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Academic literature on the topic 'Bone marrow precursors'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Bone marrow precursors"

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Vermeer, Jenny A. F., Ineke D. C. Jansen, Matangi Marthi, Fraser P. Coxon, Charles E. McKenna, Shuting Sun, Teun J. de Vries, and Vincent Everts. "Jaw bone marrow-derived osteoclast precursors internalize more bisphosphonate than long-bone marrow precursors." Bone 57, no. 1 (November 2013): 242–51. http://dx.doi.org/10.1016/j.bone.2013.08.007.

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Hackett, J., M. Bennett, and V. Kumar. "Origin and differentiation of natural killer cells. I. Characteristics of a transplantable NK cell precursor." Journal of Immunology 134, no. 6 (June 1, 1985): 3731–38. http://dx.doi.org/10.4049/jimmunol.134.6.3731.

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Abstract To study the origin and differentiation of natural killer (NK) cells, we developed an assay for the transplantable precursor of NK(YAC-1) cells present in the bone marrow. Mice were depleted of endogenous NK(YAC-1) cells by injection of anti-asialo GM1 antibody, followed by lethal whole body irradiation. Normal syngeneic bone marrow cells were transplanted into such pretreated mice. Regeneration of NK(YAC-1) activity in the recipient mice was monitored by two different assays: the ability of spleen cells to lyse YAC-1 cells in vitro and the ability to clear i.v. injected, 125IUdR-labeled YAC-1 cells from the lungs. With both assays, a dose-response relationship between the number of bone marrow cells injected and the degree of NK(YAC-1) activity generated could be demonstrated. However, the lung clearance assay appeared superior because the NK regeneration could be detected earlier and with lower numbers of injected marrow cells. With this assay, several characteristics of the NK precursors and their differentiation could be defined. 1) The generation of mature, lytic NK cells from their transplantable precursor requires an intact "marrow microenvironment" in the recipient mice, because differentiation failed to occur in mice rendered osteopetrotic by estradiol treatment. 2) The NK(YAC-1) precursors lack the surface antigens (NK-2.1, asialo GM1, Qa-5, Thy-1) that are characteristically seen on mature NK cells. 3) The NK-precursors could be eliminated from the bone marrow with anti-Qa-2 or anti-H-2 antisera + complement, indicating that these two antigens are expressed on the precursors. The relationship between NK(YAC-1) precursors and multipotent myeloid stem cells (CFU-S) was investigated by utilizing W/Wv and Sl/Sld mutant mice. Bone marrow cells of W/Wv anemic mice, although markedly deficient in CFU-S, have a normal frequency of NK(YAC-1) precursors. Sl/Sld mice that lack a suitable microenvironment for the development of CFU-S allowed normal differentiation of NK(YAC-1) precursors when transplanted with normal bone marrow cells. Together, these data suggest that multipotent myeloid progenitor cells, as defined by the CFU-S assay, and the NK(YAC-1) precursors are not closely related.
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Mori, Shinichiro, Ken Shortman, and Li Wu. "Characterization of thymus-seeding precursor cells from mouse bone marrow." Blood 98, no. 3 (August 1, 2001): 696–704. http://dx.doi.org/10.1182/blood.v98.3.696.

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Abstract The nature of the cells that seed the thymus of an irradiated recipient after intravenous (IV) transfer of bone marrow (BM) cells was investigated using 2 approaches. First, direct entry of a small number of donor BM cells into the thymus was tracked using a Ly-5 marker. Second, secondary IV transfer of the seeded thymus cells into a secondary recipient was used as an assay for precursor activity. A range of cell types was found to enter the recipient thymus initially, including B-lineage cells and myeloid cells, but T precursors were undetectable by flow cytometry over the first few days. Although all cells initially entering the thymus proliferated, no sustained thymus reconstitution was seen until day 4, when recognizable T-lineage precursors began to appear. The secondary transfer assays revealed the presence of lymphoid precursors in the recipient thymus, including T, NKT, NK, and B precursor activity, with a notable early burst of B-lineage generative capacity. There was no evidence of sustained myeloid precursor or multipotent stem cell activity, even though these were seen if BM cells were injected directly into the recipient thymus rather than introduced into the bloodstream. It is concluded that even though many cell types may initially enter an irradiated thymus, the thymus acts as a sieve, allowing lymphoid precursors, but not multipotent stem cells, to seed the environmental niches that permit selected precursor cell development and thymus reconstitution.
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Kruger, M. G., and R. L. Riley. "The age-dependent loss of bone marrow B cell precursors in autoimmune NZ mice results from decreased mitotic activity, but not from inherent stromal cell defects." Journal of Immunology 144, no. 1 (January 1, 1990): 103–10. http://dx.doi.org/10.4049/jimmunol.144.1.103.

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Abstract The formation of B lymphocytes is abnormal in autoimmune NZB and (NZB x NZW)F1 mice. With age, the proportion of sIg- Ly-5(220)+ pre-B cells and less mature B cell progenitors in the bone marrow progressively declines, reaching only approximately one-third of normal levels in 20-wk-old NZ mice. To determine the mechanisms responsible for the deficiency of NZ B lineage precursors, the mitotic activity of sIg- Ly-5(220)+ bone marrow cells in vivo was determined in NZ and conventional inbred mice as a function of age. The proportion of sIg- Ly-5(220)+ B cell precursors in (S + G2/M) stages of the cell cycle steadily decreased with age in NZ autoimmune mice. Furthermore, upon metaphase arrest, the rate of entry of sIg- Ly-5(220)+ bone marrow cells into G2/M also decreased with age in NZ mice. Therefore, the mitotic activity of sIg- Ly-5(220)+ B cell precursors is substantially decreased in NZ mice greater than or equal to 20 wk of age. The capacity of the bone marrow stromal microenvironment of NZ mice to support B lineage precursor growth was tested in two ways: 1) the capacity of preformed NZ bone marrow stroma to support B lineage cell growth in long term bone marrow cell culture under lymphopoietic conditions was assessed and 2) the capacity of NZ bone marrow B lineage precursors to expand in vivo after sublethal (200 rad) whole body irradiation was determined. Stroma derived from adult NZ mice supported the growth and development of B lineage lymphocytes in long term bone marrow cell culture to a greater extent than did age-matched conventional murine stroma. Furthermore, sublethal irradiation of older adult NZ mice resulted in some expansion of bone marrow sIg- Ly-5(220)+ B cell precursors in vivo. Therefore, the deficiency of B cell progenitors in the bone marrow of older NZ autoimmune mice is associated with diminished mitotic activity. However, this does not result from defects in the capacity of NZ bone marrow stroma to permit B lineage cell expansion as determined by both in vitro and in vivo experiments. In the absence of a detectable stromal cell defect, it is possible that an active inhibitory process within the bone marrow influences the mitotic activity of B cell precursors in NZ mice.
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Ryan, D. H., B. L. Nuccie, C. N. Abboud, and J. L. Liesveld. "Maturation-dependent adhesion of human B cell precursors to the bone marrow microenvironment." Journal of Immunology 145, no. 2 (July 15, 1990): 477–84. http://dx.doi.org/10.4049/jimmunol.145.2.477.

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Abstract Murine B cell precursors can be induced to proliferate in culture if allowed to bind to bone marrow derived adherent cells prepared under specific conditions. We studied the binding of human B cell precursor subpopulations to various in vitro microenvironments to determine which conditions may potentially be suitable models for human B precursor differentiation. Using the markers CD10, CD34, and CD20, B lineage populations of increasing maturation were quantitated: CD10+/CD34+, CD10+/CD20-, CD10+/CD20+, and CD10-/CD20+ cells in marrow, and CD10-/CD20+ mature B cells in peripheral blood. The adhesion of subpopulations of blood and marrow-derived light density cells to adherent cell layers or matrix was studied following a 2-h incubation in 24-well plates. The absolute number of bound B lineage cells was determined by cell counts and flow cytometry analysis. The adherence of B lineage cells to passaged human marrow fibroblasts (BM-FB) was highest in the most immature CD10+/CD34+ cells (34.3 +/- 4.2%), decreasing steadily with each stage of maturation to the peripheral blood B cells (11.2 +/- 2.4%). Increased adhesion of CD10+ B cell precursors relative to CD10-/CD20+ marrow B cells was confirmed by adhesion studies using sorted cells. The two most immature B lineage cells (CD10+CD34+ and CD10+/CD20-) showed more adherence to BM-FB than any other cell type tested, except for monocytes. Only B lineage precursor cells, erythroid precursors and CD10-/CD34+ cells showed significantly greater binding to BM-FB than to plastic. B lineage precursors bound equally well to primary and passaged human marrow fibroblasts, but bound significantly less well to passaged human foreskin fibroblasts, primary human marrow stroma, extracellular matrix of marrow fibroblasts, or fibronectin. These results suggest that specific binding to marrow fibroblasts is part of the differentiation program of early B lineage precursors. This binding activity gradually and predictably decreases during B lineage differentiation, in contrast to expression of other binding receptors, such as LFA-1 and CD44, which increase during B lineage maturation.
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Li, Peng, Shobi Venkatachalam, Daniela Ospina Cordona, Lorena Wilson, Tibor Kovacsovics, Karen A. Moser, Rodney R. Miles, David B. Beck, Tracy George, and Srinivas K. Tantravahi. "A clinical, histopathological, and molecular study of two cases of VEXAS syndrome without a definitive myeloid neoplasm." Blood Advances 6, no. 2 (January 13, 2022): 405–9. http://dx.doi.org/10.1182/bloodadvances.2021005243.

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Abstract VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome is caused by somatic mutations in UBA1 and is identified by a genotype-driven method. This condition affects unrelated men with adultonset inflammatory syndromes in association with hematologic manifestations of peripheral cytopenia and bone marrow myeloid dysplasia. Although bone marrow vacuolization restricted to myeloid and erythroid precursors has been identified in patients with VEXAS, the detailed clinical and histopathological features of peripheral blood and bone marrows remain unclear. The current case report describes the characteristic hematologic findings in patients with VEXAS, including macrocytic anemia, thrombocytopenia, marked hypercellular bone marrow with granulocytic hyperplasia, megaloblastic changes in erythroid precursors, and the absence of hematogones in addition to prominent vacuoles in myeloid and erythroid precursor cells. Characterizing the clinical and hematologic features helps to raise awareness and improve diagnosis of this novel, rare, but potentially underrecognized disease. Prompt diagnosis expands the general knowledgeable and understanding of this disease, and optimal management may prevent patients from developing complications related to this refractory inflammatory syndrome and improve the overall clinical outcome.
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Schatteman, Gina C., Martine Dunnwald, and Chunhua Jiao. "Biology of bone marrow-derived endothelial cell precursors." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 1 (January 2007): H1—H18. http://dx.doi.org/10.1152/ajpheart.00662.2006.

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Over the past decade, the old idea that the bone marrow contains endothelial cell precursors has become an area of renewed interest. While some still believe that there are no endothelial precursors in the blood, even among those who do, there is no consensus as to what they are or what they do. In this review, we describe the problems in identifying endothelial cells and conclude that expression of endothelial nitric oxide synthase may be the most reliable antigenic indicator of the phenotype. The evidence for two different classes of endothelial precursors is also presented. We suggest that, though there is no single endothelial cell precursor, we may be able to use these phenotypic variations to our advantage in better understanding their biology. We also discuss how a variety of genetic, epigenetic, and methodological differences can account for the seemingly contradictory findings on the physiological relevance of bone marrow-derived precursors in normal vascular maintenance and in response to injury. Data on the impact of tumor type and location on the contribution of bone marrow-derived cells to the tumor vasculature are also presented. These data provide hope that we may ultimately be able to predict those tumors in which bone marrow-derived cells will have a significant contribution and design therapies accordingly. Finally, factors that regulate bone marrow cell recruitment to and function in the endothelium are beginning to be identified, and several of these, including stromal derived factor 1, monocyte chemoattractant factor-1, and vascular endothelial growth factor are discussed.
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Antica, M., L. Wu, K. Shortman, and R. Scollay. "Thymic stem cells in mouse bone marrow." Blood 84, no. 1 (July 1, 1994): 111–17. http://dx.doi.org/10.1182/blood.v84.1.111.111.

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Abstract There is still controversy concerning the nature of the stem cells from bone marrow that colonize the thymus during embryogenesis and continually throughout life. To identify the bone marrow stem cells that home to and populate the thymus, we screened murine bone marrow cells for the presence of a population of surface phenotype similar to the earliest known intrathymic precursor. We have identified a population characterized by expression of an intermediate level of heat stable antigen, a very low level of Thy-1, and high levels of CD44 and class I major histocompatibility complex antigens. It is negative for B- cell, granulocyte, macrophage, and erythrocyte markers (B220, Gr-1, Mac- 1, and TER 119). All these markers are common to the intrathymic precursors and bone marrow stem cells. However, this new bone marrow population is Sca-2+, similar to the intrathymic precursor, which makes a clear distinction from the Sca-2- bone marrow hematopoietic stem cells previously characterized. The frequency of the new population in the normal mouse bone marrow is about 0.25%. When transferred intrathymically or intravenously to lethally irradiated mice, it has a higher expansion potential (2 x 10(5)) than has been found for the intrathymic precursors (10(3)), but less than was found for the Sca-2- multipotent stem cell (10(7)). These transfer studies also showed that it was pluripotent, in that its precursor activity was not restricted to the production of T or B lymphocytes. However, it gave a reduced spleen colony number and smaller colonies (day-12 colony-forming unit spleen) when compared with multipotent stem cells. Thus, the cell we have identified appears to be the latest pluripotent cells so far identified in bone marrow and is therefore a good candidate for a bone marrow prothymocyte, but it appears not to be T-cell-committed.
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Antica, M., L. Wu, K. Shortman, and R. Scollay. "Thymic stem cells in mouse bone marrow." Blood 84, no. 1 (July 1, 1994): 111–17. http://dx.doi.org/10.1182/blood.v84.1.111.bloodjournal841111.

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There is still controversy concerning the nature of the stem cells from bone marrow that colonize the thymus during embryogenesis and continually throughout life. To identify the bone marrow stem cells that home to and populate the thymus, we screened murine bone marrow cells for the presence of a population of surface phenotype similar to the earliest known intrathymic precursor. We have identified a population characterized by expression of an intermediate level of heat stable antigen, a very low level of Thy-1, and high levels of CD44 and class I major histocompatibility complex antigens. It is negative for B- cell, granulocyte, macrophage, and erythrocyte markers (B220, Gr-1, Mac- 1, and TER 119). All these markers are common to the intrathymic precursors and bone marrow stem cells. However, this new bone marrow population is Sca-2+, similar to the intrathymic precursor, which makes a clear distinction from the Sca-2- bone marrow hematopoietic stem cells previously characterized. The frequency of the new population in the normal mouse bone marrow is about 0.25%. When transferred intrathymically or intravenously to lethally irradiated mice, it has a higher expansion potential (2 x 10(5)) than has been found for the intrathymic precursors (10(3)), but less than was found for the Sca-2- multipotent stem cell (10(7)). These transfer studies also showed that it was pluripotent, in that its precursor activity was not restricted to the production of T or B lymphocytes. However, it gave a reduced spleen colony number and smaller colonies (day-12 colony-forming unit spleen) when compared with multipotent stem cells. Thus, the cell we have identified appears to be the latest pluripotent cells so far identified in bone marrow and is therefore a good candidate for a bone marrow prothymocyte, but it appears not to be T-cell-committed.
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Osnos, Leah, Virginia Sheikh, Jamie Hahn, Ainhoa Perez-Diez, Irini Sereti, and Irina Maric. "Administration of rhIL-7 Is Associated with Increase in Precursor T-Cells in Bone Marrows of Patients with Idiopathic CD4 Lymphocytopenia." Blood 124, no. 21 (December 6, 2014): 2747. http://dx.doi.org/10.1182/blood.v124.21.2747.2747.

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Abstract Introduction Idiopathic CD4+ Lymphocytopenia (ICL) is a rare, likely heterogeneous syndrome characterized by persistent CD4+ lymphopenia (<300/μl) in the absence of HIV infection or other known immunodeficiency. The diverse clinical presentation may include opportunistic infections, malignancies, and autoimmune diseases. Though the etiology of ICL remains unknown, previous studies have suggested decreased production, proliferation, or survival of CD4+ T-cells. There is currently no FDA-approved therapy for ICL. Methods We analyzed bone marrow core biopsies of 12 ICL patients in a phase I/IIA NIH clinical trial designed to evaluate recombinant human Interleukin-7 (rhIL-7) as a potential therapy for ICL . Subjects received 3 injections of rhIL-7 over two 24-week periods. Bone marrow biopsies were performed at week 1 and week 24 to analyze numbers of T-cells and T-cell precursors at baseline and post rhIL-7 therapy. Peripheral blood T-cell counts were assessed in parallel. Double chromogenic immunohistochemical staining using anti-terminal deoxynucleotidyl transferase (TdT) and anti-CD3 antibodies was performed on fixed, paraffin-embedded samples using an automated stainer (Ventana). Single CD3-positive T-cells and double-positive TdT/CD3 precursor T-cells were counted in at least ten consecutive fields under a light microscope and results expressed as mean positive cell number per field before and after treatment with rhIL-7. Similar staining procedure using TdT and CD79a was performed to evaluate precursor B-cells in the same patient cohort. In addition, bone marrow biopsies from 10 healthy control subjects were analyzed in parallel. Results Compared to healthy controls, ICL patients showed no significant differences in the number of bone marrow precursor T-cells (p=0.069) but had lower levels of mature T-cells (p<0.0001) in marrow core biopsies. These data correlated with presence of peripheral blood T-lymphopenias. ICL patients had higher levels of precursor B-cells that were double positive for TdT/CD79a (p=0.016) compared to control marrows, but showed no significant differences in the number of mature B-cells (p=0.059). After treatment with rhIL-7, bone marrow precursor T-cells increased significantly between weeks 1-24 (p=0.016). Mature T-cells also increased significantly (p=0.031). Precursor B-cells and mature B-cells did not change significantly (p=0.313 and 0.375, respectively). During the same time, peripheral blood CD3+ T-cell counts and CD4+ T-cell counts also increased. Conclusion Novel histological technique for double chromogenic staining allows for the visualization of T-cell precursors in bone marrow biopsies. Our study revealed no evidence that lymphopenia in ICL patients is associated with lack of T-cell precursors in bone marrow, suggesting downstream defects in T-cell differentiation, proliferation or survival. Administration of rhIL-7 was associated with an increase in peripheral blood T-cells and increase in bone marrow precursor T-cells, while B-cell lineage cells remained unchanged. Disclosures No relevant conflicts of interest to declare.
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Dissertations / Theses on the topic "Bone marrow precursors"

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Wragg, Andrew. "Bone marrow derived cells as endothelial precursors and the role of multi-potent progenitor cells in repairing ischaemic tissues." Thesis, Queen Mary, University of London, 2007. http://qmro.qmul.ac.uk/xmlui/handle/123456789/1640.

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Introduction: Atherosclerosis and its complications are a major cause of death and disability and it remains a major challenge to develop new therapies for patients with irreversible end organ damage and ongoing ischaemia. The discovery of adult stem and progenitor cells with the ability to regenerate adult tissues holds great promise. Bone marrow is the source of both endothelial progenitor cells (EPCs) and multi-potent adult progenitor cells (MAPCs). MAPCs are rare pluripotent bone marrow derived cells with the theoretical potential to differentiate into tissues of all three germ cell layers, including endothelium. These cells may have the potential to facilitate cardiac repair. The aim of this thesis was to further characterise bone marrow derived endothelial progenitor cells including multi potent adult progenitor cells and assess their angiogenic potential and mechanisms of action in animal models of cardiovascular disease. Findings: EPCs were isolated from humans and mice and their phenotype, markers and function determined, including gene tracking experiments in mice utilising the Cre/Lox system. It was not possible to isolate cells with the same phenotype as MAPCs from rodent bone marrow. However, cells with pluri-potent properties, named rat multi-potent progenitor cells (rMPCs), were isolated from rat bone marrow. These cells had the ability to up regulate tissue specific antigens from all 3 germ cell lineages and in addition secreted multiple cytokines related to angiogenesis and inflammation. To investigate the in vivo properties of rMPCs a rat hind limb model of ischaemia was established and syngeneic rMPCs were transplanted into the ischaemic hind limbs. rMPCs engrafted selectively into the adventitia of arterioles of ischaemic muscles. However, engrafted cells did not differentiate into an endothelial or smooth muscle phenotype. Cytokine analysis of muscles 5 days after rMPC injection revealed raised levels of cytokines, including chemokines MCP1 and SDR. Limb perfusion, measured by microspheres, increased after rMPC injection. In addition a novel MRI based assessment of ischaemic muscles revealed a significant normalisation of MRI signal after rMPC transplantation. However, there was no improvement in limb function assessed by treadmill running distance 4 weeks after cell injection. These findings suggest that transplantation of rMPCs into ischaemic muscles may modulate local inflammatory and angiogenic responses through paracrine mechanisms. Conclusion: Despite the potential for stem and progenitor cells to be used for the treatment of chronic cardiac ischaemia the biology of stem cells is still relatively poorly understood, as is the mechanism of action of cells after transplantation. As set out in the aims, the work in this thesis adds further to our understanding of both EPCs and BM derived pluri-potent stem cells. In addition it provides insight into the hind limb ischaemia model and the mechanism of action of cell therapy after transplantation into ischaemic muscle.
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Long, Ezhou. "Involvement of insulin-like growth factor I and its binding proteins on proliferation and differentiation of murine bone marrow macrophage precursors." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0005/MQ29746.pdf.

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Long, Ezhou. "Involvement of insulin-like growth factor I and its binding proteins on proliferation and differentiation of murine bone marrow macrophage precursors." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=27371.

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The alteration of insulin-like growth factor I (IGF-I) and its binding proteins (IGFBP) and their effects on proliferation and differentiation of murine bone marrow-derived macrophage (BMM) precursors were investigated. Bone marrow cells exposed to 20% L929-fibroblast conditioned medium (LCM) were cultured in serum-free medium for 24 h. Western ligand blotting (WLB) analysis detected four bands in all samples. 41-kDa and 30-kDa bands were detected after 12 h and remained constant during BMM differentiation. The 28-kDa and 25-kDa proteins were almost undetectable until day 2, but accumulated significantly from day 3 to day 7. Immunoblotting analysis verified these two bands as IGFBP-4. Northern blotting analyses detected both IGFBP-4 and IGFBP-3 mRNA in the cells. The 41-kDa protein was postulated to be IGFBP-3 in a glycosylated form. The identity of the 30-kDa band is not known. Northern blotting analysis showed that IGF-I mRNA level increased in a time-dependent manner until day 3, and decreased thereafter during BMM differentiation. The effect of IGF-I and its analogs on cell proliferation was studied by ($ sp3$H) thymidine incorporation. IGF-I and its analogs enhanced cell proliferation of freshly isolated bone marrow cells. Both IGF-I and long R$ sp3$ IGF-I, but not des(1-3)IGF-I, continued to exert a stimulating effect on day 1, although to a lesser extent. The effect of IGF-I and its analogs on BMM differentiation was studied by checking morphology, non-specific esterase-1 (NSE-1) activity, and mannose receptor expression. No significant differences in morphology and NSE-1 activity were observed among the treatment groups. There was no difference of mannose receptor expression on day 4 between the IGF-I group and the control cells, whereas long R${ sp3}$ and des(1-3)IGF-I increased the receptor number by 260% and 228% respectively, with less increased K$ rm sb{d}$ values. (Abstract shortened by UMI.)
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MAREGA, MANUELA. "Molecular mechanisms for the progression of chronic myeloid leukemia." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2010. http://hdl.handle.net/10281/17737.

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Chronic myeloid leukaemia (CML) is caused by the BCR-ABL hybrid gene. The molecular mechanisms leading from chronic phase (CP) to blast crisis (BC) are not understood. However, both the presence and the levels of BCR-ABL seem to be important for CML progression. BCR-ABL is under the transcriptional control of BCR promoter. Here we focused on the gene expression control of BCR and BCR-ABL upon myeloid differentiation in healthy donors (HDs), CP and BC patients. As previously reported, BCR-ABL is downregulated during myeloid maturation in CP patients. A similar pattern was detected for BCR (but not for ABL) in CP-CML and in HD, thus suggesting that the two genes may be under a similar transcriptional control. In BC this mechanism is similarly impaired for both BCR-ABL and BCR. These data indicate the presence of an ‘in trans’ deregulated transcription of both BCR and BCR-ABL promoters, associated with CML progression. The results of the luciferase assay indicate that the region comprised between 420 and 900 bp from the coding ATG site is required to achieve a basal transcription level. Previous studies suggest that a putative SP1 binding site could have a role in the basal promoter activity. In fact, an almost complete absence of transcriptional activity was measured in delta1041 and delta1271 constructs, lacking both the main transcription start site and the putative SP1 binding region. We hypothesize that SP1 could be responsible for the basal promoter activity, present in the delta541 and in longer constructs. The ChIP assay confirmed the SP1-binding to the BCR promoter. The presence of 10 additional putative protein binding sites (PBSs), along the BCR promoter is also known from previous works. Six of these putative PBSs are localized in the region between −1443 to −1202 bp, which appears to be critical from in silico studies. In fact, only in presence of a 221 bp region upstream from delta241, a strong luciferase signal could be detected, suggesting that the promoter region between −1443 and −1202 bp from the coding ATG is indeed critical to achieve the highest level of expression.
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Manoukian, Raffi. "The microenvironmental organization of early B cell precursors in the femoral bone marrow of mutant SCID mice, SCOD/myc transgenic mice and alternate fraction x-irradiated endocolonized mice /." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=57003.

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The in situ microenvironmental organization of early precursor B cells in mouse bone marrow has been studied using three experimental models: (1) mutant mice with severe combined immunodeficiency (SCID), which develop pro-B cells but no pre-B and B cells; (2) SCID/myc transgenic mice having expanded pro-B cell populations, but no pre-B and B cells; (3) x-irradiated C3H/HeJ mice during early stages in the regeneration of pro-B cells in bone marrow seeded from a shielded marrow site. The in vivo localization of B220$ sp+$ cells was revealed by the binding of i.v. injected $ sp{125}$I-mAb 14.8 detected by light and electron microscope radioautography of femoral marrow sections. Many B220$ sp+$ pro-B cells were located in peripheral regions of SCID and SCID/myc bone marrow, often in clusters, associated with an electron dense extracellular matrix and with the processes of stromal reticular cells. Many B220$ sp+$ cells were associated with macrophages which contained numerous ingested bodies. Macrophage associations were more numerous in SCID/myc than in SCID mice, especially in the peripheral marrow regions. 3-5 day post-irradiation endocolonizing marrow contained increasing numbers of B220$ sp+$ cells in subosteal and peripheral regions, situated both within sinusoids and extravascularly, associated with stromal reticular cell processes and often close to nerve fibers. The results demonstrate that early B220$ sp+$ precursors begin to differentiate in peripheral marrow regions and develop intimate associations with reticular cells and macrophages. These findings suggest that through these associations, the bone marrow reticular cells promote the early development of the B cell lineage, while the bone marrow macrophages play a role in the elimination of aberrant precursor B cells.
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Jacobsen, Karen Ann. "Microenvironmental organization of B lymphopoiesis in mouse bone marrow : in vivo localisation of B lymphocyte precursors, molecular-interactions with stromal reticular cells, and macrophage-mediated deletion of apoptotic forms." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=41346.

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The localisation of B lymphocyte precursor cells in mouse bone marrow and their associations with stromal reticular cells and macrophages have been investigated by in vivo radioimmunolabeling combined with light and electron microscope radioautography. Many early B lineage cells expressing the B220 glycoprotein prior to the expression of surface immunoglobulin and those regenerating after sub-lethal $ gamma$-irradiation, were located in bone-associated regions of femoral marrow. Labeled B220$ sp*$ lymphoid cells of undifferentiated morphology were closely associated with complex cytoplasmic processes of stromal reticular cells. The binding of a monoclonal antibody raised against a B lymphocyte-supportive stromal cell line (mAb KMI6), was highly restricted to the interface between stromal cells and undifferentiated lymphoid cells. The VCAM-1 specific mAb M/K-2, labeled electron-dense stromal cells that contacted lymphoid cells and a variety of other hemopoietic cell lineages. Within the bone marrow of normal mice there was evidence of death of B220$ sp+$ B lineage cells by apoptosis and their removal by macrophages. Cell loss, apoptosis and macrophage deletion of B precursor cells were greatly enhanced in E$ mu$-myc transgenic mice. The results reveal a complex in vivo microenvironmental organisation of B lymphocytopoiesis characterised by intimate interactions with stromal reticular cells and macrophages which regulate the development of precursor B cells and determine the ultimate output of B lymphocytes from the bone marrow.
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Letscher, Hélène. "Étude des propriétés régulatrices d’une population de précurseurs de cellules dendritiques plasmacytoïdes conditionnée par le CpG dans le cadre de réponses auto-immune et allogénique Innate activation primes bone marrow plasmacytoid dendritic cell precursors for tolerance Rôle protecteur des CpG-pre-pDC dans le cadre d’une réponse allogénique : la maladie du greffon contre l’hôte." Thesis, Sorbonne Paris Cité, 2018. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=2171&f=13417.

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Les progéniteurs hématopoïétiques présentent la faculté de détecter des signaux infectieux et inflammatoires. Leur éducation précoce par de tels signaux au sein de la moelle osseuse avant leur sortie vers la périphérie peut influencer l'évolution des réponses immunes. Alors que les cellules dendritiques plasmacytoïdes matures peuvent soit aggraver soit améliorer des maladies auto-immunes ou allogéniques, nous avons exploré la possibilité que de tels signaux innés confèrent des propriétés immunorégulatrices à des précurseurs médullaires des pDC. Nous avons caractérisé une population médullaire émergeant après interaction avec un agoniste du Toll-like receptor-9, l'oligonucléotide CpG, qui présente le phénotype c-kit+Sca-1+B220intPDCA-1+, est engagée dans la voie des cellules dendritiques plasmacytoïdes (pDC) et l'avons dénommée CpG-pre-pDC. Nous avons évalué le potentiel immunorégulateur des CpG-prepDCs en opérant leur transfert adoptif dans deux types de pathologies murines : l'Encéphalite Auto-immune Expérimentales (EAE), un modèle de sclérose en plaques qui est une maladie auto-immune, ainsi que la maladie du greffon contre l'hôte (GVHD) qui est une réponse allogénique. Il s'est avéré que le transfert d'un nombre assez faible de précurseurs (80 000 en EAE et 200 000 en GVHD) est capable de limiter la maladie à différents temps cliniques. De façon intéressante, les CpG-pre-pDC migrent spécifiquement à la moelle épinière dans l'EAE et à la rate dans la GVHD où leur descendance conserve un phénotype de pDC encore relativement immature. Dans le cadre de l'EAE, la descendance des précurseurs injectés produit essentiellement de l'IL-27 et du TGFß et plus modestement du GM-CSF. Au niveau du système nerveux central inflammé, elles font dévier la réponse immunitaire des lymphocytes T CD4+ infiltrants d'un profil pro-inflammatoire (IFNy+ GM-CSF+ IL-17+) vers un profil anti-inflammatoire (TGFß+, IL-27+, IL-17-, GM-CSFlo). L'utilisation de précurseurs déficients dans chacune de ces deux cytokines a permis de démontrer que TGFß et IL-27 interviennent séquentiellement dans la protection conférée par les CpG-prepDCs, le TGFß à des temps précoces et l'IL-27 aux phases tardives de la maladie. Des mécanismes semblables interviennent dans la protection envers la GVHD conférée par les CpG-prepDCs, car leur descendance est toujours capable de produire du TGFß mais cette fois en association avec l'IL-12, une autre cytokine de la même famille que l'IL-27. Par ailleurs, ces cellules sont capables de diminuer la production d'IL-17 tant par les lymphocytes T CD4+ que par les CD8+. Une thérapie cellulaire avec l'équivalent humain des CpG-pre-pDCs pourrait constituer un nouvel outil thérapeutique pour le traitement à la fois de la sclérose en plaques réfractaire et de la maladie du greffon contre l'hôte soit injectés seuls soit en enrichissement des greffes de cellules souches hématopoïétiques qui sont pratiquées dans ces deux maladies
Hematopoietic progenitors can sense innate signals. Their early education by such signals within the bone marrow, prior to their egress, may have considerable impact on the outcome of immune responses. While mature plasmacytoid dendritic cells (pDC) are known to either aggravate or ameliorate disease both auto-immune and allogeneic, it remains unknown whether immune regulatory function can be stably imprinted at the precursor stage in the pDC lineage onwards. We herein investigated whether activation with the oligonucleotide CpG, a Toll-like receptor-9 agonist, confers to bone marrow pDC precursors (CpG-prepDCs) characterized by the c-kit+Sca-1+B220intPDCA-1+ phenotype the capacity to protect against two kinds of murine immune pathologies: Experimental Autoimmune Encephalomyelitis (EAE), a model of multiple sclerosis which is an autoimmune disease and graft versus host disease (GVHD), an allogeneic response. We demonstrate that the adoptive transfer of relatively low number of CpG-pre-pDCs (80.000 in EAE and 200.000 in GVHD) was able to clinically reduce both diseases. Interestingly, CpG-pre-pDCs migrated to the spinal cord in EAE and to the spleen in GVHD where their progeny retained a relatively immature pDC phenotype. In EAE, the progeny of CpG-pre-pDCs massively produces IL-27 and TGFß and moderately GM-CSF. In the inflamed central nervous system, the progeny switches the immune response of infiltrating CD4+ T cells from pro-inflammatory (IFNy+ GM-CSF+ IL-17+) to anti-inflammatory (TGFß+, IL-27+, IL-17-, GM-CSFlo). The key role of TGFß and IL-27 was assessed using precursors incapacitated for the production of each of those cytokines. These experiments demonstrated that the two soluble factors acted sequentially: TGFß ensures early phases of the immunomodulation mediated by the CpG-pre-pDC while IL-27 is required for later protection. In GVHD, the mechanisms of protection are different yet similar in some ways. As for EAE, the progeny of CpG-pre-pDCs is still able to produce TGFß but this time in combination with IL-12, another cytokine from the IL-27 family. Additionally, those cells were able to reduce the IL-17 production by both pathogenic CD4+ and CD8+ T cells. The human equivalent of CpG-pre-pDC could be a new therapeutic tool in patients with multiple sclerosis or graft versus host disease either per se or enriched in the hematopoietic stem cell transfer already implemented to treat those two immune conditions
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Tsui, Yat-ping, and 徐軼冰. "Derivation of oligodendrocyte precursor cells from adult bone marrow stromal cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/197485.

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Myelin is essential for neuronal survival and maintenance of normal functions of the nervous system. Demyelinating disorders are debilitating and are often associated with failure of resident oligodendrocyte precursor cells (OPCs) to differentiate into mature, myelinating oligodendrocytes. Derivation of OPCs, from a safe source that evades ethical issues offers a solution to remyelination therapy. We therefore hypothesized that bone marrow stromal cells (BMSCs) harbour neural progenitor cells at a pre-commitment stage and that in vitro conditions can be exploited to direct differentiation of these cells along the oligodendroglial lineage. For the current study, adult rat BMSCs used were >90% immunopositive for CD90, CD73, STRO-1 (stromal cell markers), 10% for nestin (neural progenitor marker) but negligible for CD45 (haematopoietic cell marker) as measured by flow cytometry. Transfer of the culture from a highly adhesive substratum to a moderately adhesive substratum resulted in increase in proportion of p75-positive cells but CD49b-positive cells remained at 97% and Sox 10-positive cells remained negligible. Transfer of the culture to a non-adherent substratum fostered the generation of neurospheres comprising cells that were positive for the neural stem/progenitor cell (NP) marker, nestin, and for the neural crest markers CD49b, p75 and Sox10. Prior to this stage, the BMSCs were not yet committed to the neural lineage even though transient upregulation of occasional marker may suggest a bias towards the neural crest cell lineage. The BM-NPs were then maintained in adherent culture supplemented with beta-Heregulin (β-Her), basic fibroblast growth factor (bFGF) and platelet-derived growth factor-AA (PDGF-AA) to direct differentiation along the oligodendroglial lineage. Within two weeks of glial induction, cells expressing the OPC markers - NG2, Olig2, PDGFRa and Sox10, were detectable and these could be expanded in culture for up to 3 months with no observable decline in marker expression. These BM-OPCs matured into myelinating oligodendrocytes after 2 weeks in co-culture with either dorsal root ganglion neurons or cortical neurons. In vivo myelination by BM-OPCs was demonstrated by exploitation of the non-myelinated axons of retinal ganglion cells of adult rats. By 8 weeks post-injection of BM-OPCs into the retina, myelin basic protein-positive processes were also observable along the retinal axons. The results not only suppport our hypothesis, but also provide pointers to the adult bone marrow as a safe and accessible source for the derivation of OPCs towards transplantation therapy in acute demyelinating disorders.
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Biochemistry
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Doctor of Philosophy
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Gronthos, Stan. "Stromal precursor cells : purification and the development of bone tissue." Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phg8757.pdf.

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Bibliography: leaves 152-223. Experiments were designed to identify and purify human bone marrow stromal precursor cells by positive immunoselection, based on the cell surface expression of the VCAM-1 and STRO-1 antigens. The data presented demonstrates a hierarchy of bone cell development in vitro.
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Kaminski, Eduardo Roman. "Cytotoxic T lymphocyte precursor frequencies (CTL-p) and their relevance to bone marrow transplantation." Thesis, Imperial College London, 1990. http://hdl.handle.net/10044/1/46378.

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Books on the topic "Bone marrow precursors"

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Benveniste, Patricia Kuehne. T cell differentiation from bone marrow precursors. 1989.

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Collins, Graham, and Chris Bunch. Acute leukaemia. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0286.

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Acute leukaemias are rapidly progressive, clonal haematopoietic stem cell disorders resulting in the accumulation of immature blood cell precursors (known as blasts) in the bone marrow. There are two main types, defined by the presence of myeloid lineage or lymphoid markers on the blast cells: acute myeloid leukaemia and acute lymphoblastic leukaemia. This chapter addresses the causes, diagnosis, and management of the acute leukaemias.
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Albert, Tyler J., and Erik R. Swenson. The blood cells and blood count. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0265.

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Blood is a dynamic fluid consisting of cellular and plasma components undergoing constant regeneration and recycling. Like most physiological systems, the concentrations of these components are tightly regulated within narrow limits under normal conditions. In the critically-ill population, however, haematological abnormalities frequently occur and are largely due to non-haematological single- or multiple-organ pathology. Haematopoiesis originates from the pluripotent stem cell, which undergoes replication, proliferation, and differentiation, giving rise to cells of the erythroid, myeloid, and lymphoid series, as well as megakaryocytes, the precursors to platelets. The haemostatic system is responsible for maintaining blood fluidity and, at the same time, prevents blood loss by initiating rapid, localized, and appropriate blood clotting at sites of vascular damage. This system is complex, comprising both cellular and plasma elements, i.e. platelets, coagulation and fibrinolytic cascades, the natural intrinsic and extrinsic pathways of anticoagulation, and the vascular endothelium. A rapid, reliable, and inexpensive method of examining haematological disorders is the peripheral blood smear, which allows practitioners to assess the functional status of the bone marrow during cytopenic states. Red blood cells, which are primarily concerned with oxygen and carbon dioxide transport, have a normal lifespan of only 120 days and require constant erythropoiesis. White blood cells represent a summation of several circulating cell types, each deriving from the hematopoietic stem cell, together forming the critical components of both the innate and adaptive immune systems. Platelets are integral to haemostasis, and also aid our inflammatory and immune responses, help maintain vascular integrity, and contribute to wound healing.
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Book chapters on the topic "Bone marrow precursors"

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Lee, Inchul, Eunsil Yu, Robert A. Good, and Susumu Ikehara. "Eosinophilic Precursors in the Fibroreticular Network of Human Thymus." In Bone Marrow Transplantation, 77–81. Tokyo: Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-68320-9_10.

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Scollay, Roland, and Mariastefania Antica. "Stem cells for lymphocytes: comments on the time and place of commitment of precursors for the T lineage." In Bone Marrow Transplantation, 20–27. Tokyo: Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-68320-9_3.

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Kenney, Devin, and Christelle Harly. "Purification of Bone Marrow Precursors to T Cells and ILCs." In T-Cell Development, 211–32. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2740-2_13.

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Schatteman, Gina C., Ola Awad, and Martine Dunnwald. "The Old and New of Bone Marrow - Derived Endothelial Cell Precursors." In New Frontiers in Angiogenesis, 45–78. Dordrecht: Springer Netherlands, 2006. http://dx.doi.org/10.1007/1-4020-4327-9_3.

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Rosado, M. Manuela, Marco Scarsella, Simona Cascioli, Ezio Giorda, and Rita Carsetti. "Evaluating B-Cells: From Bone Marrow Precursors to Antibody-Producing Cells." In Methods in Molecular Biology, 45–57. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-496-8_4.

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Holmes, K. L., J. S. Lee, and H. C. Morse. "Mac-1+ Bone Marrow Cells Include Precursors of B Cells and T Cells." In Current Topics in Microbiology and Immunology, 19–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-74006-0_4.

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Vladimirskaya, E., N. Zamaraeva, V. Lebedev, O. Krysianovsky, A. Roumiantsev, I. Maso, and E. Osipova. "Effect of Chemotherapy on Bone Marrow Granulocyte — Macrophage and Stormal Precursors in Children with ALL." In Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, 389–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78350-0_69.

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Togni, Mauro, and Georges J. M. Maestroni. "Hematopoietic Rescue Via αl-Adrenoceptors on Bone Marrow B Cell Precursors and Endogenous Transforming Growth Factor-β." In Molecular Biology of Hematopoiesis 5, 609–17. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0391-6_74.

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Hardy, R. R., R. Wasserman, Y. S. Li, S. A. Shinton, and K. Hayakawa. "Response by B Cell Precursors to Pre-B Receptor Assembly: Differences Between Fetal Liver and Bone Marrow." In Current Topics in Microbiology and Immunology, 25–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-57284-5_3.

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Haley, Stephen T., John G. Tew, and Andras K. Szakal. "The Monoclonal Antibody FDC-M1 Recognizes Possible Follicular Dendritic Cell Precursors in the Blood and Bone Marrow." In Advances in Experimental Medicine and Biology, 289–91. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1971-3_64.

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Conference papers on the topic "Bone marrow precursors"

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Cramer, Elisabeth M., F. John, William Vainchenker, and Janine Breton-Gorius. "PRODUCTION AND LOCALISATION OF ALPHA-GRANULE PROTEINS IN MATURING MEGAKARYOCYTES: AN OVERVIEW ON ULTRA-STRUCTURAL ASPECTS OF MEGAKARYOCYTE MATURATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642952.

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In order to study the production of α- granule proteins in maturing megakaryocytes, we used immunocytochemical techniques performed on cultured and enriched bone marrow megakaryocytes. Cultures were prepared from bone marrow CFU-MK with the methylcellulose and plasma clot techniques. Preparation of bone marrow megakaryocytes was carried out from human or pig rib marrow separated on percoll gradient and counterflow centrifugation. Megakaryocyte preparations were 90$ pure and represented 85$ of those in the whole marrow. Activation was prevented with prostacyclin and prefixation with low concentration glutaraldehyde. A panel of monoclonal and polyclonal antibodies, against different platelet membrane glycoproteins and against cytoplasmic antigens (such as von Willebrand Factor (vWF), fibrinogen (Fg) and thrombospondin (TSP)) was used and observed by immunofluorescence or by immunogold in electron microscopy.The first megakaryocytic precursors, promegakaryoblasts (PMKB) identifiable by these antibodies were found at day 5 of culture. They had the size of lymphocytes, were labelled for GP lib, Ilia, and Ilb-IIIa complex but not for GPIb which appeared later. Platelet peroxidase was also present, otherwise these cells were devoid of α- granules and only a few of them exhibited a diffuse pattern for vWF immunolabelling. One day later membrane GPIb and diffuse cytoplasmic labelling for vWF were detected in the majority of PMKB. At day 9 of culture, this pattern of labelling for vWF became more intense and granular. The same pattern was observed for TSP and platelet factor 4. Immunoelectron microscopy showed that in immature megakaryocytes isolated from human bone marrow, labelling for vWF and TSP was observed in vesicles located in the Golgi region; in addition numerous small granules less than 0.1pm in diameter, round or elongated in shape, were labelled for these antigens. In mature human megakaryocytes, the labelling for these cytoplasmic antigens was restricted to the platelet α- granules in a distribution pattern similar to that of platelet α- granules. However, the labelling for Fg was consistently less intense in the granules of immature and mature megakaryocytes than in platelets.Because in platelets α- granule immunolabelling for vWF is associated with tubular structures which are specially prominent in porcine species, we studied vWF and tubular structures in pig megakaryocytes. Standard and immunoelectron microscopy revealed the simultaneous appearance of both in the small vesicles located in the Golgi area in the small immature α- granules and later in the mature α- granules. In mature megakaryocytes, labelling for vWF was intense and restricted to the α- granules. It was distributed eccentrically as in porcine blood platelets. Gold particles were often eccentrically located at one pole of the α- granule either labelling only its periphery or outlining one side of an elongated granule. Standard electron microscopy showed that tubular structures were very numerous in the mature α-granules, regularly spaced, arranged in parallel and usually located at one side of the granule. On the other hand platelets from pigs with homozygous von Willebrand disease were found to be completely devoid of both tubular structures and immunolabelling for vWF suggesting that the tubules represent the vWF itself.In acute megakaryoblastic leukemia, several phenotypes of PMKB were found in different patients, which corresponded to the stages of maturation of cultured megakaryocytes from CFU-MK.In conclusion, immunolabelling methods combined with megakaryocyte enrichment techniques are useful tools to study the origin of megakaryocyte (and platelet) granular proteins.
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Ragonnaud, Emeline, Kanako Moritoh, Monica Bodogai, Soizic Garaud, Chen Chen, Xin Wang, Karen Willard-Gallo, and Arya Biragyn. "Abstract 4499: Cancer targets early B-cell precursors to generate metastasis-promoting Bregs by promoting their premature emigration from the bone marrow and expansion in the circulation." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-4499.

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shi, xin, Joseph S. Soblosky, Ping Zhang, and Judd E. Shellito. "THYmoPOIETIC PRECURSOR CELL PRODUCTION BY BONE MARROW IN RESPONSE TO Pneumocystis Infection." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1380.

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Li, Ling, Guitao Cao, Jun Shi, Heng Wu, and Xianxia Zhang. "Detecting immature precursor cells in pathological images of bone marrow based on morphology." In 2010 Seventh International Conference on Fuzzy Systems and Knowledge Discovery (FSKD). IEEE, 2010. http://dx.doi.org/10.1109/fskd.2010.5569552.

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Bhutani, Manisha, Esther Mena, Irina Maric, Esther Tan, Neha Korde, Alexandra R. Berg, Alex R. Minter, et al. "Abstract 369: Role of bone marrow angiogenesis in myeloma and its precursor disease: a prospective clinical trial." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-369.

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Wu, Heng, Guitao Cao, Ling Li, and Jun Shi. "Identifying Immature Precursor Cells in Bone Marrow Pathological Images Based on Distance Transform and Internal Structures of Cells." In 2010 International Conference on Multimedia Technology (ICMT). IEEE, 2010. http://dx.doi.org/10.1109/icmult.2010.5631289.

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Balaji, Swathi, Sachin S. Vaikunth, Jignesh K. Parvadia, Timothy M. Crombleholme, and Daria A. Narmoneva. "In Situ Tissue Engineering Using Angiogenic Nanoscaffold Enhances Diabetic Wound Healing in db/db Mouse Model." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192198.

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Tissue engineering offers an attractive alternative for treatment of chronic nonhealing diabetic ulcers, which account for more than 27% of the $10.9 billion total diabetic health care costs in the US annually [1]. The harsh environment of a diabetic ulcer is characterized by reduced expression of angiogenic factors, insufficient vascularization, excess protease activity, matrix degradation and hyperglycemia-induced cell apoptosis [2]. A major factor contributing to insufficient neovascularization in diabetic nonhealing wounds may be deficiency in the recruitment of endothelial cells (ECs) and endothelial precursor cells (EPCs) to the wound site [3]. Recent studies focusing on altering the wound’s cellular and molecular environment using bone-marrow-derived stem cells, growth factors (delivered either directly or using gene or cell therapy), bioengineered skin constructs, and biological matrices, such as collagen and hyaluronic acid gels had promising wound healing outcomes [4]. These studies suggest that strategies aimed at modifying the extracellular environment of the diabetic wound to enhance cell survival and angiogenesis are promising for development of new therapies for diabetic wound healing.
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Jo, Sumin, Peter van den Elzen, and Gregor S. D. Reid. "Abstract A81: Early TLR-mediated killing of leukemia in bone marrow is correlated with durable protection against B cell precursor acute lymphoblastic leukemia." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-a81.

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