Objective To explore the characteristics of type 1 diabetic mice models induced by multiple low dcee streptozotoein(MLD-STZ).Methods Type 1 diabetic mice models was induced with intraperitoneally injection of STZ(40mg/kg body weight,daily)for 5 consecutive days and detected fasting blood glucose,urine glucose and histological ehange of panereata.Results The incidence of type 1 diabetes mdlitus was 65%;compared with normal control group,blood glucose and urine glucose levels increased significantly and histological analysis of pancreata showed marked insulitis in diabetic model group,and the hyperglycemia maintained from the fourth to the eighth week after the firml STZ injection.Conelnsion Type 1 diabetie mice models could be made successfully by MLDSTZ,and the hyperglycemia could maintain for a rather long time.

Diabetic Osteoporosis is a general metabolic bone disease having fracture tendency because of osteopenia in unit volume,microstructural changes of bone tissue,decreased bone strength and increased friability,which is one of important complications of diabetes mellitus in skeletal system.Studies on bone involvement in patients with diabetes mellitus have generated conflicting results,largely because of the pathogenetic complexity of the condition.There are many factors,including advantageous and disadvantageous factors,influence the probability of osteoporotic fractures in diabetics.Adequate glycemic control,and calcium and vitamin D intakes,and the prevention and treatment of diabetic complications are key elements in the elimination of osteoporosis in diabetes mellitus.Patients with osteoporosis and diabetes should be offered the same pharmacological treatments as non-diabetics.

0.05).Conclusions: (1) The more severe of learning stress, the higher level of PMDD. (2) There was no difference in anxiety and depression between the students who suffered from PMDD and the who didn't. (3) The students who suffered from PMDD had more psychosomatic symptoms.

Objective: To investigate the change of functional marker and morphology of vascular endothelium induced by simulating diving condition. Methods:14 rabbit were put in the chamber. They stayed for 35 min under 0.55 MPa, and another 35 min under 0.7 MPa, then decompressed to 0.1 Mpa following a stage decompression schedule. Blood sample were draw at 30 min before compression and after decompression for testing endothelin-1(ET-1) and von Willebrand factor (vWF). These parameters were compared to see the change from pre-compression to post-decompression. The morphological change of vascular endothelium was observed under electrical microscope after decompression. Results: After decompression, plasma levels of ET-1 was increased from (1.33?0.23)ng/L to (2.99? 0.35)ng/L and activity of vWF was reduced from (2.35?0.47)% to (1.89?0.34)%. Swelling and defluvium of vascular endothelium was found under electrical microscope. Conclusion: Compression-decompression can cause the damage of vascular endothelium.

Objective To observe the changes in the relative indexes of vascular endothelium, blood coagulation and fibrinolysis system of rabbits with experimental severe decompression sickness (DCS), and to compare the above indexes of surviving rabbits with those of dead in order to analyze the mechanism of causes of death. Methods 14 rabbits were put into a decompression chamber. They stayed for 35 min under an atmospheric pressure of 0.55 MPa, followed by a pressure of 0.7MPa for 35min. Then they were subjected to a pressure of 0.1MPa for 4 minutes. Blood samples were drawn before the compression, under high pressure, and after decompression to determine endothelin-1 (ET-1), von Willebrand factor (vWF), fibrinogen (FIB), D-Dimer, blood coagulation factor Ⅷ(FⅧ), plasminogen (PLG), plasmin inhibitor (PL-IN), prothrombin time (PT), and activated partial thromboplastin time (APTT). The changes of above parameters of surviving rabbits were compared with those of the dead. Results After rapid decompression, 8 rabbits died within 30 minutes, while the other 6 rabbits survived and all symptoms of decompression sickness disappeared 24 hours after decompression. The plasma level of ET-1 increased from 1.33?0.33pg/ml to 2.74?0.87pg/ml after a 30min stay under 0.55MPa, while the activity of vWF increased from 2.62?0.69% to 3.64?1.48%. Compared with the surviving rabbits, those dead rabbits showed significant reduction in FIB (0.92?0.12g/L) and D-Dimer (55.63?12.12ng/ml), after rapid decompression. Conclusions There was a release of vasoactive substance in the blood of rabbits during the period when they stayed under high pressure. After rapid decompression, the most important difference between the survivors and the dead was that there were stronger coagulation activation, more consumption of FIB and weaker secondary fabrinolysis in the latter compared with the survivors.

BACKGROUND:As an important industrial solvent,benzene can cause DNA damage,chromosome aberrence,formation of DNA adducts and gene mutation. OBJECTIVE:To explore the effects of benzene on DNA and the mechanism,as well as the changes of antioxidase system it caused. DESIGN:Randomized case control study. SETTING:The Department of Clinical Laboratory of First Affiliated Hospital and Public Health College of Harbin Medical University. PARTICIPANTS:The experiment was completed in the Animal Centre in Public Health College,Harbin Medical University.Twenty-four healthy male mice of Kunming species weighed between 18 g to 22 g were chosen.The mice were provided by Experimental Animal Centre of Second Affiliated Hospital,Harbin Medical University. INTERVENTIONS:The mice were divided into control group,low dose benzene group and high dose benzene group.Inhaling benzene smoke method was used 4 hours per day to cause benzene poisoning to mice except those of the control group.The mice were executed two months later to separate marrow cells and peripheral lymphocytes and remove liver,spleen and brain to make homogenate. MAIN OUTCOME MEASURES:Single cell gel electrophoresis (SCGE) was used to assay the DNA damages of marrow cells and peripheral lymphocytes.Meanwhile,the contents of superoxide dismulase(SOD),glutathione peroxidase(GSH-Px) and malondialdehyde(MDA) in liver,spleen and brain tissues were also detected. RESULTS:The comet percentage of marrow cells and peripheral lymphocytes in two benzene poisoning groups were(83.56± 10.28),(92.54± 15.93)% ,and(41.27± 6.03)% ,(65.79± 11.62)% respectively which were much higher than those in control group[(4.13± 0.52)% ,(2.21± 0.31)% ](P< 0.01) and represented dose-response relationship.The SOD activity of liver homogenate and GSH-Px activity of high dose and low dose groups were (11 573.31± 1 938.72),(12 574.68± 1 938.72) nkat/g and (309.40± 82.85),(375.41± 55.18) nkat/g respectively which were much lower than those in control group [(16 668.67± 3 137.96),(588.62± 110.52) nkat/g] (P< 0.05).However, there was no significant difference between different dose groups. The GSH-Px activity in spleen homogenate in two experimental groups was(421.75± 124.02) and(523.10± 45.18) nkat/g respectively which was much lower than that of control group [(618.42± 57.01) nkat/g](P< 0.05) and there was significant difference between two groups (P< 0.05).In the brain homogenate of both benzene groups,the GSH-Px activity was(87.35± 19.84) and(95.02± 14.00) nkat/g respectively which was much lower than that of control group[(118.36± 7.67) nkat/g] (P< 0.05) and without difference between two groups.The MDA content in brain homogenate of high dose group was(3.99± 1.15) μ mol/mg which was much higher than that of control group [(2.58± 0.53) μ mol/g] (P< 0.05). CONCLUSION:Chronic benzene poisoning can cause DNA impairment of marrow cells and peripheral lymphocytes and reduce the activity of antioxidase.

Medical laboratories provide test data and consultation services and are engaged in ensuring test results being timely,accurate and reliable,which are satisfactory for their service recipients.A summary of the customer satisfaction theory and quality management system,and an analysis of problems found in the quality management of such laboratories,attempt to pinpoint underlying causes of service quality setbacks.Based on such studies,the quality management system is built in accordance with customer satisfaction theory and CNAS-CL02 Accreditation Criteria for the Quality and Competence of Medical Laboratories (ISO 15189:2007).Such efforts aim to continuously improve service quality and ensure customer satisfaction.