AIM:To investigate effect of recombinant human thrombopoietin on exsanguine thrombocytopenia mice. METHODS:Normal peripheral platelet counts were performed on sample obtained from the tail vein of purebred Babl/c mice including experimental and control groups before experimentation. rhTPO was injected into the mice by intraperitoneal injection once a day for 7 days. On the seventh and the fourteenth day, the mice were phlebotomized from the supra-obitalis vein in order to make exsanguine thrombocytopenia animal model. At the same time, we observed the biological activity of recombinant human thrombopoietin in vivo and the mice's death rate. RESULTS: On the seventh day and the fourteenth day, platelet counts of mice treated by rhTPO were higher than those by PBS (P＜0.05). Moreover the platelet counts of mice in experimental group of rhTPO showed increasing tendency following experimental days. In addition, death happened in two groups after those mice were phlebotomized from the supra-obitalis vein, but the death rate in negative control group was evidently higher than that in experimental group (P＜0.05). CONCLUSION:rhTPO had obvious biological activity in increasing platelet production, which resulted in the drop in thrombocytopenia mice's death rate.

AIM:To investigate the potential of differentiatng into myocytes of the granulocyte colony-stimulating factor(G-CSF)-mobilized CD34 + cells. METHODS: Three hours after intraperitoneal injecction of isoprenaline(ISO) to develop acute ischemic model, rats' bone marrow hematopoietic stem cells were mobilized to the site of myocardial infarction by G-CSF. The techniques of immunohistochemisty and HE stain were used to detect the infiltration of CD34 + cells and the regeneration of myocytes in the infarct zones. RESULTS: 24 hours after administration of ISO , a large amount of infiltrative monocytes and regenerative myocytes which were CD34 positive expression could be found in the infarct zones of the G-CSF treatment group, while majority of the infiltrative inflammatory cells in control group were neutrophils and there was no infiltrative cells and myocytes which were CD34 positive expressio, 2 weeks after administration of ISO, there were a plenty of scar in control group, but not in the G-CSF treatment group. CONCLUSION: G-CSF-mobilized CD34 + cells possess the potential to differentiate into myocytes and it may be used in treating acute myocardial infarction.

AIM:To investigate effects of thrombopoietin(TPO) and TPOⅡ on human platelet activation in vitro. METHODS:Human platelets were incubated in the phosphate-buffered saline containing rhTPO or TPOⅡ at the concentration of 100 μg/L for five minutes. In order to determine the rate of platelet activation. The CD62P and CD41 expressions on platelets were analysed by flow cytometry using fluorescence labelled monoclonal antibody to CD62P and CD41. RESULTS:The results demonstrated that expression of CD62P on platelets which were incubated with rhTPO or TPOⅡ didn't increase compared with that of contrast group. CONCLUSION:Both rhTPO and TPOⅡdidn't cause the disorder of platelet activation.

AIM: To investigate the biological activity of thrombopoietin Ⅱ(TPOⅡ) in vivo , which consists of two new kinds of ligand binding with thrombopoietin receptor. METHODS: Purified ligandⅠof TPOⅡ, artificial compound ligandⅡ of TPOⅡand rhTPO were injected into purebred Babl/c mice respectively in 7 days by intraperitoneal injection once for a day. Then the biological activity of TPOⅡ was analyzed by measuring peripheral platelet counts by the end of the seventh day. RESULTS: On the seventh day, the platelet counts of mice treated by ligandⅠof TPOⅡ were higher than that in the negative control group( P 0.05). On the fourteenth day, the platelet counts increased in two all experimental groups of TPOⅡcompared with negative control group( P 0.05). Moreover the platelet counts of mice in two experimental groups of TPOⅡ and the positive group showed increase with experimental days. CONCLUSION: The purified ligandⅠof TPOⅡ had obvious activity in increasing platelet production, which is not different from the effect of rhTPO.

AIM: To investigate effects of thrombopoietin(TPO) and TPOⅡ on human platelet activation in vitro. METHODS:Human platelets were incubated in the phosphate-buffered saline containing rhTPO or TPOⅡ at the concentration of 100 ?g/L for five minutes. In order to determine the rate of platelet activation. The CD62P and CD41 expressions on platelets were analysed by flow cytometry using fluorescence labelled monoclonal antibody to CD62P and CD41. RESULTS: The results demonstrated that expression of CD62P on platelets which were incubated with rhTPO or TPOⅡ didn't increase compared with that of contrast group. CONCLUSION: Both rhTPO and TPOⅡdidn't cause the disorder of platelet activation.

AIM: To investigate the effects of granulocyte colony-stimulating factor (G-CSF)-mobilized bone marrow stem cells on treatment of the myocardial infarction in experimental rats. METHODS: Three hours after injected with isoprenaline(ISO) interaperitoneally to develop acute ischemic model, rats' bone marrow stem cells were mobilized by G-CSF and migrated to the site of myocardial infarction. The hearts were harvested from 24 hours to 2 weeks after administration of ISO for histopathological examination. RESULTS: 24 hours after administration of ISO , myocardial infarct zones scattered in the pallium of the control group ,there were a large amoumt of inflammatory cells infiltration around the infarct zones and majority of them were neutrophils. The infarction in the G-CSF treatment group was milder, majority of the infiltrative cells were monocytoid; 48 hours after administration of ISO, infarct zones expanded greatly in control group, while that of the G-CSF treatment group increased just mildly; 2 weeks after administration of ISO, there was no significant scar in the G-CSF treatment group. We also found the regeneration of myocytes in the pallium. CONCLUSION: G-CSF treatment protected the ischemic myocardium and it may be used to treat the acute myocardial infarction.

With continuous discovery of tumor immune targets and continuous changes in antibody research and development technology, antibody drugs are becoming more and more widely used in clinical practice. However, some targets are not only expressed on tumor cells, but also on red blood cells. Therefore, the clinical application of antibodies against the corresponding targets may interfere with the detection of blood transfusion compatibility, resulting in difficulty in blood matching or delay of blood transfusion. This consensus summarizes the current solutions for the interference of CD38 monoclonal antibody (CD38 mAb) in transfusion compatibility testing. After analyzing the advantages and disadvantages of different methods, polybrene and sulfhydryl reducing agents [dithiothreitol (DTT) or 2-mercaptoethanol (2-Me)], as a solution for CD38 mAb interference in blood compatibility testing, are recommended for Chinese patients, so as to eliminate blood transfusion interference produce by CD38 mAb and further provide a pre-transfusion workflow for clinicians and technicians in Department of Blood Transfusion.