Medical Image has been increasingly applied in clinical diagnosis and treatment.It is very important to make use of large numbers of images in medical image management system in order to help clinician to analyze and diagnose.The traditional information retrieval techniques are not fit for retrieving large scale medical image databases.It is a very promising idea to introduce Content-based Image Retrieval(CBIR) technique into indexing medical image databases.The structure of the Content-based Medical Image Retrieval System(CBMIR) is introduced,and the key problems are mainly investigated,which included image segmentation,feature extraction,similarity searching and feedback mechanism.At last,the status and development of CBMIR are discussed.

Objective To prepared inclusion complex of β-cyclodextrin (β-CD) and its derivatives (methyl -β-cyclode-xtrin, 2,6-dimethyl -β-cyclodextrin, hydroxypropyl -β-cyclodextrin ) with entrcavir, and explore effect of different inclusion complex on the solubility and dissolution of entecavir.Methods Regression equation was established,prepared the inclusion complexes by a magnetic stiring method,grinding method and ultrasonic method.While inclusion rate was an index,the effects of reaction process was inquired by mole ratio, inclusion temperature, inclusion time and stirring rate and the most suitable method and technology of inclusion was optimized.Determinated the solubility with HPLC method and investigated in vitro dissolution with a small cup method.Results The regression equation was A=1.026 ×106C+4248.8, R2 =0.9999 (n=6), in the range of 0.497~4.97 g/mL, linear relationship was good.The best inclusion method was magnetic stirring, the best process conditions were: mole ratio was 1 ︰1, stirring speed was 300 r/min, inclusion time was 4 hours, inclusion temperature was 50 ℃.The four inclusion complexes all were white loose powder materials.The solubility of ETV,β-CD-ETV,HP-β-CD-ETV,RM-β-CD-ETV,2,6-DM-β-CD-ETV were 2.51, 13.4, 18.9, 37.6 and 89.5 g/L.The dissolution rates was ETV<β-CD-ETV

Objective To investigate the effects of HepG2 and HepG2.2.15 cells steatosis on the mRNA and protein expressions of suppressors of cytokine signaling-3(SOCS-3) and sterol regulatory element binding proteins (SREBP-1c).Methods The cell model of chronic hepatitis B (CHB) combined with nonalcoholic fatty liver disease (NAFLD) was successfully constructed using an oleic acid-induced HepG2 and HepG2.2.15 cells steatosis.Cells were divided into HepG2 cell control group (HepG2 cell control group), HepG2.2.15 cell control group (HepG2.2.15 cell control group), HepG2 cell steatosis group (HepG2 cell steatosis group) and HepG2.2.15 cell steatosis group (HepG2.2.15 cell steatosis group).The expression levels of SOCS-3 and SREBP-1c mRNA were detected by real-time quantitative polymerase chain reaction (PCR).Changes in protein expressions of SOCS-3 and SREBP-1c were measured by western blot.Results SOCS-3 mRNA expression level in HepG2.2.15 cell control group was significantly lower than that in HepG2 cell control group (P<0.01).The level in HepG2 cell steatosis group was also significantly lower than that in HepG2 cell control group (P<0.01).However, the level of SOCS-3 mRNA in HepG2.2.15 cell steatosis group was lower than HepG2.2.15 cell control group with no statistical significance (P=0.173).There was interaction between cells and steatosis (F=25.547, P<0.01).The expression of SREBP-1c mRNA in HepG2.2.15 cell control group was significantly lower than that in HepG2 cell control group (P<0.01), and was significantly higher in HepG2.2.15 cell steatosis group than that in HepG2.2.15 cell control group (P<0.01).There was no significant difference between HepG2 cell steatosis group and HepG2 cell control group (P=1.000).There was interaction between cells and steatosis (F=5.04, P<0.05).Western blot analysis showed that protein levels of SOCS-3 and SREBP-1c in steatosis cells at 48 h and 72 h were significantly higher than those in non-alcoholic steatosis cells.Conclusions Protein expressions of SOCS-3 and SREBP-1c are up-regulated in both steatosis groups.Factorial analysis shows that there is interaction between cells and steatosis.HBV gene could inhibit SOCS-3 mRNA expression and promote the expression of SREBP-1c mRNA in steatosis cells.

AIM:To investigate the effect of perifosine, an inhibitor of protein kinase B ( PKB/Akt) , on the cell cycle, apoptosis and autophagy in human brain glioma U251 cells, and to determine the relationship between perifos-ine-induced autophagy and apoptosis of glioma.METHODS:The cell growth inhibition was determined by MTT assay. The cell cycle distribution of U251 cells was examined by flow cytometry.The cell apoptosis was analyzed by Annexin V-FITC apoptosis detection kit.The protein expression of P21, P27, cyclin B1, caspase-9 and PARP was examined by Wes-tern blot analysis.The distribution and expression of LC3-Ⅱ, an autophagy marker, was observed to determine the effect of perifosine-induced autophagy.RESULTS:Perifosine inhibited the cell viability in a dose-dependent manner.In perifos-ine-treated U251 cells, the cell cycle was arrested in G2 phase and the expression of cyclin B1 was inhibited.Perifosine in-duced apoptosis of U251 cells through activation of caspase-9 cleavage, PARP cleavage and survivin inhibition.In addi-tion, suppression of autophagy by chloroquin, an inhibitor of autophagy, increased the number of apoptotic cells.CON-CLUSION:Perifosine inhibits cell proliferation and triggers apoptosis and autophagy in human U251 cells.Blocking auto-phagy magnifies perifosine-induced glioma cell apoptosis.

Objective To study the characteristics of neutralization antibody in mice induced by DNA vaccines of hemagglutinin(HA) of novel H1N1 influenza A virus(2009H1N1).Methods HA encoding plasmids of 2009H1N1 or 1918H1N1(2009HA or 1918HA)were constructed.25 μg or 200 μg dosage of 2009HA plasmids were used to immunize the mice,the total antibody of anti-20O9HA or cross-reactive antibody were assayed by ELISA using 2009HA or 1918HA protein as capture antigen,and the neutralizing antibody were assayed by two kinds of virus pseudo - particles(pp) of 2009H1N1 and 1918H1N1 .Results During of 4 to 16 weeks after boost immunization,in two groups of mice immunized with 25 μg or 200 μg dosage 2009HA plasmids,both total antibody of anti-2009HA and neutralizing antibody to 2009H1Nlpp reached the similar level(P ＞0.05),and there were cross-reactive antibody to 1918HA protein in two groups of mice serum,with similar titers of cross-neutralizing activity to 1918H1N1 pp(P ＞0.05),Conclusion A low dosage DNA vaccine encoding HA of 2009 H1 N1 virus is able to induce persistent and high level of neutralizing antibody,and may be potential valuable vaccine against the new emerging influenza virus.

Objective:Adenoid cystic carcinoma (ACC) is an uncommon malignant neoplasm, which mostly originates from the major and minor salivary glands of the head and neck region. This study aims to provide new information on head and neck ACC with cervical lymph node metastasis. Methods:Out of the 616 patients who underwent primary tumor resection from 1995 to 2008 in the authors' hospital, 62 cases with cervical lymph node metastasis were analyzed. Results:The general incidence rate of cervical lymph node me-tastasis in ACC was approximately 10%. The base of the tongue, mobile tongue, and mouth floor were the most frequent sites of lymph node metastasis with incidence rates of 19.2%, 17.6%, and 15.3%, respectively. Most cases exhibited the classictunnel-stylemetastatic pattern of occurrence, and the levelⅠb andⅡregions were the most frequently involved areas. Primary site and lympho-vascular invasions were significantly associated with lymph node metastasis. High patient mortality rate was also significantly correlat-ed with a high number of lymph node positive cases. Conclusion:Cervical lymph node metastasis has a high tendency of occurrence in the tongue-mouth floor complex, following the classictunnel-stylemetastatic pattern. Peritumoral lymphovascular invasion could be taken as a strong predictor for the occurrence of lymph node metastasis, which ultimately leads to poor prognosis of ACC patients. A selective neck dissection should be considered as a management in such patients.

Objective:To explore the expressions of endogenous hydrogen sulfide (H2 S)and its synthases cystathionine beta synthase (CBS)and cystathionine gamma lyase (CSE)in the cell lines of normal bladder and bladder cancer,and to clarify their mechanism in the development of bladder cancer.Methods:The bladder cancer cell lines (5637,T24,UM-UC-3,EJ)and human bladder epithelial cell line SV-HUC-1 were selected.The expressions of CBS and CSE in bladder cancer and normal cell lines were analyzed by Western blotting assay and the productivities of H2 S in cell lines were detected by sensitive sulphur electrode assay.The EJ cells were selected based on the previous experimental results and divided into groups as follows:① 10 μmol· L-1 NaHS group, 50 μmol·L-1 NaHS group,100 μmol·L-1 NaHS group and control group.After drug treatment,the cell survival rate was measured by MTT assay at 24 and 48 h.② 5 μg·L-1 cisplatin group,cisplatin (5 μg·L-1 )+ NaHS (100 μmol·L-1 )group and control group.After medicine treatment,the cell survival rate was measured by MTT assay and the cell apoptotic rate was detected by flow cytometry at 48 h. Results:Compared with the normal bladder cells (SV-HUC-1),the expression levels of CBS and CSE and the productivity of H2 S in the bladder cancer cell lines (5637,T24,UM-UC-3 and EJ)were increased obviously (P <0.05 or P <0.01).Compared with control group,exogenous H2 S promoted the cell proliferation of EJ cells.The cell survival rates were increased with the increase of drug dose (P <0.05),which showed a dose-dependent effect.The cell survival rates were increased with the prolongation of time (P <0.05),which showed a time-dependent effect.After medicine treatment,compared with cisplatin group,the cell viability in cisplatin+NaHS group was increased (P <0.05)and the apoptotic rate was decreased (P <0.05).Conclusion:Endogenous H2 S and its synthases CBS and CSE have an increased expression level in bladder cancer cell lines compared with the normal bladder cells.H2 S can enhance the proliferation of bladder cancer cells and decrease the apoptosis induced by cisplatin.

Objective To determine whether there is any difference in rocuronium-induced muscle relaxation between patients of Buyi and Han nationality.Methods Sixty ASA Ⅰ or Ⅱ patients of both sexes aged 20-55 yr,with body mass index of 20-25 kg/m2,undergoing laparoscopic or arthroscopic surgery under general anesthesia,were divided into 2 groups ( n =30 each):Han group (group H) and Buyi group (group B).Anesthesia was induced with midazolam,fentanyl and TCI of propofol (Cp=2-3 μg/ml).Tracheal intubation was facilitated with rocuronium 0.6 mg/kg.The patients were mechanically ventilated.PETCO2 was maintained at 30-35 mm Hg.Neuro-muscular (N-M) function was monitored by accelerography.N-M block was assessed by single stimulation of ulna nerve after loss of consciousness.The onset time,maximal N-M block time,clinical muscle relaxation time (from injection d rocuronium to 25％ recovery),75％ recovery time (from injection of rocuronium to 75％ recovery) and recovery index were recorded.The plasma concentration of albumin and α1-acid glycoprotein were measured by ELISA and biochemical analysis respectively.Results The onset time was significantly longer and plasma α1-acid glycoprotein concentration lower in group B than in group H.There was no significant difference in maximal N-M block time,clinical muscle relaxation time,75％ recovery time,recovery index and plasma albumin concentration between the 2 groups.Conclusion The onset time of rocuronium-induced N-M block is longer in patients of Buyi nationality as compared with patients of Han nationality.Lower plasma α1 -acid.glycoprotein concentration may be involved in the underlying mechanism.

In order to express the gene of LEN-5 β-lactamase from a Klebsiella pneumoniae strain,plasmids in the strain were extracted and an 879bp product of LEN-5 gene was obtained with PCR.After being digested with Nde I and Xho I,LEN-5 gene was cloned into pET-26b (+) vector.Then it was confirmed by digestion and DNA sequencing in recombinant plasmid before transformed into E.coli BL21 (DE3).After inducing by IPTG,LEN-5 β-lactamase was expressed.Protein extraction was processed by ultrasonic and protein activity was detected by nitrocefin.The isoelectric focusing electrophoresis showed a pI of 7.6.These results indicated that the LEN-5 gene has been cloned and expressed in prokaryote cell successfully.

Objective: To investigate the effect of transforming growth factor-β1 (TGF-β1) on HBV replication and protein expression in HepG2.2.15 cells with steatosis, as well as the association of TGF-β1 with suppressor of cytokine signaling-3 (SOCS-3) mRNA and sterol regulatory element-binding protein-1c (SREBP-1c) mRNA during the steatosis of HepG2.2.15 cells. Methods: The cells were divided into HepG2/HepG2.2.15 cell control groups (C1/C2 groups) and HepG2/HepG2.2.15 cell steatosis groups (F1/F2 groups). 5 ng/ml TGF-β1 was added to the two cell systems for intervention to establish TGF-β1 intervention groups (T1/T2 groups) and steatosis+TGF-β1 intervention groups (TF1/TF2 groups). A time-resolved fluorescence analyzer was used to measure HBsAg and HBeAg, and quantitative real-time PCR was used to measure HBV DNA, SOCS-3 mRNA, and SREBP-1 mRNA. A one-way analysis of variance and a factorial analysis were used for the statistical analysis of data. Results: TGF-β1 significantly reduced the level of HBeAg in C2 group (P = 0.034) and the levels of HBsAg (P < 0.001) and HBeAg (P = 0.004) in F2 group. There was an interaction between steatosis and TGF-β1 in inhibiting HBsAg. In addition, TGF-β1 significantly reduced the mRNA expression of SOCS-3 in C1, F1, C2, and F2 groups (P < 0.05) and significantly increased the mRNA expression of SREBP-1c in C1, F1, C2, and F2 groups (P < 0.05), suggesting that there was an interaction between steatosis and TGF-β1 in downregulating the mRNA expression of SOCS-3 and upregulating the mRNA expression of SREBP-1c. Conclusion TGF-β1 does not affect HBV duplication in HepG2.2.15 cells and can inhibit the expression of HBsAg and HBeAg. TGF-β1 can downregulate the mRNA expression of SOCS-3 and upregulate the mRNA expression of SREBP-1c.