Objective To investigate the clinical significance of the expression of fragile histidine triad (FHIT) protein in primary hepatocellular carcinoma (HCC).Methods Immunohistochemical (S-P) method was used to detect the expression of FHIT in the 46 patients with HCC and 10 normal controls.Results In the patients with HCC,the expression rate of FHIT in the tumor tissue was 56.52%,significantly lowerthan that in adjacent non-tumor tissue and normal tissue.The absence of FHIT protein was correlated neither with the size,tumor capsule,serum AFP level nor with chronic hepatitis B virus infection and cirrhosis of liver.There was significant relationship between the expression of FHIT and differentiation and thrombus in the portal vein.Conclusion The loss of FHIT gene protein is a frequent event in HCC.Furthermore,the loss is closoly related to tumor prognosis prognosis and FHIT loss.

To investigate the effect of dihydroartemisinin on apoptosis of human pancreatic cancer cell line JF-305 and the role of reactive oxygen species(ROS) in the apoptosis of JF-305 cells induced by dihydroartemisinin. MTT assays were used to detect effect of different concentrations of dihydroartemisinin on cells proliferation of JF-305 lines. Cell cycle was detected by flow cytometry, and the apoptotic morphology was observed by Hoechst 333258 fluorescence staining. Annexin V fluorescence staining was used to detect the apoptosis changes of JF-305 cells, while DCFH-DA was used to detect the changes of ROS during apoptosis process. Western blot was used to detect the protein expression changes of Bax, Bcl-2, Cleaved caspase-3, Cleaved caspase-9 and Cyto C. As compared with the control group, the JF-305 cells proliferation was inhibited significantly(P<0.05) after treatment with different concentrations of dihydroartemisimin for 48 h; cell cycle was blocked in the G2/M phase; apoptotic morphology of nuclear condensation, aggregation, and fragmentation was found, and the apoptosis ratio was increased(P<0.05). DCFH-DA detection showed that the cell ROS was increased significantly after dihydroartemisinin treatment(P<0.05). Western blot results showed that the expression of Bcl-2 protein was down-regulated; the expression of Bax protein was up-regulated; the ration of Bax/Bcl-2 was increased and the protein expression levels of Cleaved caspase-3, Cleaved caspase-9 and Cyto C were increased after dihydroartemisinin treatment. Therefore, dihydroartemisinin could induce apoptosis of JF-305 cells, and the possible mechanism may be related to the formation and increasing of ROS.

OBJECTIVE： To establish the method for PCR identification of bullwhip， and to identify the authenticity of bullwhip at the molecular level. METHODS： DNA samples of bullwhip and its counterfeits （donkey whip， pig whip， sheep whip） were extracted and their integrity， purity and concentration were detected. Using GenBank related information， using mitochondrial cytochrome b （Cyt b） gene of bullwhip as target gene， Primer-BLAST online software was used to design specific primer. PCR amplification was performed for whips of different species， and electrophoretic analysis was conducted for the product. PCR products of bullwhip samples were cloned and confirmed by DNA sequencing. The specificity and repeatability of the established PCR method were verified. RESULTS： DNA purity of the bullwhip and its counterfeits was high， and there was no protein or RNA pollution. 1.5％ agarose gel electrophoresis showed that there were obvious target gene bands of bullwhip samples at 200-300 bp， while no corresponding bands appeared in other counterfeit products. The results of DNA sequencing showed that the nucleotide sequence of the gene fragment of bullwhip was 100％ similar to that of the bullwhip in GeneBank. Results of methodological validation showed that established method was specific and reproducible. CONCLUSIONS： The established PCR identification method based on Cyt b gene in the study is simple， rapid， accurate， specific and reproducible， and can meet the requirements of analysis and identification of bullwhip and its counterfeits.

Background: Base excision repair (BER) plays an important role in the maintenance of genome integrity and anticancer drug resistance. This study aimed to explore the role of BER gene polymorphisms in response to chemotherapy for advanced non-small cell lung cancer (NSCLC) patients treated with platinum-based chemotherapy. Methods: During the period from November 2009 to January 2016, a total of 152 patients diagnosed with NSCLC Stage IIIB and IV in the First Hospital of Jilin University were admitted into this study. The XRCC1 G28152A, MUTYH G972C, HOGG1 C1245G, and PARP1 T2444C polymorphisms of all the patients were detected by mass spectrometry. The logistic regression was used for statictical analysis. All tests were bilateral test, and a P < 0.05 was considered statistically significant. Results: The logistic regression model showed that the response rate of chemotherapy of the PARP1 T2444C polymorphisms, CC genotype (odds ratio [OR]: 5.216, 95% confidence interval [CI]: 1.568-17.352, P = 0.007), TC genotype (OR: 2.692, 95% CI: 1.007-7.198, P = 0.048), as well as the genotype of TC together with CC (OR: 3.178, 95% CI: 1.229-8.219, P = 0.017) were significantly higher than those of TT wild type. There was no relationship between the MUTYH G972C, XRCC1 G28152A, and HOGG1 C1245G gene polymorphisms and chemosensitivity. Conclusions The PARP1 2444 mutation allele C might be associated with the decreased sensitivity to platinum-based chemotherapy in advanced NSCLC. These findings may be helpful in designing individualized cancer treatment.
Antineoplastic Agents ; therapeutic use ; Carcinoma, Non-Small-Cell Lung ; drug therapy ; genetics ; DNA Repair ; DNA-Binding Proteins ; Female ; Genotype ; Humans ; Lung Neoplasms ; drug therapy ; genetics ; Male ; Middle Aged ; Polymorphism, Genetic ; Polymorphism, Single Nucleotide ; Retrospective Studies ; X-ray Repair Cross Complementing Protein 1 ; genetics

Humans ; Joint Dislocations ; Lunate Bone ; Wrist Injuries

Objective To establish a cell model based on calcium-activated chloride channel (CaCC) that could sensitively detect the second messenger Ca

The aim of the present study was to investigate the effect of Sophoral flavones on proliferation of cardiac fibroblasts (CFb) induced by high glucose and its underlying mechanism. Cardiac fibroblasts were exposed to different concentration of D-glucose (15, 25 and 35 mmol·L^-1) at different time point (24, 48 and 72 h) in order to determine cell proliferation, and the model group was established by culturing CFb with 25 mmol·L^-1D-glucose for 48 h. Sophoral flavones (12.5, 25 and 50 mg·L^-1) were employed for intervention. The cell viability was measured by MTT assay, and the levels of transforming growth factor-β₁ (TGF-β₁), matrix metalloproteinase-2 (MMP-2), collagen Ⅰ and collagen Ⅲ were measured by ELISA. In addition, flow cytometry was employed to detect the cell cycle; while the protein expression of prohibitin (PHB) was observed via immunocytochemistry and Western blot. This animal experiment had been approved by Jilin Medical University Experiment Animal Ethics Review Committee. The results showed that 25 mmol·L^-1 glucose could promote the proliferation of CFb; and the contents of TGF-β₁, MMP-2, collagen Ⅰ and collagen Ⅲ in the model group were higher than that of control (P<0.05). The number of cells in S and G₂ phase increased under high glucose condition. In the model group, PHB translocation occurred at 6 h and protein expression decreased at 48 h (P<0.01). Compared with the model group, 12.5-50 mg·L^-1 Sophoral flavones reduced the contents of TGF-β₁, MMP-2, collagen Ⅰ and collagen Ⅲ, increased the number of G₁ phase cells, and increased the expression of PHB protein at 48 h (P<0.05), with no effect on the nuclear translocation of PHB. These results indicated that Sophoral flavones could prevent the proliferation of CFb induced by high glucose, the mechanism of which may be related to increasing the expression of PHB protein.

Objective : To investigate the effect of CD147 on reducing hydrogen peroxide - induced oxidative stress injury in prostate cancer LNCaP cells. Methods : The lentiviral system was used to establish a CD147 ⁃silencing prostate cancer cell model (LNCaP/shCD147 cells) and a negative control cell (LNCaP/Scramble cell) , and RT⁃qPCR was performed for verification. By detecting the activity of reactive oxygen species ( ROS) , superoxide dismutase (SOD) , glutathione peroxidase ( GSH⁃PX) and malondialdehyde ( MDA) in LNCaP/shCD147 and LNCaP/Scramble cells to verify the changes of oxidative stress and antioxidant enzymes in prostate cancer cells after silencing CD147 ; hydrogen peroxide( H2 O2 ) was added to the cells and the cell growth was detected by CCK⁃8 ; Western blot was used to detect the expression changes of nuclear factor E2 related factors (Nrf2) and heme oxygenase⁃1 (HO⁃1) to verify the relationship between the oxidative stress that occurs in prostate cancer cells after silencing CD147 and the PI3K/AKT signaling pathway. Results : Successfully constructed a CD147⁃silencing prostate cancer cell model. Compared with LNCaP/Scramble cells , the expression of CD147 in mRNA was reduced (P <0. 01) . The results of oxidative stress showed that the content of ROS and MDA in cells increased after silencing CD147 (ROS , P < 0. 01 ; MDA , P < 0. 05) , while the activities of SOD and GSH⁃PX decreased(P < 0. 01) , indicating that after silencing CD147 , LNCaP/shCD147 cells undergo oxidative stress. In addition , with the increase of H2O2 concentration , the survival rate of LNCaP/shCD147 group cells decreased (P < 0. 01) . After inhibiting the PI3K/AKT signaling pathway , the expressions of Nrf2 and HO⁃1 in the LNCaP/shCD147 group were reduced (P < 0. 01) , indicating that CD147 inhibits the oxidative stress injury of prostate cancer cells through the PI3K/AKT pathway. Conclusion CD147 can reduce the oxidative stress damage of PCa cells , and its inhibitory mechanism may be related to the PI3K/AKT signaling pathway.