Bibliografías temáticas / Hematopoiesis

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Literatura académica sobre el tema "Hematopoiesis"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 9 de junio de 2025

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Artículos de revistas sobre el tema "Hematopoiesis"

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Sood, Raman, Milton English, Christiane Belele, Rebecca Haskins, Anthony Burnetti, Jagman Chahal, and Pu Paul Liu. "Identification of Three Phases of Hematopoieisis in Zebrafish and Their Differential Requirements for Runx1 and Gata1 Functions." Blood 110, no. 11 (November 16, 2007): 202. http://dx.doi.org/10.1182/blood.v110.11.202.202.

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Abstract Primitive hematopoiesis in the zebrafish takes place in the intermediate cell mass (ICM), while definitive hematopoiesis takes place in the kidney. Recently, a new transition site called caudal hematopoietic tissue (CHT), or posterior blood island (PBI) was identified. Using lineage tracing the hematopoietic cells originating from ICM were shown to transit through CHT and eventually populate kidney and thymus. However, the lineage relationship of the cells at these sites and the genetic control of early hematopoiesis in the zebrafish remain to be resolved. Transcription factors Gata1 and Runx1 are required for primitive and definitive hematopoiesis respectively in mammals, and are likely candidates as key hematopoietic regulators in the zebrafish. By ENU mutagenesis and reverse genetic screening, we have generated a zebrafish runx1 mutant line with a truncation mutation, W84X, in the runt homology domain and a hypomorphic gata1 mutant line with a missense mutation, T301K, in the C-terminal zinc finger domain. We used hypomorphic allele in combination with the previously characterized gata1 null mutation, vlad tepes (vlt) to assess the requirements for gata1 during primitive and definitive hematopoiesis. Gel-shift analysis showed that the T301K gata1 protein had reduced binding affinity for DNA as opposed to complete lack of binding by the vlt mutant protein. This reduced activity is sufficient for hematopoieisis since gata1T301K/T301K embryos had normal circulation at all stages and survived to adulthood, while gata1vlt/vlt embryos never developed circulation and died around 11–15 days post fertilization (dpf). On the other hand, compound heterozygous gata1T301K/vlt embryos lacked circulation until 7 dpf, regained circulation around 8–11dpf and survived to adulthood. Analysis of markers for definitive hematopoiesis by in situ hybridzationan and crossing with transgenic Tg(cd41-GFP) fish indicated that definitive hematopoiesis was normal. These data suggest dosage effect of gata1 function during primitive and definitive stages of hematopoiesis, indicating that partial gata1 activity was sufficient for definitive hematopoiesis. Furthermore, we identified two phases of definitive hematopoiesis by characterization of the runx1 truncation mutation. runx1W84X/W84X embryos had normal circulation until 7dpf, gradually lost circulation around 8–11dpf, stayed bloodless until 20–25dpf and the surviving embryos regained circulation, while majority of them died during the bloodless phase. Approximately twenty percent of runx1W84X/W84X embryos survived to adulthood. By in situ hybridization, definitive hematopoietic stem cell markers, runx1 and c-myb, were not detectable in the runx1 mutant embryos. However, crossing with transgenic Tg(cd41-GFP) fish showed that cd41+ stem cells of definitive hematopoiesis were retained in the runx1W84X/W84X embryos and migrated from ICM to CHT and then to kidney as wildtype clutch-mates. In runx1W84X/W84X mutant Tg(gata1-GFP) and Tg(cd41-GFP) embryos the bloodless phase was accompanied by lack of gata1-GFP+ erythroid cells and cd41-GFP+ circulating thrombocytes, which reappeared after recovery of circulation. These data suggest that there are two phases of definitive hematopoiesis: larval and adult, and that runx1 is absolutely required for the larval stage. In conclusion, we have identified three stages of hematopoiesis in the zebrafish and revealed the differential dosage requirement for gata1 and runx1 during these three stages.
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Wu, Jiang, Weiwei Zhang, Qian Ran, Yang Xiang, Jiang F. Zhong, Shengwen Calvin Li, and Zhongjun Li. "The Differentiation Balance of Bone Marrow Mesenchymal Stem Cells Is Crucial to Hematopoiesis." Stem Cells International 2018 (2018): 1–13. http://dx.doi.org/10.1155/2018/1540148.

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Bone marrow mesenchymal stem cells (BMSCs), the important component and regulator of bone marrow microenvironment, give rise to hematopoietic-supporting stromal cells and form hematopoietic niches for hematopoietic stem cells (HSCs). However, how BMSC differentiation affects hematopoiesis is poorly understood. In this review, we focus on the role of BMSC differentiation in hematopoiesis. We discussed the role of BMSCs and their progeny in hematopoiesis. We also examine the mechanisms that cause differentiation bias of BMSCs in stress conditions including aging, irradiation, and chemotherapy. Moreover, the differentiation balance of BMSCs is crucial to hematopoiesis. We highlight the negative effects of differentiation bias of BMSCs on hematopoietic recovery after bone marrow transplantation. Keeping the differentiation balance of BMSCs is critical for hematopoietic recovery. This review summarises current understanding about how BMSC differentiation affects hematopoiesis and its potential application in improving hematopoietic recovery after bone marrow transplantation.
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Gerosa, Rahel C., Steffen Boettcher, Larisa V. Kovtonyuk, Annika Hausmann, Wolf-Dietrich Hardt, Juan Hidalgo, César Nombela-Arrieta, and Markus G. Manz. "CXCL12-abundant reticular cells are the major source of IL-6 upon LPS stimulation and thereby regulate hematopoiesis." Blood Advances 5, no. 23 (December 2, 2021): 5002–15. http://dx.doi.org/10.1182/bloodadvances.2021005531.

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Abstract Hematopoiesis is maintained by hematopoietic stem and progenitor cells that are located in the bone marrow (BM) where they are embedded within a complex supportive microenvironment consisting of a multitude of various non-hematopoietic and hematopoietic cell types. The BM microenvironment not only regulates steady-state hematopoiesis by provision of growth factors, cytokines, and cell–cell contact but is also an emerging key player during the adaptation to infectious and inflammatory insults (emergency hematopoiesis). Through a combination of gene expression analyses in prospectively isolated non-hematopoietic BM cell populations and various mouse models, we found that BM CXCL12-abundant reticular (CAR) cells are a major source of systemic and local BM interleukin-6 (IL-6) levels during emergency hematopoiesis after lipopolysaccharide (LPS) stimulation. Importantly, although IL-6 is dispensable during the initial phase of LPS-induced emergency hematopoiesis, it is required to sustain an adequate hematopoietic output during chronic repetitive inflammation. Our data highlight the essential role of the non-hematopoietic BM microenvironment for the sensing and integration of pathogen-derived signals into sustained demand-adapted hematopoietic responses.
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4

Ozbudak, Irem H., Konstantin Shilo, Sabine Hale, Nadine S. Aguilera, Jeffrey R. Galvin, and Teri J. Franks. "Alveolar Airspace and Pulmonary Artery Involvement by Extramedullary Hematopoiesis: A Unique Manifestation of Myelofibrosis." Archives of Pathology & Laboratory Medicine 132, no. 1 (January 1, 2008): 99–103. http://dx.doi.org/10.5858/2008-132-99-aaapai.

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Abstract Pulmonary extramedullary hematopoiesis is a rare manifestation of myelofibrosis. We encountered a unique case of pulmonary extramedullary hematopoiesis occurring in a 59-year-old white man, where in addition to the typical foci of interstitial hematopoietic cells, a surgical lung biopsy showed airspace and arterial wall involvement. Airspace foci were associated with acute and organizing alveolar hemorrhage, while within arteries the hematopoietic elements had a striking predilection for the vascular intima. The hematopoietic foci included erythroid precursors, myeloid precursors, and megakaryocytes, which were immunoreactive with hemoglobin, myeloperoxidase, and CD61, respectively. Whether extramedullary hematopoiesis represents in situ embryonic stem cell differentiation or a compensatory seeding of hematopoietic cells from the bone marrow remains to be elucidated. However, familiarity with these findings in the lung could be helpful in uncovering occult hematological disorders accompanied by extramedullary hematopoiesis. Extramedullary hematopoiesis should also be considered as a cause of pulmonary hemorrhage, especially in the setting of myelofibrosis.
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Zon, LI. "Developmental biology of hematopoiesis." Blood 86, no. 8 (October 15, 1995): 2876–91. http://dx.doi.org/10.1182/blood.v86.8.2876.bloodjournal8682876.

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The cellular and environmental regulation of hematopoiesis has been generally conserved throughout vertebrate evolution, although subtle species differences exist. The factors that regulate hematopoietic stem cell homeostasis may closely resemble the inducers of embryonic patterning, rather than the factors that stimulate hematopoietic cell proliferation and differentiation. Comparative study of embryonic hematopoiesis in lower vertebrates can generate testable hypotheses that similar mechanisms occur during hematopoiesis in higher species.
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6

Smith, Clayton. "Hematopoietic Stem Cells and Hematopoiesis." Cancer Control 10, no. 1 (January 2003): 9–16. http://dx.doi.org/10.1177/107327480301000103.

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Background The highly orchestrated process of blood cell development and homeostasis is termed “hematopoiesis.” Understanding the biology of hematopoietic stem cells as well as hematopoiesis is important to developing improved treatments for hematologic malignancies, congenital disorders, chemotherapy-related cytopenias, and blood and marrow transplants. Methods The author reviews the current state of the art regarding hematopoietic stem cells and hematopoiesis. Results Several new concepts, including stem cell plasticity, suggest the possibility that stem cells may have the ability to differentiate into other tissues in addition to blood cells. Conclusions While much is known about hematopoietic stem cells and hematopoiesis, much remains to be clarified about the environmental and genetic processes that govern the growth and development of the blood system. In addition, careful studies remain to be conducted to determine whether hematopoietic stem cells can differentiate into extra-hematopoietic tissues.
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7

Wei, Chuijin, Pei Yu, and Lin Cheng. "Hematopoietic Reprogramming Entangles with Hematopoiesis." Trends in Cell Biology 30, no. 10 (October 2020): 752–63. http://dx.doi.org/10.1016/j.tcb.2020.07.006.

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Zon, LI. "Developmental biology of hematopoiesis." Blood 86, no. 8 (October 15, 1995): 2876–91. http://dx.doi.org/10.1182/blood.v86.8.2876.2876.

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Abstract The cellular and environmental regulation of hematopoiesis has been generally conserved throughout vertebrate evolution, although subtle species differences exist. The factors that regulate hematopoietic stem cell homeostasis may closely resemble the inducers of embryonic patterning, rather than the factors that stimulate hematopoietic cell proliferation and differentiation. Comparative study of embryonic hematopoiesis in lower vertebrates can generate testable hypotheses that similar mechanisms occur during hematopoiesis in higher species.
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9

Testa, Ugo, Germana Castelli, and Elvira Pelosi. "CLONAL HEMATOPOIESIS: ROLE IN HEMATOLOGIC NON-HEMATOLOGIC." Mediterranean Journal of Hematology and Infectious Diseases 14, no. 1 (August 27, 2022): e2022069. http://dx.doi.org/10.4084/mjhid.2022.069.

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Hematopoietic stem cells (HSCs) ensure the coordinated and balanced production of all hematopoietic cell types throughout life. Aging is associated with a gradual decline of the self-renewal and regenerative potential of HSCs and with the development of clonal hematopoiesis. Clonal hematopoiesis of indeterminate potential (CHIP) is a term defining the clonal expansion of genetically variant hematopoietic cells bearing one or more gene mutations and/or structural variants (such as copy number alterations). CHIP increases exponentially with age and is associated with cancers, including hematologic neoplasia, cardiovascular and other diseases. The presence of CHIP consistently increases the risk of hematologic malignancy, particularly in individuals who have CHIP in association with peripheral blood cytopenia.
 
 Key words: hematopoiesis, hematopoietic stem cells, clonal hematopoiesis, gene mutations, next generation sequencing.
 
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Papa, Veronica, Luisa Marracino, Francesca Fortini, Paola Rizzo, Gianluca Campo, Mauro Vaccarezza, and Francesco Vieceli Dalla Sega. "Translating Evidence from Clonal Hematopoiesis to Cardiovascular Disease: A Systematic Review." Journal of Clinical Medicine 9, no. 8 (August 2, 2020): 2480. http://dx.doi.org/10.3390/jcm9082480.

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Some random mutations can confer a selective advantage to a hematopoietic stem cell. As a result, mutated hematopoietic stem cells can give rise to a significant proportion of mutated clones of blood cells. This event is known as “clonal hematopoiesis.” Clonal hematopoiesis is closely associated with age, and carriers show an increased risk of developing blood cancers. Clonal hematopoiesis of indeterminate potential is defined by the presence of clones carrying a mutation associated with a blood neoplasm without obvious hematological malignancies. Unexpectedly, in recent years, it has emerged that clonal hematopoiesis of indeterminate potential carriers also have an increased risk of developing cardiovascular disease. Mechanisms linking clonal hematopoiesis of indeterminate potential to cardiovascular disease are only partially known. Findings in animal models indicate that clonal hematopoiesis of indeterminate potential-related mutations amplify inflammatory responses. Consistently, clinical studies have revealed that clonal hematopoiesis of indeterminate potential carriers display increased levels of inflammatory markers. In this review, we describe progress in our understanding of clonal hematopoiesis in the context of cancer, and we discuss the most recent findings linking clonal hematopoiesis of indeterminate potential and cardiovascular diseases.
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Tesis sobre el tema "Hematopoiesis"

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Javier, Jose Emmanuel F. "Increased TGF-beta Signaling Drives Different Hematopoietic Disease Outcomes following Stress Hematopoiesis." University of Cincinnati / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1617109578665394.

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Lin, Xionghui. "Hematopoiesis in a Crustacean." Doctoral thesis, Uppsala universitet, Jämförande fysiologi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-121000.

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Hemocytes (blood cells) play an important role in the immune response in invertebrates, and thus the regulation of hemocyte homeostasis (hematopoiesis) is essential for the host survival against pathogens. Astakine 1, a homologue to vertebrate prokineticins, was first identified in the freshwater crayfish Pacifastacus leniusculus as a cytokine, and was found to be necessary for new hemocyte synthesis and release in vivo, and also to induce spreading and proliferation of Hematopoietic tissue cells (Hpt cells, precursor of hemocytes) in vitro. The work of this thesis is aimed to further our understanding of the molecular mechanisms involved in astakine 1 induced hematopoiesis. Crayfish transglutaminase (Tgase) has been identified in the hemocytes, and is essential for the coagulation reaction. Interestingly this enzyme is exceedingly abundant in the Hpt cells, and the spreading of Hpt cells induced by astakine 1 was accompanied by sequential loss of TGase activity from the surface of these cells. This loss of TGase activity may be an important effect of astakine 1, resulting in recruiting new hemocytes into the circulatory system. Although astakine 1 contain a prokineticin domain, it lacks the conserved N-terminal AVIT motif present in its vertebrate homologues. This motif is important for vertebrate prokineticins to interact with their receptors, indicating a different receptor interaction for crayfish astakine 1. Astakine 1 was indeed found to interact with a completely different receptor, the β-subunit of ATP synthase, on a portion of Hpt cells, and subsequently block its extracellular ATP formation. Surface ATP synthase has been reported on numerous mammalian cells, but now for the first time in an invertebrate. The activity of ATP synthase on the Hpt cells may be important for the survival and proliferation of Hpt cells, but the underlying mechanisms remain further study. With the finding of a second type of astakine in crayfish, invertebrate astakines can be divided into two groups: astakine 1 and astakine 2. The properties of astakine 2 are different from those of astakine 1 both in structure and function. In primary cell culture of Hpt cells, only astakine 1 can promote proliferation as well as differentiation into semigranular cells, whereas astakine 2 may play a potential role in the maturation of granular cells. Moreover, a novel cysteine rich protein, Pacifastacus hematopoiesis factor (PHF), was found to be one target gene of astakine 1 in Hpt cells. Down regulation of PHF results in increased apoptosis in Hpt cells in vitro, and in vivo silencing PHF leads to a severe loss of hemocytes in the animal. Therefore astakine 1 acquires the anti-apoptosis ability by inducing its downstream gene PHF in the Hpt cells. With its ability to promote the survival, proliferation and differentiation of Hpt cells, astakine 1 is proven to be an important hematopoietic growth factor.
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3

Benson, Eric Ashley. "Loss of SIMPL increases TNFalpha sensitivity during hematopoiesis." Connect to resource online, 2008. http://hdl.handle.net/1805/1851.

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Thesis (Ph. D.)--Indiana University, 2008.<br>Title from screen (viewed June 24, 2009). Department of Biochemistry and Molecular Biology, Indiana University-Purdue University Indianapolis (IUPUI). Advisor(s): Maureen Harrington. Includes vita. Non-Latin script record. Includes bibliographical references (leaves 126-132).
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4

Urbieta, Maitee. "Regulatory T Cells and Hematopoiesis in Bone Marrow Transplantation." Scholarly Repository, 2010. http://scholarlyrepository.miami.edu/oa_dissertations/463.

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CD4+CD25+FoxP3+ regulatory T cells (Treg) possess the capacity to modulate both adaptive and innate immunity. Due to their suppressive nature, Treg cells have been studied and tested in a variety of scenarios in an attempt to ameliorate undesired immune responses. While graft versus host disease (GVHD) has in fact emerged as the first clinical application for human Treg cells (Riley et al. 2009), equally important are issues concerning hematopoietic engraftment and immune reconstitution. Currently, little is known about the effect(s) that regulatory T cells may exert outside the immune system in this context. Based on cytokine effector molecules they can produce we hypothesized that Treg cells could regulate hematopoietic phenomena. The studies portrayed in this dissertation demonstrate that Treg cells can differentially affect the colony forming activity of myeloid and erythroid progenitor cells. In-vitro as well as in-vivo findings demonstrate the ability of Tregs to inhibit and augment the differentiation of primitive and intermediate myeloid (interleukin (IL)-3 driven) and late erythroid (erythropoietin driven) hematopoietic progenitor cells, respectively. The inhibitory and enhancing affects appeared to be mediated by independent pathways, the former requiring cell-cell contact, major histocompatibility complex (MHC) class II expression on marrow cells and involving transforming growth factor beta (TGF-beta), whereas the latter required interleukin (IL)-9 and was not contact dependent. Strikingly, we observed that in addition to regulating hematopoietic activity in normal primary BM cells, Tregs were also capable of suppressing colony forming activity by the myelogenous leukemia cell line NFS-60. Furthermore, studies involving endogenous Treg manipulations in-situ (i.e. depletion of these cells) resulted in elevated overall myeloid colony activity (CFU-IL3) and diminished colony numbers of erythroid precursors (CFU-E) in recipients following BMT. Consistent with these results, it was found that upon co-transplant with limiting numbers of bone marrow cells, exogenously added Treg cells exert in-vivo regulation of myeloid and erythroid CFU activity during the initial weeks post-transplantation. This regulation of hematopoietic activity by freshly generated Tregs upon transplantation led to the elaboration of a second hypothesis; following lethal total body irradiation (TBI) the host microenvironment facilitates regulatory T cell activation/effector function. Substantial evidence has accumulated in support of this hypothesis, for example we demonstrate up-regulation of surface molecules such as GARP and CD150/SLAM, which have been previously reported as indicators of Treg activation following TCR signaling and co-stimulation, occurs in donor (reporter) Treg populations. Acquisition of an activated phenotype and hence of effector/modulatory function is consistent with the previous in-vivo observations, indicating that both recipient and donor Treg cells can influence hematopoietic progenitor cell activity post-transplant. Finally, the present studies may be of great relevance in the emerging field of Treg cell based immunotherapy for prevention and/or treatment of HSCT complications.
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Syrjänen, R. (Riikka). "TIM family molecules in hematopoiesis." Doctoral thesis, Oulun yliopisto, 2014. http://urn.fi/urn:isbn:9789526204246.

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Abstract Hematopoietic cells, i.e., erythrocytes, platelets and white blood cells, differentiate from hematopoietic stem cells in a process that is similar in vertebrates. Hematopoiesis is regulated by molecules expressed by both the hematopoietic stem and progenitor cells and the surrounding microenvironments. Knowledge of these molecules is important since many of the genes involved in normal hematopoiesis are mutated in leukemia. Furthermore, this information can be utilized in more efficient isolation and expansion of hematopoietic cells in vitro. However, these molecules are not yet sufficiently characterized. Transmembrane immunoglobulin and mucin domain (TIM) genes form a known family of immunoregulators. In mammals, TIM-4 is expressed by antigen presenting cells, while TIM-1, TIM-2 and TIM-3 are expressed by T cells, in which they regulate differentiation of TH cells. The role of TIM molecules in hematopoiesis has not yet been investigated. The aim of this thesis work was to identify and analyze novel molecules involved in embryonic hematopoiesis using chicken and mouse as model organisms. This was carried out by generating a cDNA library of hematopoietic stem and progenitor cells from embryonic chicken para-aortic region. Both previously known and novel candidate genes were identified from the library. Among them, we found homologs to tim genes. Their expression and role in hematopoiesis was studied further. TIM-2 expression was shown to be tightly governed during B cell development. It is expressed by common lymphoid progenitors and highly proliferative large-pro and large pre-B cells during both fetal liver and adult bone marrow hematopoiesis. In mouse, tim-4 expression was restricted to fetal liver CD45+F4/80+ cells. Furthermore, two distinct populations were identified: F4/80hiTIM-4hi and F4/80loTIM-4lo. The results suggest that the F4/80hiTIM-4hi cells are yolk sac-derived macrophages and the F4/80loTIM-4lo cells myeloid progenitors. This work shows for the first time that TIM family molecules are expressed during hematopoiesis. TIM-2- and TIM-4 are expressed by specific cell types during hematopoietic cell development, and in the future they may be utilized as markers in isolation of hematopoietic progenitor cells<br>Tiivistelmä Verisolut eli punasolut, verihiutaleet ja immuunipuolustuksessa tärkeät valkosolut kehittyvät alkion veren kantasoluista prosessissa, joka on kaikissa selkärankaisissa samankaltainen. Veren kanta- ja esisolujen sekä ympäröivän mikroympäristön tuottamat molekyylit säätelevät hematopoieesia eli verisolujen kehitystä. Näiden molekyylien tunteminen on tärkeää, sillä useat normaalia verisolujen kehitystä säätelevät geenit ovat osallisena myös verisyöpien synnyssä. Lisäksi tätä tietoa on mahdollista hyödyntää verisolujen tehokkaammassa eristämisessä ja kasvattamisessa hoitoja varten. Immuunipuolustuksen solut, kuten syöjäsolut eli makrofagit ja T-solut, ilmentävät TIM-molekyylejä (Transmembrane Immunoglobulin and Mucin). Ne toimivat immunologisen vasteen säätelyssä sekä solusyönnissä, mutta niiden roolia verisolujen kehittymisessä ei ole selvitetty aikaisemmin. Tässä väitöstutkimuksessa etsittiin uusia hematopoieesiin vaikuttavia geenejä käyttäen mallieläiminä sekä kanaa että hiirtä. Tutkimuksessa luotiin geenikirjasto kanan alkion para-aortaalisen alueen veren kanta- ja esisoluista. Kirjastosta tunnistettiin useita ennalta tiedettyjä sekä uusia verisolujen kehitykseen vaikuttavia geenejä. Tutkimuksessa analysoitiin tarkemmin kirjastosta löytyneiden TIM-geeniperheen jäsenten ilmentymistä ja roolia verisolujen kehityksessä. Tutkimuksessa osoitettiin, että TIM-2 proteiinin ilmentymistä säädellään tarkasti B-solujen kehityksen aikana. Lymfosyyttien yhteiset esisolut sekä suuret pro-B- ja pre-B-solut ilmentävät TIM-2 proteiinia B-solukehityksen aikana sekä alkion maksassa että aikuisen luuytimessä. Hiiren alkiossa tim-4 geenin ilmentyminen oli rajoittunut maksaan, jossa erottui kaksi erillistä solupopulaatiota: F4/80hiTIM-4hi ja F4/80loTIM-4lo. Tutkimuksen tulokset viittaavat siihen, että maksan F4/80hiTIM-4hi solut ovat ruskuaispussista lähtöisin olevia syöjäsoluja ja F4/80loTIM-4lo solut myeloidisen linjan esisoluja. Tämä tutkimus on ensimmäinen osoitus TIM-molekyylien ilmentymisestä kehittyvissä verisoluissa. Havaitsimme, että TIM-2 ja TIM-4-molekyylejä ekspressoidaan tietyissä soluissa verisolujen erilaistumisen aikana, joten tulevaisuudessa niitä on mahdollista käyttää merkkiproteiineina hematopoieettisten solujen esiasteita eristettäessä
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Kuchenbauer, Florian. "MiRNAs in hematopoiesis and leukemogenesis." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/16752.

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MicroRNAs (miRNAs) have been shown to play important roles in physiological as well as multiple malignant processes including acute myeloid leukemia (AML). In an effort to gain further insight into the role of miRNAs in AML, we have applied the Illumina massively parallel sequencing platform to carry out an in depth analysis of the miRNA transcriptome in a murine leukemia progression model, based on the engineered over-expression of the nucleoporin 98(NUP98)-homeobox HOXD13 fusion gene (ND13), followed by conversion into AML inducing cells upon transduction with the oncogenic collaborator Meis1. Of the over 307 identified miRNA/miRNA* species in both libraries, sequence counts varied between 2 and 136,558, indicating a remarkable expression range. Our finding of extensive sequence variations (isomiRs) for almost all miRNA and miRNA* species adds additional complexity to the miRNA transcriptome. A stringent target prediction analysis coupled with in-vitro target validation revealed the potential for miRNA-mediated release of oncogenes that facilitates leukemic progression from the preleukemic to leukemia inducing state. Besides over 50 putative novel miRNAs, we found a high abundance of miRNA* species, implying a functional role for these. To further elucidate the function of miRNA*s, we took advantage of 9 deep sequencing libraries from a variety of cell lines to determine the most abundant complementary strand of know miRNAs. Comparing miRNA/miRNA* ratios across the miRNA sequence libraries revealed that most ratios remain constant across tissues and species, allowing a novel classification of miRNAs into α-duplexes, miRNAs duplexes with a dominant strand and β-duplexes with both strands being abundant. However, certain ratios were highly variable across the libraries examined as exemplified for the ratio of miR-223/miR-223*. Bioinformatics as well as functional analysis revealed a possible supporting function of miR-223* to the differentiating role of miR-223 in normal normal bone marrow as well as AML. Taken together, by using deep sequencing we provided deep insight into the changes of the miRNA transcriptome in the development of AML. Furthermore, we propose a new classification for miRNA duplexes and provide evidence for a possible role a miRNA* in the development of acute myeloid leukemia.
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Hysenaj, Lisiena. "Alterations of hematopoiesis during brucellosis." Thesis, Aix-Marseille, 2019. http://www.theses.fr/2019AIXM0251.

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La brucellose est une maladie qui se transmet de l’animal à l’homme. Elle est causée par la bactérie Brucella. Lors de ma thèse, j’ai montré que Brucella persiste dans les cellules de la moelle osseuse des animaux infectés. Ces observations sont très importantes car la moelle est un organe responsable de la génération des cellules du système immunitaires et c’est la principale niche des cellules souches hématopoïétiques. Au cours de ma thèse, j'ai montré que la protéine de la membrane externe 25 de Brucella (Omp25) est capable de lier au récepteur SLAMF1, une molécule exprimée par les cellules souches hématopoïétiques. Cette interaction conduit à la génération d'un plus grand nombre de cellules myéloïdes par les cellules souches hématopoïétiques. Les cellules myéloïdes sont la niche préférée de Brucella. Ainsi, cette stratégie permet à la bactérie d'envahir l’hôte et d'établir une infection chronique de longue durée. SLAMF 1 apparaît comme une nouvelle cible thérapeutique pour le contrôle des maladies infectieuses chroniques, ce qui représenterait une avancée importante dans la génération de nouveaux médicaments<br>Brucellosis is a disease that is transmitted from animals to humans. It is caused by the pathogenic bacterium Brucella. During my thesis, I showed that Brucella persists in the bone marrow cells of infected animals. These observations are very important because the bone marrow is an organ of the immune system responsible for the generation of the immune cells, as it is the principal niche of hematopoietic stem cells. During my thesis, I showed that Brucella outer membrane 25 (Omp25) is able to bind SLAMF1, a hematopoietic stem cell molecule. This interaction leads to the production of more myeloid cells by the hematopoietic stem cell. Myeloid cells are the favorite niche of Brucella. Thus, this strategy allows the bacteria to invade the host and establish a long lasting chronic infection. SLAMF 1 appears as a new therapeutic target for controlling chronic infectious diseases, which would represent an important advance in the generation of new drugs
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8

Bilotkach, Kateryna. "Quest for early hematopoietic stem cell precursors." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/33056.

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The first transplantable hematopoietic stem cells (HSC) arise in the aorta-gonad mesonephros region (AGM) during early stages of embryo development. Specifically, ventral aspect of embryonic dorsal aorta (DA) contains HSC that upon transplantation into irradiated recipients can reconstitute all lineages of the haematopoietic system [Medvinsky et al. 1993; Muller and Medvinsky, 1994; Medvinsky and Dzierzak, 1996; Cumano et al., 1996; Tavian et al., 1996; Peault and Tavian, 2003; Taoudi and Medvinsky, 2007; Ivanovs et al., 2011, 2014]. The ventral aspect of DA bears so-called intra-aortic cell clusters (IAC), the appearance of which coincides with the emergence of HSC [Babovic and Eaves, 2014; Bhatia, 2007; Boisset et al., 2010, 2011; Bollerot et al., 2005; de Bruijin et al., 2002; Bertrand et al., 2010]. According to recent reports, HSC are a heterogeneous population of cells [Dykstra et al., 2007; Seita and Weissman, 2010; Muller-Sieburg et al., 2012]. It is unclear whether all HSC precursors originate from the same location, for example, DA lining, IAC or sub-aortic tissues; or HSC precursors migrate into DA lining from other parts of the embryo [Tavian et al., 1999; Yoder et al., 1997; Oberlin et al., 2002; Peault and Tavian, 2003; Dzierzak, 2003; Samokhvalov et al., 2007; Medvinsky et al., 2011]. To elucidate ontogeny of early HSC precursors (pro-HSC), two approaches were applied in this PhD project. First, we mapped potential pro-HSC in pre-circulation mouse embryos (embryonic day 6-8.5, E6-E8.5). We defined potential pro-HSC as cells co-expressing the transcription factor Runx1, endothelial markers (VE-Cad or CD31) and/or haematopoietic markers (CD45, CD41) [Oberlin et al., 2002; de Bruijn and Dzierzak, 2012; Liakhovitskaia et al., 2009, 2014]. In E6-E8 mouse embryo, prospective pro-HSC were found to be located in chorionic plate, yolk sac and in allantoic core domain. In early somitic mouse embryo (E8-8.5) cells with pro-HSC phenotype (Runx1+CD31+CD41+) were found to be in cell clusters in forming vessel of confluence and in nascent dorsal aortae lining. Pro-HSC are not directly transplantable [Cumano et al., 1996., 2001; Godin et al., 1993; 1995; Batta et al., 2016; Matsuoka et al., 2001; Nishikawa et al., 1998]. Therefore, cells and tissues containing prospective pro-HSC were initially matured using several in-vitro culture systems. According to our results, E8 mouse embryo pro-HSC are only preserved in explant cultures, but not in co-aggregate cultures with stroma cells. After culture, cells were transplanted into sub-lethally irradiated recipients. Six weeks after transplantation 19 out of 82 transplanted recipients had donor derived blood cells' chimerism at the level of 0.1-0.3%. Forty six percent of these grafts were derived from rostral part of the embryo tissues (head, heart, upper somites). Only one out of 82 recipients had donor cells contribution above 1% (1.2 %). This recipient was engrafted with cells derived from the E8 mouse embryo head and heart region. Recipients having blood chimerism at the range of 0.1-0.3% had mainly lymphoid donor derived cells in their peripheral blood. The only recipient showing the high donor cells contribution (1.2%) had contribution mainly to myeloid lineage. Recorded low levels of blood chimersims are in line with those reported by Rybtsov et al. (2014) for early E9 mouse embryos. Donor derived cells formed clearly distinguishable populations on cytometry plots. This population of cells were absent from control engraftment experiments with carrier cells only. Previously, lymphoid potential was detected in paraaortic spnanchnopleura (P-Sp) of E8.5-9 mouse embryos, but not in E8 mouse embryos (0-5 somites, pre-circulation) and later in yolk sac [Cumano et al., 1996; Nishikawa et al., 1998; Fraser et al., 2002; Yokota et al., 2006]. However, prior works used different criteria to establish recipient reconstitution. Therefore, it is possible that recipients repopulated with E8 derived cells at the level of 0.1% were not considered as repopulated and hence, presence of lymphoid lineage precursors was overlooked in early somitic mouse embryos. The only recipient showing substantial myeloid cells contribution (73% Mac1+Gr1+ cells of donor derived cells) received engrafted cells from an older (6-13 sp) embryo and therefore potentially has yolk sac derived myeloid cells. Yolk sac cell contribution to myeloid lineage, specifically to the brain microglia was reported in prior works [Samokhvalov et al., 2007]. Our data show that early E8 AGM cells do not expand in in vitro conditions. While in AGM, cells from E9 mouse embryo expand in culture [Rybtsov et al., 2014]. We have analysed Runx1 expression pattern and dorsal aorta morphology at the time when E9 HSC precursors acquire ability to expand in in vitro culture. Runx1 expression becomes clearly polarised at the time point (22-26 sp), when paired dorsal aortae fusion is initiated. We envision that intimate connection between DA fusion events and induction of pro-HSC maturation exists. According to prior reports, Bmp, Shh and VEGF signalling regulate DA fusion [Garriock et al., 2010]. Thereofore, to enhance in vitro HSC maturation system, DA fusion triggers (for example, Bmp4) might be added to culture. Since, pro-HSC maturation methods established to date are not efficient to expand and differentiate E8 pro-HSC into potent HSC, another approach had to be implemented to study HSC ontogeny. The second approach we utilized was to trace the origin of HSC in chicken embryo, starting from the very beginning of cell fate specification, i.e. from gastrulation stages. Chick embryo haematopoiesis is similar in both human and mouse: precursors of HSC arise in the embryo proper in AGM, and IAC are formed in DA ventral aspect [Dieterlen-Lièvre, 1975; Dieterlen-Lièvre and Martin, 1981; Dieterlen-Lièvre and Jaffredo, 2009; Jaffredo et al., 2000; Le Douarin and Dieterlen-Lièvre, 2013]. In contrast to mammals, chick embryo develops ex vivo, making direct labelling and cell tracing possible. We aimed to identify cells giving rise to regions of DA that produce IAC. Therefore, segments of primitive streak (PS) were labelled with lipophilic dyes or by substituting segments of host PS with PS sections derived from transgenic (GFP+) stage matched chicken embryos. Our results show that in an 18-25h chicken embryo (Hamburger and Hamilton developmental stage 4-6, HH4-6) cells giving rise to DA ingress through the wide region of PS (35-60% of its length) [Hamburger and Hamilton, 1951]. We identified that the section of DA producing HSC is formed by cells ingressing through PS in region of 40-55% of its length at 18-25h of chick embryo development. Regardless of the embryo development stage (HH4-6), in chimeras grafted at 40-55% of PS length, GFP+ cells contributed to DA and to the IAC. Within GFP+ labelled areas, we observed clusters consisting entirely of GFP+ and clusters having a mixture of GFP+ and GFP- cells. Entirely GFP+ clusters were found in the stretch of DA that had the entire aortic endothelial lining labelled. Clusters formed on the mosaic (GFP+/GFP-) aortic endothelium also had mosaic nature. According to our data, multiple descendants of PS contribute to the same stretch of dorsal aorta. This explains mosaicity of dorsal aorta lining and IAC labelling. Since we encountered clusters with mixture of GFP+ and GFP- cells, we conclude that IAC are not clonal formations. Mosaicity of IAC also does not exclude a scenario when cells migrate in and out of a cluster. Further tracing experiments are required to establish HSC nature of cells within a cluster.
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Gronthos, Stan. "Stromal precursor cells : purification and the development of bone tissue." Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phg8757.pdf.

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Bibliography: leaves 152-223. Experiments were designed to identify and purify human bone marrow stromal precursor cells by positive immunoselection, based on the cell surface expression of the VCAM-1 and STRO-1 antigens. The data presented demonstrates a hierarchy of bone cell development in vitro.
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Huang, Hsuan-Ting. "Epigenetic Regulation of Hematopoiesis in Zebrafish." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10175.

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The initiation of the hematopoietic program is orchestrated by key transcription factors that recruit chromatin regulators in order to activate or inhibit blood target gene expression. To generate a complete compendium of chromatin factors that establish the genetic code during developmental hematopoiesis, we conducted a large-scale reverse genetic screen targeting 425 chromatin factors in zebrafish and identified over 30 novel chromatin regulators that function at distinct steps of embryonic hematopoiesis. In vertebrates, developmental hematopoiesis occurs in two waves. During the first and primitive wave, mainly erythrocytes are produced, and we identified at least 15 chromatin factors that decrease or increase formation of \(scl^+\), \(gata1^+\), and \(\beta-globin e3^+\) erythroid progenitors. In the definitive wave, HSCs capable of self-renewal and differentiation into multiple lineages are induced, and we identified at least 18 chromatin factors that decrease or increase the formation of \(c-myb^+\) and \(runx1^+\) stem and progenitor cells in the aorta gonad mesonephros (AGM) region, without disruption of vascular development. The majority of the chromatin factors identified from the screen are involved in histone acetylation, histone methylation, and nucleosome remodeling, the same modifications that are hypothesized to have the most functional impact on the transcriptional status of a gene. Moreover, these factors can be mapped to subunits of chromatin complexes that modify these marks, such as HBO/HAT, HDAC/NuRD, SET1A/MLL, ISWI, and SWI/SNF. One of the strongest phenotypes identified from the screen came from knockdown of chromodomain helicase DNA binding domain 7 (chd7). Morpholino knockdown of chd7 resulted in increased primitive and definitive blood production from the induction of stem and progenitor cells to the differentiation of myeloid and erythroid lineages. This expansion of the blood lineage is cell autonomous as determined by blastula transplantation experiments. Though chromatin factors are believed to function broadly and are often expressed ubiquitously, the combined results of the screen and chd7 analysis show that individual factors have very tissue specific functions. These studies implicate chromatin factors as playing a major role in establishing the programs of gene expression for self-renewal and differentiation of hematopoietic cells.
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Libros sobre el tema "Hematopoiesis"

1

Gutti, Ravi Kumar. Hematopoiesis. Boca Raton: Apple Academic Press, 2023. http://dx.doi.org/10.1201/9781003413059.

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Baron, Margaret H. Developmental Hematopoiesis. New Jersey: Humana Press, 2004. http://dx.doi.org/10.1385/1592598269.

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Brown, Geoffrey, and Rhodri Ceredig. Cell determination during hematopoiesis. New York: Nova Biomedical Books, 2009.

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Mihich, Enrico, and Donald Metcalf, eds. Normal and Malignant Hematopoiesis. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1927-0.

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Wickrema, Amittha, and Barbara Kee, eds. Molecular Basis of Hematopoiesis. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-85816-6.

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Dygai, A. M., and V. V. Zhdanov. Theory of Hematopoiesis Control. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-08584-5.

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1963-, Brown Geoffrey, and Ceredig Rhodri, eds. Cell determination during hematopoiesis. Hauppauge, NY: Nova Science Publishers, 2009.

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J, Fairbairn Leslie, and Testa Nydia G. 1938-, eds. Hematopoiesis and gene therapy. New York: Kluwer Academic/Plenum Publishers, 1999.

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Amittha, Wickrema, and Kee Barbara Lynne 1966-, eds. Molecular basis of hematopoiesis. New York, NY: Springer, 2009.

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I, Zon Leonard, ed. Hematopoiesis: A developmental approach. New York: Oxford University Press, 2001.

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Capítulos de libros sobre el tema "Hematopoiesis"

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Rai, Geeta, Doli Das, Khushbu Priya, and Hiral Thacker. "Clinical Outcomes of Defective Hematopoiesis." In Hematopoiesis, 143–59. Boca Raton: Apple Academic Press, 2023. http://dx.doi.org/10.1201/9781003413059-7.

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Dahariya, Swati, Sanjeev Raghuwanshi, and Ravi Kumar Gutti. "Systems Biology Approaches Toward Understanding Human Long Noncoding RNA in Hematopoietic Cells." In Hematopoiesis, 125–42. Boca Raton: Apple Academic Press, 2023. http://dx.doi.org/10.1201/9781003413059-6.

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Kalle, Arunasree M., and Debasmita Naik. "Epigenetics of Hematopoiesis: Role of HATs and HDACs." In Hematopoiesis, 109–23. Boca Raton: Apple Academic Press, 2023. http://dx.doi.org/10.1201/9781003413059-5.

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Gautam, Dushyant Kumar, Anuradha Venkatakrishnan Chimata, Ravi Kumar Gutti, and Indira Paddibhatla. "Investigative Tools to Study Blood Cells: A Focus on Single Cell Isolation and Analysis." In Hematopoiesis, 19–49. Boca Raton: Apple Academic Press, 2023. http://dx.doi.org/10.1201/9781003413059-2.

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Singh, Anula Divyash, and Rasmita Samal. "Circulating Messengers of Blood and Their Clinical Applications." In Hematopoiesis, 161–82. Boca Raton: Apple Academic Press, 2023. http://dx.doi.org/10.1201/9781003413059-8.

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Subramani, Arun Kumar, Keyur Raval, and Ritu Raval. "Evaluation of Chitosan and Its Derivatives in Immunomodulating Blood Sentinel Cells." In Hematopoiesis, 51–71. Boca Raton: Apple Academic Press, 2023. http://dx.doi.org/10.1201/9781003413059-3.

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Prajapati, Akhilesh. "Hematopoiesis and Cancer Stem Cells: The Seed and the Soil Crosstalk." In Hematopoiesis, 183–92. Boca Raton: Apple Academic Press, 2023. http://dx.doi.org/10.1201/9781003413059-9.

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Wasnik, Samiksha, Lakshmi Manasay Chaturvedula, and Chaturvedula Tripura. "Proteoglycans and Glycosaminoglycans Regulating Functions of the Hematopoietic Stem Cell Niche." In Hematopoiesis, 73–107. Boca Raton: Apple Academic Press, 2023. http://dx.doi.org/10.1201/9781003413059-4.

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Chakraborty, Aparajita. "Unrevealing the Mechanism of Zebrafish Hematopoiesis: A Novel Approach." In Hematopoiesis, 1–17. Boca Raton: Apple Academic Press, 2023. http://dx.doi.org/10.1201/9781003413059-1.

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Choudhary, Anpreet, Rekha Sharma, Raghunath Manchala, K. Rajender Rao, Satti Vishnupriya, Suvir Singh, Obul Reddy Bandapalli, Prashant Suravajhala, Raghunadharao Digumarthi, and Sugunakar Vuree. "Minimal Residual Disease (MRD) as a Prognostic Marker in Acute Myeloid Leukemia." In Hematopoiesis, 229–73. Boca Raton: Apple Academic Press, 2023. http://dx.doi.org/10.1201/9781003413059-11.

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Actas de conferencias sobre el tema "Hematopoiesis"

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Nelson, Darlene R., and Jay H. Ryu. "A Case Of Pleuropulmonary Extramedullary Hematopoiesis." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6678.

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Grubač, Siniša, Marko Cincović, Jože Starič, Marinković Došenović, Biljana Delić-Vujanović, and Jasna Prodanov-Radulović. "The relationship of the metabolism of iron, organic matter and phlebotomy with the erythropoiesis of ruminants." In Zbornik radova 26. medunarodni kongres Mediteranske federacije za zdravlje i produkciju preživara - FeMeSPRum. Poljoprivredni fakultet Novi Sad, 2024. http://dx.doi.org/10.5937/femesprumns24012g.

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Erythropesis is the process of making red blood cells and it is related to numerous factors in the body. Iron is important because of its role in the process of making hemoglobin. In addition to the mentioned iron, it is an indirect indicator of inflammation and is regulated at the systemic and cellular level, so its lack speaks of the overall health status of individuals. Fe deficiency in the body takes place through three phases. In the first phase, there is emptying of tissue depots, but its total amount in the circulation increases, then follows the second phase or the phase of real deficit with decreasing concentration of serum iron and hemoglobin, and the third phase is the phase in which the significance of iron deficit is clinically seen. Iron deficiency disrupts all aspects of erythropoiesis. Therefore, first the iron reserves are used up, then with the decrease of transported iron, erythropoiesis changes, and when the availability of this iron is completely reduced, anemia will occur due to iron deficiency. Lipid metabolism also plays a very important role in the functioning of hematopoietic stem cells. Fatty acid oxidation is the main catabolic pathway by which energy is produced in hematopoietic stem cells. Long-chain fatty acids are activated in the cytosol and transported to the mitochondria by the transport system. In them, beta oxidation takes place through several known stages, creating acetyl coenzyme A, which starts the cycle of tricarboxylic acids. Deletion of the gene for regulation of fatty acid oxidation causes hematopoiesis stem cells to lose their potential to reconstruct and maintain themselves. Due to the importance of lipolysis in ruminants and the fact that stem cells are found in the lipidrich niches of bone marrow, we will also consider the relationship between bone marrow adipocytes and hematopoiesis. Chronic phlebotomy in rams or Fe deficiency due to inflammation and fatty liver in cows lead to specific changes in red blood cell and blood metabolites. All of the above shows that it is necessary to know the metabolic flows in order to better understand erythropoiesis in ruminants.
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Huang, Kuan-Lin, Mingchao Xie, Yige Wu, Reyka Jayasinghe, Rajees Varghese, R. Jay Mashl, Song Cao, et al. "Abstract 3424: Genomic alterations in clonal hematopoiesis." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3424.

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Al-Qadi, M. O., M. Hunsucker, and J. Akulian. "Acute Myeloid Leukemia Arising from Pleural Extramedullary Hematopoiesis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6702.

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Guang Zheng, Juping Chen, Lingru Wang, Ruimin Qin, Xi Zhang, and Kanni Gao. "Pathway enrichment analysis of Dang-gui for hematopoiesis." In 2015 12th International Conference on Fuzzy Systems and Knowledge Discovery (FSKD). IEEE, 2015. http://dx.doi.org/10.1109/fskd.2015.7382108.

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Djema, Walid, Frederic Mazenc, and Catherine Bonnet. "Lyapunov stability analysis of a model describing hematopoiesis." In 2015 European Control Conference (ECC). IEEE, 2015. http://dx.doi.org/10.1109/ecc.2015.7330947.

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Kim, Eunhee, Stephen S. Chung, Jae H. Park, Young Rock Chung, Piro Lito, Julie Feldstein, Wenhuo Hu, et al. "Abstract 3140: Context specific effects of the BRAFV600E mutation on hematopoiesis identifies novel models of BRAF mutant hematopoietic disorders." 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.am2014-3140.

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Djema, Walid, Frederic Mazenc, and Catherine Bonnet. "Stability of immature cell dynamics in healthy and unhealthy hematopoiesis." In 2016 American Control Conference (ACC). IEEE, 2016. http://dx.doi.org/10.1109/acc.2016.7526631.

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Moore, Finola E., Virginie Esain, Riadh Lobbardi, Jessica S. Blackburn, Trista E. North, and David M. Langenau. "Abstract A33: Role for the tumor suppressor phf6 in hematopoiesis." In Abstracts: AACR Special Conference on Hematologic Malignancies: Translating Discoveries to Novel Therapies; September 20-23, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.hemmal14-a33.

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Bhullar, Jasjeet, and Vincent E. Sollars. "Abstract 2964: YB-1 expression in early hematopoiesis and leukemic cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2964.

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Informes sobre el tema "Hematopoiesis"

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Taub, Floyd E., and Richard E. Weller. Proline-Rich Polypeptide 1 and GX-NH2: Molecular and Genetic Mechanisms of Hematopoiesis Regulation. Office of Scientific and Technical Information (OSTI), September 2011. http://dx.doi.org/10.2172/1025686.

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Taub, Floyd, and Richard Weller. Proline-Rich Polypeptide 1 and GX-NH2: Molecular and Genetic Mechanisms of Hematopoiesis Regulation. Office of Scientific and Technical Information (OSTI), September 2011. http://dx.doi.org/10.2172/1035210.

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Coltman, Charles A., and Jr. Clonal Hematopoiesis as a Marker of Genetic Damage Following Adjuvant Chemotherapy for Breast Cancer: Pilot Study to Evaluate Incidence. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada378125.

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Iwata, Mineo. Redefining the Hematopoietic Microenvironment. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada573826.

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Iwata, Mineo. Redefining the Hematopoietic Microenvironment. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada583988.

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Felsher, Dean W. Nanoscale Proteomic Analysis of Oncoproteins in Hematopoietic Cancers. Fort Belvoir, VA: Defense Technical Information Center, May 2012. http://dx.doi.org/10.21236/ada587676.

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Abel, Gregory, Haesook Kim, Thomas Walsh, Vincent Ho, and Robert Soiffer. Shared Care: Patient-Centered Management after Hematopoietic Cell Transplantation. Patient-Centered Outcomes Research Institute (PCORI), September 2024. http://dx.doi.org/10.25302/09.2024.ihs.151133081.

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Dorshkind, Kenneth. Effects of Hematopoietic Stem Cell Age on CML Disease Progression. Fort Belvoir, VA: Defense Technical Information Center, March 2006. http://dx.doi.org/10.21236/ada451341.

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Sytkowski, Arthur J. Development of Hematopoietic Growth Factors for Use in Military Personnel. Fort Belvoir, VA: Defense Technical Information Center, August 1990. http://dx.doi.org/10.21236/ada238603.

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Sytkowski, Arthur J. Development of Hematopoietic Growth Factors for Use in Military Personnel. Fort Belvoir, VA: Defense Technical Information Center, July 1991. http://dx.doi.org/10.21236/ada242475.

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