Objective: To study the protective mechanism of Donepezil on apoptosis of PC12 cells induced by amyloid beta protein. Methods: PC12 cells were cultured as previously,then amyloid beta protein and Donepezil were used to treat PC12 cells.Morphology observation,TUNEL and immunocytochemistry were employed to investigate the damage of PC12 cells induced by A?,protection of Donepezil on apoptosis of PC12 cells and the expression of Bcl2 and Caspase-3 in A?-treated group and Donepezil-treated group. Results: A? induced apoptosis of PC12 cells in a dose-dependent way;Compared to the group treated with A? only and the group post-treated with donepezil, the apoptosis index of PC12 cells(17.29?0.83)% and expression of Caspase-3(26.46?2.87)% were significantly downregulated in the group pretreated with donepezil(P0.05). Conclusion: This study demonstrated that Donepezil can protect PC12 cells against apoptosis induced with amyloid protein,which was closely related to the time of interference.The mechanism of protection was involved with the expression of Bcl-2 and Caspase-3.

Varieties of chemotherapeutic regimens based on fluorouracil have been recently developed.This review summarized widely used regimens of fluorouracil based chemotherapy in this decade.The common side effects,their mechanisms and clinical prevention and symptomatic treatment for these adverse reactions were also discussed.Therefore,this review will provide guidance for regimen selections,and improve the efficacy and safety of chemotherapy.In addition,the detailed information and data presented in this paper may be helpful in the development of new chemotherapy regimens.

?Silent information regulator protein 1 ( SlRT1 ) is a kind of histone deacetylases class lll on which cell metabolism coenzyme NAD+ is dependent. By the transcriptional regulation, it participates in the regulation of gene transcription, energy metabolism and cell aging process, which can prolong the lifespan of organisms and delay the development of various age-related diseases and has attracted much attention in the field of anti - aging research. ln recent years, studies have shown that SlRT1 occupies an important position in the pathogenesis of many ophthalmic diseases, especially in ocular surface diseases, glaucoma, cataracts, uveitis, and ocular fundus diseases, etc. There is a possibility that the promotion of SlRT1 activity would be the new drug target of ophthalmic therapy. The paper will review studies on SlRT1 and ophthalmic diseases.

Epithelial-mesenchymal transition (EMT) is a process by which the epithelial cells change to a mesenchymal phenotype.The highly conserved and fundamental process is integral in development, wound healing and contributes pathologically to fibrosis and cancer progression.The process can be activated by many transcription factors, growth factors or protein molecules, which involves complex molecular mechanism and signal transduction pathways.This paper reviews the development of molecular mechanisms of epithelial-mesenchymal transition and briefly summarizes the research progress of natural compounds targeting the EMT.

〔Abstract〕 Taking Wuxi People′s Hospital Affiliated to Nanjing Medical University as an example, the paper introduces the constitu-tion, software architecture and main functions of Clinical Decision Support System ( CDSS) .The system is integrated with Electronic Medical Records ( EMR) system, providing scientific and acurate information support for clinicians in the whole diagnosis process.It has positive significance to improve the work quality and reduce medical errors.

Advanced-stage Hodgkin's lymphoma (HL) has become a curable disease in the majority of patients.ABVD is considered to be the standard therapy,but debates continue regarding the role of radiation therapy(RT)in this patient population. The incorporation of interim positron emission tomography (PET) imaging, and characterization of HL on cellular and molecular levels are emerging as tools for treatment stratification and predictors of disease status. Therapeutic advances over the past 3 decades have resulted in the cure of the majority of the patients with advanced-stage HL.Several questions have emerged when considering what constitutes optimal therapy with a balance between a high cure rate and minimizing shortand long-term toxicity.This review focuses on 3 key elements:what is the optimal chemotherapy? What is the role of radiation therapy(RT)in advanced HL? Can therapy based on clinical biological risk factors be adapted?

BACKGROUND:Tetramethylpyrazine (TMP) can inhibit the expression of vascular endothelial growth factor (VEGF), but it is uncertain that TMP inhibit the growth and proliferation of HL-60 leukemic cells induced by VEGF.OBJECTIVE:To observe the effect of TMP on the proliferation of HL-60 leukemic cells induced by VEGF.DESIGN:Repetitive measurement and observation.SETTING:School of Medicine, Wuhan University of Science and Technology.MATERIALS:The experiment was carried out in the Molecular Biology Laboratory Center, School of Medicine, Wuhan University of Science and Technology from March to June in 2007. Human leukemic cell line HL-60 cells were purchased from Shanghai Institute of Cell Biology. TMP hydrochloride injection was produced by Wuxi Seventh Pharmaceutical Products Limited (Lot number:011014), protamine sulfate injection was produced by Shanghai First Biochemical Pharmaceuticals (Batch number:010302), and immunohistochemistry kit was purchased from Boster company.METHODS:①Human leukemic cell line HL-60 cells at log phase were used for the experiments. Cells were treated with 100 μg/L VEGF, and then TMP at final concentrations of 1.5, 15, 150 mg/L was added into culture medium. While the cells in medium without TMP were taken as blank control group, and the cells in medium with 20 mg/L protamine as positive control group. Meanwhile cells without treatment of VEGF were served as VEGF control group. After cells were incubated for 48 hours, the growth inhibiting rate of HL-60 cells was detected by MTT assay.②After HL-60 cells were treated with TMP at the final concentrations of 1.5, 15, 150 mg/L for 24 hours, the protein expression of VEGF in HL-60 cells was examined by SP immunohistochemistry.MAIN OUTCOME MEASURES:①Growth inhibiting rate of HL-60 cells.②Protein expression of VEGF.RESULTS:①Growth inhibiting rate of HL-60 cells:After HL-60 cells induced by VEGF were treated with 15 and 150 mg/L TMP, the absorbance value was significantly lower than that in VEGF control group (P < 0.05).②Protein expression of VEGF:After HL-60 cells were treated with TMP for 24 hours, the protein expression of VEGF was down-regulated with increasing TMP concentration in a dependent manner. Significant differences were observed in the protein expression of VEGF between cells treated by TMP and the controls (P < 0.01).CONCLUSION:TMP can inhibit the proliferation of HL-60 cells stimulated by VEGF and down-regulate the expression of VEGF.

BACKGROUND:Adult central nervous system lacks the ability to regenerate,so it is of great significance to find a new source of neural stem cells.OBJECTIVE:To investigate the differences between basic fibroblast growth factor(bFGF)and epidermal growth factor(EGF)in inducing bone marrow mesenchymal stem cells(MSCs)to differentiate into neurons in vitro.METHODS:MSCs were isolated from normal human bone marrow using density gradient centrifugation and cell attachment method.MSCs were plated in 96-well culture plates at a density of 0.25×108/L and cultured with 200 μL DMEM/F12 for 0,1,2,3,4,5,6,and 7 days,with 20 μL MTT(5 mg/mL)in 5 wells at each time point.The supernatant was removed and 100 μL dimethyl sulphoxide was added to each well for 4 additional hours of incubation.In addition,some cells were exposed to bFGF and EGF.Growth curve was determined with MTT method.Telomerase activity were examined by TRAP(PCR)-ELISA.Additionally,the functional differences of the two cytokines were checked by RT-PCR.RESULTS AND CONCLUSION:RT-PCR revealed that nestin,glial fibrillary acidic protein(GFAP)and neurofilament subunit M (NF-M)mRNA were expressed in un-induced MSCs of passage 4.Nestin expression reduced at 7 days.The expression of micro-tubule-associated protein-2(MAP2)mRNA was not detected until the induction,and increased thereafter.The expression of MAP2 mRNA was greater in bFGF+EGF and bFGF alone groups compared with EGF alone group,and the expression of GFAP in EGF alone group was greater than other groups.Results showed that MSCs can be cultivated,proliferated and differentiated into neural stem cells in vitro.The differentiated neural stem cells have the activity of proliferation,but not have the ability of infinite proliferation as tumor cells.

Objective To analysis the differences of age, prostate volume, serum PSA and PSAD, IPSS between the BPH and BPH with prostatitis. Methods Clinical data of 100 patients whom received surgical treatments with a pathologic diagnosis of BPH were retrospectively analyzed. The occurrence of prostatitis was determined by pathology. The differences of age, prostate volume, serum PSA and PSAD, IPSS between the BPH cases and BPH with prostatitis cases were analyzed. The capability of B-ultrasound in diagnosis of the prostatitis combined with BPH was evaluated. Re-suits 66% BPH patients were found combined with prostatitis. There was a significant correlation between inflammatory infiltration grade and aggressiveness grade (r= 0. 772, P<0. 001). There was a moderate correlation between prostate volume and patient age(r= 0. 420, P<0. 001). There was a low correlation between serum PSA and patient age (r= 0. 258, P<0. 01) while no significant correla-tion between PSAD and age. The patient age of BPH combined with prostatitis group was significantly higher than BPH group (P<0. 05). Average prostate volume of combined with prostatitis group was significantly higher than BPH group (P<0. 05). There was a significant correlation between prostate volume and inflammatory infiltration grade(r=0. 292, P=0. 003), PSA and aggressiveness grade(r=0. 254, P=0.007). Both average PSA and PSAD of BPH combined with prostatitis group were signif-icantly higher than the BPH group (P<0. 05). When the factor of difference in age distribution was considered, the conclusion were still valid (P<0.05). On α= 0.05 level, relatively low correlations were found between PSA and inflammatory infiltration grade(r=0. 319, P=0. 001), PSA and aggres-siveness grade(r=0. 214, P=0. 032), PSAD and inflammatory infiltration grade ( r=0. 212, P=0. 034). There was no significant correlation between PSAD and aggressiveness grade(r=0.081 ,P=0.425). Average IPSS of combined with prostatitis group were significantly higher than BPH group. On diagnosis of the combined prostatitis in BPH, the sensitivity of ultrasonic was 21.2% with a speci-ficity of 82.4%. Conclusions Prostatitis is often found in more than half BPH samples. The BPH with prostatitis usually has bigger prostate volume, higher PSA, PSAD and may present relatively se-verer clinic syndromes.

Objective To facilitate a better understanding of the progress in the research, diagnosis and treatment of Peutz Jeghers syndrome (PJS).Methods Almost all the papers related to PJS from various magazines published in English and Chinese in recent years were reviewed. Current progresses in PJS research and related diagnosis and treatment were discussed in this review.Results PJS is a rare inherited disease with autosomal dominant trait, which is characterized by the presence of hamartomatous gastrointestinal polyps and mucocutaneous pigmentation of the lips, buccal mucosa, and digits. This syndrome is commonly complicated with intestinal obstruction, bleeding, or intussusception,and patients with this disease are at high risk for the development of both GI and extraintestinal malignancies. STK11 on chromosome 19p13.3 are responsible for most cases of PJS. The polyps of PJS tend to have a high incidence of malignant change, and the recurrence of malignancy after treatment is also high. Conclusion The STK11 has been identified as one of the main genes responsible for PJS and has close correlation with formation and development of tumors. Patients with PJS are at high risk for the development of both GI and extraintestinal malignancies.