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Pesquisa : A11.284.295.588.500 [Categoria DeCS]
Referências encontradas : 2137 [refinar]
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  1 / 2137 MEDLINE  
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[PMID]:28467294
[Au] Autor:van der Pol E; Harrison P
[Ad] Endereço:a Biomedical Engineering & Physics , Academic Medical Centre, University of Amsterdam , Amsterdam , The Netherlands.
[Ti] Título:From platelet dust to gold dust: physiological importance and detection of platelet microvesicles.
[So] Source:Platelets;28(3):211-213, 2017 05.
[Is] ISSN:1369-1635
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Plaquetas/química
Micropartículas Derivadas de Células/metabolismo
Integrina beta3/genética
Trombose/fisiopatologia
[Mh] Termos MeSH secundário: Transporte Biológico/fisiologia
Biomarcadores/metabolismo
Plaquetas/ultraestrutura
Comunicação Celular/fisiologia
Micropartículas Derivadas de Células/genética
Micropartículas Derivadas de Células/ultraestrutura
Expressão Gênica
Ouro/química
Seres Humanos
Imuno-Histoquímica
Integrina beta3/metabolismo
Nanopartículas Metálicas/química
Tamanho da Partícula
Ativação Plaquetária/fisiologia
Trombose/genética
Trombose/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (ITGB3 protein, human); 0 (Integrin beta3); 7440-57-5 (Gold)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1080/09537104.2017.1282781


  2 / 2137 MEDLINE  
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[PMID]:27778450
[Au] Autor:Zwicker JI
[Ad] Endereço:Division of Hemostasis and Thrombosis, Division of Hematology-Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
[Ti] Título:Scattering the spotlight on microparticles.
[So] Source:J Thromb Haemost;15(1):185-186, 2017 01.
[Is] ISSN:1538-7836
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Micropartículas Derivadas de Células
Espalhamento de Radiação
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1111/jth.13552


  3 / 2137 MEDLINE  
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[PMID]:29266056
[Au] Autor:Liwski RS; Gebel HM
[Ad] Endereço:Department of Pathology, Dalhousie University, Halifax, Nova Scotia, Canada.
[Ti] Título:Of Cells and Microparticles: Assets and Liabilities of HLA Antibody Detection.
[So] Source:Transplantation;102(1S Suppl 1):S1-S6, 2018 01.
[Is] ISSN:1534-6080
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The evolution of antibody detection from cell- to bead-based technology has positively impacted the ability to allocate organs in a safe and timely manner. The devil, of course, is in the details that delineate how these assays are performed and applied and to recognize that while there have been some truly amazing technological advances (assets), they are still imperfect and subject to error (liabilities). This review identifies the strengths of HLA antibody assays, highlights their weaknesses and offers approaches for standardization.
[Mh] Termos MeSH primário: Micropartículas Derivadas de Células/imunologia
Antígenos HLA/imunologia
Teste de Histocompatibilidade/métodos
Isoanticorpos/metabolismo
[Mh] Termos MeSH secundário: Biomarcadores/metabolismo
Teste de Histocompatibilidade/normas
Seres Humanos
Transplante de Órgãos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (HLA Antigens); 0 (Isoantibodies)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE
[do] DOI:10.1097/TP.0000000000001818


  4 / 2137 MEDLINE  
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[PMID]:29197574
[Au] Autor:Li C; Li S; Zhang F; Wu M; Liang H; Song J; Lee C; Chen H
[Ad] Endereço:Department of Cardiology, Peking University People's Hospital, Beijing, 100044, China; Beijing Key Laboratory of Early Prediction and Intervention of Acute Myocardial Infarction, Peking University People's Hospital, Beijing, 100044, China; Center for Cardiovascular Translational Research, Peking Uni
[Ti] Título:Endothelial microparticles-mediated transfer of microRNA-19b promotes atherosclerosis via activating perivascular adipose tissue inflammation in apoE mice.
[So] Source:Biochem Biophys Res Commun;495(2):1922-1929, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Microparticles(MPs) are the major carriers of circulating microRNAs. Our previous study has shown that microRNA (miR)-19b in endothelial cell-derived microparticles (EMPs) is significantly increased in patients with unstable angina. However, little is known about the relationship between miR-19b in EMPs and the progression of atherosclerosis. The aim of the present study was to define the role and potential mechanism of miR-19b incorporated in EMPs in the development of atherosclerosis. Western-diet-fed apoE mice were injected with phosphate buffered solution(PBS), EMP carrying microRNA control(EMP ) or miR-19b mimic (EMP ) intravenously. Systemic treatment with EMP significantly accelerated carotid artery atherosclerosis progression by increasing lipid, macrophages and smooth muscle cells and decreasing collagen content in atherosclerotic plaque. Fluorescence-labelled EMP injection proved that miR-19b could be transported into perivascular adipose tissue(PVAT) by EMPs. EMP treatment also promoted inflammatory cytokines secretion and macrophages infiltration in PVAT. In further experiment, apoE mice were divided into 3 groups: EMP PVAT(+), EMP PVAT(+) and EMP PVAT(-), based on removing or keeping pericarotid adipose tissue and injected with EMP or EMP . Loss of PVAT attenuated EMP -mediated effects on increasing carotid atherosclerosis formation and inflammatory cytokines level in plaque. EMP inhibited suppressor of cytokine signaling 3 (SOCS3) expression in PVAT. Our findings demonstrate that miR-19b in EMPs exaggerates atherosclerosis progression by augmenting PVAT-specific inflammation proceeded by downregulating SOCS3 expression.
[Mh] Termos MeSH primário: Tecido Adiposo/imunologia
Aterosclerose/imunologia
Micropartículas Derivadas de Células/imunologia
Endotélio Vascular/imunologia
MicroRNAs/imunologia
Paniculite/imunologia
[Mh] Termos MeSH secundário: Animais
Apolipoproteínas E/genética
Masculino
Camundongos
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (MIRN19 microRNA, mouse); 0 (MicroRNAs)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171204
[St] Status:MEDLINE


  5 / 2137 MEDLINE  
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[PMID]:28452069
[Au] Autor:Chao OS; Chang TC; Di Bella MA; Alessandro R; Anzanello F; Rappa G; Goodman OB; Lorico A
[Ad] Endereço:College of Medicine, Roseman University, Las Vegas, Nevada, 89135.
[Ti] Título:The HDAC6 Inhibitor Tubacin Induces Release of CD133 Extracellular Vesicles From Cancer Cells.
[So] Source:J Cell Biochem;118(12):4414-4424, 2017 Dec.
[Is] ISSN:1097-4644
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tumor-derived extracellular vesicles (EVs) are emerging as an important mode of intercellular communication, capable of transferring biologically active molecules that facilitate the malignant growth and metastatic process. CD133 (Prominin-1), a stem cell marker implicated in tumor initiation, differentiation and resistance to anti-cancer therapy, is reportedly associated with EVs in various types of cancer. However, little is known about the factors that regulate the release of these CD133 EVs. Here, we report that the HDAC6 inhibitor tubacin promoted the extracellular release of CD133 EVs from human FEMX-I metastatic melanoma and Caco-2 colorectal carcinoma cells, with a concomitant downregulation of intracellular CD133. This effect was specific for tubacin, as inhibition of HDAC6 deacetylase activity by another selective HDAC6 inhibitor, ACY-1215 or the pan-HDAC inhibitor trichostatin A (TSA), and knockdown of HDAC6 did not enhance the release of CD133 EVs. The tubacin-induced EV release was associated with changes in cellular lipid composition, loss of clonogenic capacity and decrease in the ability to form multicellular aggregates. These findings indicate a novel potential anti-tumor mechanism for tubacin in CD133-expressing malignancies. J. Cell. Biochem. 118: 4414-4424, 2017. © 2017 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Antígeno AC133/metabolismo
Anilidas/farmacologia
Micropartículas Derivadas de Células/metabolismo
Desacetilase 6 de Histona/antagonistas & inibidores
Inibidores de Histona Desacetilases/farmacologia
Ácidos Hidroxâmicos/farmacologia
Proteínas de Neoplasias/metabolismo
Neoplasias/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Desacetilase 6 de Histona/metabolismo
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AC133 Antigen); 0 (Anilides); 0 (Histone Deacetylase Inhibitors); 0 (Hydroxamic Acids); 0 (Neoplasm Proteins); 0 (PROM1 protein, human); 02C2G1D30D (tubacin); EC 3.5.1.98 (HDAC6 protein, human); EC 3.5.1.98 (Histone Deacetylase 6)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180102
[Lr] Data última revisão:
180102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1002/jcb.26095


  6 / 2137 MEDLINE  
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[PMID]:28748286
[Au] Autor:Klaihmon P; Vimonpatranon S; Noulsri E; Lertthammakiat S; Anurathapan U; Sirachainan N; Hongeng S; Pattanapanyasat K
[Ad] Endereço:Graduate Program in Immunology, Department of Immunology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.
[Ti] Título:Normalized levels of red blood cells expressing phosphatidylserine, their microparticles, and activated platelets in young patients with ß-thalassemia following bone marrow transplantation.
[So] Source:Ann Hematol;96(10):1741-1747, 2017 Oct.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Bone marrow transplantation (BMT) serves as the only curative treatment for patients with ß-thalassemia major; however, hemostatic changes have been observed in these BMT patients. Aggregability of thalassemic red blood cells (RBCs) and increased red blood cell-derived microparticles (RMPs) expressing phosphatidylserine (PS) are thought to participate in thromboembolic events by initially triggering platelet activation. To our knowledge, there has been no report providing quantitation of these circulating PS-expressing RBCs and RMPs in young ß-thalassemia patients after BMT. Whole blood from each subject was fluorescently labeled to detect RBC markers (CD235a) and annexin-V together with the known number TruCount™ beads. PS-expressing RBCs, RMPs, and activated platelets were identified by flow cytometry. In our randomized study, we found the decreased levels of three aforementioned factors compared to levels in patients receiving regular blood transfusion (RT). This study showed that BMT in ß-thalassemia patients decreases the levels of circulating PS-expressing RBCs, their MPs, and procoagulant platelets when compared to patients who received RT. Normalized levels of these coagulation markers may provide the supportive evidence of the effectiveness of BMT for curing thalassemia.
[Mh] Termos MeSH primário: Plaquetas/metabolismo
Transplante de Medula Óssea
Micropartículas Derivadas de Células/metabolismo
Eritrócitos/metabolismo
Fosfatidilserinas/sangue
Ativação Plaquetária
Talassemia beta
[Mh] Termos MeSH secundário: Adolescente
Aloenxertos
Anexina A5/sangue
Criança
Feminino
Seres Humanos
Masculino
Talassemia beta/sangue
Talassemia beta/terapia
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A5); 0 (Phosphatidylserines)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171129
[Lr] Data última revisão:
171129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-017-3070-2


  7 / 2137 MEDLINE  
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[PMID]:28471598
[Au] Autor:Aharon A; Brenner B
[Ad] Endereço:Microvesicles Research Laboratory, Department of Hematology and Bone Marrow Transplantation, Rambam Health Care Campus, Haifa, Israel.
[Ti] Título:Microvesicles in Thrombosis and Inflammation.
[So] Source:Isr Med Assoc J;18(9):530-533, 2016 Sep.
[Is] ISSN:1565-1088
[Cp] País de publicação:Israel
[La] Idioma:eng
[Mh] Termos MeSH primário: Micropartículas Derivadas de Células/metabolismo
Inflamação/patologia
Trombose/patologia
[Mh] Termos MeSH secundário: Vesículas Extracelulares/metabolismo
Feminino
Seres Humanos
Placenta/metabolismo
Gravidez
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


  8 / 2137 MEDLINE  
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[PMID]:28466387
[Au] Autor:Zhao Z; Zhou Y; Tian Y; Li M; Dong JF; Zhang J
[Ad] Endereço:Department of Neurosurgery, Tianjin Institute of Neurology, Tianjin Medical University General Hospital, Tianjin, 300052, China.
[Ti] Título:Cellular microparticles and pathophysiology of traumatic brain injury.
[So] Source:Protein Cell;8(11):801-810, 2017 Nov.
[Is] ISSN:1674-8018
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. The finding that cellular microparticles (MPs) generated by injured cells profoundly impact on pathological courses of TBI has paved the way for new diagnostic and therapeutic strategies. MPs are subcellular fragments or organelles that serve as carriers of lipids, adhesive receptors, cytokines, nucleic acids, and tissue-degrading enzymes that are unique to the parental cells. Their sub-micron sizes allow MPs to travel to areas that parental cells are unable to reach to exercise diverse biological functions. In this review, we summarize recent developments in identifying a casual role of MPs in the pathologies of TBI and suggest that MPs serve as a new class of therapeutic targets for the prevention and treatment of TBI and associated systemic complications.
[Mh] Termos MeSH primário: Astrócitos/metabolismo
Lesões Encefálicas Traumáticas/fisiopatologia
Micropartículas Derivadas de Células/metabolismo
Coagulação Intravascular Disseminada/fisiopatologia
Microglia/metabolismo
Neurônios/metabolismo
[Mh] Termos MeSH secundário: Animais
Astrócitos/patologia
Transporte Biológico
Fatores de Coagulação Sanguínea/genética
Fatores de Coagulação Sanguínea/metabolismo
Encéfalo/metabolismo
Encéfalo/patologia
Encéfalo/fisiopatologia
Lesões Encefálicas Traumáticas/genética
Lesões Encefálicas Traumáticas/metabolismo
Lesões Encefálicas Traumáticas/patologia
Micropartículas Derivadas de Células/química
Micropartículas Derivadas de Células/patologia
Citocinas/sangue
Citocinas/genética
Modelos Animais de Doenças
Coagulação Intravascular Disseminada/genética
Coagulação Intravascular Disseminada/metabolismo
Coagulação Intravascular Disseminada/patologia
Regulação da Expressão Gênica
Seres Humanos
Microglia/patologia
Neurônios/patologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Blood Coagulation Factors); 0 (Cytokines)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1007/s13238-017-0414-6


  9 / 2137 MEDLINE  
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[PMID]:28465231
[Au] Autor:Wang Y; Luo L; Mörgelin M; Thorlacius H
[Ad] Endereço:Department of Clinical Sciences, Malmö, Section for Surgery, Lund University, Sweden.
[Ti] Título:Rac1 regulates sepsis-induced formation of platelet-derived microparticles and thrombin generation.
[So] Source:Biochem Biophys Res Commun;487(4):887-891, 2017 06 10.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dysfunctional coagulation aggravates clinical outcome in patients with sepsis. The aim of this study was to define the role of Rac-1 in the formation of platelet-derived microparticles (PMPs) and thrombin generation (TG) in abdominal sepsis. Male C57BL/6 mice underwent cecal ligation and puncture (CLP). Scanning electron microscopy and flow cytometry were used to quantify PMPs. TG was determined by use of a fluorimetric assay. It was found that CLP increased Rac1 activity in platelets, which was abolished by administration of the Rac1 inhibitor NSC23766. Sepsis-induced TG in vivo was reflected by reduced capacity of plasma from septic animals to generate thrombin ex vivo. Administration of NSC23766 increased peak and total TG in plasma from CLP mice indicating that Rac-1 regulates sepsis-induced formation of thrombin. The number of circulating PMPs was markedly elevated in animals with abdominal sepsis. Treatment with NSC23766 significantly decreased formation of PMPs in septic mice. Platelet activation in vitro caused release of numerous MPs. Notably, NSC23766 abolished PMP formation in activated platelets in vitro. These findings suggest that Rac-1 regulates PMP formation and TG in sepsis and that inhibition of Rac1 activity could be a useful target to inhibit dysfunctional coagulation in abdominal sepsis.
[Mh] Termos MeSH primário: Plaquetas/citologia
Plaquetas/metabolismo
Micropartículas Derivadas de Células/metabolismo
Neuropeptídeos/metabolismo
Sepse/metabolismo
Trombina/biossíntese
Proteínas rac1 de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Animais
Masculino
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Neuropeptides); 0 (Rac1 protein, mouse); EC 3.4.21.5 (Thrombin); EC 3.6.5.2 (rac1 GTP-Binding Protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


  10 / 2137 MEDLINE  
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[PMID]:28409836
[Au] Autor:Wang Y; Zhang S; Luo L; Norström E; Braun OÖ; Mörgelin M; Thorlacius H
[Ad] Endereço:Department of Clinical Sciences, Section for Surgery, Lund University, Malmö, Sweden.
[Ti] Título:Platelet-derived microparticles regulates thrombin generation via phophatidylserine in abdominal sepsis.
[So] Source:J Cell Physiol;233(2):1051-1060, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sepsis is associated with dysfunctional coagulation. Recent data suggest that platelets play a role in sepsis by promoting neutrophil accumulation. Herein, we show that cecal ligation and puncture (CLP) triggered systemic inflammation, which is characterized by formation of IL-6 and CXC chemokines as well as neutrophil accumulation in the lung. Platelet depletion decreased neutrophil accumulation, IL-6, and CXC chemokines formation in septic lungs. Depletion of platelets increased peak thrombin formation and total thrombin generation (TG) in plasma from septic animals. CLP elevated circulating levels of platelet-derived microparticles (PMPs). In vitro generated PMPs were a potent inducer of TG. Interestingly, in vitro wild-type recombinant annexin V abolished PMP-induced thrombin formation whereas a mutant annexin V protein, which does not bind to phosphatidylserine (PS), had no effect. Administration of wild-type, but not mutant annexin V, significantly inhibited thrombin formation in septic animals. Moreover, CLP-induced formation of thrombin-antithrombin complexes were reduced in platelet-depleted mice and in animals pretreated with annexin V. PMP-induced TG attenuated in FXII- and FVII-deficient plasma. These findings suggest that sepsis-induced TG is dependent on platelets. Moreover, PMPs formed in sepsis are a potent inducer of TG via PS exposure, and activation of both the intrinsic and extrinsic pathway of coagulation. In conclusion, these observations suggest that PMPs and PS play an important role in dysfunctional coagulation in abdominal sepsis.
[Mh] Termos MeSH primário: Coagulação Sanguínea
Plaquetas/metabolismo
Micropartículas Derivadas de Células/metabolismo
Fosfatidilserinas/sangue
Sepse/sangue
Trombina/metabolismo
[Mh] Termos MeSH secundário: Animais
Anexina A5/sangue
Antitrombina III
Plaquetas/imunologia
Plaquetas/microbiologia
Plaquetas/ultraestrutura
Micropartículas Derivadas de Células/imunologia
Micropartículas Derivadas de Células/microbiologia
Micropartículas Derivadas de Células/ultraestrutura
Quimiocinas CXC/metabolismo
Modelos Animais de Doenças
Inflamação/sangue
Inflamação/imunologia
Inflamação/microbiologia
Interleucina-6/metabolismo
Pulmão/imunologia
Pulmão/metabolismo
Pulmão/microbiologia
Masculino
Camundongos Endogâmicos C57BL
Infiltração de Neutrófilos
Peptídeo Hidrolases/sangue
Sepse/imunologia
Sepse/microbiologia
Sepse/patologia
Transdução de Sinais
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A5); 0 (Chemokines, CXC); 0 (Interleukin-6); 0 (Phosphatidylserines); 0 (antithrombin III-protease complex); 0 (interleukin-6, mouse); 9000-94-6 (Antithrombin III); EC 3.4.- (Peptide Hydrolases); EC 3.4.21.5 (Thrombin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170415
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25959



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