Objective: To investigate the effects and mechanism of transhinone on calcium overloaded injuried models.Methods: Three injured models induced by caffeine, KCI, and NMDA, respectively, were used to assay the action of tanshinone in cultured primary cortex neurone of baby rats. Results: It was found that tanshinone possessed obvious protective effects on primary neurone in injured models by the way of morphological examination. Crystal violet staining and lactic dehydrogenase (LDH) measurement in supernate also indicated that tanshinone increased number of live neurone and reduced the extent of cell injury significantly.Conclusion: Tanshinone protected rat cortex cells from three kinds of calcium overloadied injured effectively in vitro.

Objective: To investigate the protective effect and mechanism of total peaony glycoside (TPG) on calium overloading injury of nerve cells in rat models. Methods: The nerve cells of cerebral cortex of primary rats were subject to tissue culture,and the calcuim-overloading injury models were induced by caffeine,KCl and NMDA respectively. Results:TPG possessed obvious protective effects on the nerve cells in rat models, increased the number of survival nerve cells and reduced the content of LDH released nerve cells.Conclusion: TPG can protect rat nerve cells with calium-overloading injuriy.

AIM To investigate protective effects and mechanism of tanshinones on ischemia-like injury models. METHODS Six ischemia models including hypoxia, hypoglucose, oxidant injury, caffeine injury, nitric oxide neurotoxicity and excitatory amino acid injury were used to assay the anti-ischemic roles of tanshinones in cultured primary cortex neurons. The changes of injuried cortex neurons were observed by the way of morphological examination, and live neurons of crystal violet staining were measured according to absorbent index. RESULTS it was found that tanshinones possessed obvious protective effects on primary neurons in injury models by the way of morphological e~nation. Crystal violet staining also indicated that tanshinones increased number of live neurons in injury models significantly. The protective effects of tanshinones on models of oxidant injury, caffeine injury and NMDA injury were superior to other injury models. CONCLUSIONS 83.0 ?mol? L- 1 tanshinones protected rat cortex cells fm all injury models effectively in vitro.

AIM　To investigate protective effects and mechanism of tanshinones on ischemia-like injury models. METHODS　Six ischemia models including hypoxia, hypoglucose, oxidant injury, caffeine injury, nitric oxide neurotoxicity and excitatory amino acid injury were used to assay the anti-ischemic roles of tanshinones in cultured primary cortex neurons. The changes of injuried cortex neurons were observed by the way of morphological examination, and live neurons of crystal violet staining were measured according to absorbent index. RESULTS　It was found that tanshinones possessed obvious protective effects on primary neurons in injury models by the way of morphological examination. Crystal violet staining also indicated that tanshinones increased number of live neurons in injury models significantly. The protective effects of tanshinones on models of oxidant injury, caffeine injury and NMDA injury were superior to other injury models. CONCLUSIONS　83.0 μmol*L-1 tanshinones protected rat cortex cells from all injury models effectively in vitro.

Clinical hematology and hematologic examination is a strong practical curriculum, and experimental class is very important in the aspects of teaching.In order to improve the quality of teaching and train compound laboratory talents with high quality,several effective reform mea-sures were carried out based on the years of teaching practice by the department:improving the methods of experimental teaching;using modern means of teaching;emphasizing on the analysis of experimental results,formulating the rigorous experimental evaluation system and starting the second class etc.

Objective To study the clinical value of human kallikrein 2 detection on the early diagnosis ,prognosis and therapeu‐tic means of patients with prostate cancer .Methods 25 patients with prostate cancer and 25 patients with benign prostatic hyper‐plasia who were treated in affiliated hospital of Guangzhou Medical University between January 2015 and December 2015 were se‐lected as research objects .Their human kallikrein 2 and prostate specific antigen level were detected by ELISA and RIA .25 cases of prostatic cancer after operation of our hospital in synchronization were randomly selected as research objects and their human kal‐likrein 2 level was detected and analysed .All the data was modeling processed by SPSS21 .0 .Results Human kallikrein 2 level of PCa group ,BPH group and healthy group was(75 .5 ± 24 .5)ng/L ,(23 .3 ± 5 .8)ng/L and(22 .2 ± 3 .56)ng/L respectively ,which of PCa group was higher than that of BPH group and healthy group .The difference had statistical significance(P<0 .05) .The specific and accuracy of hK2 detecting PCa was 89% and 78% .Compared with before operation[(80 .2 ± 24 .5)ng/L] ,hK2 level of 25 pa‐tients with prostate cancer[(34 .4 ± 10 .5)ng/L] significantly decreased and the difference had statistical significance(P<0 .05) . Conclusion On diagnosing prostate cancer ,human kallikrein 2 can improve specific detection ,reduce unnecessary detected rate and provide the new direction for early clinical detection ,prognosis and therapy .It deserves further promotion .

Aim To investigate protective effects and mechanism of TPG on ischemia_like injury models. Methods Six ischemia models including hypoxia, hypoglucose, oxidant injury, calcium overload, nitric oxide neurotoxicity and excitatory amino acid injury were used to assay the anti_ischemic roles of TPG in cultured primary cortex neurons. Results It was found that TPG possessed obvious protective effects on primary neurons in injury models by the way of morphological examination. Crystal violet staining also indicated that TPG increased number of life neurons in injury models significantly. Couclusions 50～200 ?g?ml-1 TPG protected rat cortex cells from all injury models effectively in vitro.