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This review will highlight the importance of bone marrow microenvironment in maintaining bone marrow HS/PC populations and the contribution of these key populations in microvascular repair during the natural history of diabetes.
Previous studies indicate an important homeostatic role of Cxcl5 in maintaining bone marrow neutrophil numbers [ 34].
This suggests that the graft exerts a greater effect on maintaining bone marrow remission and that peripheral leukaemic cells may evade detection leading to relapse.
Although the role of individual ECM component in maintaining bone marrow niches has not been precisely defined, dynamic interaction of adhesion molecules, growth factors, and chemokines with receptors on cell surface are involved in lodging and homing of hematopoietic progenitors and effector B cells [ 31, 33, 36, 37].
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As HSPCs, the source of the blood cells in the bone marrow, are primarily responsible to maintain bone marrow homeostasis, we further analyzed a subset of HSPCs (Lin−, Sca-1+, c-Kit+, hereafter referred to as LSK cells).
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.
Prophylaxis was started concomitantly with the induction chemotherapy or the conditioning regimen (HCT), and was maintained until bone marrow recovery or fever.
They are maintained within bone marrow (BM) stem cell niches and released upon induced mobilization (see below), as firstly demonstrated by Asahara and colleagues [ 12].
To achieve osteogenic differentiation and maintain bone mass, MSCs within the bone marrow (BM) proceed through a number of functional stages including proliferation, matrix maturation and mineralization.
Mesenchymal stem cells (MSCs) from the bone marrow are progenitors of osteoblasts, the cells that build and maintain bone tissue.
For example, the actin reorganization required for phagocytosis was fully maintained in bone marrow-derived murine macrophages subjected to prolonged LT treatment (strain C57Bl/6; unpublished observations).
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