The tumor marker(TM) is widely applied in early screening, thus providing further diagnostic hint of cancer, guiding the choice of therapy protocols for various tumor and evaluating the prognosis and therapeutic effects. However, there are some problems in TM application:There has still been no satisfactory early determinant TM, none test method of TM has been standardized, and the diagnostic capability of TM has not been evaluated reasonably. It is necessary to depend on the advanced scientific administration and technique, cooperate with clinical and basic disciplines actively, try to find out the new satisfactory TM and improve as well as exert important roles in the prevention, early diagnosis and treatment of 8 main catepories of cancers in our country.

It is confirmed that the adult cells can be re-programmed to embryonic stem cells(ESCs) by presenting some certain factors in oocytes in the clone process of animals. In recent years, some transcription factors that can induce pluripotent stem cells(iPS) have been identified and which made it possible to obtain induced pluripotent stem cells similar to embryonic stem cells. iPS provides a unique platform to study the pluripotent mechanism and to establish some specific disease models. This major scientific discovery can not only avoid the use of ES which involves ethics debate, but also lead the stem cell research to a new field.

Serum adiponectin levels in type 1 diabetic patients are higher than those in the normal population.We reviewed the influencing factors of serum adiponectin levels in type 1 diabetic patients,the relationship between adiponectin and adverse type 1 diabetic clinical features,complications,concurrent condition,and all-cause mortality,as well as potential mechanisms and research directions.

Objective To investigate the loss of heterozygosity (LOH) of 3p D3S1300 and D3S1289 loci of plasma DNA of lung cancer (LC) patients and evaluate its value for a tumor marker of lung cancer.Methods Two microsatellite markers,D3S1300 and D3S1289,were analyzed by PCR and silver staining to investigate LOH of the plasma DNA and cancer tissue DNA from 69 cases of primary lung cancer,and the plasma DNA from 40 control subjects.Results The percentages of D3S1300 LOH detected in the tumor tissue and plasma DNA of LC patients were 40.6% and 29.0% respectively,while the percentages of D3S1289 LOH were 31.9% and 24.6% respectively.In contrast,only 2 cases of D3S1300 LOH and 3 cases of D3S1289 LOH were found in plasma DNA of control group (P

Objective To study the functions of GPⅠa/Ⅱa and GPⅣduring the course of platelet adhesion to collagen. Methods Reaction system which contains anti-GPⅠa/Ⅱa antibody ,anti-GPⅣantibody or no blocking antibody was analyzed by flow cytomety. PE labeled anti-CD42b antibody was used to select platelet and fluorescence intension of fluorescein isothiocyanate ( FITC) was detected during the course of platelet adhesion to FITC-labeled collagen. Results The antibody against GPⅠa/Ⅱa inhibited platelet adhesion to collagen, especially to activated platelet(P 0. 05 ). Conclusion GPⅠa/Ⅱa plays an important roles in platelet adhesion to collagen. Blocking GPⅠa/Ⅱa may decrease the adhesion. GPⅣmay be helpful for acceleration of platelet adhesion to collagen at early stage.

Objective To investigate the function of GPⅠa/Ⅱa in the platelet-collage adhesion and the platelet granules release induced by collagen. Methods With the flow cytometry, in either presence or absence of the anti-GPⅠa/Ⅱa antibody: (1) PE-labeled anti-CD42b antibody was used for selecting platelet and FITC fluorescence intension was detected during the course of platelet adhered to FITC-labeled collagen. (2) PerCP-labeled anti-CD61 antibody was used for selecting platelet and detecting CD62P with PE-labeled CD62P antibody during platelet granule release induced by collagen. Results Anti-GPⅠa/Ⅱa antibody inhibited the platelet-collagen adhesion, especially the activated platelet-collagen adhesion (P0.05). Conclusion GPⅠa/Ⅱa plays an important role in platelet-collagen adhesion. Blocking GPⅠa/Ⅱa can decrease the platelet-collagen adhesion, but has no effects on platelet granule release reaction.

Objective To investigate the clinical application of Cystatin C as a biological marker for monitoring hepatic pathological change in patients with virus hepatitis.Methods Two hundred and seven patients infected with hepatitis B or C virus(HBV, HCV)were divided into cirrhosis group(group A),chronic HBV group(group B),chronic HCV group(group C),and liver cancer group(group D). 32 healthy controls(group H) were recruited . The serum TIMP-1,TIMP-2,and Cystatin C as well as some traditional markers for monitoring liver function and renal function including creatinine, creatinine clearance rate, alanine transaminase, and aspartate transaminase were determined.Results In these groups, serum Cystatin C(F=28.334, P

Objective To investigate the effects of quercetin on the growth of lung cancer cell line A549 and the expression of hTERT gene. Methods The number of viable cells was ascertained by trypan blue dye exclusion test. Morphological changes of apoptotic cells were observed by electronic microscopy and DNA ladder assay. The telomerase activity was analyzed by PCR-TRAP assay and hTERT mRNA expression was detected by quantitative RT-PCR. Results Quercetin had a significant inhibition on the proliferation of A549 cells in a dose-dependent manner. The IC50 was 22.5 ?mol/L after exposure to quercetin for 48 h. The results from electron microscopy and DNA ladder showed that apoptosis occurred in the A549 cells of treatment groups. The results of quantitative RT-PCR and PCR-TRAP revealed that the expression of hTERT mRNA was significantly inhibited by quercetin and telomerase activity was decreased. Conclusion Quercetin inhibits the growth of lung cancer cell line A549 in a dose-dependent manner,and induce their apoptosis. The down-regulated expression of hTERT,suppression of telomerase activity and destruction of telomere stability may all contribute to the mechanism of apoptosis induction.

Objective:To prepare monoclonal antibodies(McAb)against cystatin C(Cys C)and to establish the particle enhanced turbidimetric immunoassay(PETIA)for determining human serum Cys C.Methods:The prokaryotic expression vector pET32a(+)/Cys C was constructed and Cys C expression was induced.McAbs against Cys C were prepared with the hybridoma technique after mice were immunized with the purified recombinant protein.Then the McAbs were covalently attached to uniform microparticles,PETIA method for determination of human serum Cys C was established,and primary evaluation tests of methodology were performed.Results:Three hybridoma cell lines were obtained successfully,the secreted antibodies were isotype of IgG1,and Western blot confirmed that the antibodies reacted specifically to the Cys C protein.After one of the hybridoma cell lines was injected into mice abdominal cavity,the ascites abundant for McAb was obtained.The titer of the McAb against the purified protein was 1∶4?106.With the self-made McAb,PETIA for human serum Cys C was established.The primary evaluation tests of methodology revealed that self-established PETIA method had a satisfactory performance,which was equal to the import kit.Conclusion:The prepared McAb against Cys C is prepared,which could be used to establish PETIA for determining human serum Cys C.

Objective To explore the mechanism of siRNA targeted hTERT gene to inhibit bladder cancer T24 cell growth by decreasing c-myc and TGF-?1 expression. Methods shRNA-hTERT-pTZU6+1 vectors were constructed by RNAi-DNA vector technique, then the vectors were transfected into bladder cancer T24 cells,and the most effective vector and its optimal concentration were screened using RT-PCR to detect hTERT expression in T24 cells.The T24 cell growth, the alternative of cell phase,the expression of hTERT,c-myc and TGF-?1 were detected by flow cytometry,RT-PCR and immunohistochemistry. Results Three shRNA-hTERT-pTZU6+1 vectors were successfully constructed.The most effective vector was ph2-shRNA vector,and its optimal concentration was 1.0 ?g.This vector decreased the cell growth and the cell number of S phase from 65.2% to 38.6%,increased the cell number of G0/G1 phase from 32.0% to 57.9%,and attenuated both mRNA and protein expressions of hTERT,c-myc and TGF-?1 in T24 cells. Conclusions Targeted hTERT gene with siRNA may inhibit the cell proliferation of bladder cancer;down-regulating hTERT expression by attenuating the expression of c-myc and TGF-?1 is probably involved in the mechanism.