The bone marrow compartment contains several cell populations, including mesenchymal stem cells (MSCs) that are capable of differentiating into adipogenic, osteogenic, chondrogenic, and myogenic cells.
Bone marrow failure syndromes (BMFS) typically present with a marked reduction of peripheral blood cells due to a destroyed or dysfunctional bone marrow compartment.
We predict that the ability to tissue engineer a morphologically intact and functional large-volume bone organ with a humanized bone marrow compartment will help to further elucidate physiological or pathological interactions between human HSCs and their native niches.
Retroviral gene therapy combined with bone marrow stem cell transplantation can be used to generate mice with ectopic gene expression in the bone marrow compartment in a quick and cost effective manner when compared to generating and maintaining transgenic mouse lines.
Moreover, 18F-FLT PET/CT was characterized by high background activity in the bone marrow compartment, further complicating the evaluation of bone marrow lesions.
Interestingly, two patients with the initial diagnosis of SMM demonstrated focal bone marrow lesions and were classified as symptomatic MM. 18F-FLT PET/CT was characterized by high background activity in the bone marrow compartment (Fig. 2).
Another finding of our analysis is the high background 18F-FLT activity in the bone marrow compartment, which further complicates the evaluation of bone marrow lesions in 18F-FLT PET/CT.
Normal 18F-FLT distribution is characterized by high background activity by the bone marrow compartment (e.g., vertebral column, pelvic skeleton, proximal femora) reflecting the high proliferative activity of hematopoietic cells Fig. 3 Transaxial 18F-FDG PET/CT (a) and 18F-FLT PET/CT (b) images at the pelvic level of a 65-year-old male patient with initial diagnosis of MM.
Splenomegaly often reflects an expansion of cellular proliferation outside of the bone marrow compartment, and is called extramedullary hematopoiesis (EMH).
MSCs are also essential for the proliferation and differentiation of hematopoietic cells within the bone marrow compartment [3] [5].
Thus, arginase activation by diclofenac happens either in differentiated macrophages or the mediators needed for promoting diclofenac- induced- activation of arginase do not reach the bone marrow compartment.
