The amount of ~3H-TdR incorporation into D?A of FRTL5 cells was expressed as CPM/?gD?A. THe responsibity of FRTL5 cells to stimulators such as TSH was expressed as % against thJ control CPM/?gDNA of the experimental group divided by that of the control. The responsibilities of FRTL5 cells which were recovered after being fr-o zen under-180℃ for a long time, to TSH 200?g/ml were 2741% and 3028% respectively, and the responsibilities of cells cultured in TSH media continuously for a long time, to TSH 200?u/ml and 2000?u/ml were 736% and 719% respectively. There was statistically significant differences between the two groups of the cells mentioned above. This showed that freezing FRTL5 Cells for a long time Such as 2 months was able to recover the decreased responsibility of the Cells due to a long continuous TSH culture.

Aiming at status of training the rural order directed free medical educational talents, we should improve the understanding of training the free medical students, perfect the relevant management system, strengthen medical ethics education of students, pay attention to humanistic care of students,strengthen the continuing education of students, standardize the access system of students, reform the medical distribution system, to ensure the quality of training free medical students.

Objective To explore the acute toxic reactions of memantine in neonatal rats. Methods Based on Completely Lethal dose(LD_(100)) and median lethal dose (LD_(50))of memantine in SD neonatal rats acquired in a preliminary test of death dose, 60 neonatal rats were randomly divided into normal group which were given water injection intraperitoneally and 5 study groups which were given different doses of memantine intraperitoneally.LD_(50) was calculated with Bliss method and the toxic reactions of memantine were observed in all neonatal rats of 6 groups after administration of memantine. Results LD_(50) of memantine in SD neonatal rats was((74.386?2.811)) mg/kg with 95% confidence at the range of 59.334-93.257 mg/kg.Side effects occurred at 1-4 minutes after administration. Excitatory jitteriness,ataxia,decreased respiratory rate and passivity were usually observed in groups with a lower dosage (52.0 mg/kg,61.2 mg/kg,72.0 mg/kg);some of them also manifested side lying, cyanosis and respiratory failure.While neonatal rats with a higher dosage (85 mg/kg,100 mg/kg)mainly manifested visible symptoms of inhibition, respiratory failure,side (lying) and cyanosis.However,no jitteriness and ataxia were observed in them.The neonatal rats usually died around 1 hour after memantine administration;survival rats usually returned to normal 4-5 hours after administration.Conclusion There is a positive correlation between toxic reactions and the mortality with memantine dosage in neonatal rats.

Objective To explore the effect of the JAK/STAT signal pathway on the apoptosis-related gene in the synovial tissue of rat rheumatoid arthritis (RA).Methods Fifty rat models of collagen-induced arthritis,whose arthritis index was more than 2,were divided into the model group,the low dose of AG490 group,the medium dose of AG490 group and the high dose of AG490 group.In addition,6 rats were treated intraperitoneal injection.Then,the arthritis index and the change of apoptosis-related genes were compared.Multiple-sample average was analyzed by single-factor x2 test and LSD-t or Tamhane's T 2 test were used for two-two comparison.Results The arthritis index of the model group increased evidently,and the apoptosis inhibitor Bcl-2,Bcl-xl gene and protein expression was up-regulated,which was significantly different when compared with that of the control group(0.931±0.035 vs 0.351±0.024,0.920±0.037 vs 0.271±0.029,0.322±0.047 vs 0.230±0.031 ).The expression of apoptosis promoting factor Bax wasslightly up-regulated.The blockage of JAK/STAT pathway cotld down-regulate the expression levels of the gene and protein of survivins Bcl-2 and Bcl-xl,and up-regulate the gene and protein expressions of Bax.Conclusion In the process of RA development,apoptosis inhibitor Bcl-2,Bcl-xl gene and protein expression is up-regulated.JAK/STAT signal transduction pathway regulates the apoptosis process.

Objective To investigate the serum superoxide dismutase( SOD) ,malondialdehyde ( MDA) , and nitric oxide( NO) level in generalized anxiety disorder ( GAD) patients for exploring the importance of oxida?tive stress in etiology of GAD. Methods 42 cases of first episode patients with GAD ( GAD group) and 42 cases of health ( control group) matched with age and gender were included . Serum levels of SOD,MDA ,and NO were tested to analyze for a control study.Results GAD patients had significantly higher levels of SOD,MAD and NO than health controls ((858.09±137.32)×102 U/L vs (745.40±119.19) ×102 U/L;(10.92±3.42)mmol/L vs (7.52±2.32)mmol/L;(74.32±12.34) μmol/L vs(65.22±14.29) μmol/L), t=4.036,5.368,3.297;P=0.000, 0.000,0.003) . A positive relationship between SOD and total score of Hamilton Anxiety Scale( HAMA ) ,psychotic anxiety factor of HAMA,or somatic anxiety factor of HAMA was found in GAD group ( r=0.331,0.370,0.318;P=0.029,0.016,0.040).The level of MAD correlated with total score or psychotic anxiety factor of HAMA( r=0.311, 0.320;P=0.042,0.039).Conclusion It is suggested that the dysfunction of oxidative stress may play a role in pathogenesis of generalized anxiety disorder.