Erythroid-specific 5-aminolevulinate synthase (ALAS2) catalyzes the rate-limiting step in heme biosynthesis.
红系特异的5-氨基酮戊酸合成酶（ALAS2）是血红素生物合成的限速酶。
Easily pumped liquid bone marrow aspiration showed erythroid hyperplasia mainly.
骨髓吸液易抽，示红系增生为主。
Note the presence of megakaryocytes, erythroid islands, and granulocytic precursors.
可见巨核细胞，红细胞岛和粒细胞前体细胞。
Moreover, erythroid colonies could be grown from blood samples without the need for exogenous erythropoietin.
此外，在没有促红细胞生成素的血样中红细胞可以繁殖。
To investigate effect of plasma of patients with different dialysis modes on marrow erythroid progenitors of mice.
目的观察不同透析方法治疗的尿毒症患者的血浆对小鼠骨髓红系造血祖细胞的影响。
Erythroid-specific 5-aminolevulinate synthase (ALAS2) catalyzes the rate-limiting step in heme biosynthesis of erythroid cells.
红系特异的5-氨基酮戊酸合成酶（ALAS2）是红系细胞血红素生物合成的限速酶。
Objective: to understand the changes in hematopoietic growth factor receptors during erythroid differentiation of pluripotent cells.
目的：了解多潜能造血祖细胞向红系分化过程中造血因子受体的改变。
The results suggested that the two fragments contain enhancer-like elements and they function in a certain erythroid-specific manner.
结果说明这两段顺序均有增强子活性，并且这种活性具有一定的红细胞特异性。
Objective To investigate the growth of endogenous erythroid colony (EEC) in polycythemia vera (PV) patients and its clinical significance.
目的了解真性红细胞增多症(PV)患者内源性红系集落(EEC)生长情况及其临床意义。
Methods Induce the differentiation of erythroleukemia cell line HB60-5 to mature erythroid cells by altering the culture condition and plot a cell growth curve.
方法利用红白血病细胞株hb60 - 5的生长特性，通过改变培养条件，促使细胞向成熟细胞分化。
This is the appearance of normal bone marrow smear at high magnification. Note the presence of megakaryocytes, erythroid precursors, and granulocytic precursors.
高倍镜下的正常骨髓涂片，可见巨核细胞，红细胞前体细胞和粒细胞前体细胞。
Objective To investigate the roles of mouse erythroid differentiation and denucleation factor (MEDDF), newly cloned in our laboratory, in erythroid terminal differentiation.
研究小鼠红细胞分化去核分化因子（MEDDF）在红细胞终末分化中的功能。
The absence of ALAS2 leads to maturation arrest of primitive erythroid cells. Heritable mutations of ALAS2 gene are responsible for the human X-linked sideroblastic anemia (XLSA).
ALAS2的缺失能导致红细胞发育的停滞，ALAS2基因的遗传性突变能引起X-连锁的成高铁红细胞贫血（XLSA）。
The absence of ALAS2 leads to maturation arrest of primitive erythroid cells. Heritable mutations of ALAS2 gene are responsible for the human X-linked sideroblastic anemia (XLSA).
ALAS2的缺失能导致红细胞发育的停滞，ALAS2基因的遗传性突变能引起X-连锁的成高铁红细胞贫血（XLSA）。
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