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[PMID]:26849716
[Au] Autor:Ali S; Shetty S; Ghosh K
[Ad] Endereço:Department of Haemostasis and Thrombosis, National Institute of Immunohaematology, 13th Floor, KEM Hospital, Parel, Mumbai, Maharashtra, India.
[Ti] Título:A novel mutation in GP1BA gene leads to mono-allelic Bernard Soulier syndrome form of macrothrombocytopenia.
[So] Source:Blood Coagul Fibrinolysis;28(1):94-95, 2017 Jan.
[Is] ISSN:1473-5733
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Inherited macrothrombocytopenia is one of the subgroup of inherited thrombocytopenias with variable bleeding tendencies presenting with low platelet count and giant platelets and different gene mutations are involved in its molecular pathophysiology and affect various cell functions. Herein, we describe a family with an isolated giant platelet disorder with variable bleeding diathesis with autosomal mode of inheritance.
[Mh] Termos MeSH primário: Síndrome de Bernard-Soulier/genética
Complexo Glicoproteico GPIb-IX de Plaquetas/genética
Trombocitopenia/genética
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Mutação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Platelet Glycoprotein GPIb-IX Complex)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160206
[St] Status:MEDLINE
[do] DOI:10.1097/MBC.0000000000000530


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[PMID]:27478199
[Au] Autor:Léon C; Dupuis A; Gachet C; Lanza F
[Ad] Endereço:UMR_S949, INSERM, Strasbourg, France Etablissement Français du Sang-Alsace (EFS-Alsace), Strasbourg, France Université de Strasbourg, France Fédération de Médecine Translationnelle de Strasbourg (FMTS), France catherine.leon@efs.sante.fr.
[Ti] Título:The contribution of mouse models to the understanding of constitutional thrombocytopenia.
[So] Source:Haematologica;101(8):896-908, 2016 Aug.
[Is] ISSN:1592-8721
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Constitutional thrombocytopenias result from platelet production abnormalities of hereditary origin. Long misdiagnosed and poorly studied, knowledge about these rare diseases has increased considerably over the last twenty years due to improved technology for the identification of mutations, as well as an improvement in obtaining megakaryocyte culture from patient hematopoietic stem cells. Simultaneously, the manipulation of mouse genes (transgenesis, total or conditional inactivation, introduction of point mutations, random chemical mutagenesis) have helped to generate disease models that have contributed greatly to deciphering patient clinical and laboratory features. Most of the thrombocytopenias for which the mutated genes have been identified now have a murine model counterpart. This review focuses on the contribution that these mouse models have brought to the understanding of hereditary thrombocytopenias with respect to what was known in humans. Animal models have either i) provided novel information on the molecular and cellular pathways that were missing from the patient studies; ii) improved our understanding of the mechanisms of thrombocytopoiesis; iii) been instrumental in structure-function studies of the mutated gene products; and iv) been an invaluable tool as preclinical models to test new drugs or develop gene therapies. At present, the genetic determinants of thrombocytopenia remain unknown in almost half of all cases. Currently available high-speed sequencing techniques will identify new candidate genes, which will in turn allow the generation of murine models to confirm and further study the abnormal phenotype. In a complementary manner, programs of random mutagenesis in mice should also identify new candidate genes involved in thrombocytopenia.
[Mh] Termos MeSH primário: Trombocitopenia/etiologia
Trombocitopenia/metabolismo
[Mh] Termos MeSH secundário: Animais
Autoantígenos/metabolismo
Síndrome de Bernard-Soulier/etiologia
Síndrome de Bernard-Soulier/metabolismo
Plaquetas/metabolismo
Diferenciação Celular/genética
Citoesqueleto/metabolismo
Modelos Animais de Doenças
Regulação da Expressão Gênica
Seres Humanos
Iodeto Peroxidase/metabolismo
Proteínas de Ligação ao Ferro/metabolismo
Megacariócitos/citologia
Megacariócitos/metabolismo
Camundongos
Receptores de Trombopoetina/metabolismo
Transdução de Sinais
Trombocitopenia/diagnóstico
Trombopoese
Fatores de Transcrição/metabolismo
Síndrome de Wiskott-Aldrich/etiologia
Síndrome de Wiskott-Aldrich/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Autoantigens); 0 (Iron-Binding Proteins); 0 (Receptors, Thrombopoietin); 0 (Transcription Factors); 143641-95-6 (MPL protein, human); EC 1.11.1.7 (TPO protein, human); EC 1.11.1.8 (Iodide Peroxidase)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170707
[Lr] Data última revisão:
170707
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160802
[St] Status:MEDLINE
[do] DOI:10.3324/haematol.2015.139394


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[PMID]:27405675
[Au] Autor:Peyvandi F; Hayward CP
[Ad] Endereço:Angelo Bianchi Bonomi Hemophilia and Thrombosis Center, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.
[Ti] Título:Genomic approaches to bleeding disorders.
[So] Source:Haemophilia;22 Suppl 5:42-5, 2016 Jul.
[Is] ISSN:1365-2516
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The genes encoding the coagulation factors were characterized over two decades ago. Since then, significant progress has been made in the genetic diagnosis of the two commonest severe inherited bleeding disorders, haemophilia A and B. Experience with the genetic of inherited rare bleeding disorders and platelet disorders is less well advanced. Rare bleeding disorders are usually inherited as autosomal recessive disorders, while it is now clear that a number of the more common platelet function disorders are inherited as autosomal dominant traits. In both cases, DNA sequencing has been useful since most of these disorders are due to mutations located at the coding regions or splice sites of genes encoding the abnormal protein. However, in 5-10% of patients affected with severe clotting factor deficiencies, no genetic defect can be identified and until recently, the genetic characterization of inherited platelet disorders had been confined to the more prevalent conditions such as Glanzmann disease and Bernard-Soulier syndrome. In patients with no gene mutations identified, so far, the role of next-generation sequencing as well as of other new genomic technologies will very likely have increasing importance. However, such methods require extensive bioinformatics analysis that, in turn will require critical revision of our current diagnostic infrastructure.
[Mh] Termos MeSH primário: Transtornos Herdados da Coagulação Sanguínea/genética
Genômica
[Mh] Termos MeSH secundário: Síndrome de Bernard-Soulier/diagnóstico
Síndrome de Bernard-Soulier/genética
Transtornos Herdados da Coagulação Sanguínea/diagnóstico
Transtornos Plaquetários/diagnóstico
Transtornos Plaquetários/genética
Genótipo
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Fenótipo
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170216
[Lr] Data última revisão:
170216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160714
[St] Status:MEDLINE
[do] DOI:10.1111/hae.12998


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[PMID]:27346198
[Au] Autor:Lopez-Onieva L; Montes R; Lamolda M; Romero T; Ayllon V; Lozano ML; Vicente V; Rivera J; Ramos-Mejía V; Real PJ
[Ad] Endereço:Gene Regulation, Stem Cells and Development Group, Department of Genomic Oncology, GENYO: Centre for Genomics and Oncological Research Pfizer-University of Granada-Junta de Andalucía, PTS, Granada 18016, Spain. Electronic address: lourdes.lopez@genyo.es.
[Ti] Título:Generation of induced pluripotent stem cells (iPSCs) from a Bernard-Soulier syndrome patient carrying a W71R mutation in the GPIX gene.
[So] Source:Stem Cell Res;16(3):692-5, 2016 May.
[Is] ISSN:1876-7753
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We generated an induced pluripotent stem cell (iPSC) line from a Bernard-Soulier Syndrome (BSS) patient carrying the mutation p.Trp71Arg in the GPIX locus (BSS1-PBMC-iPS4F4). Peripheral blood mononuclear cells (PBMCs) were reprogrammed using heat sensitive non-integrative Sendai viruses containing the reprogramming factors Oct3/4, SOX2, KLF4 and c-MYC. Successful silencing of the exogenous reprogramming factors was checked by RT-PCR. Characterization of BSS1-PBMC-iPS4F4 included mutation analysis of GPIX locus, Short Tandem Repeats (STR) profiling, alkaline phosphatase enzymatic activity, analysis of conventional pluripotency-associated factors at mRNA and protein level and in vivo differentiation studies. BSS1-PBMC-iPS4F4 will provide a powerful tool to study BSS.
[Mh] Termos MeSH primário: Síndrome de Bernard-Soulier/patologia
Células-Tronco Pluripotentes Induzidas/citologia
Complexo Glicoproteico GPIb-IX de Plaquetas/genética
[Mh] Termos MeSH secundário: Animais
Síndrome de Bernard-Soulier/metabolismo
Diferenciação Celular
Células Cultivadas
Reprogramação Celular
Feminino
Seres Humanos
Células-Tronco Pluripotentes Induzidas/metabolismo
Células-Tronco Pluripotentes Induzidas/transplante
Cariótipo
Leucócitos Mononucleares/citologia
Leucócitos Mononucleares/metabolismo
Camundongos
Camundongos Endogâmicos NOD
Camundongos SCID
Mutação
Teratoma/metabolismo
Teratoma/patologia
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Platelet Glycoprotein GPIb-IX Complex); 0 (Transcription Factors); 0 (adhesion receptor)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160628
[St] Status:MEDLINE


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[PMID]:27100304
[Au] Autor:Kaur H; Borhany M; Azzam H; Costa-Lima C; Ozelo M; Othman M
[Ad] Endereço:aDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada bDepartment of Hematology, Hemostasis and Thrombosis, National Institute of Blood Disease and Bone Marrow Transplantation (NIBD), Karachi, Pakistan cDepartment of Clinical Pathology, Mansoura University, Mansoura, Egypt dINCT do Sangue Hemocentro Unicamp, Department of Internal Medicine, Faculty of Medical Sciences, University of Campinas, Campinas, SP, Brazil eSchool of Baccalaureate Nursing, St Lawrence College, Kingston, Ontario, Canada.
[Ti] Título:The utility of International Society on Thrombosis and Haemostasis-Bleeding Assessment Tool and other bleeding questionnaires in assessing the bleeding phenotype in two platelet function defects.
[So] Source:Blood Coagul Fibrinolysis;27(5):589-93, 2016 Jul.
[Is] ISSN:1473-5733
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The main objective of this study is to investigate the utility of International Society on Thrombosis and Haemostasis-Bleeding Assessment Tool (ISTH-BAT) in comparison with the condensed form of Molecular and Clinical Markers for the Diagnosis and Management of type 1 and WHO BATs, in assessing bleeding in two well known and clinically significant platelet function defects. Thirty-eight patients previously diagnosed with Glanzmann's thrombasthenia and 10 with Bernard-Soulier syndrome (BSS) were analyzed. Bleeding scores were significantly higher than that of controls using both electronic bleeding questionnaire (eBQ) and ISTH-BAT with no significant difference between both tools. ISTH-BAT had a sensitivity, specificity, positive predictive value and negative predictive value of 100%, 76.2%, 0.9 and 1. This was closely similar to eBQ. Both ISTH-BAT and eBQ are efficient in BSS and Glanzmann's thrombasthenia. However, given the ISTH recommendation, ISTH-BAT should be adopted. Larger study including other platelet defects will enhance its utility and support the integration of bleeding scores with standardized laboratory testing to allow for a universal diagnostic approach to patients with suspected bleeding disorders.
[Mh] Termos MeSH primário: Síndrome de Bernard-Soulier/diagnóstico
Hemorragia/diagnóstico
Trombastenia/diagnóstico
Trombose/diagnóstico
[Mh] Termos MeSH secundário: Adolescente
Adulto
Síndrome de Bernard-Soulier/sangue
Síndrome de Bernard-Soulier/patologia
Plaquetas/metabolismo
Plaquetas/patologia
Estudos de Casos e Controles
Criança
Pré-Escolar
Autoavaliação Diagnóstica
Feminino
Hemorragia/sangue
Hemorragia/patologia
Seres Humanos
Lactente
Masculino
Meia-Idade
Inquéritos e Questionários
Trombastenia/sangue
Trombastenia/patologia
Trombose/sangue
Trombose/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160422
[St] Status:MEDLINE
[do] DOI:10.1097/MBC.0000000000000496


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[PMID]:26635054
[Au] Autor:Smaoui M; Elleuch S; Abidi S; Ellouze Y; Louati D; Loumi M; Kolsi K
[Ad] Endereço:Service d'anesthésie réanimation, Hôpital Hedi Chaker, Sfax, Tunisie.
[Ti] Título:[Bernard-Soulier syndrome and pregnancy: a case report].
[Ti] Título:Syndrome de Bernard-Soulier et grossesse : à propos d'un cas..
[So] Source:Ann Biol Clin (Paris);73(6):737-40, 2015 Nov-Dec.
[Is] ISSN:1950-6112
[Cp] País de publicação:France
[La] Idioma:fre
[Ab] Resumo:Bernard-Soulier syndrome is an inherited bleeding disorder. Due to the rarity of the combination of this syndrome and pregnancy, data on the clinical course and outcome of pregnancy in women with Bernard-Soulier syndrome is scattered in individual case reports and there is no consensus in the management of SBS. In some patients, the pregnancy course was uneventful while in others post partum hemorrhage was the most common complication. We report our experience about the perioperative management of a pregnant woman with Bernard-Soulier syndrome.
[Mh] Termos MeSH primário: Síndrome de Bernard-Soulier/terapia
Complicações Hematológicas na Gravidez/terapia
[Mh] Termos MeSH secundário: Adulto
Síndrome de Bernard-Soulier/complicações
Síndrome de Bernard-Soulier/patologia
Transfusão de Sangue
Cesárea
Feminino
Morte Fetal
Seres Humanos
Hemorragias Intracranianas/patologia
Hemorragia Pós-Parto/etiologia
Hemorragia Pós-Parto/terapia
Gravidez
Complicações Hematológicas na Gravidez/patologia
Ácido Tranexâmico/uso terapêutico
[Pt] Tipo de publicação:CASE REPORTS; ENGLISH ABSTRACT; JOURNAL ARTICLE
[Nm] Nome de substância:
6T84R30KC1 (Tranexamic Acid)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:151204
[Lr] Data última revisão:
151204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151205
[St] Status:MEDLINE
[do] DOI:10.1684/abc.2015.1101


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[PMID]:26275786
[Au] Autor:Qiao J; Davis AK; Morel-Kopp MC; Ward CM; Gardiner EE; Andrews RK
[Ad] Endereço:Australian Centre for Blood Diseases, Monash University, Melbourne, Australia. jianlin.qiao@gmail.com.
[Ti] Título:Low levels of CD9 coincidental with a novel nonsense mutation in glycoprotein Ibß in a patient with Bernard-Soulier syndrome.
[So] Source:Ann Hematol;94(12):2069-71, 2015 Dec.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Mh] Termos MeSH primário: Síndrome de Bernard-Soulier
Mutação
Complexo Glicoproteico GPIb-IX de Plaquetas/genética
Tetraspanina-29/sangue
[Mh] Termos MeSH secundário: Síndrome de Bernard-Soulier/sangue
Síndrome de Bernard-Soulier/genética
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:CASE REPORTS; LETTER
[Nm] Nome de substância:
0 (Platelet Glycoprotein GPIb-IX Complex); 0 (Tetraspanin-29)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150816
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-015-2473-1


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[PMID]:26226975
[Au] Autor:Okoli S; Madan B; Mwirigi A; Moore G; Drew A; Mitchell MJ; Cutler JA
[Ad] Endereço:Haematology, Guys & St Thomas NHS foundation Trust, London, UK.
[Ti] Título:A diagnostic dilemma: variant Bernard-Soulier syndrome, a difficult clinical and genetic diagnosis.
[So] Source:Haemophilia;21(6):e510-3, 2015 Nov.
[Is] ISSN:1365-2516
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Síndrome de Bernard-Soulier/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Síndrome de Bernard-Soulier/patologia
Síndrome de Bernard-Soulier/terapia
Feminino
Seres Humanos
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; LETTER
[Em] Mês de entrada:1608
[Cu] Atualização por classe:151023
[Lr] Data última revisão:
151023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150801
[St] Status:MEDLINE
[do] DOI:10.1111/hae.12777


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[PMID]:26133172
[Au] Autor:Li J; Dai K; Wang Z; Cao L; Bai X; Ruan C
[Ad] Endereço:Jiangsu Institute of Hematology, The First Affiliated Hospital of Soochow University, Key Laboratory of Thrombosis and Hemostasis of Ministry of Health, 188 Shizi Street, Suzhou, 215006, China. lijiaming007007@126.com.
[Ti] Título:Platelet functional alterations in a Bernard-Soulier syndrome patient with filamin A mutation.
[So] Source:J Hematol Oncol;8:79, 2015 Jul 02.
[Is] ISSN:1756-8722
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Defects in filamin A (FLNA) gene could lead to low platelet counts and decreased surface expression of glycoprotein (GP) Ibα. Here, we report and investigate the FLNA genomic alteration of a case with Bernard-Soulier syndrome (BSS), a rare hereditary bleeding disorder caused by quantitative or qualitative abnormalities in the GP Ib-IX-V receptor. DNA sequencing analysis reveals the presence of a GP Ibα c.987G > A mutation and a FLNA c.1582 G > A mutation in this patient. Transient transfection studies show that GP Ibα c.987G > A mutation abolishes the surface expression of GP Ibα on the transfected CHO cells. On the other hand, abnormal responses to collagen, including the platelet aggregation, secretion, and GP VI signaling pathways, are associated with FLNA c.1582G > A mutation. Our findings confirm a central role for FLNA in platelet-adhesive functions. The interaction between FLNA and GP Ibα in platelets deserves to be investigated.
[Mh] Termos MeSH primário: Plaquetas/metabolismo
Filaminas/metabolismo
Trombocitopenia/metabolismo
[Mh] Termos MeSH secundário: Síndrome de Bernard-Soulier
Seres Humanos
Mutação
[Pt] Tipo de publicação:LETTER; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Filamins)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:150710
[Lr] Data última revisão:
150710
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150703
[St] Status:MEDLINE
[do] DOI:10.1186/s13045-015-0171-z


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[PMID]:26044173
[Au] Autor:Shlebak A; Poles A; Manning R; Almuhareb S; De La Funte J; Mitchell M; Lucas G
[Ad] Endereço:Haemostasis and Thrombosis Unit, Imperial College Healthcare, St. Thomas' Hospital, London, UK.
[Ti] Título:A Novel Homozygous c.800C>G Substitution in GP1BA Exon 2 in a Kuwaiti Family with Bernard-Soulier Syndrome.
[So] Source:Acta Haematol;134(3):193-8, 2015.
[Is] ISSN:1421-9662
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Bernard-Soulier syndrome (BSS) is a congenital bleeding disorder characterised by thrombocytopenia, giant platelets and decreased platelet adhesion resulting from genetic alterations of the glycoprotein (GP) Ib/IX/V complex. OBJECTIVES: Three sisters with a lifelong bleeding history and a provisional diagnosis of BSS were referred for further characterisation of their bleeding diathesis. The siblings' symptoms varied in severity from skin and gum bleeding to menorrhagia associated with iron-deficiency anaemia requiring regular transfusion of red cells and platelets. The parents were consanguineous but did not demonstrate any bleeding disorder. METHODS: The family were investigated using standard haematological techniques, platelet aggregometry, platelet membrane GP analysis and DNA sequencing of the genes encoding the GPIb/IX complex. RESULTS: All 3 sisters had thrombocytopenia and giant platelets. Platelet aggregation and flow cytometry studies confirmed the lack of aggregation with ristocetin and a markedly reduced GPIb/IX surface expression. Molecular analysis demonstrated a novel homozygous c.800C>G substitution in GP1BA exon 2 leading to a serine 267 Ter stop codon in all 3 siblings. CONCLUSIONS: A novel, nonsense mutation was identified as the cause of the bleeding disorder in this family. This is the first reported BSS mutation identified in a family from Kuwait.
[Mh] Termos MeSH primário: Síndrome de Bernard-Soulier/genética
Códon sem Sentido
Éxons
Homozigoto
Complexo Glicoproteico GPIb-IX de Plaquetas/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Criança
Feminino
Citometria de Fluxo
Seres Humanos
Kuweit
Masculino
Meia-Idade
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Codon, Nonsense); 0 (Platelet Glycoprotein GPIb-IX Complex); 0 (adhesion receptor)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:150919
[Lr] Data última revisão:
150919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150606
[St] Status:MEDLINE
[do] DOI:10.1159/000381328



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