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Objective To compare the clinical effect of ifosfamide in combination with liposomal doxorubicin and dexamethasone (CDD) in the treatment of relapsed/refractory multiple myeloma (MM) with or without extramedullary plasmacytoma (EMP). Methods The clinical data of 71 relapsed/refractory MM patients treated with CDD regimen from January 2011 to December 2016 were retrospectively analyzed, including 48 patients with EMP(group A)and 23 patients without EMP (group B).One cycle of the CDD treatment was 21 d or 28 d and efficacy analysis was performed after every two cycles.Results The overall response rate in group A was 43.8%(21/48)and the complete remission and near complete remission rate was 8.3%(4/48);the overall response rate in group B was 65.2%(15/23)and the complete remission and near complete remission rate was 13.0% (3/23). There were no statistically significant differences between the two groups(χ2=1.203,0.659,P>0.05).The progression-free survival (PFS)time in group A was(8.6 ± 3.3)months, while the PFS time in group B was(7.9 ± 2.5)months and there was no significant difference between the two groups(t=1.009,P>0.05).There was no significant difference about incidence rate of adverse effects between the two groups(P>0.05).Conclusions CDD regimen can be used for the treatment of relapsed/refractory MM with or without EMP, the PFS and drug related adverse effects are similar, especially in patients with EMP.
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Currently, platelet transfusion is the primary treatment for thrombocytopnia which results from intensive chemotherapy and radiotherapy of cancer. While repeated platelet transfusions are associated with several problems. The clinical availability of safe and effective platelet growth factors is eagerly awaited. Currently, a mumber of hematopoietic growth factors with thrombopoietic activity have been identified. This review discusses the biological characteristics and the clinical trial investigation development of platelet growth factors.
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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.
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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.
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AIM: To explore whether granulocyte colony-stimulating factor (G-CSF) has the function of curing ischemia cerebral infarction in rats. METHODS: Rat cerebral infarction model was stablished by line occlusion and G-CSF 60 ?g/kg was injected into abdominal cavity an hour later. The technique of TTC and HE staining and immunohistochemistry were used to detect the volume of infarction and pathological change and the infiltration of CD34 positive cells, respectively. RESULTS: The infarction volume of the rat brain was smaller in G-CSF-therapy group than infarction group 24 hours later and the pathological damage is slighter. Both CD34 positive mono-nucleus cells and CD34 positive neuron-like cells were detected in the rat brain of G-CSF-therapy group but not in the control one 24 hours later. CONCLUSIONS: G-CSF can relieve the ischemia degree and reduce the infarction volume. The possible mechanism is that G-CSF plays protection role on the ischemic neuron cells and moblizes stem cells in bone marrow, then stimulates the regeneration and plerosis of brain tissues.
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AIM: To investigate the effects of in situ transplantation of mobilized autologous bone marrow stem cells on infarction size and cardiac function in patients with acute myocardial infarction. METHODS:25 patients with first acute myocardial infarction were randomly divided into stem cells in situ transplantation group and control group, 12 patients in stem cells in situ transplantation group were injected subcutaneously with 300 ?g granulocyte colony-stimulating factor(G-CSF) daily for four days in addition to standard therapy. 13 patients in control group were treated with standard therapy alone. The conventional 12 leads electrocardiogram were recorded on 1, 28 days after admission and the cardiac function was scored by the QRS scoring system proposed by Wagner. Furthermore, the infarction size was assessed by radionuclide myocardial perfusion imaging 7, 28 days after admission. RESULTS:4 weeks after admission, the QRS scores decreased, the infarction size reduced significantly in the stem cells in situ transplantation group (from 36.0%?8.3% to 18.0%?5.8%, P
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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.
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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.
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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.