Objective To investigate the clinical distribution and antimicrobial resistant characteristics of Pseudomonas aeruginosa(PA)in the northern area of Guangdong.Provide the reference for clinical to prevent infection and reasonable choice of antibiotics and reduce the production of drug resistance strains.Methods The separation and identification of PA were performed by conventional methods during the data of drug 2013 and 2014.The data of sensitivity test of PA were analyzed by WHONET 5.6 and SPSS19.0 softwares.Results The 584 strains PA were mainly distributed in ICU,department of orthopaedics and respiratory medicine.Specimens were mainly from sputum and wound secretion.The detection of PA to 12 antibacterial agents showed different resistance.The antimicrobial with highest resistance was the gentamicin and lower resistance rates to fluoroquinolones,carbapenems,enzyme inhibitors.And a downward trend was shown in drug resistance to CIP,FEP,LEV,SCF.Conclusion PA mainly cause lung and wound infection,especially those old patients that come from ICU,department of orthopaedics and respiratory medicine.Although the drug resistance rates of PA to the commonly used antibiotics are relatively low,The clinicians should reasonably use antibiotics so as to reduce the resistant strains,especially the produce of MDR-PA and PDR-PA.

AIM: To investigate the mechanism of the AP-1 signal transduction pathway inhibited by JIP in nasopharyngeal carcinoma cells. METHODS: AP-1 activity was triggered by Dox-induced LMP1 expression in Tet-on-LMP1-HNE 2 cells (L7). The retention of phospho-JNK in the cytoplasm caused by JIP was examined with immunofluroscence assay. RESULTS: 24 h after transfection of L7 cells with the JIP expression plasmid, the translocation of activated JNK was inhibited, which resulted in the retention of phospho-JNK in the cytoplasm and down-regulation of the AP-1 activity. CONCLUSION: JIP down-regulates the activity of AP-1 through the inhibition of the translocation of JNK.

OBJECTIVE: To elucidate which one of &mgr;, delta and kappa opioid receptors is involved in the cardiovascular depression following traumatic hemorrhagic shock. METHODS: With traumatic hemorrhagic shock rat models, the changes of myocardial and brain &mgr;, delta and kappa opioid receptors and cardiovascular functions and their relationship with hemodynamic parameters were observed. The effects of delta and kappa opioid receptor antagonists on hemodynamic parameters of traumatic hemorrhagic shock rats were observed. RESULTS: Following traumatic hemorrhagic shock, the number of myocardial and brain delta and kappa opioid receptors significantly increased, their affinity did not alter, and the increased number of delta and kappa opioid receptors was significantly associated with the decreased hemodynamic parameters. However, &mgr; opioid receptor in heart and brain did not obviously change. delta opioid receptor antagonist ICI174,864 and kappa opioid receptor antagonist Nor-binaltorphimine (50 &mgr;g, Icv) could significantly reverse those decreased hemodynamic parameters. CONCLUSIONS: It suggests that opioid receptors, especially delta and kappa opioid receptors are closely related to the pathogenesis of traumatic hemorrhagic shock, and they play important roles in the depression of cardiovascular function following traumatic hemorrhagic shock.

OBJECTIVETo elucidate the regulation of the phosphorylation of epidermal growth factor receptor (EGFR) by the EB virus encoded latent membrane protein 1 (LMP1) in nasopharyngeal carcinoma cell line.

METHODSThe levels of EGFR expression and phosphorylation in pTet-on LMP1 HNE2 cell, a nasopharyngeal carcinoma (NPC) cell line, in the dynamic expression of LMP1 induced by different concentrations of doxycycline (Dox) were observed. The EGFR dominant negative mutant and LMP1 antisense expression plasmid were transiently transfected into pTet-on LMP1 HNE2 cells by lipofectamine, and the changes in EGFR phosphorylation were observed by immunocoprecitation and Western blot. The changes in EGFR phosphorylation were observed after EGF treatment.

RESULTSIn pTet-on LMP1 HNE2 cells, Dox-induced LMP1 upregulated EGFR expression and phosphorylation in a dose-dependent manner. After EGFR dominant negative mutant was transfected into pTet-on LMP1 HNE2 cells, the increase of EGFR phosphorylation was inhibited completely. When LMP1 antisense expression plasmid was transfected into pTet-on LMP1 HNE2 cells, the levels of EGFR phosphorylation were also inhibited significantly. Meanwhile, after EGF had been added into pTet-on LMP1 HNE2 cells, increase of EGFR phosphorylation was induced, but it was completely blocked by EGFR dominant negative mutant and the introduction of LMP1 antisense.

CONCLUSIONEB virus encoded LMP1 not only induces the dose-dependent expression of EGFR, but also the dose-dependent phosphorylation of EGFR. The phosporylation of EGFR may play a vital role in the development of nasopharyngeal carcinoma.

Blotting, Western ; Epidermal Growth Factor ; metabolism ; Herpesvirus 4, Human ; metabolism ; Humans ; Nasopharyngeal Neoplasms ; pathology ; virology ; Phosphorylation ; Receptor, Epidermal Growth Factor ; metabolism ; Tumor Cells, Cultured ; Viral Matrix Proteins ; metabolism

A biosynthetic gene cluster for the bioactive fungal sesterterpenoids variecolin ( 1) and variecolactone ( 2) was identified in Aspergillus aculeatus ATCC 16872. Heterologous production of 1 and 2 was achieved in Aspergillus oryzae by expressing the sesterterpene synthase VrcA and the cytochrome P450 VrcB. Intriguingly, the replacement of VrcB with homologous P450s from other fungal terpenoid pathways yielded three new variecolin analogues ( 5- 7). Analysis of the compounds' anticancer activity in vitro and in vivo revealed that although 5 and 1 had comparable activities, 5 was associated with significantly reduced toxic side effects in cancer-bearing mice, indicating its potentially broader therapeutic window. Our study describes the first tests of variecolin and its analogues in animals and demonstrates the utility of synthetic biology for creating molecules with improved biological activities.