B7-H3 gene transfection may promote the metabolism and proliferation of prostate cancer cells,and thereby increase the 18F-FDG uptake and 18F-FLT uptake.

Objective To improve the quality standard ofZushima Plaster.Methods TLC was used to do qualitative identification of daphnetin and 7-hydroxycoumarin inZushima Plaster. The contents of daphnetin and 7-hydroxycoumarin inZushima Plaster were determined by HPLC. The chromatographic column was Agilent Eclipse Plus C18 (4.6 mm×250 mm, 5μm), and the mobile phase consisted of acetonitrile-0.1% phosphoric asid (15∶85, V/V) at a flow rate of 1.0 mL/min. The column temperature was maintained at 30℃, and the detection wavelength was set at 327 nm. Results Characteristic spots of daphnetin and 7-hydroxycoumarin could be detected by TLC from the samples, and the spots were clear and specific without interference from negative samples. The calibration curve of daphnetin and 7-hydroxycoumarin were linear in the ranges of 0.180-1.800μg and 0.100-1.00μg (r=0.999 1,r=0.999 2), and the average recovery rates were 98.99% and 101.48%, RSDwere1.43% and 1.32%, respectively (n=9).Conclusion The established method appears easy to use, accurate and specific, and therefore can be used for the quality control ofZushima Plaster.

Objective To establish a CLCN3/MMTV-PyMT double transgenic mouse model of spontaneous breast tumor with simultaneously overexpressing ClC-3.Method CLCN3 transgenic mice were crossed with MMTV-PyMT spon-taneous mammary tumor model mice.The genotype was determined by PCR.The expression of ClC-3 in tissues was detec-ted by immunofluorescence and Western blot.Results CLCN3 and MMTV-PyMT transgenic mice were bred and CLCN3/MMTV-PyMT hybrid mouse model was successfully established.The ClC-3 expression in CLCN3/MMTV-PyMT hybrid mice was higher than that in the MMTV-PyMT mice, assessed by immunofluorescence and Western blot analysis.Conclu-sions Transgenic mouse models of spontaneous breast cancer with simultaneously overexpressing ClC-3 are successfully es-tablished.The double transgenic mice provide a good animal model for further research of ClC-3 in tumor growth and metas-tasis.

Background and purpose:MiR-224 is overexpressed in hepatocellular carcinoma, and participate in invasion and metastasis of cancer. The aim of this study was to investigate the effects of miR-224 antisense oligonucleotide (ASO) on the proliferation and apoptosis of Hep3B cells.Methods:After transfection with miR-224 ASO, and detecting the miR-224 mRNA expression of Hep3B cells by real-time quantitative PCR; the miR-224 expression in Hep3B cells was measured and cell proliferation was analyzed by MTT assay and the colony formation experimentin vitro andin vivo. The cell apoptosis was analyzed by flow cytometry.Results:Compared with the control group, miR-224 ASO significantly reduced the miR-224 mRNA expression in the Hep3B cell(P<0.05), MTT assay results showed that Hep3B cells survived rate decreased greatly after transfection with miR-224 ASO. Clone formation assay revealed that the colony formation rate in miR-224 ASO group was significantly lower than that in the control group.In vivo study further confirmed that miR-224 ASO could inhibit the proliferation of Hep3B cells,and miR-224 ASO group grew substantially slow compared with the negative control. Flow cytometry indicated that miR-224 ASO group promoted apoptosis significantly.Conclusion:miR-224 was overexpressed in Hep3B cells. Reducing the expression of miR-224 can effectively inhibit the growth of Hep3B cells and promote apoptosis. miR-224 may become a new target for the regulation of gene expression in hepatocellular carcinoma.