The improvement of diagnostics teaching system,including the establishment of curriculum system and evaluation system,is the base of promoting clinical- medicine teaching.Our study showed that the theoretical knowledge and clinical skill of medical students could be improved by constructing clinical diagnostics curriculum system and improving organization management and assessment system,which could pave the way for the transition from medical students to clinicians.

Objective To explore the effect of core stability training (CST) on motor of upper limbs after stroke. Methods 60 patients with stroke were divided into observation group (n=30) and control group (n=30). Both groups accepted routine medicine and motor relearning program, and the observation group accepted CST before training. They were assessed with Simple Test for Evaluating Hand Function (STEF), modified Barthel index (MBI), and the Trunk Control Test (TCT) before and 4 weeks after treatment. Results The scores of STEF,MBI, and TCT improved after treatment in both groups (P<0.01), and improved more in the observation group than in the control group (P<0.01). Conclusion CST may facilitate the motor recovery of upper limbs after stroke.

H2S has a role of protecting neurons from ischemia-reperfusion injury and significantly reducing the cerebral infarction area, but high concentration of H2S can induce neurotoxicity. Memantine, a N-methyl-D-aspartic acid(NMDA)receptor antagonist, could reduce the neurotoxicity of H2S at high concentration. Nine novel structures(compounds I1-I9)were designed by coupling(4-hydroxy phenyl)-3H-1, 2-dithiole-3-thione(ADT-OH)with memantine through alkanes as linkers and synthesized by four-step reactions from ADT-OH. Their neuroprotection against damage induced by glutamate on HT-22 cells was evaluated by MTT method. The results indicated that these compounds markedly increased the survival rates of damaged HT-22 cells at the concentration of 1 μmol/L(P< 0. 01), which suggested that these compounds could preferably protect neurons against damage induced by glutamate.