Relevant bibliographies by topics / Circulating progenitor cells

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Circulating progenitor cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 February 2022

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Journal articles on the topic "Circulating progenitor cells"

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Anversa, Piero, Jan Kajstura, and Annarosa Leri. "Circulating Progenitor Cells." Circulation 110, no. 20 (November 16, 2004): 3158–60. http://dx.doi.org/10.1161/01.cir.0000148679.30170.78.

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Schwartzenberg, Shmuel, Varda Deutsch, Sofia Maysel-Auslender, Sarina Kissil, Gad Keren, and Jacob George. "Circulating Apoptotic Progenitor Cells." Arteriosclerosis, Thrombosis, and Vascular Biology 27, no. 5 (May 2007): 1079. http://dx.doi.org/10.1161/atvb.27.5.1079.

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Garmy-Susini, B., and J. A. Varner. "Circulating endothelial progenitor cells." British Journal of Cancer 93, no. 8 (September 27, 2005): 855–58. http://dx.doi.org/10.1038/sj.bjc.6602808.

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Susini, Sandrine, Séverine Mouraud, Elodie Elkaim, Julien Roullier, Sonia Luce, Olivier Pellé, Julie Bruneau, Marina Cavazzana, and Isabelle Andre-Schmutz. "From the Bone Marrow to the Thymic Niche." Blood 124, no. 21 (December 6, 2014): 5123. http://dx.doi.org/10.1182/blood.v124.21.5123.5123.

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Abstract To generate T cells throughout adult life, the thymus must import hematopoietic progenitor cells from the bone marrow via the blood. The cellular and molecular mechanisms governing the circulation of thymus-seeding progenitor cells are well characterized in mice but not in humans. The aim of the present study was to characterize the molecular mechanisms and cellular components involved in thymus colonization by lymphoid progenitors (CD34+/CD10+/CD7-/CD24-) and the early steps of thymopoiesis under physiological conditions in humans. Our results demonstrate that circulating lymphoid progenitor cells express CCR9 and CXCR4 chemokine receptors, VLA-4, VLA-5 and VLA-6 integrins and PSGL-1 and CD44 adhesion molecules. We used in vitro migration and adhesion assays to validate the functional status of these markers. As in the mouse, human circulating progenitor cells enter the thymus at the corticomedullary junction (CMJ). Once in the thymus, crosstalk with thymic epithelial cells causes the circulating progenitors to commit to the T-cell differentiation pathway. In order to characterize thymic niches and interactions between circulating progenitors and the thymic stroma, we undertook a chemokine/chemokine-receptor-focused gene expression analysis of sorted lymphoid progenitor cells and CMJ epithelial cells (based on the expression of EpCAM and Delta-like-4). We observed an unexpected gene expression profile for chemokines and chemokine regulators in thymus-seeding CD34+/CD10+/CD7-/CD24- cells and epithelial cells at the CMJ. The present results should help us to highlight candidate genes involved in the early steps of human thymopoiesis. Disclosures No relevant conflicts of interest to declare.
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Gomer, Richard H. "Circulating progenitor cells and scleroderma." Current Rheumatology Reports 10, no. 3 (June 2008): 183–88. http://dx.doi.org/10.1007/s11926-008-0031-8.

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Díaz del Moral, Sandra, Silvia Barrena, Ramón Muñoz-Chápuli, and Rita Carmona. "Embryonic circulating endothelial progenitor cells." Angiogenesis 23, no. 4 (July 1, 2020): 531–41. http://dx.doi.org/10.1007/s10456-020-09732-y.

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Wang, Chunlin, Chunhua Jiao, Heather D. Hanlon, Wei Zheng, Robert J. Tomanek, and Gina C. Schatteman. "Mechanical, cellular, and molecular factors interact to modulate circulating endothelial cell progenitors." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 5 (May 2004): H1985—H1993. http://dx.doi.org/10.1152/ajpheart.00431.2003.

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It appears that there are two classes of human circulating endothelial cell (EC) progenitors, CD34+and CD34–CD14+cells. Attention has focused on CD34+cells, yet CD34–CD14+monocytic cells are far more abundant and may represent the most common class of circulating EC progenitor. Little is known about molecular or physiological factors that regulate putative CD34–CD14+EC progenitor function, although factors secreted by other blood and cardiovascular cells to which they are exposed probably affect their behavior. Hypoxia and stretch are two important physiological stimuli known to trigger growth factors in cardiovascular cells and accordingly may modulate EC progenitors. To investigate the impact of these environmental parameters on EC progenitors, EC production in CD34–CD14+cultures was evaluated. Our data indicate that neither stretch nor hypoxia alters EC production by EC progenitors directly but do so indirectly through their effects on cardiovascular cells. Conditioned media (CM) from coronary artery smooth muscle cells inhibit EC production in culture, and this inhibition is stronger if the coronary smooth muscle cells have been subjected to cyclic stretch. In contrast, cardiomyocyte CM increases EC cell number, an effect that is potentiated if the myocytes have been subjected to hypoxia. Significantly, EC progenitor responses to CM are altered by the presence of CD34–CD14–peripheral blood mononuclear cells (PBMCs). Moreover, CD34–CD14–PBMCs attenuate EC progenitor responsiveness to the angiogenic factors basic fibroblast growth factor (FGF-2), vascular endothelial cell growth factor-A165, and erythropoietin while inducing EC progenitor death in the presence of transforming growth factor-β1in vitro
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Jönsson, Daniel, Thomas Spinell, Anastasios Vrettos, Christin Stoecklin-Wasmer, Romanita Celenti, Ryan T. Demmer, Moritz Kebschull, and Panos N. Papapanou. "Circulating Endothelial Progenitor Cells in Periodontitis." Journal of Periodontology 85, no. 12 (December 2014): 1739–47. http://dx.doi.org/10.1902/jop.2014.140153.

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Samman Tahhan, Ayman, Muhammad Hammadah, Heval Mohamed Kelli, Jeong Hwan Kim, Pratik B. Sandesara, Ayman Alkhoder, Belal Kaseer, et al. "Circulating Progenitor Cells and Racial Differences." Circulation Research 123, no. 4 (August 3, 2018): 467–76. http://dx.doi.org/10.1161/circresaha.118.313282.

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Bonsignore, Maria R., Giuseppe Morici, Alessandra Santoro, Maria Pagano, Lucia Cascio, Anna Bonanno, Pietro Abate, et al. "Circulating hematopoietic progenitor cells in runners." Journal of Applied Physiology 93, no. 5 (November 1, 2002): 1691–97. http://dx.doi.org/10.1152/japplphysiol.00376.2002.

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Because endurance exercise causes release of mediators and growth factors active on the bone marrow, we asked whether it might affect circulating hematopoietic progenitor cells (HPCs) in amateur runners [ n = 16, age: 41.8 ± 13.5 (SD) yr, training: 93.8 ± 31.8 km/wk] compared with sedentary controls ( n = 9, age: 39.4 ± 10.2 yr). HPCs, plasma cortisol, interleukin (IL)-6, granulocyte colony-stimulating factor (G-CSF), and the growth factor fms-like tyrosine kinase-3 (flt3)-ligand were measured at rest and after a marathon (M; n = 8) or half-marathon (HM; n = 8). Circulating HPC counts (i.e., CD34+cells and their subpopulations) were three- to fourfold higher in runners than in controls at baseline. They were unaffected by HM or M acutely but decreased the morning postrace. Baseline cortisol, flt3-ligand, IL-6, and G-CSF levels were similar in runners and controls. IL-6 and G-CSF increased to higher levels after M compared with HM, whereas cortisol and flt3-ligand increased similarly postrace. Our data suggest that increased HPCs reflect an adaptation response to recurrent, exercise-associated release of neutrophils and stress and inflammatory mediators, indicating modulation of bone marrow activity by habitual running.
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Dissertations / Theses on the topic "Circulating progenitor cells"

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Ensley, Ann Elizabeth. "Functional evaluation of circulating endothelial progenitor cells for vascular tissue engineering." Diss., Available online, Georgia Institute of Technology, 2006, 2006. http://etd.gatech.edu/theses/available/etd-04042006-145611/.

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Thesis (Ph. D.)--Biomedical Engineering, Georgia Institute of Technology, 2006.
Vito, Raymond, Committee Member ; Nerem, Robert, Committee Chair ; Eskin, Suzanne, Committee Member ; Hanson, Stephen, Committee Member ; Gibbons, Gary, Committee Member.
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Thomas, Honey. "A clinical investigation of circulating endothelial progenitor cells in cardiovascular repair." Thesis, University of Newcastle upon Tyne, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.490148.

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Background Endothelial progenitor cells (EPCs) are circulating progenitor cells involved in vascular repair and regeneration. I investigated the role of EPCs in cardiac transplant recipients, to establish whether reduced EPCs are associated with cardiac allograft vasculopathy (CAV), and to investigate whether patients receiving older donor hearts have lower EPCs than those receiving hearts from younger donors. I carried out a study to 'determine whether controlled vascular damage occurring at percutaneous coronary intervention (pCI) results in EPC release. Finally I assessed whether EPCs show diurnal variation in healthy individuals. Methods and Results I used flow cytometry quantification of absolute EPC counts with all the commonly used phenotypes from whole peripheral blood. The methods underwent extensive optimisation stages and reproducibility studies. I did not find any difference EPC numbers between cardiac transplant patients with and without CAV. There was no reduction in EPCs in patients with older donor hearts. There was no evidence of EPC mobilisation in the first 24 hours after PCI, rather there was a fall in EPCs in the first 6 hours. This is similar to the pattern ofdiurnal variation found in healthy volunteers sampled at 3 time points who showed a fall in EPCs between 8am and 3pm and a subsequent rise at lOpm. Conclusions My work has shown that EPCs are not reduced in CAV which highlights the pathophysiological differences from coronary disease. It provides evidence supporting the theory that age related decline in EPCs is not due to aging of the target tissues. also challenge the existence of a vascular injury specific mobilisation ofEPCs following PCI. Finally I have demonstrated a significant diurnal variation in EPCs which is important both in underst&lding EPC kinetics and also for the interpretation and conduction of future clinical studies.
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Dotsenko, Olena. "Bone marrow resident and circulating progenitor cells in patients undergoing cardiac surgery." Thesis, St George's, University of London, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.530510.

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Murray, Neil A. "Circulating megakaryocyte progenitor and precursor cells in the healthy and thrombocytopenic neonate." Thesis, University of Aberdeen, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337398.

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Background: Thrombocytopenia is common in sick preterm babies in the first day of life. Despite this, platelet production in thrombocytopenic preterm babies has rarely been assessed. Methods: To address this problem I have developed miniaturised assays to study circulating megakaryocyte (MK) progenitors (BFU-MK and CFU-MK), total cultured MK precursors and mature MK, by culturing mononuclear cells purified from 0.5-1ml of preterm peripheral blood. MK lineage colonies and cells are identified by a MK specific anti-glycoprotein IIb/IIIa antibody (CD61) by APAAP. Results: i) Normal values for these cells at birth were established in cord blood from healthy term and preterm babies. ii) Circulating BFU-MK/CFU-MK, total cultured MK precursors and mature MK were then prospectively studied in 63 preterm babies (gestational age 24-34 wks). iii) At birth 18 (69%) of the thromocytopenic babies were also neutropenic. Conclusion: These data indicate that the principal cause of the thrombocytopenia and neutropenia in the preterm babies studied was reduced platelet and neutrophil production occurring as a consequence of reduced numbers of MK and neutrophil progenitors respectively. Taken together these data suggest the haematological abnormalities characteristic of new-born born to mothers with PIH or with IUGR (thrombocytopenia, neutropenia and polycythaemia) are a consequence of dysregulation of fetal haemopoiesis occurring proximal to committed MK and neutrophil progenitors, most likely at the level of the primitive multipotent haemopoietic stem cell (CFU-GEMM). Finally the value of miniaturised MK progenitor and precursor assays in evaluating rare or unusual cases of neonatal thrombocytopenia has been demonstrated. In the three examples investigated this approach provided unique insights into the pathogenesis of the thromocytopenia in each case.
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李晓 and Xiao Li. "Macrophage migration inhibitory factor and circulating progenitor cells: relevance and implications inperiodontal medicine." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B45894267.

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Watson, Timothy J. "Circulating progenitor cells in atrial fibrillation : Relationship to endothelial dysfunction, thrombogenesis and inflammation." Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/1253/.

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Atrial fibrillation (AF) is the most common arrhythmia encountered in clinical practice with rapidly rising prevalence and incidence predominantly due to advancing age in Western populations. Of particular concern however is the strong relationship between AF and stroke. This relates to a number of factors, but there is an emerging body of evidence to suggest that AF confers a hypercoagulable state. Disruption of endothelial homeostasis (damage vs. repair) is thought to be central to this process. The endothelium appears to be damaged both by AF and various other vascular diseases (e.g. hypertension) that frequently co-exist with the arrhythmia, with similar disruption to endothelial repair (normally effected by endothelial progenitor cells). Endothelial damage seems to be an essential prerequisite to thrombogenesis in AF. Significantly, the endothelium also links a number of processes including inflammation, growth factors, the renin-angiotensin-aldosterone system among others, which may directly or indirectly lead to activation of the coagulation cascade. This thesis investigates the relationship between the temporal pattern of AF (paroxysmal, persistent, permanent) and established markers of endothelial dysfunction (vonWillebrand factor, vWf; soluble E-selectin, sEsel), angiogenesis (vascular Endothelial Growth Factor, VEGF), apoptosis (soluble Fas/Fas ligand, sFas/sFasL) and inflammation (C-reactive protein, CRP; Interleukin-6, IL-6) in AF with particular reference to circulating progenitor cells (CPCs) as a novel marker of endothelial health/angiogenesis. Additionally the impact of restoration of sinus rhythm using electrical cardioversion on these indices and the relevance of the AF arrhythmia burden in influencing these markers is investigated. In conclusion, the endothelium seems to be a central link through which all three components of Virchow’s triad interact in AF. This thesis finds a possible link for CPCs to interact with various other reported aberrancies of the hypercoagulable state in this process. Also reported is a modest alteration in CPC counts following restoration of sinus rhythm, however, only limited numbers of patients were assessed and this requires examination with a more in depth study. Finally, the thesis has also examined the role of paroxysmal AF in influencing surrogate markers of the hypercoagulable state, but failed to find any significant differences on the basis of the arrhythmia burden. These findings must however been considered in light of numerous study limitations, the most notable of which is limited statistical power.
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Webster, Katie Elizabeth. "Angiogenesis in endometriosis : the role of circulating angiogenic cells and the endometrium." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:33c8921c-8320-4559-8298-52d85c8a2987.

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Endometriosis is a common cause of subfertility and pelvic pain, affecting up to 10% of women of reproductive age. It is characterised by the presence of endometrial-like tissue outside the uterus. The development of the disease is still poorly understood and, currently, the diagnosis relies on visualisation of typical lesions during surgery. There is great interest in identifying biomarkers to assist in diagnosis and disease management. Blood vessel development is known to be a crucial feature of endometriosis, but the mechanisms involved in angiogenesis are not well described for this disease. Most vessel development relies on the proliferation and migration of pre-existing endothelial cells. However, there may also be roles for cells derived from peripheral blood (circulating angiogenic cells) and surrounding stromal cells. In this thesis, the contribution of these different cell types to vessel development in endometriosis is assessed. In chapter 2, a robust protocol was optimised to identify circulating angiogenic cells (CACs) with flow cytometry. The reliability of the protocol was verified, and the level of these cells was found not to fluctuate with the menstrual cycle in healthy women (P=0.279, F=1.359, 3 d.f.). In chapter 3, levels of CACs in women with and without endometriosis were found to be equivalent (0.0835% ± 0.0422 compared to 0.0724% ± 0.0414), demonstrating that they have no use as a disease biomarker. In chapter 4, isolation and culture of endothelial cells from the endometrium was attempted. However, a pure culture of endometrial endothelial cells could not be obtained, which may be due to contamination by other cell types or cellular transdifferentiation. Finally, in chapter 5, the contribution of endometrial stromal cells to vessel development was considered. Stromal cells were found not to differentiate towards an endothelial cell phenotype, but were able to participate in tube formation assays. However, the presence of endometriosis did not influence this behaviour.
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Sakamori, Yuichi. "Increase in circulating endothelial progenitor cells predicts response in patients with advanced non-small-cell lung cancer." Kyoto University, 2016. http://hdl.handle.net/2433/215446.

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Martins, Sandra Cristina Pinto. "Evaluation of circulating endothelial progenitor cells by multicolor flow cytometry in chronic kidney disease patients." Master's thesis, Universidade de Aveiro, 2015. http://hdl.handle.net/10773/16135.

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Mestrado em Biologia Molecular e Celular
Endothelial dysfunction and impaired endothelial regenerative capacity play a key role in the pathogenesis of cardiovascular disease, which is one of the major causes of mortality in chronic kidney disease (CKD) patients. Circulating endothelial cells (CEC) may be an indicator of vascular damage, while circulating endothelial progenitor cells (EPC) may be a biomarker for vascular repair. However, the simultaneously evaluation of CEC and EPC circulating levels and its relation were not previously examined in CKD population. A blood sample (18ml) of healthy subjects (n=10), early CKD (n=10) and advanced CKD patients (n=10) was used for the isolation of early and late EPCs, CECs, and hematopoietic cells, identified by flow cytometry (BD FACSCanto™ II system) using a combination of fluorochrome-conjugated primary antibodies: CD31-PE, CD45-APC Cy7, CD34-FITC, CD117-PerCp Cy5.5, CD133-APC, CD146-Pacific Blue, and CD309-PECy7. Exclusion of dead cells was done according to a fixable viability dye staining. This eightcolor staining flow cytometry optimized protocol allowed us to accurate simultaneously identify EPCs, CECs and hematopoietic cells. In addition, it was also possible to distinguish the two subpopulations of EPCs, early and late EPCs subpopulation, by CD45intCD31+CD34+CD117-CD133+CD309-CD146- and CD45intCD31+CD34+CD117-CD133-CD309+CD146- multiple labeling, respectively. Moreover, the identification of CECs and hematopoietic cells was performed by CD45-CD31+CD34-/lowCD117-CD133-CD309-CD146+ and CD34+CD117+, respectively. The levels of CECs were non-significantly increased in early CKD (312.06 ± 91.34) and advanced CKD patients (191.43±49.86) in comparison with control group (103.23±24.13). By contrast, the levels of circulating early EPCs were significantly reduced in advanced CKD population (17.03±3.23) in comparison with early CKD (32.31±4.97), p=0.04 and control group (36.25 ± 6.16), p=0.03. In addition the levels of late EPCs were significantly reduced in both advanced (6.60±1.89), p=0.01, and early CKD groups (8.42±2.58), p=0.01 compared with control group (91.54±29.06). These results were accompanied by a dramatically reduction in the recruitment, differentiation and regenerative capacity indexes in CKD population. Taken together, these results suggest an imbalance in the process of endothelial repairment in CKD population, and further propose that the indexes of recruitment, differentiation and regenerative capacity of EPCs, may help to select the patients to benefit from guiding intervention strategies to improve cardiovascular health by inducing vascular protection.
A disfunção endotelial e as alterações nos processos de regeneração endotelial podem desempenhar um papel determinante na patogénese da doença cardiovascular, que é uma das principais causas de mortalidade na doença renal crónica (DRC). As células endoteliais circulantes (CEC) podem ser um indicador de dano vascular, enquanto que as células progenitoras endoteliais circulantes (CPEC) pode ser um biomarcador de reparação vascular. No entanto, a avaliação simultânea dos níveis de CECs e de CPECs e sua relação não foram previamente avaliados numa população de doentes renais crónicos. Amostras de sangue (18 mL) foram recolhidas a partir de indivíduos saudáveis (n = 10), e a partir de doentes renais crónicos em estadios precoces (n=10) e em estádios avançados (n=10), para se proceder ao isolamento de populações de CPECs imaturas e maduras, CECs e células hematopoiéticas. Estas populações de células foram identificadas por citometria de fluxo (sistema BD FACS Canto II) usando uma combinação de anticorpos primários conjugados com fluorocromos: CD31-PE, CD45-APC Cy7, CD34-FITC, CD117-PerCp Cy5.5, CD133-APC, CD309-PE Cy7 e CD146-Paciific blue. Para a exclusão das células mortas recorreu-se a um marcador de viabilidade (“fixable viability dye”). Este protocolo otimizado de citometria de fluxo de oito cores permitiu identificar simultaneamente e com precisão as subpopulações de CECs, CPECs e células hematopoiéticas. Além disso, também foi possível distinguir as duas subpopulações de CPECs, imaturas e maduras, por marcação múltipla CD45intCD31+ CD34+ CD117-CD133+ CD309-CD146- e CD45intCD31+ CD34+CD117- CD133-CD309+ CD146-, respetivamente. Adicionalmente, a identificação de CECs e células hematopoiéticas foi realizada por CD45-CD31+ CD34-/lowCD117- CD133-CD309- CD146+ e CD34+ CD117+, respetivamente. Os níveis de CECs foram mais elevados em pacientes em estadios precoces de DRC (312,1±91,3) e em estadios avançados (191,4±49,9) comparativamente com o grupo controlo (103,23±24,13), n.s. Para além disso, os níveis de CPECs imaturas foram significativamente diminuídos em estadios avançados de DRC (17,1±3,2) em comparação com estadios precoces (32,3±4,9), p=0,04, e com o grupo controlo (36,3±6,2), p=0,03. Os níveis de CPECs maduras foram significativamente reduzidos em estadios avançados de DRC (6,6±1,9), p=0,01 e em estadios precoces (8,4±2,6), p=0,01, em comparação com o grupo controlo (91,5±29,1). Estes resultados foram acompanhados por uma diminuição acentuada nos índices de capacidade de recrutamento, diferenciação e regeneração na população de doentes renais crónicos. Globalmente, estes resultados sugerem um desequilíbrio no processo de reparação endotelial na DRC, e sugerem ainda, que os índices de recrutamento, diferenciação e regeneração podem ajudar na seleção de pacientes que possam beneficiar de estratégias de intervenção para melhorar a saúde cardiovascular induzindo proteção vascular.
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Laterza, Claudio <1980&gt. "Circulating Endothelial Progenitor Cells: isolation and biological characterization of EPCs from healthy subjects and nephropatic patients." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2012. http://amsdottorato.unibo.it/4745/.

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Nel 1997 venne isolata una popolazione cellulare con caratteristiche appartenenti a cellule endoteliali mature e a cellule progenitrici ; le cellule appartenenti a queste popolazione furono denominate EPCs (cellule endoteliali progenitrici circolanti) e fu messa in evidenza la loro capacità di dare origine a vasculogenesi postnatale. Lo scopo dello studio è stata la caratterizzazione di tale popolazione cellulare in termini biologici e la valutazione delle differenze delle EPCs in soggetti sani e nefropatici in emodialisi. È stata infine valutata l’eventuale capacità della Vitamina D di influenzare le capacità delle Late EPCs in termini di formazione di colonie in vitro e di attività anticalcifica in soggetti in insufficienza renale cronica.
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Books on the topic "Circulating progenitor cells"

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International Workshop "Novel Angiogenic Mechanisms" (2002 Columbus, Ohio). Novel angiogenic mechanisms: Role of circulating progenitor endothelial cells. New York: Kluwer Academic/Plenum, 2003.

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I, Moldovan Nicanor, ed. Novel angiogenic mechanisms: Role of circulating progenitor endothelial cells. New York: Kluwer Academic/Plenum, 2003.

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Moldovan, Nicanor I. Novel Angiogenic Mechanisms: Role Of Circulating Progenitor Endothelial Cells. Springer, 2012.

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Moldovan, Nicanor I. Novel Angiogenic Mechanisms: Role of Circulating Progenitor Endothelial Cells (Advances in Experimental Medicine and Biology). Springer, 2003.

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Correa, Paulo Norberto *. An improved serum-free medium for the growth of normal human circulating erythroid progenitor cells and its application to the study of erythropoiesis in "Polycythemia vera". 1991.

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Cahill, Thomas J., and Paul R. Riley. Epicardial and coronary vascular development. Edited by Miguel Torres. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0009.

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The coronary circulation is essential for human life. In embryonic development, abnormal formation of the coronary vasculature can cause death in utero or after birth. In adulthood, atherosclerosis of the coronary arteries is the commonest cause of death worldwide. The last decade has witnessed significant strides forward in our understanding of coronary development. Multiple sources of coronary endothelial cells have been identified using genetic tools for fate mapping. The epicardium, the outermost layer of the developing heart, has emerged as both a source of cell progenitors and key signalling mediators. Knowledge of the specific genes underlying formation, function, and heterogeneity of the epicardium is expanding. Significant challenges remain, however, in understanding the spatiotemporal signalling patterns required for organized migration, differentiation, and patterning of the vasculature. In addition, dissecting how coronary development is perturbed in patients with congenital coronary anomalies is a major ongoing focus of research.
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Book chapters on the topic "Circulating progenitor cells"

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Schmid, Michael C., and Judith A. Varner. "Circulating Endothelial Progenitor Cells (CEPC)." In Methods in Molecular Biology, 139–55. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-241-0_8.

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Murrow, Jonathan R., and Arshed A. Quyyumi. "Circulating Endothelial Progenitor Cells: Mechanisms and Measurements." In Asymptomatic Atherosclerosis, 151–67. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-179-0_11.

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Anand-Apte, Bela. "Dysfunction of Circulating Endothelial Progenitor Cells in Diabetic Retinopathy." In Studies on Retinal and Choroidal Disorders, 517–28. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-606-7_25.

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Schaafsma, M. R., J. H. F. Falkenburg, N. Duinkerken, D. van der Harst, A. Brand, S. Osanto, C. R. Franks, R. Willemze, and W. E. Fibbe. "High Levels of Circulating Hematopoietic Progenitor Cells after Continuous Infusion of High Dose Interleukin-2 in Cancer Patients." In Advances in haemapheresis, 189–96. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3904-9_23.

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Mancuso, Patrizia, Angelica Calleri, and Francesco Bertolini. "Circulating Endothelial Cells and Circulating Endothelial Progenitors." In Recent Results in Cancer Research, 163–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-28160-0_14.

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Ferratge, S., J. Boyer, N. Arouch, F. Chevalier, and G. Uzan. "Perspective of Therapeutic Angiogenesis Using Circulating Endothelial Progenitors from Umbilical Cord Blood." In Perinatal Stem Cells, 111–19. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-2703-2_10.

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"Circulating Progenitor Cells." In Encyclopedia of Cancer, 865. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_1181.

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"Circulating Endothelial Progenitor Cells." In Handbook of Disease Burdens and Quality of Life Measures, 4169. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-0-387-78665-0_5312.

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Ciurea, Stefan O., and Ronald Hoffman. "The polycythaemias." In Oxford Textbook of Medicine, 4264–74. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.220308.

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Polycythaemia or erythrocytosis is characterized by an abnormal increase in the numbers of red blood cells, leading to an elevation in the haemoglobin concentration and haematocrit (>52% in men and >48% in women). The cause may be either (1) primary—due to an intrinsic defect of haemopoietic stem cells; or (2) secondary—due to extrinsic stimulation of progenitor erythroid cells by circulating growth factors; and the condition needs to be distinguished from (3) pseudopolycythaemia—in which haematocrit is raised because the plasma volume is decreased....
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Emmett, Stevan R., Nicola Hill, and Federico Dajas-Bailador. "Non- malignant haematology and allergy." In Clinical Pharmacology for Prescribing. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780199694938.003.0020.

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Anaemia is very common, affecting over one- third of the world’s population and can be defined as a reduction in the haemoglobin content of red blood cells (RBC). The normal range varies slightly according to the population being tested, but typically in the UK anaemia in males can be diagnosed if the haemoglobin falls to below 135 g/ L and in females below 115 g/ L. In addition to a reduction in the haemoglobin concentration there is usually an as­sociated reduction in the number of circulating red cells and a low haematocrit. Anaemia is not a diagnosis, it is an abnormality that has an underlying cause and, therefore, a determination of that cause must be made before effective treatment can begin. The production of red cells is termed ‘haematopoiesis’ and occurs in the bone marrow (liver and spleen in foetal life). The bones involved in production change as we age from almost all bones in neonates to long bones, pelvis, and thoracic cage when we reach our 4th decade. As with all blood cells, production of RBCs begins with a pluripotent stem cell that is capable of forming many progenitor cells, including those of the erythroid (red cell) lineage (Figure 12.1). It is estimated that a single pluripotent stem cell, fol­lowing 18– 20 successful divisions, is able to produce 10 million mature erythrocytes. For this process to occur a number of growth factors (GF) are required, which act in synergy and enable the process of haematopoiesis to follow a stepwise maturation process, ending in the release of mature erythrocytes into the blood stream. Examples of such factors include the interleukins (IL), i.e. IL- 1, IL- 3, IL- 4, IL- 5, and IL- 6. Growth factors also act on the bone marrow stromal cells, enabling the correct environment for cell maturation and development. Tumour necrosis factor (TNF) and IL- 1 are particularly important stromal acting growth factors and can stimulate the stromal cells to produce many of the IL factors described above. The GF erythropoietin (EPO) is required for successful red cell maturation. Many of the growth factors work by binding to cell sur­face receptors.
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Conference papers on the topic "Circulating progenitor cells"

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Obi, Syotaro, Kimiko Yamamoto, Joji Ando, Haruchika Masuda, and Takayuki Asahara. "Differentiation of circulating endothelial progenitor cells induced by shear stress." In 2012 International Symposium on Micro-NanoMechatronics and Human Science (MHS). IEEE, 2012. http://dx.doi.org/10.1109/mhs.2012.6492452.

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Ooi, AT, DW Nickerson, DA Elashoff, SM Dubinett, and BN Gomperts. "Circulating Epithelial Progenitor Cells May Predict Onset and Severity of Lung Cancer." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2673.

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Cribbs, SK, DJ Sutcliffe, WR Taylor, M. Rojas, KL Brigham, K. Easley, L. Tang, and GS Martin. "Circulating Endothelial Progenitor Cells Are Inversely Associated with Organ Dysfunction in Sepsis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4711.

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Pizarro, Sandra, Victor I. Peinado, Marta Vives, Marta Diez, Elisabet Ferrer, Laureano Molins, Roberto Rodríguez-Roisin, Josep Roca, and Joan Albert Barberà. "ENDOTHELIAL PROGENITOR CELLS IN COPD: RELATIONSHIP BETWEEN CIRCULATING CELLS AND THEIR PRESENCE IN PULMONARY ARTERIES." 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.a5251.

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Musri, MM, M. Diez, JA Barbera, E. Ferrer, and VI Peinado. "Circulating Vascular Progenitor Cells Undergo Endothelial to Mesenchymal Transition Mediated by TGFbeta RI." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5358.

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Anjum, Fatima, Satish Gowda, Keval Joshi, Ghassan Jamaleddine, Spiro Demetis, Joe Zein, Jason Lazar, and Raj Wadgaonkar. "Characterization Of Altered Patterns Of Circulating Endothelial Progenitor Cells In Sickle Cell Disease Induced Pulmonary Hypertension." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1992.

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Sucur, A., Z. Jajic, M. Artukovic, M. Ikic Matijasevic, F. Grubisic, B. Anic, S. Ivcevic, D. Flegar, and D. Grcevic. "AB0026 Chemokine signals are critical for homing and enhanced differentiation of circulating osteoclast progenitor cells." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.2317.

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Pollok, Karen E., Shanbao Cai, Haiyan Wang, Barbara J. Bailey, Anthony L. Sinn, Jayne M. Silver, Myka L. Estes, Julie A. Mund, David A. Ingram, and Jamie Case. "Abstract 1954: Human circulating progenitor cells of hematopoietic origin promote tumor growth in melanoma xenograft models." 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.am10-1954.

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Tepper, Robert S., Chris Tiller, Julie Mund, Jamie Case, and David A. Ingram. "Infants With Bronchopulmonary Dysplasia (BPD) Have Fewer Pro-Angiogenic Circulating Progenitor Cells And Decreased Pulmonary Diffusion." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2511.

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Nowak, Kai, Elena Joas, Grietje Beck, Neysan Rafat, and Peter Hohenberger. "Abstract 365: Circulating bone marrow-derived VEGFR-2+ progenitor cells in benign and malignant soft tissue tumors." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-365.

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Reports on the topic "Circulating progenitor cells"

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Tiwari, Raj K. Estrogen Mobilizes Circulating Bone Marrow Progenitor Cells to Promote Tumor Neovasculature: Lessions from Ischemic Model Provide a Novel Breast Cancer Target. Fort Belvoir, VA: Defense Technical Information Center, September 2007. http://dx.doi.org/10.21236/ada479232.

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Lee, Adrian V. Novel Transgenic Mouse Model for Testing the Effect of Circulating IGF-I on Mammary Stem/Progenitor Cell Number and Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, August 2008. http://dx.doi.org/10.21236/ada494145.

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Lee, Adrian V. Novel Transgenic Mouse Model for Testing the Effect of Circulating IGF-I on Mammary Stem/Progenitor Cell Number and Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, August 2007. http://dx.doi.org/10.21236/ada474677.

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