Medicine as a global profession should undoubtedly possess a common set of value, scientific knowledge and skill. Based on such agreement, many national or international organizations are recently trying to create standards for medical education. These standards can be basically classified into"process standard"and"content standard", the latter emphasizes the results of so-called outcome assessment, the educational evaluation of which must be more substantial. The Institute for International Medical Education(IIME), an international organization established in 1999 in New York, is striving to defy the Global Minimum Essential Requirements in Medical Education, test their validity and feasibility in a few countries and popularize them to the medical cycle in the future.

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.

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 whether AT2 receptor is expressed in skeletal muscular vasculature, and the expression of angiotensin Ⅱ receptors in pulmonary circulation of children with left-to-right shunt but without obstructive pulmonary hypertension. METHODS: Lung and skeletal muscular tissue were obtained from 20 children with left-to-right shunt by biopsy during operation. These skeletal muscular tissues were detected by reverse transcriptase/polymerase chain reaction (RT-PCR ) and immunohistochemistry techniques for AT2 receptors. mRNA of AT1 and AT2 receptors in lung tissues were detected by RT-PCR and analyzed semi-quantitatively. RESULTS: In all of the skeletal muscular tissues, mRNA of AT2 receptor was found by RT-PCR, and the results of immunohistochemistry staining for AT2 receptor of vessels were positive. In the lung tissues, the level of mRNA of AT2 receptor was different to AT1 receptor, and the former was higher than the latter (P