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DNA from bone marrow samples was genotyped on the Precision Medicine Research Array and biogeographical ancestry was quantitatively assessed using the Geographic Population Structure Origins tool.
Finally, colony formation in methylcellulose ex vivo of NF1 null CD34+/CD38- cells sorted from AML bone marrow samples was inhibited by low-dose rapamycin.NF1 null states are present in 7 of 95 (7%) of adult AML and delineate a disease subset that could be preferentially targeted by Ras or mammalian target of rapamycin-directed therapeutics.
Non-amplified RNA from the transduced murine primary bone marrow samples was used for validation with quantitative RT-PCR (qRT-PCR).
In children, microscopic detection on bone marrow samples was positive in 15/18 (83,3%).
Among the tools used for VL diagnosis, Giemsa staining and microscopic examination of bone marrow samples was the most frequently used technique (48/65 episodes, 73%).
DNA from placenta and bone marrow samples was extracted by using the DNeasy Blood and Tissue Kit (QIAGEN, Hilden, Germany) according to the manufacturer's instructions.
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Bone marrow samples were obtained at the beginning and end of the harvest.
Bone marrow samples were obtained from nine human donors after informed consent.
Bone marrow samples were tested for the presence of FeLV proviral DNA to determine FeLV latent infection.
Bone marrow samples were collected from the lesion site (P) and the iliac crest (IC) of 7 patients affected by CPT and type 1 neurofibromatosis (NF1+) and 6 patients affected by CPT without NF1 (NF1−).
In brief, bone marrow samples were accessed from the femurs and tibias of rats and diluted using low glucose DMEM containing 10% FBS.
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