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In these diseases, there is an increase in DNA damage and a risk of progression to acute leukemia.

该病中DNA损伤和发展为急性白血病的风险增加。

Some leukemogenesis has been shown to be aberrance of epigenetic modification.

白血病的发生和发展与表观遗传修饰异常直接相关。

INHIBITORY EFFECTS OF ANTHRAQUINONE DERIVATIVES ON P 388 LEUKEMIA IN MICE

蒽醌衍生物对小鼠P388白血病的抑制作用

The significance of combined therapy of arsenic trioxide and alltrans retinoic acid in treating acute promyelocytic leukemia.

全反式维甲酸联合三氧化二砷治疗初发急性早幼粒细胞白血病的疗效观察。

Objective:To observe the therapeutic efficacy and side effect of all-trans retinoic acid combined with arsenic trioxide(As2O3)on newly-diagnosed patients with acute promyelocytic leukemia.

目的:观察全反式维甲酸联合三氧化二砷(As2O3)治疗初发急性早幼粒细胞白血病的疗效和不良反应。

An D-dimeride analysis of the therapeutic effects and reactions in treating acute promyelocytic leukemia with intravenous arsenic trioxide or all-trans retinoic acid.

三氧化二砷不同给药方法治疗急性粒细胞白血病的临床观察和随访。

To investigate the mechanism of Arsenic Trioxide treatment to Leukemia.

目的 探讨三氧化二砷(As2O3)治疗白血病的作用机制。

Immunohistochemical method was used to detect avian leukosis virus subgroup J from egg-type chicken, which was preliminarily diagnosed to appear subgroup J avian leukosis. The organs from these chickens were examined by ALV-J gp85 monoclonal antibody, these organs included marrow, liver, spleen, kidney, lung, heart, pancreas, oviduct, ovary, ventriculus glanduaris, skeletal muscle, cerebrum, ischiacticus nerve.

采用免疫组化法,对病理学初步诊断为蛋用型鸡 J亚群白血病的自然发病鸡的肿瘤、骨髓、肝脏、脾脏、肾脏、肺脏、心脏、胰脏、输卵管、卵巢、腺胃、骨骼肌、大脑、坐骨神经,用特异性抗 J亚群禽白血病病毒囊膜糖蛋白gp85的单克隆抗体进行检测,待检的组织切片中均检出阳性抗原,免疫组化的研究结果与病理学诊断结果相一致。

Yelodysplastic syndromes,as a disease of dyspoiestichematopoietic stem cell,have a disturbance of DNA synthesis,cellsdifferentiation and some leudemic characterization.It's marrow cell displaylike megaloblastic change,so we postulated that folate receptor have adifference of both quantitative and quanlititive in megalolbastic anemia,MDSand lenkemia.

DS作为异常干细胞克隆性增生疾病,在DNA的合成及细胞分化异常,表现出白血病的某些特征和骨髓细胞具有不同程度的巨幼变,因而我们推测巨幼贫、白血病和MDS的叶酸受体不但有量的改变,而且有质的变化。

Meanwhile,HDAC1 acetylation level is significantly increased.The overexpression of HDAC1 can promote erythroid cell proliferation and inhibits induced differentiation,the knockdown of HDAC1 or 2 inhibits erythroid cell proliferation and promotes induced differentiation.We also found that HDAC1 affects GATA1 mediated transcription activity.Thus our data revealed that HDAC1 may negatively regulate GATA1 mediated transcription and suggest that the dynamic regulation of GATA1 associated NuRD/MeCP1/HDAC1/HDAC2 complex may determine the onset of erythroid differentiation programs.Moreover,this study will eventually help to design new therapeutic approaches in treatment of leukemia.

研究发现在被诱导分化的小鼠红细胞白血病细胞中与GATA1相结合的HDAC1被乙酰化并失去活性,在血细胞中过表达HDAC1能够促进血细胞的增殖并抑制分化,反之在血细胞中敲除HDAC1或HDAC2能抑制血红细胞的增殖并促进分化,而且HDAC1能够负调控GATA1的转录活性,GATA1与NuRD/MeCP1复合体之间的动态调控,决定血红细胞分化的发生和发展,并为探索白血病的致病机理奠定了理论基础。

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