Objective To investigate the expression of NF-κB and epithelial-mesenchymal transition (EMT) related markers E-cadherin and Vimentin proteins in human pancreatic cancer tissues and its relation with the malignant features. Methods The expression of NF-κB、E-cadherin and Vimentin proteins in 62 cases of pancreatic cancer tissues were detected by using immunohistochemistry and compared with the clinicopathological data of pancreatic cancer. Results The positive expression rate of NF-κB was 81% (50/62), Vimentin protein increased of expression was 61% (38/62), and E-cadherin protein loss of expression was 55 % (34/62) in pancreatic cancer. The positive expression rate of NF-κB was significantly related with the lymph node metastasis (x2=11.761, P＜0.05), distant metastasis (x2=9.225, P＜0.05), the absent expression of epithelial marker E-cadherin protein (r =0.352, P ＜0.05) and the positive expression of mesenchymal marker Vimentin protein (r=0.343, P ＜0.05), but there was no relation with the patients gender,age, tumor location, tumor type and tumor differentiation (P ＞0.05). In addition, the significant correlation of E-cadherin expression loss and Vimentin expression with tumor lymph node metastasis and distant metastasis was found (x 2= 6.914, 4.984, 7.753, 5.144, P ＜0.05). Conclusion The overexpression of NF-κB in pancreatic cancer may accelerate invasion and metastasis of pancreatic cancer through inducing EMT.

Objective To study the changes of insulin resistance due to severe short-term fluctuations of body mass in simple obese patients. Methods 94 women with simple obesity, were treated by low caloric and high protein diet for two months. A series of examinations were taken before and after the treatment. Results After two months, weight, body mass index (BMI), waist, hip, fasting serum insulin and HOMA-IR reduced significantly ( P <0. 01 or P < 0.05 ). But after 6 months follow-up,these data began to regain. After 12 months ,these data were not significantly different. Fasting serum insulin and HOMA-IR increased ( P < 0. 05). Conclusions The low caloric and high protein diet combined acupuncture or cupping could reduce weight. But 44% patients weight rebound, and HOMA-IR increased.

Hepatic carcinoma is one of the most common malignant tumors in China.Autophagy activity and the change of Nrf2-ARE pathway play an important role in the process of liver tumors.Nrf2 which is an important regulator to liver cancer belongs to the CNC family.Research discovered that after the inhibition of autophagy,Nrf2-ARE pathway activation contributes to the progression of hepatocellular carcinoma.This article summarizes the relationship between autophagy and the Nrf2-ARE pathway and its impact on the hepatic carcinoma.

Objective To explore the influence of HepG2 cells' proliferation and autophagy by the Nrf2-ARE pathway,and provide the experimental basis for clinical exploring effective liver cancer treatment.Methods Hepatic carcinoma HepG2 cells were cultured,and its proliferation inhibition rates and the change of cell cycle' s in each phase were explored by the MTT assay and flow cytometry.The hepatoma cells' autophagy was qualitative observed by inverted phase contrast microscope and fluorescence microscope.Results Inhibitory rate of HepG2 cells was obviously higher in the Nrf2 inhibitor BML-111 group than control group (P ＜ 0.05),and the control group was aslo obviously higher than the Nrf2 inducer EGb group (P ＜ 0.05).Flow cytometric analysis showed that G1 phase cells in the cell cycle increased,S phase cells reduced and G2/M period cells relatively increased in the Nrf2 inhibitor BML-111 group.But G1 phase cells reduced,S phase cells increased and G2/M period cells relative reduced in the Nrf2 inducer EGb group.Inverted phase contrast microscope and fluorescence microscope checked that ranging from the size of the bubble and autophagosome formed in Hepatoma HepG2 cytoplasmic of the Nrf2 inhibitor BML-111 group.Conclusions The Nrf2-ARE pathway played an reverse inhibition on HepG2 cells' proliferation and autophagy.After the inhibition of Nrf2-ARE pathway,HepG2 cells mostly stayed in the G1 phase of the cell cycle.

Objective To found sensitive and reliable method to identify trophoblastic tumor cells in the peripheral blood of the patients suffered from gestational trophoblastic tumor.Methods Given numbers of JAR cell from ten to million were mixed into 10ml non pregnant peripheral blood as a model. Detection of ? hCG mRNA with fluorescence quantitative reverse transcription polymerase chain reaction (FQ RT PCR) and then estimation of the numbers of tumor cell in the blood. Nine cases of peripheral blood were collected from the pretreatment patients of gestational trophoblastic tumor to assay ? hCG mRNA with FQ RT PCR, then to estimate the numbers of tumor cell in the circulation blood. Results FQ RT PCR could detect ? hCG mRNA when ≥10 2 JAR cells were mixed into 10ml non pregnant peripheral blood. Four cases of bloods had been detected ? hCG mRNA expression in 9 cases of gestational trophoblastic tumor, and the numbers of tumor cell from 10 4 to 10 7 per 10ml blood. Conclusion FQ RT PCR of which primers and probe are designed for ? hCG had been proved to be very sensitive detection means, it could be used to detect gestational trophoblastic tumor cells from patient preipheral blood; With FQ RT PCR the tumor cells had been detected in some patients of gestational trophoblastic tumor.

Histone methyltransferase SMYD3 (SET and MYND domain containing 3) is a protein which has the function of histone methylation found in recent years,it has an important role in transcriptional regulation.The research shows that SMYD3 inhibit apoptosis and promote cell proliferation,invasion and metastasis.More and more data shows SMYD3 highly expressed in liver cancer and is low in normal tissues which is even undetectable.SMYD3 level was significantly associated with prognosis,and gene silencing experiments in SMYD3 tumor cell growth was inhibited.Therefor,SMYD3 is closely related with the development and prognosis of HCC occurrence,which suggests that people can suppress the expression SMYD3 to block tumor cell growth,migration and improve prognosis to provide new goals and direction for the future of cancer treatment.

AIM: To investigate the growth inhibition of Candida albicans mediated by vaginal epithelial cells and determine if estrogen affects the anti-fungal activity. METHODS: C_ 57BL/6J mice vaginae from estrogen treatment group, diestrus group and ovariectomized group were excised, respectively. The vaginae were dissociated into single cell suspension by dispase and collagenaseⅠ. The epithelial nenriched cells were used as effector cells. Blastoconidia of C. albicans were used as target cells. After coincubation of effector with target for 9 h, the target cells growth density was observed, percent growth inhibition was calculated, and ultra-structural changes were observed. RESULTS: After coincubation of effector cells with target cells for 9 h, growth density of C. albicans was visibly reduced and it's growth activity was inhibited. Compared to ovariectomized group and diestrus group, vaginal epithelial cells from estrogen-treated mice had less ability to inhibit the growth of C. albicans (P

Hepatocellular carcinoma (HCC) greatly threatens human health. In clinical treatment, the therapeutic strategies for HCC are attracting more attention. With the research advances in the pathogenesis of HCC and the rapid development of molecular biology techniques, the therapies with molecular-targeted antitumor drugs for advanced HCC have become a hot research topic, and significant efficacy has been achieved in clinical practice. This article summarizes the research advances in clinical application of molecular-targeted drugs for the treatment of HCC and related issues, discusses the future perspectives of therapeutic strategies, and provides a new direction and reference for the clinical treatment of HCC.

Objective To investigate the protective effect of retigabine (a M-type potassium channel opener) on brains and its mechanism in male mice after acute cerebral ischemia reperfusion(I/R)injury.Methods Seventy male C57BL/6J mice were randomly divided sham-operated group (n=10),middle cerebral artery occlusion (MCAO) group (n=10) and prevention group (n=50) according to the random number table method;mice in the prevention group were then divided into XE991 (a M-type potassium channel blocker) group,RTG-treatment 0 h group,RTG-treatment 1 h group,RTG-treatment 3 h group,and RTG-treatment 6 h group (n=10).The MCAO models were established by suture method,and reperfusion was performed 90 min after cerebral ischemia.In RTG-treatment groups,a single dose of 10.5 mg/kg RTG was injected at the designated varying time points (0,1,3 and 6 h after the reperfusion);in XE991 group,a single dose of 3.0 mg/kg XE991 was injected after the reperfusion;mice in the sham-operated group and MCAO group received the same volume of saline.Twenty-four h after model making,infarct size was measured by TTC staining.HE staining was used to observe the morphological changes of neurons in hippocampal CA1 regions.The apoptotic neurons level and membrane protein CD40L expression in the ischemic penumbra were detected by TUNEL staining and Western blotting.Results In the sham-operated group,brain tissues had no obvious change,no infarction was observed,there was no CD40L expression,and TUNEL staining positive neurons were hardly found.(1) Cerebral artery territory infarction was visible in the MCAO group and intervention group;however,the infarction volume of the RTG-treatment groups was significantly lower than that in the MCAO group (P＜0.05);the infarction volume of the RTG-treatment 6 h group was increased as compared with that of the RTG-treatment 0 h group,RTG-treatment 1 h group,and RTG-treatment 3 h group,without significant difference (P＞0.05).(2) HE staining showed that hippocampal neurons were obviously swollen and necrotic in the MCAO group and XE991 group,while the pathological damages such as brain edema and neuron necrosis were ameliorated significantly in the RTG-treatment groups.(3) As compared with those in the MCAO group,the number of TUNEL staining positive neurons in the RTG-treatment 0 h group,RTG-treatrnent 1 h group,and RTG-treatment 3 h group and CD40L number in the RTG-treatment 0 h group and RTG-treatment 3 h group were decreased significantly (P＜0.05);as compared with that in the MCAO group,the number of TUNEL staining positive neurons increased significantly in the XE991 group (P＜0.05).Conclusion RTG has protective effect on cerebral I/R,and its mechanism might relate to reducing cell excitability and inflammation,thereby inhibiting cell apoptosis;these protection would be less effective when RTG is used outside a defined critical period of time.

Breast cancer is one of the most common cancers in women,but there is currently a lack of accurate prognos-tic assessment systems.The Naples Prognostic Score(NPS)is a prognostic prediction system that incorporates inflammatory and nutritional indicators.It has been proven to have important clinical utility in predicting the prognosis of patients with malignancies such as colon cancer,gallbladder cancer,endometrial cancer,and lung cancer.In recent years,research has found that NPS may be superior to TNMstaging in predicting the prognosis of breast cancer patients.It is an independent predictor of overall sur-vival(OS)and progression-free survival(PFS)in breast cancer patients.This suggests that NPS has great potential for applica-tion in predicting the prognosis of breast cancer.