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A possible explanation for our findings in BMDMs is that the aging bone marrow microenvironment causes cellular defects during differentiation, but not at the early progenitor stage.
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The activation can also trigger leukemia cell movement to the marrow microenvironment, where CXCL12 pushes leukemia cells in close contact with marrow stromal cells that lead to growth and drug resistance signals.
Even sub-lethal doses cause a deficit to the bone marrow microenvironment, including a decline in hematopoietic cells, and this deficit occurs in a dose dependent fashion.
Therefore, the ability to maintain the bone marrow microenvironment would hinder much of the trabecular bone loss caused by radiation exposure, ultimately decreasing some comorbidities in patients exposed to radiation.
The presence of a plasma cell clone in the unique microenvironment of the bone marrow causes multiple organ dysfunction through the production of the amyloidogenic light chains, while within the bone marrow microenvironment the plasma cells interact with either cellular or non-cellular components of the bone, but no data exist about this interaction.
Interestingly, bone marrow microenvironment is also a critical reservoir for DTCs.
BCP-ALL cells critically depend on interactions with the bone marrow microenvironment.
Upon infection, however, neutrophils are recruited from the bone marrow microenvironment and lose these pro-survival signals.
The decline in total bone marrow hematopoietic cells is accompanied with elevated adipocytes into the marrow cavity, thereby inhibiting hematopoiesis and recovery of the bone marrow microenvironment.
These malignancies affect normal homeostasis and reshape the bone marrow microenvironment.
The bone marrow microenvironment is vital to the development, differentiation, and regulation of the lymphohematopoietic system.
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