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勞錦輝 and Kam-fai Simon Lo. "Cytomegalovirus and bone marrow transplantation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31215609.
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Lo, Kam-fai Simon. "Cytomegalovirus and bone marrow transplantation /." Hong Kong : University of Hong Kong, 1997. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19471142.
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Fadini, Gian Paolo. "Bone marrow dysfunction in diabetes." Doctoral thesis, Università degli studi di Padova, 2013. http://hdl.handle.net/11577/3422580.
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Background. Diabetes mellitus (DM) increases cardiovascular disease (CVD) and this is attributed, at least in part, to shortage of vascular regenerative cells derived from the bone marrow (BM). Indeed, the BM harbours several subsets of progenitor cells for endothelial, smooth muscle cells and cardiomyocytes, which derive from a common CD34+ ancestor. Recent data from experimental models of type 1 and type 2 diabetes highlight BM pathologies that include microangiopathy, neuropathy, altered gene expression and niche dysfunction.
Aims. The set of experiments herein described aim to portray the alterations of BM function in clinical and experimental diabetes.
Methods. The approaches are diversified and include: 1) A prospective trial of direct BM stimulation with human recombinant granulocyte colony stimulating factor (G-CSF) in diabetic and non diabetic patients; 2) A meta-regression analysis of trials using G-CSF to stimulate cardiovascular repair in diabetic and non diabetic patients; 3) A study of stem/progenitor cell compartmentalization in the BM and peripheral blood (PB), in relation to diabetes; 4) An animal study to dissect the role of DPP-4 dysregulation in the impaired stem/progenitor cell mobilization induced by diabetes.
Results. Part 1: in response to G-CSF, levels of CD34+ cells and other progenitor cell phenotypes increased in non DM subjects. DM patients had significantly impaired mobilization of CD34+, CD133+, CD34+CD133+ hematopoietic stem cells and CD133+KDR+ endothelial progenitors, independently of potential confounders. The in vivo angiogenic capacity of circulating mononuclear cells increased after hrG-CSF in non DM controls, but not in DM patients. DM was associated with inability to upregulate CD26/DPP-4 on CD34+ cells, which is required for the mobilizing effect of G-CSF.
Part 2: for the meta-regression analysis 227 articles were screened, 96 were retrieved for evaluation and 24 retained for the analysis of the primary end-point. There was a strong negative correlation between prevalence of diabetes and achieved CD34+ cell levels after G-CSF stimulation (r=-0.68; p<0.0001), while there was no correlation with other traditional risk factors. A multiple regression analysis showed that the correlation between diabetes and mobilization was independent. In 13 articles reporting pre- and post-G-CSF cell counts, the increase in CD34+ cells was also negatively correlated with prevalence of diabetes (r=-0.82; p<0.0001).
Part 3. PB and BM CD34+ cell counts were directly correlated, and that most circulating CD34+ cells were viable, non-proliferating and derived from the BM. Then, PB and BM CD34+ cell levels were analyzed in a 2-compartment model in 72 patients with or without cardiovascular disease. Self organizing maps showed that disturbed compartmentalization of CD34+ cells was associated with aging and cardiovascular risk factors, especially diabetes. High activity of DPP-4, a regulator of the mobilizing chemokine SDF-1α, was associated with altered stem cell compartmentalization. The role of DPP-4 in the BM mobilization response of diabetic rats was then assessed. Diabetes differentially affected DPP-4 activity in PB and BM and impaired stem/progenitor cell mobilization after ischemia or G-CSF administration. DPP-4 activity in the BM was required for the mobilizing effect of G-CSF, while in PB it blunted ischemia-induced mobilization. Indeed, DPP-4 deficiency restored ischemia (but not G-CSF) -induced stem cell mobilization and improved vascular recovery in diabetic animals.
Conclusion. Evidences from multiple clinical and experimental approaches indicate that diabetes impairs the mobilization of stem/progenitor cells from the BM to PB. This primary BM defect is related to a maladaptive and tissue-specific DPP-4 dysregulationPresupposti. Il diabete mellito (DM) aumenta il rischio cardiovascolare e ciò viene attribuito almeno in parte alla riduzione delle cellule vasculo-rigenerative di origine midollare. Infatti il midollo osseo contiene precursori per cellule endoteliali, muscolari lisce e cardiomiociti, che derivano da un progenitore CD34+. Dati recenti ottenuti da modelli sperimentali di diabete tipo 1 e tipo 2 indicano l’esistenza di difetti midollari che includono microangiopatia, neuropatia, alterazione dell’espressione genica e disfunzione della nicchia staminale. Obiettivi. Questo set di esperimenti ha avuto l’obiettivo di descrivere in dettaglio le alterazioni della funzione midollare nel diabete clinico e sperimentale. Metodi. Gli approcci metodologici sono diversificati e comprendono: 1) un trial di stimolazione midollare diretta con G-CSF ricombinante umano in pazienti con e senza diabete; 2) un’analisi di meta-regressione dei trials in cui il G-CSF è stato somministrato per indurre rigenerazione cardiovascolare in pazienti con e senza diabete; 3) lo studio della compartimentalizzazione delle cellule staminali/progenitrici nel midollo e nel sangue periferico, in relazione al diabete; 4) un modello animale per la definizione del ruolo di DPP-4 nel difetto di mobilizzazione midollare associato al diabete. Risultati. Parte 1: in risposta al G-CSF, le cellule CD34+ circolanti aumentavano significativamente nel paziente non diabetico, ma non nel diabetico, che mostrava anche una difettosa mobilizzazione di cellule ematopoietiche CD133+ e CD34+CD133+, nonché di cellule progenitrici endoteliali CD133+KDR+, indipendentemente dai possibili fattori confondenti. La capacità angiogenica in vivo delle cellule mononucleate aumentava significativamente dopo G-CSF nei soggetti diabetici ma non nei non diabetici, rispetto al basale. Il diabete risultava associato ad una incapacità di upregolare DPP-4 sulle cellule CD34+ in risposta al G-CSF. Parte 2: per la meta-regressione sono stati individuati 227 articoli, recuperati 96 e trattenuti 24 per l’analisi primaria. È stata identificata una forte correlazione negativa tra prevalenza del diabete all’interno di ogni trial e livello delle cellule CD34+ raggiunte dopo mobilizzazione con G-CSF (r=-0.68; p<0.0001). Una analisi di regressione multipla ha confermato che il risultato era indipendente da possibili fattori confondenti. In 13 articoli contenenti dati sui livelli di cellule CD34+ pre- e post-G-CSF, la correlazione negativa tra prevalenza del diabete e mobilizzazione appariva ancora più stretta (r=-0.82; p<0.0001). Parte 3: i livelli delle cellule CD34+ nel midollo e nel sangue periferico risultano essere direttamente correlati e la maggior parte delle cellule CD34+ erano di origine midollare, non proliferanti e non apoptotiche. Lo studio della compartimentalizzazione delle cellule CD34+ in 72 pazienti con e senza malattia cardiovascolare mediante l’uso delle mappe auto-organizzanti ha permesso di rilevare alterazioni della mobilizzazione in presenza di diabete ed elevato rischio cardiovascolare. Inoltre, un’elevata attività plasmatica di DPP-4 si associava ad alterata compartimentalizzazione delle cellule CD34+. In ratti diabetici rispetto ai controlli, l’attività di DPP-4 risultava significativamente aumentata nel sangue periferico e ridotta nel midollo osseo. Lo studio di ratti geneticamente deficienti dell’enzima DPP-4 ha permesso di stabilire che l’alterazione tessuto-specifica di DPP-4 nel diabete è responsabile del difetto di mobilizzazione post-G-CSF e post-ischemia. La delezione di DPP-4 ripristinava la mobilizzazione post-ischemica di cellule staminali ematopoietiche e progenitrici endoteliali e favoriva il recupero del tessuto ischemico nel diabete. Conclusioni. Diversi tipi di evidenze sperimentali indicano chiaramente che il diabete induce un difetto nella mobilizzazione delle cellule staminali/progenitrici midollari. Questo difetto primitivo del midollo osseo nel diabete è correlato ad una disregolazione tessuto-specifica dell’attività dell’enzima DPP-4
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Fisher, Maya. "Bone marrow regeneration follwing tibial marrow ablation in rats is age dependent." Thesis, Atlanta, Ga. : Georgia Institute of Technology, 2008. http://hdl.handle.net/1853/26526.
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Thesis (M. S.)--Biology, Georgia Institute of Technology, 2009.Committee Chair: Boyan Barbara; Committee Member: Guldberg Robert; Committee Member: Lovachev Kiril; Committee Member: Schwartz Zvi. Part of the SMARTech Electronic Thesis and Dissertation Collection.
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Jackson, G. H. "Long term bone marrow culture studies of patients with lymphoid malignancies undergoing autologous bone marrow transplantation." Thesis, University of Newcastle Upon Tyne, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309068.
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Schmidt-Mende, Jan Georg. "Bone marrow apoptosis in myelodysplastic syndromes." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=96939781X.
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McIntosh, Bryan James. "Regulation of thrombopoietin in bone marrow." Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2007. http://wwwlib.umi.com/cr/ucsd/fullcit?p3284334.
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Thesis (Ph. D.)--University of California, San Diego, 2007.Title from first page of PDF file (viewed January 9, 2008). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 50-58).
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Funaki, Hilde. "Psychological responses to bone-marrow-transplantation." Thesis, City University London, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283269.
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Sebastian, Anil. "Recreating bone marrow tissues in vitro." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.528263.
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Davison, Glenda Mary. "Immune reconstitution post bone marrow transplantation." Master's thesis, University of Cape Town, 2000. http://hdl.handle.net/11427/3376.
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Bibliography: leaves 82-95.The aims of this project were therefore: to document the immune reconstitution following T-cell depleted bone marrow and peripheral blood stem cell transplantation and to compare this with the recovery following autologous grafts. to document the cell surface expression of CD95 in an attempt to comment on the role played by FAS mediated apoptosis in the post transplant immune deficiency.
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Weber, Matthew Charles. "Engineering human bone marrow stromal cells." Case Western Reserve University School of Graduate Studies / OhioLINK, 1991. http://rave.ohiolink.edu/etdc/view?acc_num=case1055867071.
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Avera, Emily. "Transplant anxieties : discourses about bone marrow." Master's thesis, University of Cape Town, 2008. http://hdl.handle.net/11427/10038.
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Includes bibliographical references (leaves 89-94).This minor dissertation examines the various discourses in the Bone Marrow Transplant (BMT) network in South Africa. The organisations in the network which were observed using participant observation were the South African Bone Marrow Registry and the Sunflower Fund to complement this, the researcher interviewed staff members at these organisations as well as at a public hospital haematology unit in the Cape Town area that conducts BMT. Additionally patients, donors, and their family members were interviewed. Some media related to the BMT network was also analysed. Informed heavily by Troy Duster's work on genetic and social feedback loops, it was found that the discourses reflect a complex interweaving of biological materiality, ethnicity, culture, mortality, health resource rationing, South African nationhood, and the limits of bodily integrity. There is extensive discussion of how the BMT discourses demonstrate the necessity of engagement with several issues: the hybridity of expert and lay intercultural communication, health inequalities, human rights, and the prioritisation of first and third world medicine, the meanings of race, culture, ethnicity, and nationhood in a diverse South Africa, conceptions of donor shortage, and the imperative of saving lives through medical practise.
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Mancini, Richard Anthony. "Factors affecting beef bone marrow discoloration /." Search for this dissertation online, 2004. http://wwwlib.umi.com/cr/ksu/main.
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Hussein, Hayam. "Cathepsin K Inhibition In Bone And Bone Marrow In Horses." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1449218489.
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LACAVA, GIOVANNA. "A Comprehensive Study on Homeostatic Bone and Bone Marrow Mediators." Doctoral thesis, Università degli Studi di Camerino, 2019. http://hdl.handle.net/11581/428952.
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Bone marrow is an extremely complex tissue, whose function is to accommodate the hematopoietic and the bone stem/progenitor cells. In particular, the bone marrow stromal microenvironment consists of several different types of cells, including bone lining osteoblasts, endothelial cells, reticular adventitial cells, neuronal cells and mesenchymal stem cells. Here, this large number of different populations coexist and exchange several signals in order to preserve bone marrow homeostasis. Accordingly, it is necessary to highlight that changes in the bone marrow steady-state may lead to localized and/or systemic diseases.
The characteristics and the properties in the bone and bone marrow environment have been well elucidate for a number of factors, while less is known about other molecules, although they play critical functions within these tissues. Among them, the p62 multidomain protein has been associated with the osteoclastogenic processes, but not well-defined information is, so far, present in the literature regarding its function in the fine-tuned processes underling the bone and bone marrow metabolic features.
Recently, we demonstrated that p62 regulates osteoblasts differentiation and that p62 deficiency inhibits the bone turnover rate.
Consistently, our studies aimed at analyzing the bone marrow features of p62 KO mice. We showed that a significant adipocyte infiltration, particularly evident during the aging. This observation, together with the finding of a decreased osteolineage cell pools, impaired CXCL12/CXCR4 signaling and hemosiderin accumulation, demonstrated that p62 deficiency is able to disrupt bone marrow niche homeostasis overall in aged mice.
The other molecule here studied is the soluble cytokine IFN-γ. By means of administration of a plasmid coding for IFN-γ (pINF-γ) both in ovariectomized (osteopenic) and in the sham-operated mice, we demonstrated that pINF-γ injections induced pathologic bone and bone marrow alterations, characterized by cortical and trabecular bone loss, increased proinflammatory cytokine release and impaired mesenchymal stem cells (MSCs) osteoblastogenic differentiation. In addition, the reduction of CXCL12+ cell number and the observation of hypercellular areas in the bone marrow of sham-operated and ovariectomized mice administered with pINF-γ, further suggest that IFN-γ is an important mediator of bone catabolism.
During my PhD course we also investigated the therapeutic effects of a new hyaluronic acid-based hydrogel in a mouse model of knee osteoarthritis. Our results demonstrated that hydrogel administration allowed for the controlled and sustained release of hyaluronic acid, prolonging so the exposure of osteoarthritic knees to this biopolymer and promoting cartilage and subchondral bone regeneration. We also proved that hyaluronic acid-bearing hydrogels were able to counteract osteoarthritis by decreasing on the one hand the expression of pro-inflammatory mediators, while on the other hand by inducing MSCs differentiation and maturation into chondroblasts.
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Clutter, Suzanne Davis. "Chemotherapy disrupts bone marrow stromal cell function." Morgantown, W. Va. : [West Virginia University Libraries], 2006. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=4528.
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Thesis (Ph. D.)--West Virginia University, 2006.Title from document title page. Document formatted into pages; contains x, 180 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.
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Baki, Mert. "Bone Marrow Targeted Liposomal Drug Delivery Systems." Master's thesis, METU, 2011. http://etd.lib.metu.edu.tr/upload/12613251/index.pdf.
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Homing is the process that stem cells move to their own stem cell niches under the influence of chemokines like stromal-derived factor-1&alpha(SDF-1&alpha
) upon bone marrow transplantation (BMT). There is a need for increasing homing efficiency after BMT since only 10-15% of the transplanted cells can home to their own niches and a limited amount of donor marrow can be transplanted. In this study, we aimed to develop and characterize bone marrow targeted liposomal SDF-1&alpha
delivery system prepared by extrusion method. Alendronate conjugation was chosen to target the liposomes to bone marrow microenvironment, particularly the endosteal niche. Optimization studies were conducted with the model protein (
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Fletcher, Joanne L. "Bone Marrow Progenitors in Vascular Tissue Engineering." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.518451.
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Bågesund, Mats. "Salivary function after pediatric bone marrow transplantation /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4110-6/.
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Amofah, Eunice. "Bone marrow stem cells in liver disease." Thesis, Imperial College London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497234.
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袁國勇 and Kwok-yung Yuen. "Infectious complications in bone marrow transplant recipients." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31981689.
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Chandran, Priya. "Bone Marrow Microenvironment in Acute Myleoid Leukemia." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24301.
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Acute myeloid leukemia (AML) often remains refractory to current chemotherapy and transplantation approaches despite many advances in our understanding of mechanisms in leukemogenesis. The bone marrow “niche” or microenvironment, however, may be permissive to leukemia development and studying interactions between the microenvironment and leukemia cells may provide new insight for therapeutic advances. Mesenchymal stem cells (MSCs) are central to the development and maintenance of the bone marrow niche and have been shown to have important functional alterations derived from patients with different hematological disorders. The extent to which MSCs derived from AML patients are altered remains unclear. The aim of this study was to detect changes occurring in MSCs obtained from human bone marrow in patients with AML by comparing their function and gene expression pattern with normal age-matched controls.
MSCs expanded from patients diagnosed with acute leukemia were observed to have heterogeneous morphological characteristics compared to the healthy controls. Immunohistochemistry and flow data confirmed the typical cell surface immunophenotype of CD90+ CD105+ CD73+ CD34- CD45-, although MSCs from two patients with AML revealed reduced surface expression of CD105 and CD90 antigens respectively. Differentiation assays demonstrated the potential of MSCs from AML patients and healthy donors to differentiate into bone, fat and cartilage. However, the ability of MSCs from AML samples to support hematopoietic function of CD34+ progenitors was found to be impaired while the key hematopoietic genes were found to be differentially expressed on AML-MSCs compared to nMSCs.
These studies indicate that there exist differences in the biologic profile of MSCs from AML patients compared to MSCs derived from healthy donors. The results described in the thesis provide a formulation for additional studies that may allow us to identify new targets for improved treatment of AML.
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McWilliam, Nicola A. "The fibrinolytic system of human bone marrow." Thesis, University of Aberdeen, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337476.
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The fibrinolytic system of normal and leukaemic bone marrow was examined. Normal bone marrow had a very active fibrinolytic system due to abundant free t-PA, with negligible contribution from u-PA. High levels of PAI-2 antigen were observed in addition to PAI-1. Plasminogen, the precursor of plasmin was detected, mainly in complex with α2-AP, indicating that plasmin had been generated. The balance of the fibrinolytic system in normal bone marrow contrasted with the system in plasma, where plasmin is not normally generated. In bone marrow the t-PA level was greater than that of the inhibitors while in plasma t-PA circulates in complex with PAI-1. t-PA, u-PA, u-PAR, PAI-1 and PAI-2 were localised to cells of the myeloid, monocytic, megakaryocytic and T-lymphoid lineages in normal marrow. In contrast, cells of the B-lymphoid lineage did not possess the antigens of interest. In addition, non-haematopoietic cells in the marrow were examined, and it was observed that osteocytes, endothelial cells, smooth muscle cells and adipocytes contained the antigens of the fibrinolytic system. PAI-1, PAI-2, u-PA, u-PAR and probably t-PA were synthesised by the cells of the marrow, while plasminogen and α2-AP arose from the general circulation. The activity and antigen levels of the components of the fibrinolytic system differed between normal and leukaemic bone marrow. In leukaemic marrow, u-PA was observed, while t-PA and PAI-2 were decreased compared with normal bone marrow. PAI-1, plasminogen, α2-AP and plasmin-α2-AP complex were similar to normal bone marrow. The appearance of u-PA was probably associated with the malignant phenotype and may confer an invasive advantage on the leukaemic cell. In addition, the profile of the fibrinolytic system observed in leukaemic bone marrow may contribute to the haemorrhagic symptoms associated with certain forms of leukaemia.
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Elfer, Jane. "Emotional impact of sibling bone marrow donors." Thesis, University of East London, 2017. http://roar.uel.ac.uk/7137/.
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This thesis reports on a study of the emotional impact on sibling bone marrow donors. lt considers in particular donation that takes place during their adolescence and was prompted by the concern of medical and nursing colleagues managing the treatment of young people with cancer. The study interviewed five donors and discusses these interviews using the lens of psychoanalytic theory to offer a deeper understanding of these donors' experiences. Understood in this way, particularly using the psychoanalytic concept of projective identification, a main finding of the study is that whilst these donors would not have refused to donate, based on the love and duty of a filial relationship, the donation evoked complex emotions arising from the sense of the physiological merging of two people. The study makes some recommendations to change current practice within the hospital where I work in order to improve the psychological management and care of sibling bone marrow donors.
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Rehman, Haroon, Asha Chepkorir Segie, Kanishka Chakraborty, and Devapiran Jaishankar. "Bone Marrow Wars: Attack of the Clones." Digital Commons @ East Tennessee State University, 2020. https://dc.etsu.edu/asrf/2020/presentations/33.
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Multiple myeloma is characterized by the malignant proliferation of clonal plasma cells producing monoclonal paraproteins, leading to multi-organ damage. On the other hand monoclonal B-cell lymphocytosis (MBCL) is characterized by the malignant proliferation of clonal B-lymphocytes, with potential to develop into chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL). CLL/SLL can result in visceromegaly, anemia, thrombocytopenia, fevers, night sweats and unintentional weight loss. Literature review demonstrates these two malignant clonal bone marrow disorders are most frequently seen independently in patients; however, we report one rare diagnostic challenge where both clonal disorders were identified in a single patient concurrently. A 64-year-old man initially presented with worsening back pain. Thoracic spine x-ray revealed a T11 compression fracture, confirmed by magnetic resonance imaging. Complete blood count revealed a white blood cell count of 7.3 K/uL with 54% lymphocyte predominance and peripheral smear demonstrated a population of small lymphocytes with round nuclei and an atypical chromatin pattern suggestive of CLL/MBCL. Flow cytometry revealed a monoclonal B-cell CD5 positive, CD23 positive, CD10 negative population with an absolute count of 1.6 K/uL. Due to the instability and pain associated with the spinal fracture, patient had kyphoplasty performed and intraoperative bone biopsies were taken from both T11 and T12 vertebrae. Interestingly each bone biopsy revealed involvement by both a kappa-light chain restricted plasma cell neoplasm, ranging from 15% to 30% cellularity, as well as a CD5-positive B-cell lymphocyte population. It suggested two concurrent but pathologically distinct pathologies including plasma cell myeloma and a separate B-cell lymphoproliferative disorder with immunophenotypic features suggestive of CLL/MBCL. Bone marrow biopsy was performed for definitive evaluation and confirmed multiple myeloma with 15-20% kappa-restricted plasma cells identified, and also confirmed concurrent MBCL with CD5 and CD23-positive, kappa-restricted B-cells identified on bone marrow flow cytometry. Adding an additional layer of complexity, bone marrow molecular genetics revealed presence of a MYD88 mutation, raising concern for possible lymphoplasmacytic lymphoma (LPL). However, secondary pathologic review ruled out LPL, as the immunophenotypic pattern of the clonal B-cells was not consistent with that of LPL, and although the MYD88 mutation is predominantly seen in LPL, it has also been seen in a small percentage of CLL/SLL cases and exceedingly rarely described in MM as well. Serum protein electrophoresis with immunofixation, serum quantitative immunoglobulins and serum quantitative free light chain assay revealed findings consistent with IgG kappa multiple myeloma and systemic CT imaging was negative for any lymphadenopathy, confirming MBCL. Patient was started on first-line multiple myeloma systemic therapy for transplant eligible patients and has demonstrated an excellent response to treatment thus far. This patient case serves to demonstrate the importance of maintaining a broad differential when approaching hematological problems; It also underlines the necessity for a complete diagnostic evaluation to identify rare clinical conundrums such as with our patient, allowing for proper and timely treatment. While we use “Occam’s razor” to explain multiple problems with a single unifying diagnosis the rare possibility of divergent diagnosis is to be always entertained.
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Yuen, Kwok-yung. "Infectious complications in bone marrow transplant recipients." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19929614.
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Lloyd, Brandon R. "Comparison of Bone Marrow Mesenchymal Stem Cells from Limb and Jaw Bones." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1458678153.
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Hall, Brett Matthew. "Effects of high dose chemotherapy on the bone marrow microenvironment." Morgantown, W. Va. : [West Virginia University Libraries], 2002. http://etd.wvu.edu/templates/showETD.cfm?recnum=2558.
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Thesis (Ph. D.)--West Virginia University, 2002.Title from document title page. Document formatted into pages; contains ix, 173 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 163-169).
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Lu, King-hei Crosby. "A single centre, randomised trial on harvest cell yield and marrow engraftment using haemopoietic growth-factor primed bone marrow." Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B25176481.
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Bailey, Amy. "A systemic approach to paediatric bone marrow transplantation." Thesis, University of Birmingham, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408830.
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Gray, Caroline J. "Distress and emotional state throughout bone marrow transplantation." Thesis, University of British Columbia, 1991. http://hdl.handle.net/2429/29729.
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Bone marrow Transplantation causes a variety of symptoms and emotional states which change throughout the treatment. The purpose of this descriptive correlational, repeated measures study was to describe the type and degree of symptom distress and the emotional states experienced by BMT patients at the time of admission, through the administration of chemotherapy and radiotherapy, bone marrow infusion, waiting for engraftment to 25 days following the infusion of bone marrow. In addition, this study investigated the relationship between symptom distress and emotional states of the BMT patient. The conceptual framework was based on Lazarus and Folkman's (1984) theory of stress, appraisal, and coping. The design involved administering McCorkle and Young's (1978) Symptom Distress Scale, McNair, Lorr, and Droppleman's (1971) Profile of Mood States, and two Data Collection Guides to ten patients at five times during the BMT procedure. A convenience sample of 12 subjects participated in the study.
Overall, the participants experienced moderate degrees of symptom distress. Distress related to insomnia and appetite problems caused high levels of distress with moderate amounts of distress reported for distress related to nausea, pain, fatigue, bowel changes, concentration, and outlook. The least amount of distress was associated with appearance, breathing, and coughing problems. Symptom distress changed significantly over time with increased levels during the administration of chemotherapy and radiotherapy, one and seven days post-infusion and decreased to near baseline levels 25 days following the bone marrow infusion in all symptoms except outlook. Outlook distress was high initially and gradually declined over the course of the treatment. Significant changes were shown in nausea existence, appetite, insomnia, bowel, and concentration distress. The levels and changes seemed to reflect the clinical course of the BMT procedure.
The participants showed moderate levels of emotional disturbance during the BMT with vigor and fatigue reaching high levels, tension and confusion reaching moderate levels, and depression and anger remaining fairly low. Emotional disturbance changed significantly over the course of the BMT for total emotional state and for all the emotional subscales except depression.
The findings indicate that during times of intensive treatment emotional disturbance is greater. Total symptom distress and emotions showed no correlation except one day following bone marrow infusion; however, all six specific emotion components were correlated with at least one of the following distressful symptoms: outlook, pain, appearance, concentration, or fatigue.
The findings suggest that symptom distress and emotions are closely linked to clinical events such as medications, blood transfusions, chemotherapy, radiotherapy, infections, nutritional deficits, but were tempered by coping abilities and lack of risk factors for emotional disturbance. Implications from the findings suggest specific times for the nurse to be particularly cognizant of specific symptom distress and emotional states and their patterns during the BMT. In addition, the nurse must be aware that there are complicated and uncomplicated courses for the BMT. The nurse must be adept at assessing the BMT patients for particular symptom distress and emotions when they are most likely to be problematic and to intervene appropriately.Applied Science, Faculty of
Nursing, School of
Graduate
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Barron, Mary Anne. "Vitamin K deficiency in paediatric bone marrow transplantation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0008/MQ40822.pdf.
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Rodriguez, Francisco Jose. "Oral mucositis in children receiving bone marrow transplantation." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2008m/rodriguez.pdf.
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Al-Khaldi, Abdulaziz A. "Therapeutic angiogenesis using autologous bone marrow stromal cells." Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=32749.
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Objectives. To study marrow stromal cells (MSCs) induced angiogenesis. To examine the possible mechanisms involved in the process. To evaluate neovascularization following implantation of MSCs in ischemic hind limb model.Methods and result. Using murine Matrigel angiogenesis model, we compared MSCs related angiogenesis to that produced by vascular endothelial growth factor (VEGF) and basic fibroblast growth factor. We found that MSCs result in an efficient and organized angiogenesis, arteriogenesis and vasculogenesis. MSC-related angiogenesis is VEGF dependent. MSCs in vivo produce VEGF that through paracrine effect induces local angiogenesis and through an autocrine loop stimulates FLK1+MSCs to differentiate into endothelial cells. MSCs implanted into ischemic hind limb resulted in marked improvement in blood flow and collateral vessels formation.
Conclusion. MSCs spontaneously induce efficient and mature angiogenesis in ischemic/hypoxic tissues with significant arteriolar component resulting in increased blood flow. They are also capable of spontaneous differentiation into endothelium. VEGF appears to be necessary for MSC-related angiogenesis and vasculogenesis.
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Vig, Pamela. "Bone marrow stem cell contribution to liver regeneration." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.427949.
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Burdon, Peter Charles Edward. "Regulation of neutrophil mobilisation from the bone marrow." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289739.
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Powell, Timothy Jack. "Characterisation of rat bone marrow derived dendritic cells." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298613.
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Kallis, Yiannis Nicolaou. "The bone marrow in liver fibrosis and regeneration." Thesis, Imperial College London, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.528283.
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Porter, Christopher John Hamilton. "Targeting collodial drug carriers to the bone marrow." Thesis, University of Nottingham, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.315061.
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Cavanagh, Gary. "The role of CD31 in bone marrow transplantation." Thesis, University of Newcastle Upon Tyne, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404955.
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Fegan, C. D. "The gut mucosal barrier following bone marrow transplantation." Thesis, University of Newcastle Upon Tyne, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308776.
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Wadoodi, Ashar. "The role of bone marrow in thrombus resolution." Thesis, King's College London (University of London), 2012. https://kclpure.kcl.ac.uk/portal/en/theses/the-role-of-bone-marrow-in-thrombus-resolution(2983faec-0618-4c4f-8897-7816419c55bd).html.
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Deep vein thrombosis (DVT) is a common condition affecting 1-2% of the population. It can be further complicated by serious sequelae such as life threatening pulmonary embolus and the chronically debilitating post-thrombotic syndrome. The main treatment modalities available for DVT are only able to limit disease progression, with resolution occurring physiologically. Natural resolution of DVT occurs through a process of thrombus retraction and recanalisation which is comparable to progenitor mediated neovascularisation. The focus of this project was to examine the circulating progenitor cell response to venous thrombosis and to profile the underlying cytokine response. This data was ultimately used, to manipulate the number of circulating progenitor cells and expression of cytokines to enhance the recanalisation process. The presence of venous thrombus produced a bimodal circulating haematopoietic progenitor cell response whilst in the bone marrow compartment progenitor cells were simultaneously depleted. GCSF, GMCSF, VEGF, PIGF and SDF1 were expressed differentially in thrombus, vein wall and plasma, with the laparotomy wound mirroring the cytokine profile of the resolving thrombus. The expression pattern of PIGF in the resolving thrombus was however, unusually specific and not seen in the healing laparotomy wound.
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Davies, Julie Theresa. "Activation of adhesion of bone marrow stromal cells." Thesis, St George's, University of London, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.656858.
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Osteoblasts, the bone-forming cells, derive from multipotential bone marrow stromal precursors called colony-forming units-fibroblastic (CFU-F). CFU-F rapidly adhere to plastic upon culture ex vivo, adhesion of such stromal precursors to bone in vivo is likely to be an early event in the anabolic response to bone stimulatory factors. It has been suggested that osteoclasts are involved in the activation of bone formation during bone remodelling. In order to test this, osteoclast conditioned medium was prepared from osteoclasts cultured on either plastic or bone. It was then used as culture medium for bone marrow cells. It was found that the conditioned medium was unable to increase the adherence of bone marrow cells and therefore the number of CFU-F when cultured in 6-well plates. The ability of parathyroid hormone (PTH) to enhance bone formation has recently been exploited in the treatment of osteoporosis. However, the underlying mechanisms are unknown. PTH and other possible osteoblast activating factors were tested for the ability to activate adhesion of CFU-F in vitro. For this, bone marrow cells were incubated in PTH for varying times. Non-adherent cells were then removed, and the adherent cells were incubated in PTH-free medium for 14 days to assess, as colony formation, the number of CFU-F that had adhered in the preceding period. Incubation in PTH caused a substantial increase in the number of CFU-F that adhered within 24 h. This increase was abrogated by peptidic inhibitors of integrins. The increase did not appear to be mediated through a PTHinduced increase in interleukin-6, since interleukin-6 had no effect on CFU-F numbers when substituted for PTH. Similarly, adhesion was unaffected by incubation of bone marrow cells in dibutyryl cyclic AMP, nor by inhibitors or donors of nitric oxide. However, activation of CFU-F in vitro by PTH was strongly inhibited by indomethacin and mimicked by Prostaglandin E2 (PGE2). To test the effects of PTH in vivo, the number of CFU-F that could be extracted from murine bone marrow after administration of an anabolic dose of PTH were measured. A dramatic reduction in the number of CFU-F that could be extracted from their bone marrow commenced within 2 h of treatment. It was also found that indomethacin reversed the PTH mediated reduction of CFU-F that could be extracted from mouse bone marrow. Intermittent PTH administered over a 6 day period increased the dynamic parameters associated with bone formation and there was a concomitant increase in the number of osteoblasts on bone surfaces. These results suggested that PTH rapidly activates adhesion of CFU-F to plastic or bone surfaces. This activation may represent an early event in the anabolic response of bone cells to PTH.
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Bennett, Jonathan Hilary. "The differentiation of osteogenic cells from bone marrow." Thesis, University of Oxford, 1991. http://ora.ox.ac.uk/objects/uuid:3460f26e-a124-4605-8601-2e300241de14.
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Roulson, Jo-An. "Bone marrow endothelial transmigration of prostate carcinoma cells." Thesis, University of Manchester, 2008. https://www.research.manchester.ac.uk/portal/en/theses/bone-marrow-endothelial-transmigration-of-prostate-carcinoma-cells(997acbf2-bbbc-455b-bb84-b439ffb9f839).html.
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Lyndina, Yu. "Histological features of red bone marrow in rats." Thesis, Sumy State University, 2016. http://essuir.sumdu.edu.ua/handle/123456789/46296.
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Bone marrow is the flexible tissue in the interior of bones. In humans, red blood cells are produced by cores of bone marrow in the heads of long bones in a process known as hematopoiesis. The hematopoietic component of bone marrow produces approximately 500 billion blood cells per day, which use the bone marrow vasculature as a conduit to the body's systemic circulation. Bone marrow is also a key component of the lymphatic system, producing the lymphocytes that support the body's immune system. Information about the normal structure of the bone marrow is a key step in understanding its changes under the influence of negative environmental factors.
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Gowers, Kate Hayley Christine. "Characterisation of bone marrow progenitor cells in disease." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/11068.
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The bone marrow serves as a reservoir for leukocytes and stem cells, from where cells can be mobilised into the circulation and can be recruited to sites of inflammation. Mobilisation of cells out of the bone marrow is dependent on their migration across the bone marrow sinusoidal endothelium, which is thought to be structurally and functionally different to endothelial cells from other vascular beds. In order to characterise the bone marrow endothelium and to study the molecular mechanisms involved in the mobilisation of cells, a protocol to isolate bone marrow endothelial cells and to grow them in vitro was developed. The bone marrow contains a number of distinct progenitor cell populations, including endothelial progenitor cells (EPCs) and mesenchymal stem cells (MSCs). Whether these populations of stem cells are recruited from the bone marrow to the lungs was investigated in two contrasting models of lung disease: the house dust mite (HDM) model of allergic airways disease and the bleomycin model of pulmonary fibrosis. In the HDM model increased recruitment of EPCs to the inflamed lungs was associated with increased peribronchial angiogenesis, and reduced EPC numbers in the bone marrow. Blocking VEGF inhibited EPC recruitment to the inflamed lungs and reduced the associated peribronchial angiogenesis. In this model, no recruitment of MSCs to the inflamed lungs was observed. However, in the bleomycin model, a significant elevation in MSC numbers was observed in the circulation, lung tissue and BAL fluid. Experiments to block the recruitment of MSCs to the lungs in response to bleomycin injury were performed, along with investigations into the recruitment of exogenously administered MSCs to the injured lungs. A population of MSCs residing in the naïve lungs was identified, which are phenotypically similar to bone marrow MSCs, but can be distinguished by their size and expression of specific cell surface antigens.
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Langford-Smith, Kia Jane. "Non-myeloablative bone marrow transplantation for Mucopolysaccharide diseases." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/nonmyeloablative-bone-marrow-transplantation-for-mucopolysaccharide-diseases(5d3fd9c5-01f2-42aa-81ed-a2ce6ef140fe).html.
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The Mucopolysaccharide (MPS) diseases are a group of lysosomal storage disorders, caused by a lack of the enzymes required for catabolism of glycosaminoglycans (GAGs), leading to severe neurological decline, skeletal deformities, organomegaly, cardiac and respiratory compromise, and premature death. The severe form of MPS I, Hurler syndrome, can be successfully treated using haematopoietic stem cell transplantation (HSCT), but the risks associated with myeloablation and immune suppression limit the broader application of HSCT to attenuated diseases. Successful engraftment in MPS I has been difficult to achieve, and requires fully myeloablative conditioning, whilst reduced intensity conditioning is a risk factor for graft rejection. Non-myeloablative conditioning generating reliable graft acceptance and high donor chimerism could increase safety and applicability of HSCT in genetic disease, therefore the aim of this research was to identify such a regimen in a clinically relevant mouse model of HSCT.Conditioning regimens developed in existing mouse models of HSCT have had limited clinical success, and often require clinically unachievable high cell doses or less stringent strain combinations to overcome allogeneic transplant rejection. To improve clinical relevance we used CBA donors and C57BL/6 recipients, which require full myeloablation with busulfan and immune suppression using non-depleting anti-CD4 and anti-CD8 monoclonal antibodies for engraftment of low cell doses across a major histocompatibility complex barrier. In syngeneic transplant donor chimerism was improved by generating a greater ratio of donor:recipient haematopoietic cells in the bone marrow initially, therefore we tested granulocyte colony stimulating factor (G-CSF), high cell dose and stem cell niche disruption and compared this to anti-CD40L costimulatory blockade in allogeneic transplant performed with a reduced dose of busulfan that was insufficient for graft acceptance. Despite improvements in initial engraftment with some of these treatments, only combined signal 1 and 2 T cell blockade were effective in reducing the dose of busulfan required for long-term graft acceptance. Early detection of MPS is important in treatment success; good disease biomarkers are vital, and biomarkers suitable for monitoring treatment outcome in MPS are lacking. We evaluated serum heparin cofactor II-thrombin (HCII-T) complex for MPS. We determined optimal sample collection and storage conditions, assay limitations and developed measurement in dried blood spots. Dermatan sulphate has a greater effect on in vivo HCII-T complex formation than heparan sulphate, thus in the MPS mouse models HCII-T is a reliable biomarker for MPS I, but not MPS IIIA or IIIB. HCII-T is greatly elevated in MPS I, II and VI patients, who all store dermatan sulphate, but it is also elevated by a small but significant amount in MPS III patients, who store heparan sulphate. HCII-T was also measured longitudinally in MPS I, II and VI patients, compared to an existing clinical biomarker, and validated against clinical outcomes to show that it is a good biomarker of short-term treatment outcomes and responds rapidly to perturbations in treatment. Finally, we determined whether an engraftment defect was observed in the MPS I mouse model, and show that this is present following both syngeneic and allogeneic HSCT. The effect of enzyme replacement therapy (ERT) and anti-inflammatory treatment prior to allogeneic HSCT was investigated, and initial results suggest that ERT, but not ibuprofen, may improve HSCT outcome. Overall, a clinically relevant mouse model of allogeneic HSCT has been developed and used to determine a non-myeloablative conditioning regimen that generates high levels of donor chimerism with a minimal dose of busulfan and blockade of both signal 1 and 2 of T cell activation. The conditions required to observe an engraftment defect in MPS I mice have also been defined, and preliminary studies have suggested that ERT, but not anti-inflammatory treatment, may overcome the engraftment defect in MPS I. Alongside this work, the HCII-T biomarker has been evaluated in MPS mouse models and patients, determining that it correlates well with short-term treatment outcomes. The techniques and models developed here will provide an excellent basis for further work in developing non-myeloablative conditioning for bone marrow transplant in MPS I.
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Tandy, Corinne B. "Time line of decomposition of porcine bone marrow." Thesis, Boston University, 2011. https://hdl.handle.net/2144/38104.
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Thesis (M.S.)--Boston UniversityPLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
The postmortem interval, or time since death, is a significant factor in medicolegal death investigations. Currently, the techniques used to assess time since death are subjective, phase-based qualitative methods. Recently, legal decisions and best practice recommendations have encouraged increasing quantitative assessment of forensic techniques. The purpose of this research is to determine ifbone marrow biopsy can be used as a quantifiable predictive indicator of time since death. Bone marrow plug biopsies were acquired from six pigs (Sus scrofa) during decomposition through skeletonization (28 days) and examined microscopically. The appearance of 122 marrow sections were scored and analyzed in light of time since death and accumulated degree-days. This pilot study suggests that there is a strong relationship between bone marrow appearance and the postmortem interval and the results encourage further research into a potential quantitative predictive tool to be utilized in medicolegal death investigations.
2031-01-01
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Porter, Ryan Michael. "Examination of Glucocorticoid Treatment on Bone Marrow Stroma: Implications for Bone Disease and Applied Bone Regeneration." Thesis, Virginia Tech, 2002. http://hdl.handle.net/10919/36365.
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Long-term exposure to pharmacological doses of glucocorticoids has been associated with the development of osteopenia and avascular necrosis. Bone loss may be partially attributed to a steroid-induced decrease in the osteoblastic differentiation of multipotent progenitor cells found in the bone marrow. In order to determine if there is a change in the osteogenic potential of the bone marrow stroma following glucocorticoid treatment, Sprague-Dawley rats were administered methylprednisolone for up to six weeks, then sacrificed at 0, 2, 4, or 6 weeks during treatment or 4 weeks after cessation of treatment. Femurs were collected and analyzed for evidence of steroid-induced osteopenia and bone marrow adipogenesis. Although glucocorticoid treatment did inhibit bone growth, differences in ultimate shear stress and mineral content were not detected. The volume of marrow fat increased with increasing duration of treatment, but returned to near control levels after cessation of treatment. Marrow stromal cells were isolated from tibias, cultured in the presence of osteogenic supplements, and analyzed for their capacity to differentiate into osteoblast-like cells in vitro. Glucocorticoid treatment diminished the absolute number of isolated stromal cells, but did not inhibit the relative levels of bone-like mineral deposition or osteocalcin expression and secretion.
Although pharmacological glucocorticoid levels induce bone loss in vivo, physiologically equivalent concentrations have been shown to enhance the formation of bone-like tissue in vitro. However, glucocorticoids have also been reported to inhibit proliferation and type I collagen synthesis in marrow stromal cell cultures. In order to assess the effects of intermittent dexamethasone treatment on the progression of osteogenesis in rat marrow stromal cell culture, this synthetic glucocorticoid was removed from the culture medium after a variable period of initial supplementation. Cell layers were analyzed for total cell number, collagen synthesis, phenotypic marker expression, and matrix mineralization. Prolonged supplementation with dexamethasone decreased proliferation, but did not significantly affect collagen synthesis. Furthermore, increased treatment duration was found to increase bone sialoprotein expression and mineral deposition. The duration of glucocorticoid treatment may be a key factor for controlling the extent of differentiation in vitro.Master of Science