Bone marrow stromal antigen 2 (BST-2) is a kind of host restriction factor. Since it was discovered to be responsible for the defect in virion release of HIV-1 mutants lacking the accessory gene vpu in 2008, it was thought to mainly restrict the viruses by directly tethering viral particles at the plasma membrane. Recent reports suggest that BST-2 also can inhibit the the release of HBV particles, which are budding in the intracellular vesicles, expanding the antiviral spectrum of BST-2. Futhermore, the machanism that BST-2 used to restrict HBV release in multivesicular bodies (MVBs) is similar to that used to restrict HIV at the plasma membrane. However, HBV have evolved strategies to antagonize the antiviral action of BST-2. There are two different opinions about the antagonist. One is HBV inactivated BST-2 by HBx requiring a hepatocyte-specific environment. Another thought envelope protein HBs counteract the antiviral action of BST-2. In this review, we focus on the current advances in the anti-HBV activity of BST-2.
Animals ; Antigens, CD ; genetics ; immunology ; GPI-Linked Proteins ; genetics ; immunology ; Hepatitis B ; genetics ; immunology ; virology ; Hepatitis B virus ; genetics ; physiology ; Host-Pathogen Interactions ; Humans ; Virus Release

Objective To understand the molecular epidemiology characteristics and its drug resistance of methicillin-resistant Staphylococcus aureus (MRSA) in the urban area of Jilin and to provide important basis for guiding the clinical medication and prevention of the MRSA infection. Methods One hundred and three strains of MRSA from July 2013 to July 2014 in the urban area of Jilin were selected. The polymerase chain reaction (PCR) technology and multiple polymerase chain reaction were used to detect mecA gene and Staphylococcus chromosomal cassette mec typing (SCCmec) genotype of MRSA. The drug sensitivity test for 13 kinds of clinical common antibacterial drugs were detected by using the K-B method. And the source of the strains were analyzed. Results The results of SCCmec genotype of MRSA showed that SCCmecⅢtype were 62 strains, accounting for 60.2%;SCCmecⅡtype were 39 strains, accounting for 37.9%; failing to parting were 2 strains,accounting for 1.9%. Drug susceptibility test results showed that all of 103 MRSA strains were resistant to cefoxitin, cefazolin, penicillin and benzene, and drug resistance rate was 100.0%. The resistant rate to erythromycin, levofloxacin, ciprofloxacin, tetracycline, gentamicin and rifampin were 96.1%, 93.2%, 95.1%, 91.3%, 90.3%and 55.3%receptively;the resistant rate to sulfamethoxazolewas was only 1.9%;and the resistant strains to vancomycin and teicoplanin were not detected. The top three department of the distribution of the strains source were department of neurosurgery (31.1%), ICU (19.4%) and burn plastic surgery (17.5%). Conclusions The SCCmecⅢtype is the main MRSA epidemic strains, and SCCmec type II is a minor epidemic strainin the urban area of Jilin. The antibiotic resistance of MRSA is a serious problem with multiple drug resistance, but MRSA is sensitive to vancomycin and teicoplanin.

Objective To establish an LC-MS/MS method for the detection of landiolol concentration in human blood.Methods After pretreatment with neostigmine and a deproteinization procedure, landiolol and the internal standard venlafaxine were eluted isocratically using a mobile phase consisting of acetonitrile and 10 mmoL·L-1 ammonium acetate with 0. 1% formic acid in a ratio of 3664 ( V/V ) . Separation of the respective compounds was achieved on a Waters XTerra? RP18 column (150 mmí4. 6 mm,5 μm). Quantitative analysis of landiolol was conducted by a triple-quadrupole mass spectrometer with positive-electrospray ionization source,monitored under a multiple reaction monitoring ( MRM) mode. The extracted ions monitored following MRM transitions were m/z 510. 5→423. 1 for landiolol and m/z 278. 2→215. 1 for the internal standard venlafaxine. ResultsThe calibration curve of landiolol in human blood showed good linear relationship in the range of 1. 010-2 020 μg·L-1 . The lower limit of quantitation was 1. 010 μg · L-1 . The RSD of within-day and between-day precision was less than 6. 5% and 4. 8%, respectively. The recovery rate was 92. 6%-100. 9%. Conclusion The method is proven to be simple,rapid and reliable,and can be applied to study the pharmacokinetics of landiolol hydrochloride in healthy Chinese volunteers.

Objective To study the 18F-FDG PET/CT features of tuberculous and malignant diffuse peritoneal lesions and to discuss the diagnostic value of 18F-FDG PET/CT in diagnosing and differentiating the lesions. Methods The 18F-FDG PET/CT features of 72 patients with tuberculous peritonitis,28 primary serous papillary carcinoma of the peritoneum and 135 peritoneal metastases confirmed by clinic and/or histopathology, were retrospectively reviewed. The peritoneal thickening features of tuberculous and malignant peritoneal lesions were observed. The maximal standardized uptake value (SUVmax) of peritoneal lesions and ascites, ascites SUVmax/liver SUVmax (T/NT) were compared between tuberculous peritonitis and cancerous peritonitis. The ROC curve was used to analyze the diagnostic efficiency of T/NT, SUVmax of peritoneal lesions and ascites. Results The typical 18F-FDG PET/CT features of tuberculous peritonitis were uniformity thickening of parietal peritoneum, mesenteric and omental stain like changes, widely and even distribution of the peritoneal 18F-FDG, while the cancerous peritonitis was obvious uneven thickening of parietal peritoneum, mesenteric and omental nodules and pie-shape changes, uneven distribution of the peritoneal 18F-FDG. The degree of 18F-FDG uptake was increased in all peritoneal lesions, and there was no significant difference between the tuberculous group (SUVmax=10.53±5.44) and the cancerous group (SUVmax=11.45±6.78, t=1.017, P>0.05). The 18F-FDG concentration in malignant ascites (SUVmax=1.88±0.65,T/NT=0.73± 0.18) was obvious higher than that of tuberculous ascites (SUVmax=1.67±0.69,T/NT=0.57±0.27, t=2.243 and 5.045,both P<0.05). The area under the ROC curve of T/NT, SUVmax of ascites, SUVmax of peritoneal lesions were 0.707, 0.593, 0.536, respectively. Conclusion The 18F-FDG PET/CT imaging can reflect the morphology and metabolic changes of peritoneal lesions. It is important to combine the SUVmax of ascites in order to improve the efficiency of diagnosing the diffuse peritoneal diseases.

Background:SEMA3B is a candidate tumor suppressor gene,which plays an essential role in tumorigenesis and progression of a wide variety of cancer. Aims:To explore preliminarily the influence of DNA methylation on regulation of SEMA3B gene expression in gastric cancer. Methods:Real-time PCR was used to determine the expression of SEMA3B mRNA in six human gastric cancer cell lines(SGC7901,AGS,MGC803,BGC823,MKN45,and HGC27),one gastric epithelial cell line(GES-1),and 41 gastric cancer tissue and paired adjacent noncancerous tissue specimens. Methylation specific PCR was used to detect the promoter methylation of SEMA3B gene,and correlation between methylation of SEMA3B gene and clinicopathological characteristics of gastric cancer was analyzed. After treated with a demethylation agent,5-Aza-dC(10μmol/L),for 72 hours,the methylation and mRNA expression of SEMA3B gene were re-examined in above-mentioned cell lines. Results:SEMA3B mRNA expression was significantly lower in six gastric cancer cell lines and gastric cancer tissues than that in GES-1 cells(P <0. 001)and paired adjacent noncancerous tissues(P <0. 01). Promoter methylation of SEMA3B gene could be detected in all six gastric cancer cell lines but not GES-1 cells. Frequency of SEMA3B gene methylation was significantly higher in gastric cancer tissues than in paired adjacent noncancerous tissues (67. 6% vs. 32. 4%,P <0. 01),and the frequency was correlated with differentiation and lymph node metastasis of gastric cancer(P<0. 05). After treated with 5-Aza-dC,hypermethylation of SEMA3B gene in 5 gastric cancer cell lines was decreased,accompanied by up-regulation of SEMA3B mRNA expression. Conclusions:Hypermethylation in promoter of SEMA3B gene might be one of the mechanisms accounting for the reduced expression of SEMA3B,and being involved in tumorigenesis and progression of gastric cancer. SEMA3B might be a potential biomarker for diagnosis and prognostic assessment for gastric cancer and a promising epigenetic therapeutic target.

Objective To detect the serum prohibitin protein(PHB)level in children with renal interstitial damage and analyze the correlation between PHB and renal interstitial fibrosis(RIF). Methods Serum PHB protein levels were determined by Western blot analysis in 36 children with kidney diseases,and 30 healthy children were studied as control. Levels of BUN,Scr,and urinary microprotein series(including ALBU/Cr,NAGU/Cr,IgG U/Cr,α1-MU/Cr)were studied by automatic biochemical analyzer. Renal interstitial damage was semiquantitatively graded according to Katafuchi's method. The correlation between serum levels of serum PHB protein and those of BUN,Scr as well as urine microprotein were analyzed. Results Serum PHB protein was positive in children with diverse kidney diseases however it was negative in the normal controls(P ＜ 0.05). Serum PHB levels were significantly higher in children with proliferative glomerulonephritis than those with non-proliferative glomerulonephritis(P ＜ 0.05). Statistical analysis indicated that serum PHB levels positively correlated with the degree of tubulointerstitial lesions(r ＝ 0.868,P ＜ 0.001)as well as the glomerular injuries(r ＝ 0.753,P ＜ 0.001). And,serum PHB levels were also positively correlated with urinary microprotein including NAG(r ＝ 0.586,P ＜ 0.001)and IgG(r ＝ 0.341,P ＜ 0.001). Conclusions Serum PHB levels were significantly increased in children with kidney diseases and were positively correlated with the degrees of renal interstitial damage,suggesting that PHB might be a potential clinical marker for detecting tubulointerstitial lesions.

Objective To construct S6K1 shRNA gene recombinant adenovirus(S6K1 Ax)and evaluate its gene silencing effects on mouse cell lines and C57 BL/6J mice level.Methods Three S6K1 shRNA gene sequences were designed and spliced from pcPUR plasmid,pcDNA3.1 plasmid to cosmid plasmid and transfected into adenovirus.S6K1 Ax which has best gene silencing effect was selected and proliferated in 293 cell.Silencing effect of S6K1Ax was checked on mice AML12,C2C12,3T3-L1 cell lines.C57BL/6J liver was obtained after S6K1 Ax was injected into mice tail vein six days later.S6K1 was evaluated by qRT-PCR and Western blot.Alanine transferanse(ALT)was examined before and after S6K1 Ax injected.Results S6K1Ax can silence S6K1 expression of mouse AML12,C2C12 and 3T3-L1 cell lines and liver of C57 BL/6J mice on Western blot.S6K1 mRNA expression of C57BL/6J liver were control group 1.39±0.21 vs S6K1Ax group 0.63±0.09,t=6.132.P<0.01.ALT of mice hepatic function did not change after S6K1Ax injected:before(15.15±4.43)U/L,after(17.32±4.22)U/L,t=1.451,P>0.05.Conclusion Construction of shS6K1 Ax can knockdown S6K1 gene on mice cell lines and C57BL/6J mice liver,it provides a good tool to study the function of S6K1.

AIM:To investigate the effect and mechanism of liver ischemia/reperfusion(I/R)injury on the changes of cardiac energy metabolism and structure.METHODS:48 healthy Wistar male rats were randomly divided into 6 groups as follows(n=8 in each group):control group(CTL),simply ischemia for 30 min without reperfusion(I group);reperfusion following ischemia for 30 min(I/R group);2 h reperfusion following ischemia for 30 min(I/R 2 h group);4 h reperfusion following ischemia for 30 min(I/R 4 h group)and 6 h reperfusion following ischemia for 30 min(I/R 6 h group).The level of serum endotoxin was measured.The levels of insulin and insulin antibody in heart were detected by radioimmunoassay.The contents of MDA,MPO and lactic acid in heart were also determined.RESULTS:During the process of liver I/R injury,the level of endotoxin increased in I group and I/R group and declined gradually for long time during reperfusion,but was still longer than that in CTL group(P0.05).CONCLUSION:During the process of liver I/R injury,endotoxin is absorbed from intestine and impairment of liver detoxication leads to endotoxemia,which might play a role in the changes of the energy metabolism and structure in heart.

Background and purpose: Lysine specific demethylase 1(LSD1) is an important chromatin modifier. It epigenetically regulates gene expression pattern through chromatin modification and participates in maintenance of tumor malignant properties, such as oncogenesis, development, invasion, migration and metabolic transformation. SIRT3 (sirtuin 3) is a mitochondria localized tumor suppressor and regulates tumor metabolic transformation and oxidative stress. The correlation between LSD1 and SIRT3 has never been reported before. This study aimed to elucidate the correlation between LSD1 and SIRT3 with gene transcriptional regulation methods. Methods: RNA interference technique, co-immunoprecipitation assay(CoIP), chromatin immune-precipitation assay(ChIP) and ifrelfy luciferase activity assay were employed to elucidate the correlation between LSD1 and SIRT3 in pancreatic cancer. Results:mRNA and protein levels of SIRT3 were signiifcantly elevated in LSD1 knock-down PANC-1 cells. LSD1 interacts with PGC-1α, an important regulator of SIRT3 gene expression. LSD1 and PGC-1αoccupied the same region in SIRT3 promoter region through ChIP analysis. Luciferase activity assay validated LSD1 as a negative regulator of PGC-1αin SIRT3 gene transcriptional regulation. Conclusion:LSD1, as an important tumor promoter, negatively regulates the expression of tumor suppressor gene SIRT3, these results provide important clues for the role that LSD1 plays in aberrant metabolism and oxidative stress.

Objective To explore a rapid bacterial identifying method based on the 16S rRNA gene sequence analysis technology to provide the scientific basis for the diagnosis and treatment of unknown pathogenic bacteria.Methods The pure colonies were iso-lated and cultured directly from a clinical patient′s sputum sample.The colony as a template for PCR amplification with universal primers to amplify 16S rRNA gene fragments of unknown bacteria.The product of PCR was sequenced directly,then the sequence result was compared by using the BLAST of NCBI and the pathogen was identified based on the sequence homology.Results 1 strain of unknown pathogen was identified as ochrobactrum by this test and confirmed by ABI bacterial rapid identification sys-tem.Conclusion This study simplifies the isolation and identification procedures of unknown pathogen from the clinical samples and establishes a simple method for the rapid identification of pathogens by using 16S rRNA gene amplification.