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The data suggest that Desertliving Cistanche Polysaccharides may promote the bone marrow cellcycle transition and the recovery of Hematopoietic function in bone marrow depressed anemia mice, accelerate haematogenesis in rubrum strain and macronucleus strain.

肉苁蓉多糖可能通过促使骨髓抑制贫血小鼠骨髓细胞细胞周期的转化,促进骨髓造血功能的恢复,并促进红系巨核系造血。

The data suggest that Desertliving Cistanche Polysaccharides may promote the hone marrow cellcycle transition and the recovery of Hemstopoietic function in bone marrow depressed anemia mice, accelerate haematogenesis in rubrum strain and macronucleus strain.

肉苁蓉多糖可能通过促使骨髓抑制贫血小鼠骨髓细胞细胞周期的转化,促进骨髓造血功能的恢复,并促进红系巨核系造血。

Objective To investigate the role of antiapoptotic Bcl-x protein in megakaryocyte differentiation and maturation.

目的 研究抗凋亡蛋白Bcl-x在巨核细胞分化和成熟过程中的作用。

hNUDC may play an important role in megakaryocyte proliferation and differentiation.

hNUDC对促进造血干细胞增殖和分化为巨核细胞具有重要作用。

To investigate the prognostic significance of bone marrow megakaryocyte in patients with Idiopathic thrombocytopenic purpura.

目的 探讨特发性血小板减少性紫癜患者骨髓巨核细胞数与预后的关系。

He results indicate that both of them have the same MK-CSA and can potentiate IL-3dependent megakaryocyte colony formation.

PO与IL-3和IL-6同时存在时,能够进一步促进巨核细胞集落的生成。

These results propose that GSNO can facilitate platelet production from megakaryocyte, and it may be partly through cGMP pathway.

这些结果提示,GSNO可以促进脐带血 CD34+细胞来源的巨核细胞产生具有一定功能的血小板,其产生的机制可能部分与 cGMP途径有关。

The intrinsic defect of megakaryocyte progenitor cell is considered to be a primary pathogenesis of APATP.

巨核祖细胞的内在缺陷是APATP的主要发病机制。

Pathogenic mechanism is mainly by inhibiting bone marrow and megakaryocyte function, direct destruction of platelets and induce allergic work.

致病机制主要是通过抑制骨髓和巨核细胞的功能,直接破坏血小板和诱导机体变态反应起作用。

Objective:To study the capacity of differentiate committedly of recombinant human thrombopoietin on megakaryocyte progenitor cells in peripheral stem cells.

摘 要 目的:探讨重组人促血小板生成素对外周造血干细胞中巨核系祖细胞的定向诱导分化能力。

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