Background and purpose:Extraovarian peritoneal serous papillary carcinoma(EPSPC) originats from peritoneum with rare incidence, sometimes may affect the surface of ovary and have multi-focal lesions, whose standard therapy have not been established. In this study, we preliminarily reviewed the clinical characteristics, treatment and prognosis of EPSPC in 11 cases. Methods:The clinical characteristics of 11 cases with EPSPC were first retrospectively analyzed. All the patients underwent cytoreduction surgery followed by chemotherapy. Finally, short-term and long-term effi cacy, time to progression (TTP) and overall survival were evaluated by RECIST, respectively. Results:Abdominal pain, distention and ascites were the most common presenting symptoms, but tumors could be palpable in only 18.2% of the patients. The positive rate of ascites, abdomen B ultrasound,MRI scan and ascending CA125 level in the plasma and ascites was 100%,45.5%,100%,72.7%,81.2%,respectively. The successful rate of cytoreduction surgery was 45.5% for the EPSPC. After chemotherapy, the cases of complete remission, partial remission, stable disease and progression disease were 1(11.1%,1/9),3(33.3%,3/9),2(22.2%,2/9) and 3(33.3%,4/9), respectively. TTP was 5-14 months for all the patients and the median TTP was 8.6 months. The 1,2,3-year overall survival was 72.7%,18.2%,0%, respectively and the median overall survival was 14.6 months. Conclusions: Ascite, abdomen MRI scan and CA125 level are the most meaningful factor to diagnose EPSPC. EPSPC is a carcinoma of poor prognostic with non-specific clinical characteristics, low successful rate of cytoreduction surgery and is chemotherapy-resistent.

The binding of the nuclear factor erythroid 2 related factor 2(Nrf2)to the antioxidant response elements(ARE)can start the expression of batches of antioxidant proteins,anti-inflammatory factors and detoxification enzymes. Nrf2/ARE signalling plays a pivotal role in anti-inflammation and in preventing xenobiotics induced lesions. Besides involvenment in physiological processes,such as regulating nutrient metabolism,Nrf2/ARE signalling also functions in the pathogenesis of various dieases. This review outlines the strcuture,functions,and regulation of Nrf2/ARE signal pathways.

The description of the circulation of qiand blood in twelve meridians and the symptoms of diseases in which they dominate inMiraculous Pivot·Meridianshas a certain guiding significance for clinical diagnosis and treatment. But in the book, six yang meridians “dominating in bodily diseases is considered as “fluid”, “humor”, “qi”, “blood”, “sinew” and “bone” dominating in bodily diseases. That is puzzling and prone to doubt. The authors perform a multi-angle analysis from the characteristics of circulation of qi and blood and functional activityof qi in meridians and give a reasonable explanation by referring also to other sections and chapters inHuangdi’s Internal Classic.

Objective To establish drug resistant models of temporal lobe epilepsy induced by amygdala kindling,and to investigate the changes of cAMP response element binding protein (CREB) and phosphorylated cAMP response element binding protein (p-CREB) expression in the hippocampus tissues in order to explore their roles in drug resistant epileptogenesis.Methods Eighty adult male SD rats were randomly divided into control group (n =10) and model group (n =70).The 70 rats were used to prepare the amygdaloid kindled model of epilepsy by chronic stimulation of amygaloid basal lateral nucleus.The successful kindled models were randomly selected as drug resistant epileptic group (n =10) and drug sensitive epileptic group (n =10) according to their response to the phenytoin and phenobarbital.On the basis of behavioral observation,electrophysiology,pathological HE staining,CREB and p-CREB expression changes,we verified the reliability of the models and explored the differences among the three groups above.The changes of CREB and p-CREB expression were detected by immunohistochemical method and Western blotting assay.Results In control group,the electroencephalogram (EEG) frequency was (8.700 ±1.494) Hz;in drug sensitive epileptic group,the EEG frequency was (14.700 ± 1.159) Hz;in drug resistant epileptic group,the EEG frequency was (19.800 ± 1.686) Hz.The frequency differences among the three groups were statistically significant (F =144.202,P =0.000).By immunohistochemical staining,a large number of CREB and p-CREB positive cells were observed in drug resistant epileptic group.As compared with the control group (CREB 0.197 ±0.058,p-CREB 0.260 ±0.176),the expression levels of CREB and p-CREB were increased in drug sensitive epileptic group (CREB 0.361 ±0.151,p-CREB 0.656 ±0.234) and in drug resistant epileptic group (CREB 0.591 ± 0.150,p-CREB 1.077 ± 0.400).The difference among the three groups had statistical significance (F =24.206,20.376,both P ＜ 0.01).Conclusions The expressions of CREB and p-CREB were significantly increased in drug resistant epileptic rats.These findings indicate that the expressions of CREB and p-CREB may play certain roles in the drugresistant epileptogenesis.

Objective To investigate a antitumor effects of mouse original monoclonal antibody against hMIC -1 as intravenous administration with human pancreatic tumor in vivo and providing experimental data .Methods The fourty-eight mice were randomized into eight groups for loaded with two pancreatic tumor cell lines panc -1 or sw1990 respectively , and individual tumor growth was observed , antitumor efficacy was evaluated after using mouse original monoclonal antibody against hMIC-1 by intravenous administration .The pathological change with formalin fixed , paraffin embedded tissues section was viewed .Results There was a significant difference in tumor volume and weigt in intravenous injection of mouse original monoclonal antibody against hMIC-1 on load pancreatic tumor with nude mice group compared with that in the control group after four week treatment , and the mouse original monoclonal antibody against hMIC-1 demonstrated a close association between inhibition of tumor volume growth and dose-effective in the two xenograft models examined .Under examined microscope , the pancreatic tumor tissue was destroyed evidently in mouse original monoclonal antibody against hMIC-1 group.Conclusions The antitumor effect of intravenous injection for mouse original monoclonal antibody against hMIC-1 is better than that of systemic using gemcitabine .

Objective To observe the quantity of drainage fluid after operation and to evaluate the application of negative pressure drainage in skin soft tissue expansion. Methods The silica gel tube of 2 mm inside diameter with multi holes on sides was set under the skin soft tissue expander in 48 patients, then drained from upper incision or another incised hole,and connected with negative pressure apparatus. Results After operation, the quantity of drainage was from less than 5 ml to no more than 50 ml, averaged 16 ml. Conclusion For an operation with expansion capability above 100～200 ml,setting the negative pressure drainage as a routine is a most simple and effective method to prevent and treat bleeding and hematoma formation.It can produce effects on reducing the early complications such as hematoma and infection.

Objective Apuinic/apyrimidic endonuclease/redox effector factor-1(APE1/Ref-1,abbreviated as APE1) is a major member of the base excision repair(BER) pathway involved in oxidative DNA damage repair.To knock down APE1 gene expression in HOS cells with pSilence APE1,and explore its effect in combination with 252Cf neutron ray radiotherapy.Methods The constructed APE1 siRNA expression vector pSilence APE1 was transfected into HOS cells by SuperFect Transfection liposome,and it was used to knock down the expression of APE1.The HOS cells and transfected HOS cells were respectively irradiated by 252Cf neutron ray,then the cell survival(D0),DNA single strand breaks(SSB) and cell apoptosis were determined by clone formation assay,alkaline comet assay and flow cytometer.Results The cell-survival curve was plotted by clone formation assay,the D0 value was 2.80 vs.1.89 and Dq value was 2.66 vs.2.00 for the control and transfected HOS cells,respectively,after being irradiated by 252Cf neutron ray.The tail moments at 2,5 and 10 Gy were 6.664?0.648 vs.7.997?0.542,20.322?1.433 vs.25.238?1.185 and 33.909?1.245 vs.39.191?1.052,respectively,for the control and transfected HOS cells,and the cell apoptosis rate at 2,5 and 10 Gy was 4.00 vs.5.68,5.91 vs.7.55 and 9.63 vs.13.51,respectively,for the control and transfected HOS cells.All these findings showed significant difference between the two groups(P

Objective To study the inhibitory effect of APE1 expression vector pSilence APE1 on growth of osteosarcoma in nude mice, and to elucidate the role of APE1 in pathogenesis and development of osteosarcoma. Methods Nude mice model bearing osteosarcoma was reproduced by implanting human osteosarcoma cell line 9901. Twenty mice were randomly divided into two groups: control group in which the mice were treated with lipofectamine, and experimental group in which the mice were treated with pSilence APE1. The tumor inhibition rate was calculated after 12 days of treatment. Meanwhile, the expression of APE1 protein, intratumor microvessel density (MVD), and proliferation index were observed by immunohistochemistry. Apoptosis index was assessed by terminal dUTP nick end labeling (TUNEL) technique. Results Down-regulation of APE1 expression of tumor cells was found in the group treated with pSilence APE1. The tumor inhibition rate was 38.23%. The intratumoral microvessel density (MVD) in experimental groups and proliferation index were significantly lower than the control group, while the apoptosis index was much higher. Conclusion Targeted knock down of APE1 by pSilence APE1 may inhibit the growth of osteosarcoma in vivo.

BACKGROUND:Gene therapy is the direction of spinal cord injury(SCI) therapy,the key of which is construction of targeting gene and vector. OBJECTIVE:To construct the recombinant adenovirus vector carrying human brain-derived neurotrophic factor(hBDNF) marked enhanced green fluorescent protein(EGFP). DESIGN,TIME AND SETTING:A single sample observation was completed in the First Affiliated Hospital of Fujian Medical University from September 2007 to June 2008. MATERIALS:Competent E. coli DH-5? was obtained from the American Stratagene Company. Plasmid pDC316-hBDNF,pDC316-mCMV-EGFP,pBHGlox_E1,3Cre and package system AdMax and 293 package cell strain were purchased from the Canadian Mixcrobix-Biosystems Company. METHODS:The hBDNF gene was constructed by PCR with plasmid pDC316-BDNF as template. With enzyme digestion,the hBDNF gene was inserted into the vector pDC316-mCMV-EGFP and the shuttle plasmid pDC316-hBDNF-mCMV-EGFP was constructed,which was cotransfected with the adenovirus skeleton plasmid pBHGlox_E1,3Cre into 293 cells to obtain the produced replication defective recombinant adenovirus vector Ad-hBDNF-EGFP. The recombinant adenovirus was propagated by repeat infection of 293 cells and purified by ion exchange method,then the virus particles were counted and the purity and titer were determined. MAIN OUTCOME MEASURES:①PCR identification of plasmid pDC316-hBDNF. ②Construction and identification of the shuttle plasmid pDC316-hBDNF-mCMV-EGFP. ③Packing,amplification and purification of recombinant adenovirus vector Ad-hBDNF-EGFP. ④PCR identification of the recombinant adenovirus. ⑤Titer of recombinant adenovirus. RESULTS:PCR amplification,restriction analysis and sequencing identified that both recombinant shuttle plasmid pDC316-hBDNF-mCMV-EGFP and recombinant adenovirus vector Ad-hBDNF-EGFP were correctly constructed. After amplification and purification,the virus particle count,A260/A280 and titer of recombinant adenovirus were 2.4?1011 VP/mL,2.0 and 0.8?1010 CCID50/mL,respectively. CONCLUSION:Recombinant adenovirus vector Ad-hBDNF-EGFP is successfully constructed,which laid a foundation for further study regarding gene function and therapy.

AIM: To investigate the effect of sodium ferulate on expression of apoptosis-related genes, bcl-2 and bax , in rat lens epithelial cells (LEC) injured by oxidation.METHODS: Eyes of SD rats were divided randomly into four groups: control group, hydrogen peroxide group (H 2O 2), pirenoxine sodium group (PS) and sodium ferulate group (SF). Eyes were excised and lenses were separated under operating microscope and sterilized condition. Lenses were incubated in CO 2 incubator for 24 h with 300 ?mol?L -1 H 2O 2 and with or rithout 5 mmol?L -1 SF. The expression of Bcl-2 and Bax protein of LEC were measured and compared by tearing the LEC anterior capsule via immunohistochemical analysis.RESULTS: (1) There were Bcl-2 and Bax expression in normal lenses of SD rates, Bcl-2 expression was stronger than Bax. (2) Bcl-2 expression decreased and Bax expression increased markedly ( P