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[PMID]:29381717
[Au] Autor:Tobolowsky FA; Wada N; Martinez-Maza O; Magpantay L; Koletar SL; Palella FJ; Brown TT; Lake JE
[Ad] Endereço:Department of Internal Medicine, Division of Infectious Diseases, University of Colorado, Denver, Colorado, United States of America.
[Ti] Título:Brief report: Circulating markers of fibrosis are associated with immune reconstitution status in HIV-infected men.
[So] Source:PLoS One;13(1):e0191606, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Lymphoid tissue fibrosis may contribute to incomplete immune reconstitution on antiretroviral therapy (ART) via local CD4+ T lymphocyte (CD4) depletion. Hyaluronic acid (HA) increases with fibrotic burden. CXCL4 concentrations increase in response to pro-fibrotic stimuli, but lower CXCL4 concentrations in HIV-infected individuals may reflect successful immune evasion by HIV. We investigated relationships between circulating HA and CXCL4 concentrations and immune reconstitution on ART in HIV-infected Multicenter AIDS Cohort Study participants. METHODS: HIV-infected men on ART for >1 year with cryopreserved plasma samples and suppressed post-ART HIV-1 RNA were included. Men with post-ART CD4 <200 cells/mm3 were defined as immunologic non-responders (n = 25). Age-/race-matched men with post-ART CD4 >500 cells/mm3 served as controls (n = 49). HA and CXCL4 concentrations were measured via ELISA. RESULTS: Median pre-ART CD4 was 297 cells/mm3 for non-responders vs 386 cells/mm3 for controls. Median post-ART CD4 was 141 cells/mm3 for non-responders and 815 cells/mm3 for controls. HIV infection duration was 23 years, with median time on ART 13 years for non-responders vs 11 years for controls. Pre-ART HA and CXCL4 concentrations did not vary by eventual immune reconstitution status. Post-ART HA concentrations tended to be higher (85 vs 36 ng/mL, p = 0.07) and CXCL4 concentrations were lower (563 vs 1459 ng/mL, p = 0.01) among non-responders. Among men with paired pre-/post-ART samples, non-responders had greater HA increases and CXCL4 decreases than controls (HA: 50 vs 12 ng/mL, p = 0.04; CXCL4: -1258 vs -405 ng/mL, p = 0.01). CONCLUSIONS: Higher circulating concentrations of HA and lower concentrations of CXCL4 are associated with failure of immune reconstitution on ART.
[Mh] Termos MeSH primário: Biomarcadores/sangue
Infecções por HIV/imunologia
[Mh] Termos MeSH secundário: Fármacos Anti-HIV/uso terapêutico
Contagem de Linfócito CD4
Fibrose
Infecções por HIV/sangue
Infecções por HIV/tratamento farmacológico
Seres Humanos
Ácido Hialurônico/metabolismo
Tecido Linfoide/patologia
Masculino
Meia-Idade
Fator Plaquetário 4/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-HIV Agents); 0 (Biomarkers); 37270-94-3 (Platelet Factor 4); 9004-61-9 (Hyaluronic Acid)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180131
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191606


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[PMID]:28991552
[Au] Autor:Jones CG; Pechauer SM; Curtis BR; Bougie DW; Irani MS; Dhakal B; Pierce B; Aster RH; Padmanabhan A
[Ad] Endereço:Medical Sciences Institute, BloodCenter of Wisconsin, Milwaukee, WI.
[Ti] Título:A Platelet Factor 4-Dependent Platelet Activation Assay Facilitates Early Detection of Pathogenic Heparin-Induced Thrombocytopenia Antibodies.
[So] Source:Chest;152(4):e77-e80, 2017 Oct.
[Is] ISSN:1931-3543
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Heparin-induced thrombocytopenia (HIT) is a dangerous complication of heparin therapy. HIT diagnosis is established by recognizing thrombocytopenia and/or thrombosis in an affected patient and from the results of serological tests such as the platelet factor 4 (PF4)/heparin immunoassay (PF4 ELISA) and serotonin release assay (SRA). Recent studies suggest that HIT antibodies activate platelets by recognizing PF4 in a complex with platelet glycosaminoglycans (and/or polyphosphates) and that an assay based on this principle, the PF4-dependent P-selectin expression assay (PEA), may be even more accurate than the SRA for HIT diagnosis. Here, we demonstrate that the PEA detected pathogenic antibodies before the SRA became positive in two patients with HIT studied serially, in one case even before seropositivity in the PF4 ELISA. In one of the patients treated with plasma exchange, persistent dissociation between the PEA and SRA test results was observed. These results support a role for the PEA in early HIT diagnosis.
[Mh] Termos MeSH primário: Anticorpos/sangue
Diagnóstico Precoce
Heparina/efeitos adversos
Fator Plaquetário 4/sangue
Trombocitopenia/diagnóstico
[Mh] Termos MeSH secundário: Idoso
Anticoagulantes/efeitos adversos
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Meia-Idade
Trombocitopenia/sangue
Trombocitopenia/induzido quimicamente
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Anticoagulants); 37270-94-3 (Platelet Factor 4); 9005-49-6 (Heparin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171010
[St] Status:MEDLINE


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[PMID]:28690072
[Au] Autor:Sena IFG; Prazeres PHDM; Santos GSP; Borges IT; Azevedo PO; Andreotti JP; Almeida VM; Paiva AE; Guerra DAP; Lousado L; Souto L; Mintz A; Birbrair A
[Ad] Endereço:Department of Pathology, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.
[Ti] Título:Identity of Gli1 cells in the bone marrow.
[So] Source:Exp Hematol;54:12-16, 2017 Oct.
[Is] ISSN:1873-2399
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Bone marrow fibrosis is a critical component of primary myelofibrosis in which normal bone marrow tissue and blood-forming cells are gradually replaced with scar tissue. The specific cellular and molecular mechanisms that cause bone marrow fibrosis are not understood. A recent study using state-of-the-art techniques, including in vivo lineage tracing, provides evidence that Gli1 cells are the cells responsible for fibrotic disease in the bone marrow. Strikingly, genetic depletion of Gli1 cells rescues bone marrow failure and abolishes myelofibrosis. This work introduces a new central cellular target for bone marrow fibrosis. The knowledge that emerges from this research will be important for the treatment of several malignant and nonmalignant disorders.
[Mh] Termos MeSH primário: Células da Medula Óssea/efeitos dos fármacos
Terapia de Alvo Molecular
Fator Plaquetário 4/genética
Mielofibrose Primária/tratamento farmacológico
Piridinas/farmacologia
Pirimidinas/farmacologia
Proteína GLI1 em Dedos de Zinco/genética
[Mh] Termos MeSH secundário: Animais
Medula Óssea/efeitos dos fármacos
Medula Óssea/metabolismo
Medula Óssea/patologia
Células da Medula Óssea/metabolismo
Células da Medula Óssea/patologia
Proliferação Celular
Modelos Animais de Doenças
Expressão Gênica
Seres Humanos
Camundongos
Camundongos Transgênicos
Fator Plaquetário 4/metabolismo
Mielofibrose Primária/genética
Mielofibrose Primária/metabolismo
Mielofibrose Primária/patologia
Proteína GLI1 em Dedos de Zinco/antagonistas & inibidores
Proteína GLI1 em Dedos de Zinco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (GANT 61); 0 (GLI1 protein, human); 0 (Pyridines); 0 (Pyrimidines); 0 (Zinc Finger Protein GLI1); 37270-94-3 (Platelet Factor 4)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170711
[St] Status:MEDLINE


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[PMID]:28596376
[Au] Autor:Beckers CML; Simpson KR; Griffin KJ; Brown JM; Cheah LT; Smith KA; Vacher J; Cordell PA; Kearney MT; Grant PJ; Pease RJ
[Ad] Endereço:From the Leeds Institute for Cardiovascular and Metabolic Medicine, LIGHT Laboratories, University of Leeds, United Kingdom (C.M.L.B., K.R.S., K.J.G., J.M.B., L.T.C., K.A.S., P.A.C., M.T.K., P.J.G., R.J.P.); and Clinical Research Institute of Montreal, McGill University, Canada (J.V.).
[Ti] Título:Cre/lox Studies Identify Resident Macrophages as the Major Source of Circulating Coagulation Factor XIII-A.
[So] Source:Arterioscler Thromb Vasc Biol;37(8):1494-1502, 2017 Aug.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To establish the cellular source of plasma factor (F)XIII-A. APPROACH AND RESULTS: A novel mouse floxed for the gene, FXIII-A (Flox), was crossed with myeloid- and platelet-cre-expressing mice, and cellular FXIII-A mRNA expression and plasma and platelet FXIII-A levels were measured. The platelet factor 4-cre.Flox cross abolished platelet FXIII-A and reduced plasma FXIII-A to 23±3% ( <0.001). However, the effect of platelet factor 4-cre on plasma FXIII-A was exerted outside of the megakaryocyte lineage because plasma FXIII-A was not reduced in the Mpl mouse, despite marked thrombocytopenia. In support of this, platelet factor 4-cre depleted FXIII-A mRNA in brain, aorta, and heart of floxed mice, where FXIII-A cells were identified as macrophages as they costained with CD163. In the integrin αM-cre.Flox and the double copy lysozyme 2-cre.cre.Flox crosses, plasma FXIII-A was reduced to, respectively, 75±5% ( =0.003) and 30±7% ( <0.001), with no change in FXIII-A content per platelet, further consistent with a macrophage origin of plasma FXIII-A. The change in plasma FXIII-A levels across the various mouse genotypes mirrored the change in FXIII-A mRNA expression in aorta. Bone marrow transplantation of FXIII-A bone marrow into FXIII-A mice both restored plasma FXIII-A to normal levels and replaced aortic and cardiac FXIII-A mRNA, while its transplantation into FXIII-A mice did not increase plasma FXIII-A levels, suggesting that a limited population of niches exists that support FXIII-A-releasing cells. CONCLUSIONS: This work suggests that resident macrophages maintain plasma FXIII-A and exclude the platelet lineage as a major contributor.
[Mh] Termos MeSH primário: Fator XIII/metabolismo
Integrases/genética
Macrófagos/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos CD/sangue
Antígenos de Diferenciação Mielomonocítica/sangue
Plaquetas/metabolismo
Transplante de Medula Óssea
Antígeno CD11b/sangue
Antígeno CD11b/genética
Células Cultivadas
Fator XIII/genética
Feminino
Regulação da Expressão Gênica
Predisposição Genética para Doença
Seres Humanos
Integrases/metabolismo
Macrófagos/transplante
Masculino
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Fenótipo
Fator Plaquetário 4/sangue
Fator Plaquetário 4/genética
RNA Mensageiro/sangue
RNA Mensageiro/genética
Receptores de Superfície Celular/sangue
Receptores de Trombopoetina/sangue
Receptores de Trombopoetina/genética
Trombocitopenia/sangue
Trombocitopenia/genética
Tirosina Quinase 3 Semelhante a fms/sangue
Tirosina Quinase 3 Semelhante a fms/genética
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (CD11b Antigen); 0 (CD163 antigen); 0 (Mpl protein, mouse); 0 (RNA, Messenger); 0 (Receptors, Cell Surface); 0 (Receptors, Thrombopoietin); 104641-95-4 (factor XIII subunit A); 37270-94-3 (Platelet Factor 4); 9013-56-3 (Factor XIII); EC 2.7.10.1 (fms-Like Tyrosine Kinase 3); EC 2.7.7.- (Cre recombinase); EC 2.7.7.- (Integrases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309271


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[PMID]:28544777
[Au] Autor:Flores RJ; Kelly AJ; Li Y; Chen X; McGee C; Krailo M; Barkauskas DA; Hicks J; Man TK
[Ad] Endereço:Texas Children's Cancer and Hematology Centers, Texas Children's Hospital, Houston, Texas.
[Ti] Título:The prognostic significance of circulating serum amyloid A and CXC chemokine ligand 4 in osteosarcoma.
[So] Source:Pediatr Blood Cancer;64(12), 2017 Dec.
[Is] ISSN:1545-5017
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Osteosarcoma (OS) is the most common pediatric bone cancer.  Despite advances in treatment regimens, the survival rate remains 60-70%.  There is an urgent need to identify prognostic biomarkers, so that targeted therapies can be developed to improve the outcome. PROCEDURE: Our laboratory has previously identified that circulating serum amyloid A (SAA) and CXC chemokine ligand 4 (CXCL4) are upregulated in patients with OS.  In this study, we tested if they could be used as prognostic biomarkers.  We used enzyme-linked immunosorbent assays to measure their concentrations in serum samples (n = 233) and immunohistochemistry to examine their expressions in primary tumors (n = 37).  Prognostic significance of the serum concentrations and tumor expressions of the biomarkers was then evaluated. RESULTS: Patients with "high SAA" and "low CXCL4" circulating levels at diagnosis significantly correlated with a worse outcome (HR = 1.68, P = 0.014), which was independent of the metastatic status.  These patients also exhibited a significantly higher rate of poor histologic response to chemotherapy.  Furthermore, low tumor expression of CXCL4 correlated with poor survival (HR = 3.57, P = 0.005). CONCLUSIONS: Our results demonstrate that circulating SAA and CXCL4 may serve as prognostic biomarkers in OS.  Targeting CXCL4 has been reported, suggesting that it may be exploited as a therapeutic target in OS.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/sangue
Neoplasias Ósseas/mortalidade
Osteossarcoma/mortalidade
Fator Plaquetário 4/sangue
Proteína Amiloide A Sérica/análise
[Mh] Termos MeSH secundário: Adolescente
Adulto
Neoplasias Ósseas/sangue
Neoplasias Ósseas/diagnóstico
Criança
Pré-Escolar
Seres Humanos
Osteossarcoma/sangue
Osteossarcoma/diagnóstico
Prognóstico
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Serum Amyloid A Protein); 37270-94-3 (Platelet Factor 4)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171122
[Lr] Data última revisão:
171122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1002/pbc.26659


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[PMID]:28515281
[Au] Autor:Silva-Cardoso SC; Affandi AJ; Spel L; Cossu M; van Roon JAG; Boes M; Radstake TRDJ
[Ad] Endereço:Laboratory of Translational Immunology, University Medical Center Utrecht, 3584 EA Utrecht, the Netherlands.
[Ti] Título:CXCL4 Exposure Potentiates TLR-Driven Polarization of Human Monocyte-Derived Dendritic Cells and Increases Stimulation of T Cells.
[So] Source:J Immunol;199(1):253-262, 2017 Jul 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chemokines have been shown to play immune-modulatory functions unrelated to steering cell migration. CXCL4 is a chemokine abundantly produced by activated platelets and immune cells. Increased levels of circulating CXCL4 are associated with immune-mediated conditions, including systemic sclerosis. Considering the central role of dendritic cells (DCs) in immune activation, in this article we addressed the effect of CXCL4 on the phenotype and function of monocyte-derived DCs (moDCs). To this end, we compared innate and adaptive immune responses of moDCs with those that were differentiated in the presence of CXCL4. Already prior to TLR- or Ag-specific stimulation, CXCL4-moDCs displayed a more matured phenotype. We found that CXCL4 exposure can sensitize moDCs for TLR-ligand responsiveness, as illustrated by a dramatic upregulation of CD83, CD86, and MHC class I in response to TLR3 and TLR7/8-agonists. Also, we observed a markedly increased secretion of IL-12 and TNF-α by CXCL4-moDCs exclusively upon stimulation with polyinosinic-polycytidylic acid, R848, and CL075 ligands. Next, we analyzed the effect of CXCL4 in modulating DC-mediated T cell activation. CXCL4-moDCs strongly potentiated proliferation of autologous CD4 T cells and CD8 T cells and production of IFN-γ and IL-4, in an Ag-independent manner. Although the internalization of Ag was comparable to that of moDCs, Ag processing by CXCL4-moDCs was impaired. Yet, these cells were more potent at stimulating Ag-specific CD8 T cell responses. Together our data support that increased levels of circulating CXCL4 may contribute to immune dysregulation through the modulation of DC differentiation.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Diferenciação Celular
Células Dendríticas/imunologia
Ativação Linfocitária
Fator Plaquetário 4/imunologia
Fator de Necrose Tumoral alfa/imunologia
[Mh] Termos MeSH secundário: Antígenos CD/genética
Antígenos CD/imunologia
Antígeno B7-2/genética
Antígeno B7-2/imunologia
Linfócitos T CD4-Positivos/efeitos dos fármacos
Linfócitos T CD4-Positivos/fisiologia
Linfócitos T CD8-Positivos/efeitos dos fármacos
Linfócitos T CD8-Positivos/fisiologia
Células Cultivadas
Técnicas de Cocultura
Células Dendríticas/efeitos dos fármacos
Células Dendríticas/fisiologia
Escherichia coli/fisiologia
Infecções por Escherichia coli/imunologia
Infecções por Escherichia coli/microbiologia
Infecções por Escherichia coli/prevenção & controle
Genes MHC Classe I
Seres Humanos
Imidazóis/farmacologia
Imunoglobulinas/genética
Imunoglobulinas/imunologia
Interleucina-12/genética
Interleucina-12/imunologia
Glicoproteínas de Membrana/genética
Glicoproteínas de Membrana/imunologia
Fenótipo
Fator Plaquetário 4/metabolismo
Fator Plaquetário 4/farmacologia
Poli I-C/farmacologia
Quinolinas/farmacologia
Tiazóis/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (B7-2 Antigen); 0 (CD83 antigen); 0 (CD86 protein, human); 0 (CL 075); 0 (Imidazoles); 0 (Immunoglobulins); 0 (Membrane Glycoproteins); 0 (Quinolines); 0 (Thiazoles); 0 (Tumor Necrosis Factor-alpha); 187348-17-0 (Interleukin-12); 37270-94-3 (Platelet Factor 4); O84C90HH2L (Poly I-C); V3DMU7PVXF (resiquimod)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1602020


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[PMID]:28416511
[Au] Autor:Arepally GM
[Ad] Endereço:Division of Hematology, Duke University Medical Center, Durham, NC.
[Ti] Título:Heparin-induced thrombocytopenia.
[So] Source:Blood;129(21):2864-2872, 2017 May 25.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Heparin-induced thrombocytopenia (HIT) is an immune complication of heparin therapy caused by antibodies to complexes of platelet factor 4 (PF4) and heparin. Pathogenic antibodies to PF4/heparin bind and activate cellular FcγRIIA on platelets and monocytes to propagate a hypercoagulable state culminating in life-threatening thrombosis. It is now recognized that anti-PF4/heparin antibodies develop commonly after heparin exposure, but only a subset of sensitized patients progress to life-threatening complications of thrombocytopenia and thrombosis. Recent scientific developments have clarified mechanisms underlying PF4/heparin immunogenicity, disease susceptibility, and clinical manifestations of disease. Insights from clinical and laboratory findings have also been recently harnessed for disease prevention. This review will summarize our current understanding of HIT by reviewing pathogenesis, essential clinical and laboratory features, and management.
[Mh] Termos MeSH primário: Autoanticorpos
Heparina/efeitos adversos
Fator Plaquetário 4
Receptores de IgG
Trombocitopenia
[Mh] Termos MeSH secundário: Autoanticorpos/sangue
Autoanticorpos/imunologia
Seres Humanos
Fator Plaquetário 4/antagonistas & inibidores
Fator Plaquetário 4/sangue
Fator Plaquetário 4/imunologia
Receptores de IgG/sangue
Receptores de IgG/imunologia
Trombocitopenia/sangue
Trombocitopenia/induzido quimicamente
Trombocitopenia/imunologia
Trombocitopenia/prevenção & controle
Trombose/sangue
Trombose/etiologia
Trombose/imunologia
Trombose/prevenção & controle
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Autoantibodies); 0 (FCGR2A protein, human); 0 (Receptors, IgG); 37270-94-3 (Platelet Factor 4); 9005-49-6 (Heparin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170419
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2016-11-709873


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[PMID]:28388835
[Au] Autor:Kuter DJ; Konkle BA; Hamza TH; Uhl L; Assmann SF; Kiss JE; Kaufman RM; Key NS; Sachais BS; Hess JR; Ness P; McCrae KR; Leissinger C; Strauss RG; McFarland JG; Neufeld E; Bussel JB; Ortel TL
[Ad] Endereço:Massachusetts General Hospital, Boston, Massachusetts, USA.
[Ti] Título:Clinical outcomes in a cohort of patients with heparin-induced thrombocytopenia.
[So] Source:Am J Hematol;92(8):730-738, 2017 Aug.
[Is] ISSN:1096-8652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Heparin-induced thrombocytopenia (HIT) is a thrombotic disorder usually prompting treatment with non-heparin anticoagulants. The benefits and risks of such treatments have not been fully assessed. METHODS: We analyzed data for 442 patients having a positive heparin-platelet factor 4 antibody test and recent heparin exposure. The primary outcome was a composite endpoint (death, limb amputation/gangrene, or new thrombosis). Secondary outcomes included bleeding and the effect of anticoagulation. FINDINGS: Seventy-one patients (16%) had HIT with thrombosis (HIT-T); 284 (64%) had HIT without thrombosis (isolated HIT); 87 (20%) did not have HIT. An intermediate or high "4T" score was found in 85%, 58%, and 8% of the three respective groups. Non-heparin anticoagulation was begun in 80%, 56%, and 45%. The composite endpoint occurred in 48%, 36%, and 17% (P = .01) of which 61%, 38%, and 40% were receiving non-heparin anticoagulation. Compared with the no HIT group, the composite endpoint was significantly more likely in HIT-T [HR 2.48 (1.35-4.55), P = .003)] and marginally more likely in isolated HIT [HR 1.66 (0.96-2.85), P = .071]. Importantly, risk increased (HR 1.77, P = .02) after platelet transfusion. Major bleeding occurred in 48%, 36%, and 16% of the three groups (P = .005). Non-heparin anticoagulation was not associated with a reduction in composite endpoint events in either HIT group. INTERPRETATION: HIT patients have high risks of death, limb amputation/gangrene, thrombosis, and bleeding. Non-heparin anticoagulant treatment may not benefit all patients and should be considered only after careful assessment of the relative risks of thrombosis and bleeding in individual patients.
[Mh] Termos MeSH primário: Heparina/efeitos adversos
Trombocitopenia/epidemiologia
Trombocitopenia/etiologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Anticoagulantes/uso terapêutico
Autoanticorpos/sangue
Autoanticorpos/imunologia
Ensaio de Imunoadsorção Enzimática
Feminino
Heparina/imunologia
Seres Humanos
Masculino
Meia-Idade
Mortalidade
Avaliação de Resultados da Assistência ao Paciente
Contagem de Plaquetas
Fator Plaquetário 4/imunologia
Modelos de Riscos Proporcionais
Estudos Retrospectivos
Trombocitopenia/diagnóstico
Trombocitopenia/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticoagulants); 0 (Autoantibodies); 37270-94-3 (Platelet Factor 4); 9005-49-6 (Heparin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170728
[Lr] Data última revisão:
170728
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170408
[St] Status:MEDLINE
[do] DOI:10.1002/ajh.24759


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[PMID]:28368308
[Au] Autor:Brown AJ; Joseph PR; Sawant KV; Rajarathnam K
[Ad] Endereço:Department of Biochemistry and Molecular Biology, and Sealy Center for Structural Biology and Molecular Biophysics, The University of Texas Medical Branch, Galveston, TX 77555, USA. aj3brown@utmb.edu.
[Ti] Título:Chemokine CXCL7 Heterodimers: Structural Insights, CXCR2 Receptor Function, and Glycosaminoglycan Interactions.
[So] Source:Int J Mol Sci;18(4), 2017 Apr 01.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Chemokines mediate diverse fundamental biological processes, including combating infection. Multiple chemokines are expressed at the site of infection; thus chemokine synergy by heterodimer formation may play a role in determining function. Chemokine function involves interactions with G-protein-coupled receptors and sulfated glycosaminoglycans (GAG). However, very little is known regarding heterodimer structural features and receptor and GAG interactions. Solution nuclear magnetic resonance (NMR) and molecular dynamics characterization of platelet-derived chemokine CXCL7 heterodimerization with chemokines CXCL1, CXCL4, and CXCL8 indicated that packing interactions promote CXCL7-CXCL1 and CXCL7-CXCL4 heterodimers, and electrostatic repulsive interactions disfavor the CXCL7-CXCL8 heterodimer. As characterizing the native heterodimer is challenging due to interference from monomers and homodimers, we engineered a "trapped" disulfide-linked CXCL7-CXCL1 heterodimer. NMR and modeling studies indicated that GAG heparin binding to the heterodimer is distinctly different from the CXCL7 monomer and that the GAG-bound heterodimer is unlikely to bind the receptor. Interestingly, the trapped heterodimer was highly active in a Ca release assay. These data collectively suggest that GAG interactions play a prominent role in determining heterodimer function in vivo. Further, this study provides proof-of-concept that the disulfide trapping strategy can serve as a valuable tool for characterizing the structural and functional features of a chemokine heterodimer.
[Mh] Termos MeSH primário: Glicosaminoglicanos/química
Simulação de Dinâmica Molecular
Domínios Proteicos
Multimerização Proteica
beta-Tromboglobulina/química
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Sítios de Ligação/genética
Cálcio/metabolismo
Quimiocina CXCL1/química
Quimiocina CXCL1/genética
Quimiocina CXCL1/metabolismo
Glicosaminoglicanos/metabolismo
Células HL-60
Heparina/química
Heparina/metabolismo
Seres Humanos
Interleucina-8/química
Interleucina-8/genética
Interleucina-8/metabolismo
Cinética
Espectroscopia de Ressonância Magnética
Oligossacarídeos/química
Oligossacarídeos/metabolismo
Fator Plaquetário 4/química
Fator Plaquetário 4/genética
Fator Plaquetário 4/metabolismo
Ligação Proteica
Homologia de Sequência de Aminoácidos
beta-Tromboglobulina/genética
beta-Tromboglobulina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL1 protein, human); 0 (Chemokine CXCL1); 0 (Glycosaminoglycans); 0 (Interleukin-8); 0 (Oligosaccharides); 0 (PPBP protein, human); 0 (beta-Thromboglobulin); 37270-94-3 (Platelet Factor 4); 9005-49-6 (Heparin); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170613
[Lr] Data última revisão:
170613
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE


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[PMID]:28323919
[Au] Autor:Maybin JA; Thiruchelvam U; Madhra M; Saunders PTK; Critchley HOD
[Ad] Endereço:MRC Centre for Reproductive Health, The University of Edinburgh, Queen's Medical Research Institute, Edinburgh EH16 4TJ, United Kingdom.
[Ti] Título:Steroids Regulate CXCL4 in the Human Endometrium During Menstruation to Enable Efficient Endometrial Repair.
[So] Source:J Clin Endocrinol Metab;102(6):1851-1860, 2017 Jun 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: Repair of the endometrial surface at menstruation must be efficient to minimize blood loss and optimize reproductive function. The mechanism and regulation of endometrial repair remain undefined. Objective: To determine the presence/regulation of CXCL4 in the human endometrium as a putative repair factor at menses. Patients/Setting: Endometrial tissue was collected throughout the menstrual cycle from healthy women attending the gynecology department. Menstrual blood loss was objectively measured in a subset, and heavy menstrual bleeding (HMB) was defined as >80 mL per cycle. Monocytes were isolated from peripheral blood. Design: CXCL4 messenger RNA (mRNA) and protein were identified by quantitative reverse transcription polymerase chain reaction and immunohistochemistry. The function/regulation of endometrial CXCL4 was explored by in vitro cell culture. Results: CXCL4 mRNA concentrations were significantly increased during menstruation. Intense staining for CXCL4 was detected in late secretory and menstrual tissue, localized to stromal, epithelial and endothelial cells. Colocalization identified positive staining in CD68+ macrophages. Treatment of human endometrial stromal and endothelial cells (hESCs and HEECs, respectively) with steroids revealed differential regulation of CXCL4. Progesterone withdrawal resulted in significant increases in CXCL4 mRNA and protein in hESCs, whereas cortisol significantly increased CXCL4 in HEECs. In women with HMB, CXCL4 was reduced in endothelial cells during the menstrual phase compared with women with normal menstrual bleeding. Cortisol-exposed macrophages displayed increased chemotaxis toward CXCL4 compared with macrophages incubated with estrogen or progesterone. Conclusions: These data implicate CXCL4 in endometrial repair after menses. Reduced cortisol at the time of menses may contribute to delayed endometrial repair and HMB, in part by mechanisms involving aberrant expression of CXCL4.
[Mh] Termos MeSH primário: Endométrio/metabolismo
Menorragia/genética
Menstruação/genética
Fator Plaquetário 4/genética
[Mh] Termos MeSH secundário: Adulto
Endométrio/citologia
Células Epiteliais/efeitos dos fármacos
Estradiol/farmacologia
Feminino
Regulação da Expressão Gênica
Seres Humanos
Hidrocortisona/farmacologia
Imuno-Histoquímica
Técnicas In Vitro
Menorragia/metabolismo
Ciclo Menstrual/genética
Ciclo Menstrual/metabolismo
Menstruação/metabolismo
Meia-Idade
Monócitos
Fator Plaquetário 4/efeitos dos fármacos
Fator Plaquetário 4/metabolismo
Progesterona/farmacologia
RNA Mensageiro
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Células Estromais/efeitos dos fármacos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 37270-94-3 (Platelet Factor 4); 4G7DS2Q64Y (Progesterone); 4TI98Z838E (Estradiol); WI4X0X7BPJ (Hydrocortisone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2016-3604



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