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1

Kojima, Seiji. "Use of granulocyte colony-stimulating factor for treatment of aplastic anemia." Nagoya University School of Medicine, 1999. http://hdl.handle.net/2237/5344.

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2

Hamzic, Edita. "Characterisation of mesenchymal stroma and discovery of biomarkers in aplastic anemia." Thesis, Kingston University, 2012. http://eprints.kingston.ac.uk/26276/.

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Haemopoietic activity in Aplastic anemia (AA) is significantly reduced and is generally attributed to failure of Haemopoietic stem cells (HSC) within the bone marrow. The extent to which Mesenchymal stromal cells (MSC) are involved in the functional restriction of HSC is largely unknown. To understand this, the physical and functional properties of AA MSC were studied in vitro. MSC were characterised by their phenotype and ability to form adherent stromal layers. The functional properties of AA MSC were assessed through proliferative, clonogenic and cross¬over culture assays. Results show seve
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3

Teo, Steve Keng Ong. "METABOLISM OF AMINO-CHLORAMPHENICOL: POSSIBLE ROLE IN CHLORAMPHENICOL-INDUCED APLASTIC ANEMIA AND LEUKEMIA." Thesis, The University of Arizona, 1985. http://hdl.handle.net/10150/291285.

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4

Wellman, Maxey Lee. "Studies on the pathogenesis of feline leukemia virus-induced erythroid aplasia /." The Ohio State University, 1986. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487268021746533.

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5

Arruda, Daisy Maria Meireles. "Aloimmunity against HLA class I antigens in patients with myelodysplastic syndrome and aplastic anemia." Universidade Federal do CearÃ, 2005. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=38.

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CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior<br>Myelodysplastic syndrome (MDS) and aplastic anemia (AA) are two of the hematological disorders which present peripheral cytopenias, with extensive clinical manifestations that vary from slight anemia to severe pancytopenia; the latter requiring continuous transfusional reposition of red cell (RC) and platelet concentrates (PC), which can induce aloimunization in patients. Such patients can develop a post-transfusional refractory state, rendering further transfusions unviable. The objective of the present study was to investigate th
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6

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

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In patients with aplastic anaemia that respond to immunosuppressive therapy, quantitative, morphological and functional haematologic derangement have been reported. To explain these findings, abnormalities in the marrow stroma or the stem cell have been postulated. To define the relative contribution of each of the latter, the integrity of the bone marrow from sixteen patients that responded to anti-lymphocyte globulin and high dose methyl prednisolone was compared to normal individuals. Bone marrow mononuclear cells were divided into two fractions. From the first, stroma was cultured in aMEM
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7

Tellechea, Maria Florencia. "Geração de células-tronco pluripotentes induzidas (iPSCs) a partir de células de pacientes com anemia aplástica adquirida." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/17/17135/tde-05122016-120214/.

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A anemia aplástica (AA) é uma doença hematológica rara caracterizada pela hipocelularidade da medula óssea, o que provoca pancitopenia. Esta pode ser de origem genética (associada a encurtamento telomérico) ou adquirida (não-associada a desgaste excessivo dos telômeros). Na forma adquirida, a ativação anormal de linfócitos T provoca a destruição das células hematopoéticas. O mecanismo que leva a essa destruição ainda não foi elucidado. Um dos tratamentos mais eficazes para repovoar a medula óssea hipocelular é o transplante com célulastronco hematopoéticas (CTHs). Porém, uma grande porcentagem
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8

MICHELOZZI, ILARIA MARINA. "The role of the bone marrow microenvironment in aplastic anaemia and acute myeloid leukaemia: from pathogenesis to chemoresistance." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2019. http://hdl.handle.net/10281/241079.

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La nicchia staminale ematopoietica è formata da molteplici tipi cellulari che contribuiscono alla regolazione dell’ematopoiesi all’interno del midollo osseo. In alcuni disordini ematopoietici il microambiente midollare risulta alterato, sebbene il suo contributo alla patogenesi non sia ancora chiaro, fornisce supporto alle cellule staminali leucemiche (LSC), a spese delle normali cellule staminali ematopoietiche, e protezione contro i chemioterapici. Dunque, per eradicare le LSC, le strategie terapeutiche devono considerare l’effetto protettivo contro i chemioterapici esercitato dal microambie
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9

Padilha, Pedro Henrique. "Variantes do gene THPO em pacientes com anemia aplástica adquirida." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/17/17154/tde-25042018-150914/.

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Introdução: A anemia aplástica (AA) adquirida é uma doença grave, caracterizada por pancitopenia e medula óssea hipocelular sem que haja associação com aumento de reticulina ou infiltração anormal na medula. Embora o mecanismo fisiopatológico não esteja totalmente elucidado, atribui-se a uma resposta imunomediada dos linfócitos T no ambiente medular. A trombopoetina (codificada pelo gene THPO) é um hormônio glicoproteico produzido pelo fígado e responsável pelo estímulo de crescimento de megacariócitos, desenvolvimento plaquetário e de demais linhagens e, quando disfuncional, contribui para o
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10

Rodrigues, Fernanda Gutierrez. "Identificação de moduladores genéticos em pacientes com anemia aplástica por sequenciamento de nova geração." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/17/17154/tde-25072018-110641/.

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A fisiopatologia das síndromes de falência da medula óssea (FMO) está relacionada a mecanismos adquiridos de destruição das células-tronco hematopoeiticas na medula ou a defeitos constitucionais em genes fundamentais para o reparo do DNA e manutenção dos telômeros. A anemia aplástica (AA), o protótipo das doenças de FMO, pode ter etiologia adquirida ou constitucional. A avaliação genética de pacientes com AA adquirida tem como objetivo a detecção de mutações somáticas que possam ser usadas como marcadores de resposta ao tratamento imunossupressor. Diferentemente, em pacientes com AA constituci
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11

Bradley, Melville D. M. D. "2,4,6-Trinitrotoluene (TNT) Air Concentrations, Hemoglobin Changes, and Anemia Cases in Respirator Protected TNT Munitions Demilitarization Workers." Scholar Commons, 2009. https://scholarcommons.usf.edu/etd/1871.

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2,4,6-Trinitrotoluene, TNT, is an explosive used in munitions production that is known to cause both aplastic and hemolytic anemia in exposed workers. Deaths have been reported secondary to both varieties of anemia. Studies have shown that TNT systemic absorption is significant by both the respiratory and dermal routes. A literature review revealed that the most recent review article on TNT exposure arguing for a TWA drop from the PEL to the TLV was in 1977 -- this article cited anemia issues in addition to other untoward effects of TNT. No studies encountered looked at hemoglobin change or an
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12

Scheinberg, Phillip. "Parâmetros preditivos de resposta hematológica, recidiva, evolução clonal e sobrevida em pacientes com anemia aplástica severa tratados com terapia imunossupressora." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5141/tde-06112018-153339/.

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A anemia aplástica severa (AAS) pode ser tratada com sucesso na maioria dos casos com terapia imunossupressora (IS) ou transplante alogenêico de medula óssea (TMO). Os principais fatores que determinam a escolha da modalidade terapêutica são a idade e a disponibilidade de um doador HLA-histocompatível. Em pacientes mais jovens, o TMO de um doador aparentado é preferível, enquanto que em pacientes acima de 40-50 anos, a terapia IS é a modalidade terapêutica de escolha. Resposta hematológica é obtida em 60-75% dos casos com terapia IS na AAS, o que correlaciona com melhor sobrevida. Recidivas oc
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13

Wei, Hsi-Ju. "TARGETING DENDRITIC CELL METABOLISM TO INDUCE IMMUNE TOLERANCE." Case Western Reserve University School of Graduate Studies / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=case1538497998943838.

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14

Sébert, Marie. "Génétique et évolution clonale des syndromes d’insuffisance médullaire." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCC271.

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Les syndromes d’insuffisance médullaire sont liés à des mutations constitutionnelles à l’origine d’une hématopoïèse déficiente chez les patients atteints. Ils représentent un groupe hétérogène de maladies syndromiques, et impliquent plusieurs familles de gènes avec des mécanismes biologiques différents conduisant à l’insuffisance médullaire. Ces maladies prédisposent à une évolution clonale somatique, avec un risque accru de développer un syndrome myélodysplasique (SMD) ou une leucémie aigüe myéloïde (LAM) au cours du temps. Nous avons séquencé et analysé l’exome d’ADN fibroblastique d’une coh
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15

Marchesi, Raquel Ferrari. "Anemia aplástica adquirida - avaliação da biópsia de medula óssea na identificação de prognóstico desfavorável, aferido pela evolução para SMD/LMA: um estudo comparativo em crianças e adultos." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5144/tde-08052018-121635/.

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Anemia aplástica adquirida (AAA) é doença rara e seu diagnóstico diferencial inclui a Síndrome mielodisplásica hipocelular (SMD-h). A evolução de AAA para SMD/LMA (Síndrome mielodisplásica/Leucemia mieloide aguda) ocorre em até 15% dos casos. Este estudo propõe-se a comparar parâmetros histológicos e imuno-histoquímicos de pacientes adultos e crianças com AAA que evoluíram e não para SMD/LMA. Seu objetivo é avaliar a ocorrência dos critérios morfológicos/imunofenotípicos nas biópsias de medula óssea do grupo pediátrico (<19 anos) com o grupo de adultos, comparar esses critérios associados à ev
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16

Azambuja, Ana Paula de. "Características clínicas e laboratoriais de pacientes que apresentam clone de hemoglobinúria paroxística noturna detectado por citometria de fluxo." reponame:Repositório Institucional da UFPR, 2013. http://hdl.handle.net/1884/31899.

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Resumo: INTRODUÇÃO: A Hemoglobinúria Paroxística Noturna (HPN) é caracterizada clinicamente por hemólise intravascular crônica, falência medular e hipercoagulabilidade levando a tromboses. A facilidade na detecção de clone HPN através do uso de técnicas sensíveis aumentou o número de pacientes com este diagnóstico, entretanto, a heterogeneidade da doença torna imprescindível a correlação clínica. OBJETIVOS: Analisar as características clínico-biológicas de uma população brasileira de pacientes com clone HPN, e avaliar as diferenças na apresentação, sobrevida global, diferença entre as categor
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17

Souza, Gisele de Paula e. Silva Carneiro Mendes de. "Caracterização epidemiológica e estudo de fármacos utilizados em pacientes submetidos ao transplante de medula óssea em um hospital público de Curitiba - Paraná." reponame:Repositório Institucional da UFPR, 2017. http://hdl.handle.net/1884/48951.

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Orientadora: Profª. Drª. Yanna Dantas Rattmann<br>Coorientador: Profª. Drª. Milene Zanoni da Silva<br>Dissertação (mestrado) - Universidade Federal do Paraná, Setor de Ciências da Saúde, Programa de Pós-Graduação em Saúde Coletiva. Defesa: Curitiba, 20/06/2017<br>Inclui referências e apêndices<br>Resumo: O transplante de medula óssea (TMO) representa uma das principais modalidades terapêuticas para os pacientes com diagnóstico de doenças oncológicas, hematológicas e congênitas. Na América Latina, o Brasil foi o pioneiro neste procedimento realizando, em 1949, no Hospital de Clínicas da Univers
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18

RONCELLI, GALLEGO FABIENNE. "Association d'une anemie aplastique et d'un osteosarcome chez une enfant de six ans." Aix-Marseille 2, 1989. http://www.theses.fr/1989AIX20275.

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19

Fagnani, Renata 1973. "Estudo epidemiologico das infecções hospitalares dos pacientes com doenças onco-hematologicas ou anemia aplastica atendidos no Hospotal das Clinicas-Unicamp." [s.n.], 2005. http://repositorio.unicamp.br/jspui/handle/REPOSIP/313471.

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Orientador: Plinio Trabasso<br>Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas<br>Made available in DSpace on 2018-08-05T09:39:08Z (GMT). No. of bitstreams: 1 Fagnani_Renata_M.pdf: 5349161 bytes, checksum: e6caf1cbb6ca03b1ded5646ba6d81269 (MD5) Previous issue date: 2005<br>Resumo: Os avanços nas técnicas de diagnósticos e na terapêutica têm aumentado a sobrevida e o número de indivíduos com alterações imunológicas, sendo a neutropenia fator predisponente para IH. Este estudo avaliou a ocorrência de IH nos pacientes com DOH ou AA acompanhados consecut
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Quiroga, Márcia Regina Silva. "Avaliação do quimerismo em pacientes com anemia aplástica severa adquirida, após 18 meses do transplante de células-tronco hematopoiéticas, submetidos a diferentes regimes de condicionamento." reponame:Repositório Institucional da UFPR, 2014. http://hdl.handle.net/1884/36311.

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Orientador: Prof. Dr. Ricardo Pasquini<br>Co-orientadora: Drª. Noemi Farah Pereira<br>Dissertação (mestrado) - Universidade Federal do Paraná, Setor de Ciências da Saúde, Programa de Pós-Graduação em Medicina Interna. Defesa : Curitiba, 01/08/2014<br>Inclui referências<br>Resumo: O resultado do transplante de células-tronco hematopoéticas (TCTH) é avaliado por meio da recuperação hematológica e da análise do quimerismo. Este estudo tem como objetivo avaliar os níveis de quimerismo em pacientes com Anemia Aplástica Severa (AAS) Adquirida com mais de 18 meses de acompanhamento pós-TCTH, que apre
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Skeppner, Gunnar. "Pure red cell aplasia in Swedish children : clinical features, epidemiological and etiological aspects of transient erythroblastopenia of childhood and of Diamond-Blackfan anemia /." Örebro ; Stockholm, 2002. http://diss.kib.ki.se/2002/91-628-5092-x/.

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22

Martins, Ana Isabel Barros Ramos. "Aplastic anemia: from pathophysiology to diagnosis, management and treatment." Master's thesis, 2015. http://hdl.handle.net/10316/30585.

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Trabalho final de mestrado integrado em Medicina (Hematologia), apresentado à Faculdade de Medicina da Universidade de Coimbra.<br>Aplastic anemia (AA) is a rare hematopoietic disease characterized by a pancytopenia and a hypoplastic bone marrow. AA can be congenital (CAA) or acquired (AAA). Acquired AA comprises those cases where a causative factor is identified (Secondary AA) and also idiopathic cases (Idiopathic AA). There was a marked improvement on treatment options in the last years that had resulted on increased overall survival rates. It is known that a correct management of this entit
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23

Chao, Yu-Hua, and 趙玉華. "The Role of Mesenchymal Stem Cells in Severe Aplastic Anemia and Sepsis." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/82511666340917484541.

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博士<br>中山醫學大學<br>醫學研究所<br>103<br>The mechanisms of idiopathic severe aplastic anemia (SAA) in children are not completely understood. Insufficiency of the bone marrow microenvironment, in which mesenchymal stem cells (MSCs) are an important element, can be a potential factor associated with hematopoietic impairment. Here we compared the properties of MSCs from 5 SAA children with those of MSCs from 5 controls, and studied whether aberrant gene expression could be found in SAA MSCs. In vitro, MSCs from SAA children and controls were similar in morphology and surface marker expression. However, S
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"The combination of karyotype analysis, HbF and p53 immunostaining is useful for the differential diagnosis between refractory anemia and aplastic anemia." Thesis, 2008. http://hdl.handle.net/2237/10682.

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岩崎, 卓識, and Takashi Iwasaki. "The combination of karyotype analysis, HbF and p53 immunostaining is useful for the differential diagnosis between refractory anemia and aplastic anemia." Thesis, 2008. http://hdl.handle.net/2237/10682.

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26

Grimaldi, Francesco. "Study of the immune reconstitution in patients receiving a reduced intensity stem cell transplantation for Aplastic Anemia." Tesi di dottorato, 2016. http://www.fedoa.unina.it/11001/1/GRIMALDI_Francesco_28.pdf.

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Aplastic anemia is a rare hematological disease, prototype of bone marrow failure syndromes, characterized by a progressive reduction of bone marrow stem cells that leads to classic histological finding of “fatty” or “empty” marrow. Clinical picture is dominated by bone marrow failure symptoms, such as fatigue, petechiae and/or fever that can rapidly deteriorate to potentially fatal bleeding, or life-threatening blood sepsis. Aplastic Anemia commonly affects 1 to 2/106 individuals per year, with an estimated incidence about 2-3 times higher in Eastern countries. Although the etiology remains u
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Chao, Yu-Hua, and 趙玉華. "Poor potential of proliferation and differentiation in bone marrow mesenchymal stem cells derived from children with severe aplastic anemia." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/39580640453422785754.

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碩士<br>中國醫藥大學<br>醫學研究所碩士班<br>97<br>Background Idiopathic severe aplastic anemia (SAA), characterized by failure of hematopoiesis, is rare and potentially life-threatening to children. However, the pathogenesis has not been completely understood, and insufficiency in the hematopoietic microenvironment can be an important factor. Mesenchymal stem cells (MSCs) play an important role in maintaining bone marrow microenvironment. Therefore, we aimed at the intrinsic defects of bone marrow MSCs derived from SAA children. Materials and Methods Bone marrow MSCs were obtained from 5 SAA children and 5 c
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Roderick, Justine E. "The roles of Notch1 and PKC-Θ in immune mediated bone marrow failure". 2011. https://scholarworks.umass.edu/dissertations/AAI3465077.

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We sought to evaluate the individual contributions of Notch1 and PKC-Theta to disease progression in a mouse model of immune-mediated bone marrow failure and to define a mechanism for their potential cellular cooperation. We transferred parental bulk splenocytes into F1-hybrid recipients to induce a robust immune-mediated bone marrow failure (BMF) that we could partially rescue by administering a pharmacological inhibitor of Notch activation. Transferring splenocytes from PKC-Theta deficent animals did not induce disease, and treating animals with a pharmacological inhibitor of PKC-Theta also
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Κακαγιάννη-Σιάσου, Θεοδώρα. "Μελέτη της αλληλεπίδρασης προγονικών αιμοποιητικών κυττάρων και κυττάρων στρώματος του μυελού στην παθογένεια της απλαστικής αναιμίας. Προσέγγιση με μεθόδους κυτταρικής και μοριακής βιολογίας". Thesis, 2006. http://nemertes.lis.upatras.gr/jspui/handle/10889/836.

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Στην επίκτητη απλαστική αναιμία (ΑΑ) ο υποκυτταρικός μυελός και η πανκυτταροπενία στο περιφερικό αίμα είναι αποτέλεσμα βλάβης των αρχέγονων αιμοποιητικών κυττάρων. Προηγούμενες μελέτες έχουν δείξει ότι κύριο χαρακτηριστικό γνώρισμα της νόσου είναι η ποσοτική αλλά και ποιοτική διαταραχή της stem cell δεξαμενής. Κλινικά και εργαστηριακά ευρήματα προτείνουν το σημαντικό ρόλο του ανοσοποιητικού συστήματος και ειδικά των Τ λεμφοκυττάρων στην ανάπτυξη της απλαστικής αναιμίας. Σήμερα, πλέον, είναι ευρύτερα αποδεκτό ότι η καταστολή του μυελού, που παρατηρείται στην ιδιοπαθή απλαστική αναιμία, είναι α
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"Estudo epidemiologico das infecções hospitalares dos pacientes com doenças onco-hematologicas ou anemia aplastica atendidos no Hospotal das Clinicas-Unicamp." Tese, Biblioteca Digital da Unicamp, 2005. http://libdigi.unicamp.br/document/?code=vtls000374847.

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