Epilepsy was arousing the attention of medical circles because of the complexity of its mechanism and the difficulty of its control.The project which used the pioneering research as the basement and was directed by the chinese medicine used the modern multidisciplinary research technologies and explored the mechanism of the brain damage in epilesy.The project′s treatment idea is different from the others,which provided a new way for seeking new medicines for treating epilepsy.The research techniques took use of the application of the behavioral methods and the electrophysiological methods creatively and the subject firstly used this way to observe it dynamically,which greatly improved the accuracy of evaluating the models and pharmacodynamics studies of the epilepsy.The research method of the project firstly observed the changing mechanism of the brain damage and the regulation of the apoptosis related genes,and even the efficiency of tsaoko-anemarrhenae decoction,which enriched the scientific intension of the decoction.The conclusions palyed a very important role in exploiting the new medicine for treating epilepsy and enriching the knowledge of the five visceras in chinese medicine.

Accidents ; Child ; Dinitrobenzenes ; poisoning ; Humans ; Male

Objective To analyze the effect of Chinese medicine differentiation syndrome combined with hormone in the treatment of nephrotic syndrome.Methods 84 children with nephrotic syndrome from May 2005 to May 2012 in our hospital were randomly divided into observation group and control group,42 cases in each group.The control group was given hormone,while the observation group was given Chinese medicine on the basis of hormone treatment.The clinical efficacy was compared between the two groups.Results After treatment,the laboratory indicators of the observation group were better than before treatment,the differences were statistically significant(P ＜ 0.05).After treatment,the laboratory parameters of the observation group were better than the control group,the differences were statistically significant(P ＜ 0.05).The total effective rate of the observation group was 83.33％,which was significantly higher than 52.38％ of the control group(P ＜ 0.05).Conclusion The clinical efficacy of Chinese medicine differentiation syndrome with hormone in treatment of children with nephrotic syndrome is clear,and it is safe and reliable,which is worth to be applied in clinical.

Objective To evaluate the relationship between serum albumin(Alb) level and short-term prognosis in patients with acute cerebral stroke.Methods The serum Alb level was examined at admission and once in two weeks during hospitalization in 242 patients with acute cerebral stroke.The mortality,incidence of complication and rate of disease improvement were compared between lower serum Alb level group (Alb

Objective To explore the effect of Jiawei Wendan decoction on whole regulating function of CaMK/MAPK signal pathway in hippocampus of depression model rats.Methods Isolated depression model rats as research object were living unpredictable chronic stress.Based on the examination of mRNA/protein expression which was the key factor of the signal pathway of CaMK/MAPK and the intersection CREB1 mRNA expression,the relationship between CaMK Ⅱ/RSK protein expression and the CREB1 mRNA expression were analyzed with relation analysis method.Results ① Bidirectional correlation analysis:the respective coefficient (r value) of CaMK Ⅱ protein expression and the CREB1mRNA expression in hippocampus of the model group,Chinese medicine treatment group and western medicine treatnent group were-0.502 (P ＜ 0.01),-0.643 (P ＜ 0.01),-0.408 (P＜ 0.05) ;the respective coefficient(r value) of RSK protein expression and the CREB1 mRNA expression in hippocampus of the model group,Chinese medicine treatment group and western medicine treatment group were 0.550 (P ＜ 0.01),0.687 (P ＜ 0.0 l),0.407 (P ＜ 0.01).②Regression analysis:the respective regression coefficient of CaMK Ⅱ protein (positive direction),RSK protein (negative direction) and CREB1 mRNA expression in the model group,Chinese nedicine treatment group and western medicine treatment group were R 2 =0.472,F =12.983(P＜0.01),R2=0.666,F=28.961(P＜0.01),R2=0.356,F=8.004(P＜0.01).Conclusion The anti-depressant effect mechanism of Jiawei Wendan decoction is to regulate the whole function of the CaMK and MAPK signal pathway and then further up-regulate CREB1 mRNA expression.

OBJECTIVE: To study the inhibitory effect of Longzhi extracts (extracts from a Chinese herbal compound) on the growth of transplanted hepatoma H22 and sarcoma S180 in mice. METHODS: Certain dosage of Longzhi extracts was dissolved into distilled water to obtain the suspension of definite concentration. The suspension of 0.2 ml was planted on the right forefoot of each mouse. The mice were randomly divided into groups 24 hours later and treated for 7 days. One day after the treatment stopped, the mice were sacrificed and the tumor masses were taken out and weighed. RESULTS: The inhibition rates of Longzhi extracts on the tumor of transplanted H22 and S180 were 63% and 41% respectively. CONCLUSION: Longzhi extracts has antitumor action.

Objective To investigate the affecting mechanism of Jie Yu No.1 Decoction(JY),which was a complex prescription with the function of adjusting spleen and stomach,on the HPA-axis function of depression model rats.Methods60 SD rats were randomly divided into the normal,the model,the Amitriptyline and the JY decoction groups,with 15 each.Isolated-living condition and chronic mild unpredictable stress were applied suceessively to set up DEP rat model.Radiative immunotherapy was used to measure the content of hormone(CRH),somatostatin(SS) and Cortisol(CORT) in the blood plasma.The correlativity was Analyzed between SS,CRH and CORT to preliminary discuss the affecting mechanism of JY on the function of SS adjusting HPA-axis,and to clarify the antidepressant mechanism of the JY.ResultsThe correlation coefficient between SS and CRH was r=-0.5094,P=0.1972,t=1.4501.The result indicated that SS and CRH had the remarkable negatively correlation.The correlation coefficient between SS and CORT was r=0.010,P=0.9613,t=0.0244.The result indicated that SS and CORT had no remarkable correlation.ConclusionThe antidepressant mechanism of JY may be as that SS reduces CRH contents and reaches the adjustment of HPA-axis function in order to play its antidepressant effect.

BACKGROUND: The study aimed to investigate the clinical characteristics of acute renal failure (ARF) caused by oral acyclovir. METHODS: A 45-year-old Chinese male patient with acyclovir-induced ARF suffered from abdominal pain for one day. The pain was extended to the epigastric area from the right lower quadrant. Transient oliguria was seen in addition to microscopic hematuria and proteinuria. The serum creatinine concentration was 304 μmol/L. Eight days before the occurrence of ARF, the patient took oral acyclovir for facial neuritis. RESULTS: His renal function was restored completely following the discontinuation of acyclovir, with continuous renal replacement therapy for 54 hours and some symptomatic treatment. CONCLUSION: The presentation of acute renal failure caused by acyclovir can be diverse, but the prognosis is good after active treatment.

Objective To investigate methylation of the P15INK4B and p27kipl genes in human mantle cell lymphoma cell line Mino,to evaluate the effects of decitabine on demethylation of p15INK4B and p27kip1 genes and on apoptosis of Mino cells and its relative mechanism. Methods Mino cells were after treated with various concentration of decitabine, the cell viability, cell cycle distribution or the apoptosis of Mino cells was respectively analyzed by trypan dye-exclusion assay or flow cytometry.The mRNA and protein expression of p15INK4B 、p27kip1 and bcl-2 were studied by RT-PCR or Western blot, respectively.Methylation of the p15INK4B and p27kip1 genes in Mino cells were determined by PCR using the methylation specific primer(MSP).Results Decitabine significantly inhibit the cell growth,induced G1 arrest and promoted apoptosis of Mino cells. The expression of p15INK4B and p27kipl mRNA were both significantly increased,wheres bcl-2 mRNA was decreased, After treatment with 6.4,3.2,1.6 mmol/L decitabine for 72 h,the methylationg of p15INK4B gene were decreased to 25.2 ％ 、48.2 ％ and 65.0 ％respectively,in the meantime,the methylationg of p27kip1 gene was decreased to 20.21％ 、50.2 ％ and 70.0 ％. Conclusion The hp15INK4B and p27kip1 genes of Mino cells are methylated and down-regulated.Decitabine can inhibit the proliferation and induce the apoptosis of Mino cell lines,with the reduction of bcl-2 gene and demethylation of p15INK4B and p27kip1 genes.

AIM:To elucidate whether ZFP580 is involved in the cardioprotective effects of hypoxic precondi-tioning (HPC) against hypoxia-reoxygenation (H/R) injury in H9c2 myocardial cells.METHODS: Rat heart-derived H9c2 cells were cultured in DMEM .H/R was induced by incubation under ischemic hypoxia for 3 h and reoxygenation for 2 h.HPC was induced by exposing the H 9c2 cells to 10 min of hypoxia and 20 min of reoxygenation for 3 cycles before H/R treatment.MTT staining and LDH leakage detection were used to evaluate the effects of HPC .Western blotting was used to detect the protein levels of ZFP580, phosphorylated ERK1/2 and cleaved caspased-3.The effects of ZFP580 overexpre-ssion or knockdown on H/R induced apoptosis were determined .RESULTS:The results of MTT staining and LDH leakage detection showed evidence of HPC cytoprotection against H /R-induced cell death in H9c2 cells.ZFP580 protein level and ERK1/2 phosphorylation were significantly increased in the HPC group compared with control group and H /R group. PD98059, an inhibitor of ERK1/2 phosphorylation , significantly suppressed the HPC-induced up-regulation of ZFP580 pro-tein expression.ZFP580 overexpression significantly inhibited apoptosis and caspase-3 activation in H9c2 cells.CON-CLUSION:HPC exhibits cytoprotection against H/R and leads to high level of ZFP 580 protein in H9c2 cells.ZFP580 is regulated by ERK1/2 activation and mediates the anti-apoptotic effect of the ERK1/2 signaling pathway in HPC cytoprotec-tion.