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Relevant bibliographies by topics / Bone marrow cells; Blood; Haematopoietic

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Academic literature on the topic 'Bone marrow cells; Blood; Haematopoietic'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Bone marrow cells; Blood; Haematopoietic"

1

Basden, K., DW Cooper, and EM Deane. "Development of the blood-forming tissues of the tammar wallaby Macropus eugenii." Reproduction, Fertility and Development 8, no. 6 (1996): 989. http://dx.doi.org/10.1071/rd9960989.

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The development of the haematopoietic tissues of the tammar wallaby Macropus eugenii follows a similar pattern to that observed in eutherian and other metatherian mammals. At birth, the liver appears to be the only site of haematopoiesis with significant numbers of neutrophils and stem cells present in the circulation. By Day 3, the spleen shows limited haematopoietic activity and by Day 12 contains areas of erythroid and myeloid cells. At two weeks after birth, the haematopoetic activity in the liver declines and small areas of haematopoiesis are apparent in the bone marrow. By the end of the first month, the bone marrow appears to be the major site of haematopoiesis.

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Haznedaroglu, Ibrahim C., and Yavuz Beyazit. "Local bone marrow renin–angiotensin system in primitive, definitive and neoplastic haematopoiesis." Clinical Science 124, no. 5 (November 12, 2012): 307–23. http://dx.doi.org/10.1042/cs20120300.

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The locally active ligand peptides, mediators, receptors and signalling pathways of the haematopoietic BM (bone marrow) autocrine/paracrine RAS (renin–angiotensin system) affect the essential steps of definitive blood cell production. Haematopoiesis, erythropoiesis, myelopoiesis, formation of monocytic and lymphocytic lineages, thrombopoiesis and other stromal cellular elements are regulated by the local BM RAS. The local BM RAS is present and active even in primitive embryonic haematopoiesis. ACE (angiotensin-converting enzyme) is expressed on the surface of the first endothelial and haematopoietic cells, forming the marrow cavity in the embryo. ACE marks early haematopoietic precursor cells and long-term blood-forming CD34+ BM cells. The local autocrine tissue BM RAS may also be active in neoplastic haematopoiesis. Critical RAS mediators such as renin, ACE, AngII (angiotensin II) and angiotensinogen have been identified in leukaemic blast cells. The local tissue RAS influences tumour growth and metastases in an autocrine and paracrine fashion via the modulation of numerous carcinogenic events, such as angiogenesis, apoptosis, cellular proliferation, immune responses, cell signalling and extracellular matrix formation. The aim of the present review is to outline the known functions of the local BM RAS within the context of primitive, definitive and neoplastic haematopoiesis. Targeting the actions of local RAS molecules could represent a valuable therapeutic option for the management of neoplastic disorders.

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Al-Drees, Mohammad A., Jia Hao Yeo, Badwi B. Boumelhem, Veronica I. Antas, Kurt W. L. Brigden, Chanukya K. Colonne, and Stuart T. Fraser. "Making Blood: The Haematopoietic Niche throughout Ontogeny." Stem Cells International 2015 (2015): 1–14. http://dx.doi.org/10.1155/2015/571893.

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Approximately one-quarter of all cells in the adult human body are blood cells. The haematopoietic system is therefore massive in scale and requires exquisite regulation to be maintained under homeostatic conditions. It must also be able to respond when needed, such as during infection or following blood loss, to produce more blood cells. Supporting cells serve to maintain haematopoietic stem and progenitor cells during homeostatic and pathological conditions. This coalition of supportive cell types, organised in specific tissues, is termed the haematopoietic niche. Haematopoietic stem and progenitor cells are generated in a number of distinct locations during mammalian embryogenesis. These stem and progenitor cells migrate to a variety of anatomical locations through the conceptus until finally homing to the bone marrow shortly before birth. Under stress, extramedullary haematopoiesis can take place in regions that are typically lacking in blood-producing activity. Our aim in this review is to examine blood production throughout the embryo and adult, under normal and pathological conditions, to identify commonalities and distinctions between each niche. A clearer understanding of the mechanism underlying each haematopoietic niche can be applied to improvingex vivocultures of haematopoietic stem cells and potentially lead to new directions for transplantation medicine.

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Sanchez-Herrero, Alvaro, Isabel A. Calvo, Maria Flandes-Iparraguirre, Marietta Landgraf, Christoph A. Lahr, Abbas Shafiee, Froilán Granero-Molto, et al. "Engineering a Humanised Niche to Support Human Haematopoiesis in Mice: Novel Opportunities in Modelling Cancer." Cancers 12, no. 8 (August 6, 2020): 2205. http://dx.doi.org/10.3390/cancers12082205.

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Despite the bone marrow microenvironment being widely recognised as a key player in cancer research, the current animal models that represent a human haematopoietic system lack the contribution of the humanised marrow microenvironment. Here we describe a murine model that relies on the combination of an orthotopic humanised tissue-engineered bone construct (ohTEBC) with patient-specific bone marrow (BM) cells to create a humanised bone marrow (hBM) niche capable of supporting the engraftment of human haematopoietic cells. Results showed that this model supports the engraftment of human CD34+ cells from a healthy BM with human haematopoietic cells migrating into the mouse BM, human BM compartment, spleen and peripheral blood. We compared these results with the engraftment capacity of human CD34+ cells obtained from patients with multiple myeloma (MM). We demonstrated that CD34+ cells derived from a diseased BM had a reduced engraftment potential compared to healthy patients and that a higher cell dose is required to achieve engraftment of human haematopoietic cells in peripheral blood. Finally, we observed that hematopoietic cells obtained from the mobilised peripheral blood of patients yields a higher number of CD34+, overcoming this problem. In conclusion, this humanised mouse model has potential as a unique and patient-specific pre-clinical platform for the study of tumour–microenvironment interactions, including human bone and haematopoietic cells, and could, in the future, serve as a drug testing platform.

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Pirillo, Chiara, Myriam Haltalli, Sara Gonzalez-anton, George Adams, Delfim Duarte, and Cristina Lo Celso. "Inhibiting Matrix Metalloproteinases Hinders Acute Myeloid Leukaemia and Prevents Healthy Stem Cell Loss." Blood 134, Supplement_1 (November 13, 2019): 2487. http://dx.doi.org/10.1182/blood-2019-129847.

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Haematopoietic stem cells (HSCs), despite being very rare (<0.015% of bone marrow haematopoietic cells), maintain the turnover of all blood cells through a balance of quiescence, self-renewal and differentiation. Disruption of HSCs function and of the bone marrow (BM) microenvironment are key aspects of Acute Myeloid Leukaemia (AML). AML develops in adults and symptoms arise due to the loss of healthy haematopoietic cells. It is unknown exactly what factors contribute to this although it is clear that there is a progressive loss of BM HSCs in this disease. One hypothesis is that HSCs are pushed out of the BM niche by competing leukaemic blasts. To explore this, we used intravital 2-photon confocal microscopy in a live mouse model of leukaemia which allows us to visualise the dynamics of healthy haematopoietc cells at various stages of the disease. We monitored the development of extramedullary haematopoiesis (EMH) during AML growth and tested the function of HSCs found in these alternative sites to determine whether EMH acts as an alternative mechanism of blood cell maintenance in response to AML. Furthermore, we investigated the influence of an extracellular matrix metalloproteinase inhibitor, Prinomastat, on the loss of HSCs in this model. Prinomastat has been studied extensively in solid organ cancers as it has been shown capable of inhibiting cancer metastasis. In this study, we examined whether it might have a function in preventing the loss of HSCs from the bone during leukaemia infiltration. C57BL/6 mice were injected with 100k of YFP-AML blasts and peripheral blood (PB) checked every four days for AML progression. Cellular dynamics were assessed by intravital microscopy (IVM) of the mouse calvarium and spleen at early (10%), medium (25%) and late (>25%) PB infiltration. To calculate the number of circulating HSCs and progenitors (HSPCs) blood was taken by cardiac puncture and analysed by flow cytometry for HSCPs absolute number. The same was done for BM, spleen and liver HSPCs. HSC functionality was determined by transplanting sorted Lin- c-Kit+ Sca-1+ CD48- CD150+ (LKS Slam) cells from CD45.1 BM, spleen and liver of AML-burdened mice into lethally irradiated C57BL/6 mice. BM reconstitution was then analysed every four weeks. To analyse the role of extracellular matrix remodelling, C57BL/6 mice were transplanted with 100k AML cells tagged with yellow-fluorescent-protein (YFP) and then administered intravenous prinomastat daily. These mice were imaged and had bone marrow analysed using flow cytometry together with a control group at early, medium and late AML based on PB infiltration. AML progression leads to a dramatic and progressive loss HSCPs in the BM. Intravital imaging showed an enhanced egress of healthy cells from the BM into the circulation. Conversely, we found a clear association between the extent of infiltration of the marrow and the number of HSCs found in the spleen and liver. Our transplantation experiments show that the extramedullary HSCs are functional and able to reconstitute the BM of lethally irradiated mice irrespective of the organ from which they were sorted. Treatment with prinomastat significantly reduced the number of HSCs and progenitors leaving the bone marrow (P=0.0001). In the treated mice, the number of BM HSCs was consistently higher at every infiltration time point when compared to untreated mice. In addition, prinomastat caused a reduction in the extent of extramedullary haematopoesis in both the spleen and liver. This study provides a unique insight into the effect of AML on the dynamics of HSCs as disease progresses. Contrary to expectations, HSCs are not lost, but rather a majority appear to migrate from the bone marrow to sites of extramedullary haematopoiesis. These cells remain functional and are capable of regenerating haematopoiesis when transplanted into a recipient mouse. Further to this, we have demonstrated that by inhibiting the function of metalloproteinases using Prinomastat it is possible to prevent this loss of HSCs thus retain these cells within the bone marrow. These findings highlight the importance of the extracellular matrix in acute myeloid leukaemia and suggest that metalloproteinase inhibitors could potentially have a significant role in resisting the perturbations caused by AML on haematopoiesis. Disclosures No relevant conflicts of interest to declare.

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Denizot, Y., V. Desplat, C. Dulery, F. Trimoreau, and V. Praloran. "Arachidonic Acid and Freshly Isolated Human Bone Marrow Mononuclear Cells." Mediators of Inflammation 8, no. 1 (1999): 31–35. http://dx.doi.org/10.1080/09629359990694.

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Arachidonic acid (AA), a fatty acid found in the human bone marrow plasma, is the precursor of eicosanoids that modulate bone marrow haematopoiesis. To further our understanding of the role of AA in the bone marrow physiology, we have assessed its incorporation in human bone marrow mononuclear cells. Gas chromatography analysis indicates the presence of AA in their fatty acid composition. In bone marrow mononuclear cells, [3H]-AA is incorporated into triglycerides and is later delivered into phospholipids, a result not observed with blood mononuclear cells. Prelabelling-chase experiments indicate a trafficking of labelled AA from phosphatidylcholine to phosphatidylethanolamine. Stimulation of prelabelled bone marrow mononuclear cells with granulocyte-macrophage colony-stimulating factor (GM-CSF) results in the release of a part of the incorporated labelled AA. Finally, exogenous AA (up to 1 μM) has no significant effect on cell growth. In conclusion, human bone marrow mononuclear cells participate to the control of marrow AA concentrations by incorporating AA into phospholipids and triglycerides. In turn, bone marrow mononuclear cells can release AA in response to the potent haematopoietic growth factor GM-CSF.

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Cuvertino, Sara, Georges Lacaud, and Valerie Kouskoff. "SOX7-enforced expression promotes the expansion of adult blood progenitors and blocks B-cell development." Open Biology 6, no. 7 (July 2016): 160070. http://dx.doi.org/10.1098/rsob.160070.

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During embryogenesis, the three SOXF transcription factors, SOX7, SOX17 and SOX18, regulate the specification of the cardiovascular system and are also involved in the development of haematopoiesis. The ectopic expression of SOX17 in both embryonic and adult blood cells enhances self-renewal. Likewise, the enforced expression of SOX7 during embryonic development promotes the proliferation of early blood progenitors and blocks lineage commitment. However, whether SOX7 expression can also affect the self-renewal of adult blood progenitors has never been explored. In this study, we demonstrate using an inducible transgenic mouse model that the enforced expression of Sox7 ex vivo in bone marrow/stroma cell co-culture promotes the proliferation of blood progenitors which retain multi-lineage short-term engrafting capacity. Furthermore, SOX7 expression induces a profound block in the generation of B lymphocytes. Correspondingly, the ectopic expression of SOX7 in vivo results in dramatic alterations of the haematopoietic system, inducing the proliferation of blood progenitors in the bone marrow while blocking B lymphopoiesis. In addition, SOX7 expression induces extra-medullary haematopoiesis in the spleen and liver. Together, these data demonstrate that the uncontrolled expression of the transcription factor SOX7 in adult haematopoietic cells has dramatic consequences on blood homeostasis.

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Manesso, Erica, José Teles, David Bryder, and Carsten Peterson. "Dynamical modelling of haematopoiesis: an integrated view over the system in homeostasis and under perturbation." Journal of The Royal Society Interface 10, no. 80 (March 6, 2013): 20120817. http://dx.doi.org/10.1098/rsif.2012.0817.

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A very high number of different types of blood cells must be generated daily through a process called haematopoiesis in order to meet the physiological requirements of the organism. All blood cells originate from a population of relatively few haematopoietic stem cells residing in the bone marrow, which give rise to specific progenitors through different lineages. Steady-state dynamics are governed by cell division and commitment rates as well as by population sizes, while feedback components guarantee the restoration of steady-state conditions. In this study, all parameters governing these processes were estimated in a computational model to describe the haematopoietic hierarchy in adult mice. The model consisted of ordinary differential equations and included negative feedback regulation. A combination of literature data, a novel divide et impera approach for steady-state calculations and stochastic optimization allowed one to reduce possible configurations of the system. The model was able to recapitulate the fundamental steady-state features of haematopoiesis and simulate the re-establishment of steady-state conditions after haemorrhage and bone marrow transplantation. This computational approach to the haematopoietic system is novel and provides insight into the dynamics and the nature of possible solutions, with potential applications in both fundamental and clinical research.

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Ramasamy, Saravana K. "Structure and Functions of Blood Vessels and Vascular Niches in Bone." Stem Cells International 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/5046953.

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Bone provides nurturing microenvironments for an array of cell types that coordinate important physiological functions of the skeleton, such as energy metabolism, mineral homeostasis, osteogenesis, and haematopoiesis. Endothelial cells form an intricate network of blood vessels that organises and sustains various microenvironments in bone. The recent identification of heterogeneity in the bone vasculature supports the existence of multiple vascular niches within the bone marrow compartment. A unique combination of cells and factors defining a particular microenvironment, supply regulatory signals to mediate a specific function. This review discusses recent developments in our understanding of vascular niches in bone that play a critical role in regulating the behaviour of multipotent haematopoietic and mesenchymal stem cells during development and homeostasis.

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Fouillard, Loic, Alain Chapel, Domnique Bories, Sandrine Bouchet Tec, Helene Rouard, Patrick Herve, Patrick Gourmelon, Dominique Thierry, and Norbert C. Gorin. "Allogeneic Related HLA Mismatch Mesenchymal Stem Cells for the Treatment of Engraftment Failure Following Autologous Hematopoietic Stem Cell Transplantation." Blood 108, no. 11 (November 16, 2006): 2560. http://dx.doi.org/10.1182/blood.v108.11.2560.2560.

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Abstract Primary graft failure is usually associated with a high mortality rate despite infusion of back up graft and haematopoietic growth factors. In animal models mesenchymal stem cells (MSC) stimulate haematopoiesis recovery after TBI and enhance engraftment of haematopoietic stem cells (Almeida-Porada et al, Exp hematol 1999). Co-infusion of autologous blood stem cells and MSC in cancer patients receiving high dose chemotherapy speed up haematopoietic recovery (Koç et al, JCO 2000). We have previously shown that MSC can engraft and improve the bone marrow microenvironment in a patient with end stage severe aplastic anaemia (Fouillard et al, Leukemia 2003). We report a patient treated with MSC for aplastic anemia secondary to engraftment failure. A 40 year old nulliparous woman with acute myeloid leukaemia received an autologous bone marrow transplantation; conditioning regimen combined a 12 Gray TBI and cyclophosphamide (120 mg/kg). Primary graft failure occurred and persited despite back up marrow infusion. Partial recovery on polymorphonuclear (PMN) and haemoglobin (Hb) was obtained with granulocyte colony stimulating factor (G-CSF) and EPO. Thrombocytopenia remained below 50x109/l. No residual leukaemic cells were detected Three years after ABMT, allogeneic MSC were infused at a dose of 2,78x106/kg. MSC were isolated from a HLA mismatched brother bone marrow (Osiris Therapeutics Inc Baltimore, MD). At time of MSC infusion, the marrow aspirate was hypocellular with no leukaemic blast cells. Blood cell counts were: PMN: 0.8x109/l, platelets: 45x109/l and Hb: 10.5 g/dl. No conditioning regimen and no prophylaxis of GVHD was given. Growth factors were discontinued. After MSC infusion, a rapid haematopoietic recovery was observed on both PMN and platelet which reached a normal level. With a follow up of 18 months, the patient is alive and well. Recovery of haematopoiesis was corroborated by an improvement of in vitro haematopoietic and stromal clonogenic assays. CFU-GM and CFU-F studied the day before MSC infusion, one month and one year after MSC infusion, increased strikingly (p<0.05). LTC-IC increased significantly one year after MSC infusion (p<0.05). There was no change in BFUE. To further characterize the effects seen on haematopoiesis, we utilized a custom RayBiotech antibody array and compared proteins secreted by MSC of recipient before and one year after infusion. This array evidenced an increased secretion of proteins implied in haematopoiesis (Flt3l, GM-CSF, G-CSF, IL1, IL6, TPO, SDF1) one year after MSC infusion. Real time PCR confirmed an up-regulation of gene expression for GCSF, GM-CSF, IL1, IL6. We studied MSC engraftment. We analysed the bone marrow biopsy extracted DNA for mesenchymal chimerism before MSC infusion, one month and one year post MSC infusion by real time quantitative PCR of the Y specific SRY gene: male DNA was not detected before infusion; a level of male DNA of 1/105 was detected one month after MSC infusion. This observation shows that MSC can induce haematopoietic tissue repair. MSC should be considered in the treatment of engraftment failure and other bone marrow failure states including severe idiopathic aplastic anaemia and accidental irradiation.

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Dissertations / Theses on the topic "Bone marrow cells; Blood; Haematopoietic"

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Emambokus, Nikla R. "Applications of the Cre-LoxP technology to the study of megakaryocytes." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325900.

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Chang, Chao-Hui. "Haematopoietic stem/progenitor cell interactions with the bone marrow vascular niche." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:452da334-bd4e-45c7-a7bd-fc8767d1239c.

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Umbilical cord blood (UCB) is used as a source of haematopoietic stem cells (HSCs) for transplantation but shows defective homing to the bone marrow niche and delayed haematological reconstitution. Following transplantation, HSCs will home to the bone marrow in response to the CXCL12 chemokine, adhere to the bone marrow sinusoidal endothelial cells and then migrate into and lodge in bone marrow niches. In addition to CXCR4, a variety of molecules have been described as being important in these processes. In this laboratory, junctional adhesion molecule-A (JAM-A) was shown to be expressed on human UCB CD133⁺/CD34⁺ cells and regulated by hypoxia. In this thesis, further phenotypic studies show that this molecule is most highly expressed on human CD41a⁺ megakaryocytes and CD14⁺ monocytes/macrophages in UCB. JAM-A was also found to be expressed on all human UCB CD133⁺ cells, which have been shown by others to encompass the HSCs and early myeloid-lymphoid precursors and on the majority of CD34⁺ haematopoietic progenitor cells (HPCs). While it is also present on bone marrow sinusoidal endothelium (BMEC), JAM-A is not detected on cultured bone marrow mesenchymal stromal cells (MSCs). JAM-A blockade, silencing and overexpression experiments showed that JAM-A contributes to, but is not solely responsible for, the adhesion of CD34⁺ haematopoietic progenitor cells to IL-1β activated BMEC-60 cells and fibronectin. Lack of significance in cell migration suggested that JAM-A is more likely to act as an adhesion molecule or a regulator of adhesion rather than as a migratory molecule in such cells. Further functional studies using the proximity ligation assay highlight a potential association of JAM-A with CXCR4 and the adhesion molecules, tetraspanin CD82 and integrin β1. Mechanistic studies were commenced to establish if JAMA could modulate CXCR4 signalling following CXCL12 stimulation, but time constraints prevented these from being completed. These preliminary experiments which were carried out first in the Jurkat cell line lacking JAM-A or transduced to express JAM-A, however, suggest that JAM-A may modulate CXCL12-induced Rap1 phosphorylation and ERK1/2 phosphorylation. The former pathway is important for integrin function and the latter pathway is important in cell adhesion. The results described here, although requiring finalisation, support the hypothesis that JAM-A acts as an adhesion molecule and also may fine tune CXCR4 and integrin mediated functions on human CD34⁺ cells, thereby potentially regulating engraftment of these cells to the bone marrow niche.

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Schuller, Christine Children's Cancer Institute Australia for Medical Research Faculty of Medicine UNSW. "Telomeres and telomerase in haematopoietic progenitors and bone marrow endothelial cells." Publisher:University of New South Wales. Children's Cancer Institute Australia for Medical Research, 2008. http://handle.unsw.edu.au/1959.4/41098.

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In normal human somatic cells, the length of telomeres (chromosomal end structures) decreases with each cell division until reaching a critically short length, which halts cell proliferation and induces senescence. The enzyme telomerase, which functions to maintain telomeres at a length that is permissive for cell division, is expressed in approximately 85% of cancer cells and some stem and progenitor cells, including haematopoietic progenitor cells (HPCs), but not most other normal somatic cells. Previous investigations have demonstrated that ectopic expression of telomerase reverse transcriptase (hTERT) reconstitutes telomerase activity, resulting in telomere elongation in some normal human cell types. However, similar experiments performed in HPCs and endothelial cells have demonstrated a dissociation between the expression of telomerase activity and telomere lengthening. This thesis is focussed on further investigating telomerase-mediated telomere length regulation in HPCs and endothelial cells. Short telomeres in bone marrow and blood leukocytes are associated with the development of disorders linked to bone marrow failure. However, to date a relationship between telomere length and myeloid cell proliferative potential has not been demonstrated. In the current investigations, the telomere length and proliferative potential of 31 cord blood-derived HPCs was determined. Regression analysis revealed a significant correlation between mean telomere length and erythroid cell expansion, but not expansion of other myeloid lineage cells. Another novel finding was that telomerase activity was upregulated in lineage-committed CD34- erythroid cells that were positive for the erythroid-specific lineage marker glycophorin A. It was also functionally demonstrated that telomerase activity facilitates the maximum expansion of erythroid cells. To address the dissociation between telomerase activity and telomere maintenance in BMECs, a dominant negative mutant of the telomere binding protein TRF1, which functions to regulate telomere accessibility, was over-expressed in hTERT-transduced BMECs. These studies showed that telomere access, as well as oncogene expression and exposure to oxidative stress, contribute to telomere length regulation in BMECs. Overall, the results from these investigations demonstrate for the first time the functional significance of telomere length and telomerase activity in ex vivo expansion of erythroid cells, and provide novel insight to the molecular complexity of telomere length maintenance in endothelial cells.

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Robinson, Simon N. "Proliferation regulation of haematopoietic stem cells in normal and leukaemic haematopoiesis." Thesis, University of St Andrews, 1992. http://hdl.handle.net/10023/14965.

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The cellular integrity of the blood is maintained by the cellular output of the haematopoietic stem cell population which produces the specialized precursors and differentiated cells which constitute the blood. The investigation of haematopoietic stem cell behaviour and regulation has been hampered by both the difficulty in their identification and the development of relevant assay systems. The purpose of this investigation was to study the behaviour and regulation of the haematopoietic stem cell population in normal and leukaemic haematopoiesis using an in vitro assay of a primitive haematopoietic precursor. The use of a combination of haematopoietic colony-stimulating factors [interleukin 3 (IL3)/multi-CSF and macrophage colony-stimulating factor (M-CSF/CSF-1)] in semi-solid agar culture of murine haematopoietic tissue, stimulated the proliferation of a haematopoietic colony-forming cell, defined as the "HPP-CFCIL3+CSF-1" population, which was characterized by a high proliferative potential, a multipotency and behavioural and regulatory properties consistent with its being a primitive haematopoietic precursor and possibly a component of the haematopoietic stem cell population. The proportion of the in vitro HPP-CFCIL3+csf-1 population in S-phase in normal murine marrow, was determined to be relatively low at approximately 10%, increasing to approximately 40% in sublethally X-irradiated, regenerating murine marrow and the respective presence of the haematopoietic stem cell proliferation inhibitor and stimulator was demonstrable by the induction of appropriate kinetic changes in the in vitro HPP-CFCIL3+CSF-1 population. In leukaemic haematopoiesis, leukaemic proliferation often occurs at the expense of apparently suppressed normal haematopoiesis. In vitro HPP-CFCIL3+CSF-1 assay of the haematopoietic stem cell proliferation regulators in a number of murine, myeloid leukaemic cell lines, failed to demonstrate either increased levels of the haematopoietic stem cell proliferation inhibitor, or evidence of a direct-acting, leukaemia- associated proliferation inhibitor, however, evidence of a leukaemia- associated impairment of inhibitor and stimulator production was observed and this may be a possible mechanism by which the leukaemic population develops a proliferative advantage over normal haematopoietic tissue. The identification of a possible mechanism of leukaemic progression and suppression of normal haematopoiesis may subsequently allow the development of potentially more effective disease treatment and management regimes. The endogenous haemoregulatory tetrapeptide: Acetyl-N-Ser- Asp-Lys-Pro [AcSDKP, Mr=487 amu] is reported to prevent the G0-G1 transition of haematopoietic stem cells into S-phase. The mechanism of action of AcSDKP and a number of related peptides, was investigated in relation to the stem cell proliferation stimulator and inhibitor. AcSDKP demonstrated no direct haemoregulatory role against the in vitro HPP-CFCIL3+CSF-1 population, which is consistent with reports that AcSDKP is not active against cells already in late G1, or S-phase, rather it appeared to act indirectly by impairing the capacity of the haematopoietic stem cell proliferation stimulator to increase the proportion of the in vitro HPP-CFCIL3+CSF-1 population in S-phase. An apparent impairment of stimulator action may explain the reported AcSDKP-associated 'block' of haematopoietic stem cell recruitment. A putative endogenous AcSDKP precursor and synthetic and degradative enzyme systems have been reported and the possible physiopathological role of AcSDKP in a number of myeloproliferative disorders has been implicated. The potential application of AcSDKP as a 'haemoprotective' agent administered prior to the use of S-phase- specific chemotherapy may be of clinical significance. The in vitro HPP-CFCIL3+CSF-1 assay of a primitive haematopoietic precursor cell population, which may be a component of the haematopoietic stem cell population, should play a significant role in the investigation of haematopoietic stem cell behaviour and regulation in both normal and aberrant haematopoiesis. With the characterization of the mechanism(s) of action of the haematopoietic stem cell proliferation inhibitor and stimulator and the haemoregulatory tetrapeptide AcSDKP, the manipulation of the haematopoietic system to clinical advantage can be envisaged, while the identification of the aberrant regulatory mechanism(s) in haematopoietic dysfunction may allow, the development of more effective disease treatment and management regimes.

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Hodby, Katharine Ailsa. "Investigating the mechanism of bone marrow failure observed in patients with acute myeloid leukaemia." Thesis, Queen Mary, University of London, 2018. http://qmro.qmul.ac.uk/xmlui/handle/123456789/36673.

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Patients with Acute Myeloid Leukaemia (AML) present with the signs and symptoms of bone marrow failure. This finding spans the genetic and phenotypic diversity of the disease. The mechanism which underlies it is poorly understood. This thesis explores the effect of AML on the normal haematopoietic stem cell (HSC) population, using primary human diagnostic bone marrow samples. Previous work from our group suggested that AML induces a state of quiescence in HSCs, producing a differentiation block responsible for the observed cytopenias1. Reversal of this process might offer an alternative to the current treatment of patients with palliative transfusions. I have developed a flow cytometry-based technique to differentiate normal HSCs from leukaemia cells, selecting cells with the CD34+38-ALDHhighCLL1- expression signature. Validation of this technique by assessment of sorted cells by FISH and PCR, suggests it is successful in 73% of AML samples. In a further 25% of samples, it selects for a population significantly enriched for normal HSCs. We used this panel to investigate the concentration of HSCs at AML diagnosis, compared to controls. We show that there is no significant difference between HSC concentration at AML diagnosis (n=38, median [HSC] 2.5 cells/μl) and controls (n=24, median [HSC] 2.4 cells/μl). HSC concentration was not significantly affected by AML karyotype, patient age or gender. However, those patients presenting with a low HSC concentration at diagnosis (< 0.1 HSC/μl) were found to have a significantly worse outcome both in terms of overall and relapse-free survival, an effect apparently independent of age, gender and underlying karyotype. HSC concentration at diagnosis with AML may therefore represent a new independent prognostic marker. We then studied CD33 expression patterns on HSCs within Core Binding Factor mutated AML (n=37) at diagnosis, and found its expression to be significantly lower than on HSCs within controls (n=9) (17% versus 58%, p=0.005). CD33 expression on HSCs from AML samples rose significantly from diagnosis to remission (n=16) (17% to 58%, p=0.0001). This mirrors previous findings from our group using CD34low AML samples, and is, we believe, the first time that the antigenic signature of normal HSCs has been shown to be modified. 6 by the presence of AML. However, an in vitro assay to test the significance of these changes in terms of the cytotoxicity of GO towards normal HSCs did not demonstrate a significant difference between HSC subgroups. Finally, we attempted to investigate the mechanism by which AML might induce HSC quiescence by studying the comparative transcriptomes of HSCs from CD34low AML (n=6) and controls (n=6) by RNA-Seq, using direct cell to cDNA synthesis, followed by amplification. A first attempt resulted in poor quality data, with a significant proportion of reads mapping to non-coding DNA regions. A repeat approach, using utilising immediate RNA extraction post sorting resulted in significantly better quality data Bioinformatics analysis revealed differential expression of 6 genes between the 2 datasets (GNPDA1, ADGRG3, MIAT, WDR31, RP11-244H3.1 and RXFP1). GO enrichment studies using David highlighted a number of pathways including the TNF signalling pathway (p=0.003; after Benjamini-Hochberg correction p=0.51). Validation of these findings by independent qPCR, and functional exploration of enriched signalling pathways remains outstanding.

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Gilmore, William Samuel. "A study of molecules involved in the regulation of the growth of haematopoietic cells and heart muscle cells in culture." Thesis, University of St Andrews, 1986. http://hdl.handle.net/10023/14970.

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The description of the molecular events responsible for the control of cell division and differentiation is, currently, one of the major goals of molecular and cellular biologists. Cell and tissue culture techniques have proved to be promising laboratory tools for the study of the regulators of cellular growth and differentiation. Most cells in culture require specific polypeptide growth factors which are supplied by the addition of a complex biological fluid such as serum or, in some instances, by the cells themselves. These growth factors usually act on their target cell via a membrane receptor to which they bind. The events which occur after the growth factor binds to the membrane receptor have not been fully described, but the phosphorylation of tyrosine residues in certain proteins has been observed. A study was made of the polypeptide growth factors responsible for the growth and differentiation of haematopoietic cells in vitro. These growth factors, called colony - stimulating factors (C.S.F.'s) were prepared from human placental conditioned medium, giant cell tumour conditioned medium and pokeweed mitogen stimulated spleen conditioned medium. A C.S.F. from human placental conditioned medium was radioiodinated and the binding of the labelled growth factor to an anti-C.S.F. antiserum was studied. The binding studies indicated that a purer C.S.F. preparation and/or a more specific antiserum was necessary in order to establish a radioimmunoassay for C.S.F. The C.S.F.'s from giant cell tumour conditioned medium were purified by ultrafiltration, hydrophobic - interaction chromatography, gel filtration and thiolpropyl - sepharose 6B chromatography. Two peaks of biological activity were observed on gel filtration. One of these peaks gave an apparent MW of 63,000 and the other peak gave an apparent MW of 30,200. The C.S.F. from pokeweed mitogen stimulated spleen conditioned medium was labelled with peroxidase and the binding of the labelled-C.S.F. to bone marrow cell membranes studied. The labelled-C.S.F. bound to the membranes and the binding exhibited a linear relationship with membrane protein content. Also a defined growth medium for chick embryonic heart cells was developed. These cells were observed to differentiate from primitive foetal cells into mature "adult-type" cells. The cells grew as a monolayer, had spontaneous activity and were seen to beat.

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Nicol, Andrew. "Analysis and in-vitro expansion of cord blood haemopoietic stem cells for transplantation." Thesis, University of Bristol, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337265.

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Prewitz, Marina. "Decellularised extracellular matrices as instructive microenvironments for bone marrow derived stem cells." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2012. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-86334.

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The regenerative potential of adult stem cell populations within the human body bears great promises for their use in regenerative medicine. The bone marrow (BM) harbours two different types of adult stem cells, haematopoietic stem and progneitor cells (HSPCs) and multipotent mesenchymal stromal cells (MSCs), which are tightly regulated in their distinct anatomically defined niches by multiple cues such as cytokines, cell-cell contacts, the extracellular matrix (ECM) and the physical microenvironment. The ex vivo expansion of these cells for applications in regenerative therapies is of great interest and several biomaterial approaches attempt to mimic the natural BM niche and its components to control stem cell maintenance and differentiation. However, as of now the complexity of such stem cell niches is hard to recapitulate. Towards this goal, this work was focussing on the ECM environment of BM stem cells and was set out to engineer improved in vitro culture systems. MSC themselves are one of the most important cell types within the BM that secrete and construct ECM-networks and thereby shape the microenvironment of the residing cells. The potential of primary human BM-MSC to secrete ECM in vitro has been exploited to generate niche-like ECM surrogates in a robust and versatile format. Application of decellularisation regimes allowed the fabrication of complex matrices which demonstrated suprastructural, compositional and physicochemical properties compareable to those of the native BM-ECM environment. Reliable stability and reproduciblity was achieved by a dedicated procedure of maleic anhydride co-polymer-mediated covalent binding of fibronectin and subsequent anchorage of cell-secreted ECM molecules. As a result of the high reproducibility, a complete proteomic register of ECM molecules was obtained in combination with determining the complex fibrillar and soft gel-like characteristics of MSC-derived matrices. Based on the established BM niche-like substrate, the impact of extracellular matrices on MSC and HSPC ex vivo behavior has been explored. Both cell types demonstrated strong adhesion to ECM substrates and depicted a changed cellular morphology upon contact with native ECM structures compared to standard culture substrates or simple ECM protein coatings, indicating an intense interplay between the cell and the microenvironment. MSC that re-grew into their own matrices have shown advantageous proliferation and cytokine secretion levels as well as enhanced differentiation intensity (upon differentiation induction) compared to MSC that were cultured on less complex substrates. Similarly, HSPC were also instructed for enhanced expansion on MSC-derived matrices without exhaustion of stem cell-marker expressing progenitor cells. The efficiency of these matrices was related to their ability to mimic the native composite suprastructure, ligand nano-topography, molecular composition and physical properties of natural BM ECM environments. The data obtained within this thesis set the ground for a more rational design of artificial stem cell niches with defined and distinct properties, offering exciting options for the in-depth analysis and understanding of stem cell regulation by exogenous cues.

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9

Taylor, Alan. "The role of leukaemia inhibitory factor and a leukaemic associated inhibitor in the control of the proliferation of haematopoietic stem cells." Thesis, University of St Andrews, 1996. http://hdl.handle.net/10023/14962.

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Activities associated with, or interacting with, leukaemic cell populations were assayed for the ability to influence in vitro haematopoiesis. The first of these, the glycoprotein leukaemia inhibitory factor (LIF), has a role in aspects of murine, non human primate and human haematopoiesis. It is thought to be particularly important in the development of megakaryocytes and is also known to induce the terminal differentiation of certain leukaemic cell lines. LIF was assayed both for direct and indirect effects on the proliferation of haematopoietic precursor cell populations in vitro. As a direct acting agent in semi-solid agar culture of haematopoietic cell populations derived from normal bone marrow or 15 day foetal liver, LIF was unable to support colony formation. In cultures of cells derived from normal bone marrow stimulated with single, or combinations of, growth factors, the addition of LIF had no statistically significant effect on the level of colony formation. In cultures of cells derived from foetal liver, stimulated with particular growth factor combinations (medium conditioned by the Wehi3B leukaemic cell line + medium conditioned by the lung fibroblast cell line, L929); GM-CSF + M-CSF; IL-la + IL-3 + M-CSF), LIF, was shown to decrease the level of colony formation. LIF did not directly alter the proportion of the population in DNA synthesis in cell populations derived from normal femoral marrow, 15 day foetal liver or y- irradiated femoral marrow. As an indirect acting agent LIF failed to block the synthesis of a stem cell stimulator, or it's action, on a population of high proliferative potential colony forming cells derived from normal femoral marrow, cloned in the presence of Wehicm+L929cm. (HPP-CFC (Wehicm + L929cm)) LIF's actions on clones of a murine myeloid leukaemia (SA2JMB1) were also assessed. LIF had no statistically significant effect on colony formation or the level of DNA synthesis in populations of SA2JMB1 leukaemic cells. A second group of associated activities was produced by the X- irradiation induced murine myeloid leukaemia (SA2JMB1). Medium conditioned by the leukaemic cells was assayed in vitro both for direct and indirect effects on the proliferation of haematopoietic cells derived from femoral marrow. As a direct acting agent in 7 and 14-day semi-solid agar culture of femoral marrow, leukaemic conditioned medium alone stimulated limited colony formation. In 7 and 14 day cultures stimulated with single and combinations of specific colony stimulating factors: (rmGM-CSF, rhM-CSF, rhIL-1a) a significant increase in colony number was noted in all cases when cultures were supplemented with leukaemic conditioned medium. SA2JMBlcm was shown to support the proliferation of an IL-3 dependent cell line (FDCP-A4 cells). The colony enhancing ability of SA2JMBlcm was shown to be blocked by pretreatment with antibodies to IL-3. This suggested that SA2JMB1 conditioned medium contained IL-3 or an IL-3 like activity, as one of its components. The conditioned medium failed to directly alter the level of DNA synthesis in a population of HPP-CFC (Wehicm+L929cm) derived from normal bone marrow or y- irradiated bone marrow. As an indirect acting agent the conditioned medium did block the action of a stem cell proliferation stimulator on normal bone marrow derived HPP-CFC (Wehicm+L929cm). This leukaemia associated activity was shown to be larger than 50KD, sensitive to heat treatment and able to act in a different manner to the stem cell inhibitor MIP-1-a. Thus this novel activity may be important in blocking stimulator action in haematopoietic stem cells and thus contribute to the haematopoietic insufficiency seen in leukaemia.

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Novitzky, Nicolas. "Interactions between the haematopoietic stem cell and the myeloid microenvironment in aplastic anaemia." Doctoral thesis, University of Cape Town, 1993. http://hdl.handle.net/11427/24943.

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In patients with aplastic anaemia that respond to immunosuppressive therapy, quantitative, morphological and functional haematologic derangement have been reported. To explain these findings, abnormalities in the marrow stroma or the stem cell have been postulated. To define the relative contribution of each of the latter, the integrity of the bone marrow from sixteen patients that responded to anti-lymphocyte globulin and high dose methyl prednisolone was compared to normal individuals. Bone marrow mononuclear cells were divided into two fractions. From the first, stroma was cultured in aMEM containing 12.5% of both horse and foetal calf serum and 10-5 M hydrocortisone at 37° C in 5% CO2 in 90% humidity. The medium was changed weekly. Upon confluence, these stromal layers were studied morphologically and with cytospin preparations stained with Sudan black, 0 red oil, alkaline and acid phosphatases. The remainder was monocyte and lymphocyte depleted, CD 34+ progenitors were selected with paramagnetic beads and the population morphologically and immunophenotypically defined. To determine the functional status, control or patient CD 34+ progenitors, were suspended for two hours on normal or aplastic stroma for adherence to take place. The non-adhesive fraction was decanted by standardised washing and cultured for fourteen days in the presence of PHA-conditioned medium in the CFU-gm assay. Strama-adherent progenitors were covered with 0.3% agar and cultured for five days. Aggregates with more than twenty cells were scored (CFU-bl). The remaining CD 34+ cells were cultured in the mixed colony assay with combinations of recombinant cytokines belonging to the G protein super-family and the tyrosine kinase group in dose response studies. Light density cells from patients with treated aplasia contained significantly fewer CD 34+ cells than those present in the control suspensions (mean 0.65%, SD 0.35% vs 1.62%, SD 1.4%; p= 0.002). Normal and aplastic stroma became confluent at three and four weeks. There was no difference on the morphology or the cytochemical stains between the two groups. Functionally, aplastic bone marrow stroma supported CFU-bl formation no differently from normal layers. However, CD 34+ precursors from the patients cultured on control stroma resulted in significantly fewer CFU-bl (p= 0.0002,) and CFU-gm (p= 0.0009). This work provides original evidence supporting the reduced clonogenicity of the corresponding populations of CFU-bl from patients with aplasia is unrelated to attachment to the stroma, but intrinsic to the CD 34+ cells. Moreover, this study shows for the first time that exposure of these progenitors to growth factors belonging to the G protein and tyrosine kinase receptor families have defective responses, correctable only at supra physiological concentrations, while effects on combinations containing c-kit ligand, appear preserved. Following immunosuppressive therapy, the bone marrow is repopulated by a hypoproliferative progenitor cell population which responds suboptimally to physiological cytokine stimulation. This suggests that abnormal interactions between receptors and their ligands or alterations in the signal transduction for cell division by the cytokines belonging to the G superfamily lead to suboptimal growth.

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Books on the topic "Bone marrow cells; Blood; Haematopoietic"

1

Pathology of bone marrow and blood cells. 2nd ed. Baltimore, Md: Lippincott William & Wilkins, 2009.

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Diggs, L. W. The morphology of human blood cells. 6th ed. Abbott Park, Ill: Abbott Laboratories, 2003.

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University of Minnesota. Blood and Marrow Transplant Program. Blood and marrow transplantation: A patient's guide. 2nd ed. Minneapolis: Fairview Press, 2010.

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Harvey, John W. Atlas of veterinary hematology: Blood and bone marrow of domestic animals. Philadelphia, PA: W.B. Saunders, 2001.

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Maziarz, Richard T., and Susan Slater. Blood and marrow transplant handbook: Comprehensive guide for patient care. New York: Springer, 2011.

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Blood and marrow transplantation long term management: Prevention and complications. Chichester, West Sussex, UK: John Wiley & Sons, 2014.

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International Conference on the Occasion of the 60th Birthday of T.M. Fliedner (1989 Schloss Reisensburg, Germany). The hemopoietic stem cell: The origin and clinical usefulness of harvested peripheral blood stem cells : repair of stem cells and their kinetic properties in recovery from marrow injury by radiation and chemicals. Ulm: Universitätsverlag Ulm, 1990.

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Hokkaido Symposium on Transfusion Medicine (6th 1994 Sapporo-shi, Japan). Transfusion and hematopoietic stem cells: Proceedings of the 6th Hokkaido Symposium on Transfusional Medicine. Oxford: Blackwell Science, 1996.

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Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, and Hassan Al-Sader. Haematopoietic stem cell transplantation. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0009.

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Haemopoietic stem cell transplantation (SCT) - Indications for haemopoietic SCT - Allogeneic SCT - Autologous STC - Investigations for BMT/PBSCT - Pretransplant investigation of donors - Bone marrow harvesting - Peripheral blood stem cell mobilization and harvesting - Microbiological screening for stem cell cryopreservation - Stem cell transplant conditioning regimens - Infusion of cryopreserved stem cells - Infusion of fresh non-cryopreserved stem cells - Blood product support for SCT - Graft-versus-host disease (GvHD) prophylaxis - Acute GvHD - Chronic GvHD - Veno-occlusive disease (syn. sinusoidal obstruction syndrome) - Invasive fungal infections and antifungal therapy - CMV prophylaxis and treatment - Post-transplant vaccination programme and foreign travel - Longer term effect post-transplant - Treatment of relapse post-allogeneic SCT - Discharge and follow-up

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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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Book chapters on the topic "Bone marrow cells; Blood; Haematopoietic"

1

Nakano, Toru, Takumi Era, Hiroaki Kodama, and Tasuku Honjo. "Development of Blood Cells from Mouse Embryonic Stem Cells in Culture." In Bone Marrow Transplantation, 9–19. Tokyo: Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-68320-9_2.

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Tanaka, Junji, Masahiro Imamura, Masaharu Kasai, Satoshi Hashino, Satoshi Noto, Sumiko Kobayashi, Keisuke Sakurada, and Masahiro Asaka. "Cytokine Gene Expression in Peripheral Blood Mononuclear Cells after Allogeneic Blood Stem Cell Transplantation." In Bone Marrow Transplantation, 142–45. Tokyo: Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-68320-9_18.

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Brenner, M. K., J. P. Grob, and H. G. Prentice. "Purging of Bone Marrow." In White cells and platelets in blood transfusion, 225–36. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2089-0_21.

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Gascon, Pere. "Bone Marrow Toxicity: Red Blood Cells." In Side Effects of Medical Cancer Therapy, 407–26. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-70253-7_15.

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Aapro, Matti S. "Bone Marrow Toxicity: White Blood Cells." In Side Effects of Medical Cancer Therapy, 427–37. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-70253-7_16.

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Gascon, Pere. "Bone Marrow Toxicity: Red Blood Cells." In Side Effects of Medical Cancer Therapy, 333–64. London: Springer London, 2012. http://dx.doi.org/10.1007/978-0-85729-787-7_8.

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Aapro, Matti S. "Bone Marrow Toxicity: White Blood Cells." In Side Effects of Medical Cancer Therapy, 365–80. London: Springer London, 2012. http://dx.doi.org/10.1007/978-0-85729-787-7_9.

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Takaue, Yoichi, Yoshifumi Kawano, Arata Watanabe, Haruhiko Eguchi, Takanori Abe, Atsushi Makimoto, Yasuhiro Okamoto, and Yasuhiro Kuroda. "Transplantation with Purified or Unmanipulated Mobilized Blood Stem Cells in Children." In Bone Marrow Transplantation, 246–49. Tokyo: Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-68320-9_30.

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Scheding, Stefan, Wolfram Brugger, and Lothar Kanz. "Transplantation of Ex-Vivo Expanded Peripheral Blood Progenitor Cells After High Dose Chemotherapy in Cancer Patients." In Bone Marrow Transplantation, 250–57. Tokyo: Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-68320-9_31.

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Mulder, P. O. M., D. Th Sleijfer, E. G. E. de Vries, P. H. B. Willemse, P. E. Postmus, J. L. M. Orie, C. Th Smit Sibinga, M. R. Halie, and N. H. Mulder. "Autologous Bone Marrow Transplantation in Solid Malignancies." In White cells and platelets in blood transfusion, 93–100. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2089-0_10.

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Conference papers on the topic "Bone marrow cells; Blood; Haematopoietic"

1

Yan, W. W., Y. Liu, and B. M. Fu. "Mechanical Mechanism of Circadian Fluctuations Regulated Haematopoietic Stems Cell Release." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53377.

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Haematopoietic stem cells (HSCs) circulate in the bloodstream under flow conditions, but the mechanical mechanisms of governing their physiological trafficking in mammals are still not yet clearly understood. The mobilization of HSCs and their progenitors into the circulation represents the basis for modern bone marrow transplantation procedures [1]. Recently, Mendez-Ferrer et al. performed experimental investigations on mice [2]. They demonstrated that the circulating HSCs and their progenitors exhibit robust circadian oscillations, and the circadian fluctuations could also be significantly altered when the HSCs were subjected to different time of lighting. These results indicated that the photic cues could affect the trafficking of HSCs in healthy animals. This implies that the light is the stimulus of HSCs release. When the HSCs are exposed to light, the HSCs release would markedly increase; when the HSCs are in darkness, the HSCs release keeps low efficiency. In this study, we numerically simulate this phenomenon to study the mechanical mechanism of circadian fluctuations regulated HSCs release under the influence of periodic lighting time.

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Moore, AP, MM Magbanua, J. Scott, D. Moore, MD Alvarado, LJ Esserman, and JW Park. "Simultaneous quantitative assessment of tumor cells in blood and bone marrow in primary breast cancer patients." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-302.

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Pincha, Mudita, Paranchai Boonsawat, Christoph Domschke, and Philipp Beckhove. "Abstract 4076: Characterizing tumor-specific memory stem like T cells in blood and bone marrow of breast cancer patients." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4076.

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Pindur, G., E. Seifried, and H. Rasche. "FIBRIN DEPOSITS IN BONE MARROW AND CHANGES IN HAEMOPOIESIS AFTER ENDOTOXIN ADMINISTRATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644256.

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Thrombotic occlusion of microcirculation during DIC has already been studied in numerous organs, but little is known about analogous findings in the bone marrow. Therefore in rats under the influence of endotoxin the defibrination was examined for its relationship to changes inthe bone marrow and haemopoiesis. Bone marrow specimens were studied histologically by fibrin staining methods. Blood cells were measured automatically on the Coulter counter, fibrinogen by clotting assay. A fall in the thrombocyte and fibrinogen level was induced through a single injection of endotoxin with a maximum after 24 hours and 48 hours. In the same phase, after a short-term drop, a marked rise in the leukocyte count in the peripheral blood was observed. Following an initial increase the erythrocytes dropped and reached their lowest level after 48 hours. In the bone marrow 24 hours after endotoxin administration a large amount of fibrin deposits were observed in the small vessels. At the same time a clear reduction in all three haemopoietic cell lines was noticed. Between days five and ten the parameters of the peripheral blood normalized. Fibrin deposits in the bone marrow were no longer evident after three days. After 28 days an increase in the granulocytopoiesis and a continuing reduction in the megakaryopoiesis was observed.lt is concluded, due to the existence of fibrin deposits in the bone marrow in the beginning phase, that the observed haematologic alterations can not only be explained by the direct effect of endotoxin, but possibly also by the temporary microcircu-latory disturbances of the bone marrow during defibrination with its adverse effects on the haemopoiesis.

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LoSurdo, Jessica L., Douglas W. Chew, Alejandro Nieponice, and David A. Vorp. "Mechanical and Chemical Stimulation of Bone-Marrow Stem Cells in a Three-Dimensional Fibrin Matrix: Preliminary Results." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193117.

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The primary goal of tissue engineering is to develop a biological, mechanically-robust, and anti-thrombogenic vascular graft to replace diseased or damaged tissue and organs [1]. For example, researchers have incorporated smooth muscle cells (SMCs) into extracellular matrix to provide a living, functional conduits with the intended purpose of replacing SMC-containing tubes, such as the blood vessel, urethra, esophagus, intestine, etc. Although the preferred source is autologous cells to avoid immunological rejection, adult SMCs are difficult to obtain and expand. An alternative source of autologous cells could be bone marrow derived stem cells (BMSCs), which differentiate toward mesenchymal and hematopoietic lineages [2].

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Ohta, Makoto, Wataru Sakuma, Toshio Nakayama, Hitomi Anzai, Makoto Ito, Katsuyuki Sado, and Shuji Nakamura. "Computational Fluid Dynamics Analysis of the Bone Marrow in Cancellous Bone as a Non-Newtonian Fluid." In ASME 2016 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/imece2016-67006.

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Stem cells in the bone marrow (BM) are used as regenerative treatment for leukemia. They are usually harvested by puncturing the cancellous bone in the ilium of the donor with a needle. However, this process can cause severe burden to the donor because of its inefficiency; the bone may require 50–100 punctures to obtain enough stem cells. Various factors affect the volume of BM harvested, and their influence can be estimated by observing the flow in the cancellous bone. Recent computational fluid dynamics (CFD) analyses of BM with 3-D reconstruction of the cancellous bone have profiled flow velocity or wall shear stress (WSS) and have shown that some parts on the surface of the cancellous bone have higher WSS and that this high WSS may tear cells from the surface of the bone. CFD analysis may therefore help determining a method for efficient stem cell harvest. However, it is difficult to validate CFD using BM structure because of its porosity. To improve the accuracy of WSS and flow pattern calculations, blood characteristics should be incorporated as key factors and the effects of non-Newtonian flow and viscosity on the flow patterns evaluated. Therefore, the purpose of this study was to evaluate CFD analyses of BM in the cancellous bone based on flow where viscosity depended on the shear rate. BM from porcine ilium bones was extracted, and the viscosities of samples, with or without anti-clotting medications, were measured at various shear rates. 3-D reconstruction of the cancellous bone was performed using micro-CT after removing BM and fat from the bone. The resolution of the reconstruction was 11.7 μm per pixel, which was sufficient to reconstruct the porous structure. The size of the bone sample was 2.5 × 2.5 × 3.5 mm. The number of mesh was approximately 4.3 million. CFD analyses were performed using 3-D reconstruction and viscosity profile at three pressure differences (5, 7, and 10 kPa). Constant pressure was applied in the outlet. The viscosity of BM could be divided into three shear rate ranges. The first corresponded with a shear rate over 100 1/s, where the viscosity was constant at less than 0.01 Pa·s. Transient curves were observed for shear rates 0.01–100 1/s. At lower shear rates, the viscosity was again constant, at over 105 Pa·s. These changes were higher than the changes in blood viscosity based on the shear rate. The CFD analyses showed that the results depended on the inlet pressure. When the pressure difference was 10 kPa, the viscosity change almost disappeared, and the velocity profile was similar to that of Newtonian flow. When the pressure difference was 5 or 7 kPa, changes in viscosity and completely changed flow patterns were observed. The WSS profile also changed with the velocity profile. Therefore, pressure can be a major factor in the velocity profile of BM in the cancellous bone. Effects of non-Newtonian flow on velocity and WSS profiles were observed under an appropriate pressure difference.

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Chebouti, Issam, Agnes Bankfalvi, Christoph Friedrich, Rainer Kimmig, and Sabine Kasimir-Bauer. "Abstract 369: Association between tumor infiltrating immune cells, circulating tumor cells in blood and disseminated tumor cells in the bone marrow in patients with primary ovarian cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-369.

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Deng, Glenn, Sujatha Krishnakumar, Marc A. Coram, Ashley A. Powell, Haiyu Zhang, Michael N. Mindrinos, Melinda L. Telli, et al. "Abstract 3528: Genotype discordance between circulating tumor cells in blood and disseminated tumor cells in bone marrow at single cell level in breast cancer patients." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3528.

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9

Grisanti, S., F. Consoli, C. Almici, F. Bertagna, R. Verardi, M. Ungari, V. Amoroso, et al. "P4-07-19: Bone Marrow Involvement Is Associated with High Numbers of Circulating Tumor Cells in Peripheral Blood of Metastatic Breast Cancer Patients." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p4-07-19.

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Adany, R., A. Kiss, J. Kappelmayer, R. J. Ablin, and L. Muszbek. "EXPRESSION OF FACTOR XIII SUBUNIT A IN DIFFERENT TYPES OF HUMAN MACROPHAGES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644651.

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In addition to plasma the presence of subunit a of blood coagulation Factor XIII (FXIIl) has been verified in platelets and megakariocytes. Most recently, we demonstrated that human peripheral blood monocytes also contain FXIII subunit a. The present study was designed 1/ to determine the stage in the maturation sequence of bone marrow monocytopoesis in which FXIII appears 2/ to establish if FXIII is retained during differentiation into macrophages 3/ to assess how general is the presence of FXIII subunit a in different types of macrophages. FXIII subunit a was immunomorphologically detected in bone marrow smears, in cytospin preparations of cells from serous cavities (pleural, peritoneal, pericardial and synovial spaces), and paraformaldehyde-fixed paraffin-embedded or frozen sections of different organs where classical types of macrophages have been described earlier (liver, lung, thymus, skin, connective tissue, prostate and developing bone) . Cells containing FXIII subunit a were intensively characterized by immunofluorescent and enzymecytochemical techniques in double and treble labeling systems. Its presence was clearly demonstrated in promonocytes of bone marrow, and in all probability, it is present in monoblasts, as well. FXIII was also found in macrophages from different serous cavities and in embryonic osteoclasts. Cells containing FXIII subunit a of connective tissue were found to be tissue histiocytes, and not fibroblasts as previously thought. Kupffer cells of the liver and Langerhans cells of the epidermis were negative supporting theories that these cells are not members of monocyte-derived macrophage cell population. Immunomorphological detection of FXIII subunit a seems to be a useful marker for labeling the continuum of monocyte/macrophage cell line from the earliest ftrais in the bone marrow to the mature forms of macrophages and might be a valuable tool in the cytological diagnosis of malignant disorders of this cell line.

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Reports on the topic "Bone marrow cells; Blood; Haematopoietic"

1

Vessella, Robert L. Does the Phenotyping of Disseminated Prostate Cancer Cells in Blood and Bone Marrow Prior to Radical Prostatectomy Provide Prognostic Information? Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada435227.

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Vessella, Robert L. Does the Phenotyping of Disseminated Prostate Cancer Cells in Blood and Bone Marrow Prior to Radical Prostatectomy Provide Prognostic Information? Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada412293.

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Vessella, Robert. Does the Phenotyping of Disseminated Prostate Cancer Cells in Blood and Bone Marrow Prior to Radical Prostatectomy Provide Prognostic Information? Fort Belvoir, VA: Defense Technical Information Center, July 2003. http://dx.doi.org/10.21236/ada418201.

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