A BASIC program was written to analyse the data from radioreceptor assay by microcomputer. Concentrations of ligand, total binding, nonspecific binding, specific binding and the ratio of specific binding (number of receptor sites) to free ligand content were calculated for each point. The receptor binding affinity constant and binding capacity were obtained by Sca-tchard analysis. Results and graphs can be displayed on the screen and/ or printed out by using a graphic printer

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Objective To explore the clinical features of patients with vertebrobasilar dolichoectasia (VBD).Methods Patients diagnosed with posterior circulation ischemia in our hospital from October 2008 to January 2012 were consecutively collected and were divided into the VBD group and the non-VBD (NVBD) group.Clinical manifestations,risk factors,hemodynamic parameters and neuroimaging features were collected.Results (1) Statistical difference was observed in dyslipidemia,hypertension and the history of diabetes in the two groups (P ＜ 0.05).(2) The cerebral hemodynamic features of the VBD patients were as the following:decreased peak systolic velocity of vertebral artery and basilar artery and decreased systolic/diastolic ratio.Statistical difference was showed in the average peak flow velocity(Vm),pulsatility index(PI) and resistance index(RI) (P =0.036,0.032,0.032,respectively).(3) The main clinical manifestations of VBD were ischemic cerebrovascular disease,hemorrhagic cerebrovascular disease,oppression,brain damage symptoms and hydrocephalus.(4) The diagnosis in most of the VBD patients was confirmed by neural imaging and MRI was the first choice.Conclusion The VBD patients have relative unique clinical features.MRI should be the first choice for neuroimaging.

Objective:To study the changes of the NKT like cells after HIV infected. Methods:We collected peripheral blood from 47 untreated HIV infected individuals and 31 healthy controls,and analyzed the expression of Annexin-V,Ki-67,HLA-DR and other surface molecules in NKT like cells by flow cytometry. Results:The NKT like cell percentage of untreated HIV infected group was (3. 03±1. 61)%,the NKT like cell percentage of normal control group was (8. 30±7. 42)%,the percentage of NKT like cells in HIV infected individuals was significantly lower than the healthy controls ( P<0. 05 );the NKT like cell HLA-DR expression of untreated HIV infected group and normal control group were (5. 40±4. 10)% and (0. 89±0. 83)%,the NKT like cell Annexin-V expression of untreated HIV infected group and normal control group were (30. 21±13. 15)% and (5. 40±8. 05)% ,and the activation and apoptosis of NKT like cells was significantly higher after HIV infection compared with health individuals (P<0. 001,P<0. 01),the degree of activation was negatively correlated with CD4 count (r=-0. 885 7,P<0. 05);and the NKT like cell Ki-67 expression of untreated HIV infected group and normal control group were (11. 15±4. 76)% and (27. 63±18. 31)%,the proliferation ability was significantly lower after HIV infection compared with healthy controls(P<0. 05). Conclusion:HIV infection can significantly reduce the number of NKT like cells and its ability to proliferate,and increase its ability to activation and apoptosis.

mRNA in ARE and GW9662 group were 2.276 ±0.534 and 0.362 ±0.026,respectively.Compared with control group,PPARγmRNA level in both of ARE and GW9662 group reached statistical significance (t =4.785,P =0.001 ;t =2.395,P =0.044).PPARγprotein expression in ARE group,GW9662 +ARE group and control group were 27 688.33 ±3 593.06,21 816.00 ±1 644.07,17 716.33 ±2 273.95,respectively,which was higher in ARE group than that in control and GW+ARE group (t =5.159,P =0.001 ;t =3.038,P =0.016). NF-κB p65 mRNA expression in GW9662 +ARE group was 0.346 ±0.149,which in ARE group and GW9662 group were 0.392 ±0.1 87 and 1 .720 ±0.338,respec-tively.The differences of NF-κB p65 mRNA expression level between ARE,and control or GW9662 group were statistically significant (t =3.592,P =0.007;t =7.851 ,P =0.000).While,the differences of Caspase-3 mRNA and protein expression levels among the four groups were not statistically significant (F =1 .1 81 ,P =0.376;F =0.647,P >0.05).Conclusion ARE may restrain NF-κB through up-regulating PPARγto inhibit the proliferation and invasive potential of LLC in vitro, which suggests that PPAR-γmay be a novel therapeutic target for lung cancer.

Tumor radioresistance is the leading cause of clinical radiotherapy failure and disease progression.Researches show that the occurrence of radioresistance is related to the cell cycle arrest,relevant gene change,tumor microenvironment change,autophagy,tumor stem cells and other factors.Studying the mechanism of radioresistance and looking for an effective method to avoid it is the key to improve the effect of radiotherapy,which can provide the probability of the prognosis of radiosensitivity.

Objective:Our purpose was to investigate the growth regulation and postreceptor signal transduction of somatostatin (SS) on human colon cancer cell line. Methods:Low differentiated clone A cells of human carcinoma were treated with different concentrations of SS and the growth status was observed. Intracellular 1,4,5-trisphosphate (IP3) and cyclic adenosine monophosphate (cAMP) were extracted, then the concentrations of them were measured by liquid scintillation technique and gamma scintillation counter.Intracellular free calcium concentration was detected by loading Fura-2 and fluorescental technique. Protein kinase C (PKC) was extracted from cytosol and membrane, then the activity of both parts was determined with TaKai method. Results:The clone A cell growth was inhibited greatly by different concentrations of SS (10-10 to 10-5　mol/L) and it is related to the doses of SS.Somatortatin could largely inhibit the production of intracellular IP3, ［Ca2+］i, and cAMP, and decrease the activity of PKC. Conclusion:The growth of Clone A cell can be inhibited by SS. The inhibition may be mediated by phosphate inositol pathway, so intracellular IP3, ［Ca2+］i decreased, or inhibited the cell growth by inhibiting the activity of PKC.On the other hand, the cell proliferation may be inhibited by adenosine cyclase pathway, that is decreasing intracellular cAMP ,inhibiting cAMP-depending protein kinase.

Objective:To screen and characterize the common epitopes recognized by monoclonal antibody 3A8,which binds several kinds of Gram negative bacteria,which were recognized by monoclonol antibody 3A8 agaisnt different strains of LPS.Methods:Phage clones binding to 3A8 were screened from C7C phage displayed peptide library,the attached phage clones were eluted by LPS2630(O111:B4).After 3 rounds of panning,the positive phage clones were identified by ELISA,and the amino acid sequences of these positive clones were deduced from DNA sequences.In order to predict how these peptide mimics interaction with 3A8,peptides(A2 and A5) based on conserved sequences of positive clones were synthesized and conjugated with KLH for further study.The binding of A2-KLH and A5-KLH to 3A8 were identified by ELISA.Results:15 of 33 phage clones were identified as positive clones and shown specific binding with 3A8.LPS2630 potently inhibited the binding of phage clone to 3A8.In analysis of the amino acid sequence,there were seven kinds of sequences containing highly hydrophilic residues,and Ser Pro Pro/Pro X Pro was the conserved sequence.The peptides A2 and A5 could bind to 3A8 specially.Conclusion:The conserved sequences containing Ser Pro Pro/Pro X Pro are obtained,which are recognized by mAb 3A8 against broad spectrum Gram negative bacteria and several strain LPS.The synthetic peptides based on the conserved sequence can bind to 3A8,indicating that the peptides can mimic a common epitope of Gram negative bacteria,which be expected as candidate epitope for vaccinization.

Objective:To find small molecular leads for inhibition on early stage of HIV infection by identification and characterization of the HIV-1 gp41 C-helix mimotopes.Methods:For identification of the gp41 C-helix mimotopes,C7C phage display peptide library was biopanning by using a synthetic peptide N36 which was derived from the gp41 N-helix as target.After three rounds of screening,positive phage clones were identified by ELISA and sequenced.Results:16 of 26 phage clones were identified to bind with peptide N36,and 10 of them were sequenced.Every clone of ten clones contains at least two hydrophobic residues,which may dock into the hydrophobic pocket in the gp41 N-helix domain.9 of the 10 clones have a conservative sequence WW,which may mimic the W628 and W631 in C-helix to interact with the hydrophobic residues in the gp41 pocket.One clone expressing the conservative sequence named clone No.8(CYWWHRLHC) was selected for characterization.The binding between the clone No.8 and N36 was blocked by free peptide N36.And the binding between clone No.8 and peptide N36 was inhibited by peptide C34(IC 50=12.5 ?g/ml).Conclusion:The short circular peptides displayed on phages containing WW residues may mimic the conformational epitope of the HIV-1 gp41 C-helix to interact with the N-helix.This information may be useful for design of HIV-1 fusion inhibitors.

OBJECTIVE: To study protection effect of trasylol on cerebral injury resulting from cerebral ischemia-reperfusion in the interference of immunological response.METHODS: 105 SD rats were randomly assigned into sham operation group,model group and trasylol group (n=35).Focal ischemia-reperfusion model were established by occluding middle cerebral artery.24 h before ischemia and at the 0 h,24 h,4 d,6 d,8 d,10 d,12 d and 14 d of reperfusion,trasylol group were given trasylol via tail vein and other two groups were given normal saline.The infiltration of CD4+ and CD8+ T lymphocytes was observed using immunohistochemistry at different stages of cerebral ischemia-reperfusion.RESULTS: As compared with sham operation group,CD4+and CD8+ T lymphocytes count in model group were increased significantly after cerebral ischemia-reperfusion injury and obtained maximum value at 10th day.CD4+ and CD8+ T lymphocytes count in trasylol group were lower than in model group after cerebral ischemia-reperfusion injury and obtained maximum value at 8th day (P