38 molars diagnosed as early cracked teeth and without pulpitis were selected to carry out the clinical observation. All the teeth were prepared and restored by metal crown under local anesthesia. After 1-15 years follow-up, the efficiency was 84.20% and all the tested teeth showed no symptoms of pulpitis and kept good chewing function. The results suggests that for the teeth diagnosed as early cracked molars and without pulp inflammation, making metal crown with less dentin loss is a safe and scientific treatment method.

Objective: To study the influence of different inhibition conditions for center of rotation (CR) and regularity variations of CR before and after orthodontic treatment of embedded and inverted impact upper central incisor. Methods:Based on clinical findings a computer model of rolling movement was established,then computer finite element Super DrawnⅡwas applied to establish an analytic analogue computing model for calculation. Results:The deeper the crown embedded by hard tissue,the more the edgewise displacement of CR;while the crown was normally exposed,the moving locus tended toward front and upward. Conclusions: Perpendicular orthodontic force to the long axis of tooth forced point that close to the incisal margin and the partly embedded crown by the alveolar bone,especially the bone of lingual aspect are the main factors for the upward moving and erectness of the root apex. Possible subsidence of CR may be avoided by suitable early stage orthodontic treatment.

Objective:To evaluate the linearity change of hard tissue of the juvenile of Class II division 1 with mandible functional retrusion by IMGA. Methods: The pre- and post- treatment cephalometric of 12 juvenile patients with IMGA were analyzed in Pancherz analysis to compare the dental position and the skeletal change. Results: After treatment, as far as OLp plane, the statistical changes were significance by pg/OLp,mi/OLp,ii/OLp, co/OLp +pg/OLp,is/OLp -ii/OLp,ms/OLp -mi/OLp,is/OLp-ss/OLp(P0.05), respectively. Conclusion: The IMGA is effective on the treatment of the juvenile patients of Class II division 1 with mandible retrusion of facial hypodivergency.

AIM: To explore the mechanism underlying inducible nitric oxide (NO) caused injury of endothelial cells during inflammation. METHODS: The activity of iso-enzymes of NO synthase (NOS), NO level and iNOS expression were examined using NADPH method, Griess reaction and RT-PCR, respectively. Furthermore, the lactate dehydrogenase (LDH) release rate, malondialdehyde (MDA) content were also measured. RESULTS:Co-administration of cytokines (TNF-? 5?10 5 U/L, IL-1? 2?10 5 U/L, INF-? 2?10 5 U/L) and LPS (10 mg/L) caused an obvious increase in NOS activity, NO levels (about two-fold) and a significant injury of the cells. At the same time, a significant increase in iNOS mRNA was also detected. Wheareas, treatment of the cells separately with cytokines or LPS for 24 h had no significant effect on NOS activity and NO level in cell lysates, however, it caused a significant increase in LDH release and MDA content. Also, the effect of cytokines and LPS on cell viability was concentration-and time-dependent. L-NMMA, a inhibitor of NOS, can suppress inducible NO production and protect cells against NO induced injury. CONCLUSION:Co-administration of cytokines (TNF-?, IL-1? and INF-?) and LPS significant activated iNOS and NO production which, in turn, induced oxidative reaction in endothelial cells.

AIM: To explore the effect of aspirin on inducible nitric oxide synthesis and gene expression under inflammation in endothelial cells. METHODS: Using NADPH, Griess methods and RT-PCR, the activity of isozymes of NO synthase (NOS), nitric oxide (NO) level, and iNOS mRNA expression were examined respectively. Also, the lactate dehydrogenase (LDH) release rate, malondialdehyde (MDA) content and cell viability were measured. RESULTS: Aspirin (3 mmol/L) reduced inducible NO production and NOS activity(P

AIM: To explore the regulatory effects of ferritin expression and intracellular iron change on aspirin resistance to oxidative damage in endothelial cells. METHODS: Using ELISA to measure the levels of ferritin expression under different aspirin concentrations, in the presence of iron cheltor desferioxamine and add to FeCl 3. Then using RNA-protein bandshift assay and RT-PCR to examine the activation of IRP and the expression of IRP 2 mRNA onaspirin induced ferritin formation. RESULTS: Aspirin at low concentration (0.1mmol/L) induced significant increase in ferritin expression in a concentration-dependent fashion up to 25% over basal levels. Aspirin induced cytoprotection from H 2O 2 damage increased significantly following ferritin formation in endothelial cells.However, in the presence of iron chelator desferrioxamine, aspirin enhanced ferritin synthesis was abrogated with a 3 fold increase in the activity of IRP and significant increase in IRP 2 mRNA level. In contrast, FeCl 3 and aspirin both increased the level of induced ferritin synthesis with significant decrease in IRP activity and IRP 2 mRNA level. CONCLUSION: The effect of aspirin induced ferritin synthesis on resistance to oxidative damage in endothelium was operated through down-regulating IRP activation and IRP 2 mRNA level.