Auswahl der wissenschaftlichen Literatur zum Thema „Activation polyclonal“
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Zeitschriftenartikel zum Thema "Activation polyclonal"
Goldman, Michel, Dana Baran und Philippe Druet. „Polyclonal activation and experimental nephropathies“. Kidney International 34, Nr. 2 (August 1988): 141–50. http://dx.doi.org/10.1038/ki.1988.159.
Der volle Inhalt der QuelleChequer-Bou-Habib, Dumith, Claudio Daniel-Ribeiro, Dalma M. Banic, Antonio C. Franciscone do Valle und Bernardo Galvao-Castro. „Polyclonal B cell activation in paracoccidioidomycosis“. Mycopathologia 108, Nr. 2 (November 1989): 89–93. http://dx.doi.org/10.1007/bf00436058.
Der volle Inhalt der QuelleDziarski, Roman. „Autoimmunity: polyclonal activation or antigen induction?“ Immunology Today 9, Nr. 11 (Januar 1988): 340–42. http://dx.doi.org/10.1016/0167-5699(88)91333-3.
Der volle Inhalt der QuelleTew, John, David Engel und Dennis Mangan. „Polyclonal B-cell activation in periodontitis*“. Journal of Periodontal Research 24, Nr. 4 (Juli 1989): 225–41. http://dx.doi.org/10.1111/j.1600-0765.1989.tb01787.x.
Der volle Inhalt der QuelleKaattari, Stephen L., und Mary A. Yui. „Polyclonal activation of salmonid B lymphocytes“. Developmental & Comparative Immunology 11, Nr. 1 (Dezember 1987): 155–65. http://dx.doi.org/10.1016/0145-305x(87)90017-6.
Der volle Inhalt der QuelleBarbieri, P., I. Olivieri, G. Benedettini, P. Marelli, M. L. Ciompi, G. Pasero und M. Campa. „Polyclonal B cell activation in ankylosing spondylitis.“ Annals of the Rheumatic Diseases 49, Nr. 6 (01.06.1990): 396–99. http://dx.doi.org/10.1136/ard.49.6.396.
Der volle Inhalt der QuelleGranholm, Norman A., und Tito Cavallo. „Autoimmunity, Polyclonal B-Cell Activation and Infection“. Lupus 1, Nr. 2 (Februar 1992): 63–74. http://dx.doi.org/10.1177/096120339200100203.
Der volle Inhalt der QuelleBurg, Debra L., und Thomas L. Feldbush. „Polyclonal activation of primed rat B cells“. Cellular Immunology 98, Nr. 2 (April 1986): 351–63. http://dx.doi.org/10.1016/0008-8749(86)90295-9.
Der volle Inhalt der QuelleNeveu, P. J., und D. Perdoux. „Polyclonal Activation of Guinea Pig Spleen Lymphocytes“. International Archives of Allergy and Immunology 78, Nr. 4 (1985): 401–5. http://dx.doi.org/10.1159/000233921.
Der volle Inhalt der QuelleDonati, Daria, Li Ping Zhang, Qijun Chen, Arnaud Chêne, Kirsten Flick, Maja Nyström, Mats Wahlgren und Maria Teresa Bejarano. „Identification of a Polyclonal B-Cell Activator in Plasmodium falciparum“. Infection and Immunity 72, Nr. 9 (September 2004): 5412–18. http://dx.doi.org/10.1128/iai.72.9.5412-5418.2004.
Der volle Inhalt der QuelleDissertationen zum Thema "Activation polyclonal"
Haidar, ahmad Hamad. „Pro-inflammatory activity and adjuvant effect of Neutrophil Extracellular Traps in physiological and pathological context“. Electronic Thesis or Diss., Paris 13, 2024. http://www.theses.fr/2024PA131004.
Der volle Inhalt der QuelleActivated neutrophils (PMNs) expel neutrophil extracellular traps (NETs). NETs serve as adefense mechanism against pathogens. However, the role of NETs extends beyond their antimicrobial function, with implications in various physiological and pathological processes, including autoimmune disorders. Increased NET formation has been reported in rheumatoid arthritis (RA); a chronic inflammatory disease affecting joints. We have previously shown that NETs are pro-inflammatory on resting macrophages. Indeed, NETs contain several molecules with immunostumulatory properties. We suggest that NETs act as damage-associated molecular patterns (DAMPs) on B lymphocytes inducing their polyclonal activation, independently of antigen specificity; a new mechanism by which NETs might contribute to immune dysregulation, particularly in the context of RA. We demonstrate by flow cytometry, ELISA and RNA sequencing (RNAseq) that NETs could directlyactivate total and naïve B cells toward a robust pro-inflammatory profile, characterized by high productionof pro-inflammatory cytokines and the upregulation of HLA-DR and the co-stimulatory molecules CD40and CD86 which are important for antigen presenting cell (APC) function. This activation is amplified in RA patients. We show also that this mechanism is modulated by the presence of C1q and LL-37 proteins, and didn't required the Toll-like receptor 9 (TLR9). Beyond B cell activation, our findings shed light on the domino effect initiated by NETs. NET-activated B cells subsequently act as APCs and trigger T cell activation, bolstering the adaptive immune response. NET-activated B cells also induce the recruitment andactivation of neutrophils. This potential crosstalk highlights the versatile nature of NETs beyond their conventional role in antimicrobial defense
Jellison, Evan Robert. „CD4 T Cell-Mediated Lysis and Polyclonal Activation of B Cells During Lymphocytic Choriomeningitis Virus Infection: A Dissertation“. eScholarship@UMMS, 2008. https://escholarship.umassmed.edu/gsbs_diss/349.
Der volle Inhalt der QuelleOuedraogo, David Eric. „Exploration du réservoir EBV chez les patients infectés par le VIH : implications pathologiques“. Thesis, Montpellier 1, 2013. http://www.theses.fr/2013MON1T001.
Der volle Inhalt der QuelleIt is assumed that circulating memory B cells including those latently infected by EBV return periodically to lymphoid nodes where they are stimulates and undergo differentiation into immunoglobulin-producing cells allowing the virus to initiate viral replication. However, the monitoring and the management of EBV reactivation and it association with lymphoid malignancies in HIV-infected patients are still being controversies and need a better understanding of the probable mechanisms involved. In this study, we proposed novel biological tools for EBV DNA quantification allowing discriminating latent and lytic reservoir. We showed that the EBV reservoir levels are closely associated with the polyclonal B-cell activation. We also observed an association between immune activation and EBV reactivation markers with the occurrence of B-cell lymphoma. Moreover, we described a long term evolution of monoclonal gammapathies in HIV-infected subjects and the persistence of the immunoglobulis monoclonal pike was found to be associated with higher EBV reservoir levels. Therefore, the B-cell activation and subsequently EBV reactivation likely play the main roles on the occurrence of B lymphocytes malignancies during HIV infection
Cangiani, Eloísa Elena. „Caracterização do padrão das citocinas e dos isótipos de imunoglobulinas produzidos na Yersiniose experimental murina /“. Araraquara : [s.n.], 2005. http://hdl.handle.net/11449/100122.
Der volle Inhalt der QuelleAbstract: Yersinia enterocolitica is an enteropathogen that can lead to the development of reactive arthritis. One of the immunomodulating mechanisms used by arthritogenic pathogens is the polyclonal activation of lymphocytes. The objective of this study was to verify if the polyclonal activation of B-lymphocytes occur and to compare the different immunoglobulin (Ig) isotypes produced during the infection with Y. enterocolitica O:8 in susceptible (BALB/c) and resistant (C57BL/6) mice strains. We also analyzed the production of pro-inflammatory and regulatory cytokines in T CD4+ and T CD8+ lymphocytes populations.
Orientador: Beatriz Maria Machado de Medeiros
Coorientador: Iracilda Zeppone Carlos
Banca: Maria Regina D'Império Lima
Banca: Phileno Pinge
Banca: Ângela Maria Victoriano de Campos Soares
Banca: Deise Pasetto Falcão
Doutor
Cangiani, Eloísa Elena [UNESP]. „Caracterização do padrão das citocinas e dos isótipos de imunoglobulinas produzidos na Yersiniose experimental murina“. Universidade Estadual Paulista (UNESP), 2005. http://hdl.handle.net/11449/100122.
Der volle Inhalt der QuelleCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Universidade Estadual Paulista (UNESP)
Yersinia enterocolitica é um enteropatógeno que pode levar ao desenvolvimento de artrite reativa. Um dos mecanismos imunomoduladores usados pelos patógenos artritogênicos é a ativação policlonal de linfócitos. O objetivo deste estudo foi verificar se ocorre ativação policlonal de linfócitos B e comparar o padrão isotípico de imunoglobulinas produzidas durante a infecção com Y. enterocolitica O:8 em linhagens de camundongos suscetíveis (BALB/c) e resistentes (C57BL/6), bem como analisar o padrão de secreção de citocinas pró-inflamatórias e regulatórias pelas populações de células T CD4+ e CD8+.
Yersinia enterocolitica is an enteropathogen that can lead to the development of reactive arthritis. One of the immunomodulating mechanisms used by arthritogenic pathogens is the polyclonal activation of lymphocytes. The objective of this study was to verify if the polyclonal activation of B-lymphocytes occur and to compare the different immunoglobulin (Ig) isotypes produced during the infection with Y. enterocolitica O:8 in susceptible (BALB/c) and resistant (C57BL/6) mice strains. We also analyzed the production of pro-inflammatory and regulatory cytokines in T CD4+ and T CD8+ lymphocytes populations.
Landgraf, Taise Natali. „Receptor de aerobactina férrica de Escherichia coli - IutA: um novo antígeno T-independente do tipo 1“. Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/17/17147/tde-30072012-174116/.
Der volle Inhalt der QuelleIndigenous bacteria may contain some virulence factors, such as siderophores iron chelator molecules and fimbriae, that allow these microorganisms to become pathogens in sites others than their normal habitat. Among the different indigenous bacterial species in the gut, Escherichia coli is one with potential to cause infections, mainly urinary tract infection (UTI). Certain strains of E. coli have a plasmid (pColV), which encode ferric aerobactin outer membrane receptor, IutA, often associated with UTI. Our group has recently described IutA as an inducer of B cell proliferation. Here, we identify the molecules and mechanisms that modulate the proliferation of B lymphocytes induced by recombinant IutA (rIutA) from E. coli. To determine whether the B cell proliferation induced by rIutA is dependent on other cell, we carried out assays with CFSE-labeled B cells cocultured separately with macrophages or dendritic cells stimulated with rIutA using transwell membranes or incubated with conditioned medium from these cells. The analysis of the results showed that rIutA indirectly induced the proliferation of B cells in a manner dependent on molecules released by accessory cells. When we analyzed the ability of rIutA in inducing proliferation of cells from mice deficient in adapter molecule MyD88, we found that this signaling molecule is crucial for signaling induced by rIutA in B cells, but not in accessory cells. A similar analysis with cells from mice deficient in Toll like receptor (TLR) 4, TLR2 or inteukin (IL-) 33 receptor revealed that these receptors were not required for rIutA signaling of any tested cells. Conversely, the pretreatment of the B cells with IL-1 receptor antagonist significantly decreased the proliferation of these cells in response to conditioned medium from cultures of IutAstimulated macrophages. Moreover, we determined that rIutA induced the expression of IL-1 in macrophages and dendritic cells stimulated with IutA. Altogether, our results suggest that IutA from E. coli induces polyclonal B-cell proliferation independently of T cells in a mechanism mediated by accessory cells such as macrophages and dendritic cells. Although the IutA-binding receptors from macrophages and dendritic cells have not been identified, we suggested that rIutA induces these cells to produce IL-1, which in turns acts on its receptor on B cells, triggering proliferation. These results open perspectives for studying IutA as a molecule that stimulates the mucosa-associated lymphoid tissue and as an immune-evasion molecule from pathogenic E. coli.
Silva, Joselli Santos. „Desestruturação da polpa branca do baço na leishmaniose visceral canina: células e citocinas envolvidas“. reponame:Repositório Institucional da FIOCRUZ, 2014. https://www.arca.fiocruz.br/handle/icict/7489.
Der volle Inhalt der QuelleMade available in DSpace on 2014-04-03T13:38:30Z (GMT). No. of bitstreams: 1 Joselli Silva. Desestruturação da polpa... 2014.pdf: 6952851 bytes, checksum: 512840eb0cc488e4f61742ce875c4837 (MD5) Previous issue date: 2014
Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Salvador, BA, Brasil / Universidade Federal da Bahia. Faculdade de Medicina da Bahia. Salvador, BA, Brasil
A leishmaniose visceral está associada às alterações arquiteturais esplênicas e redistribuição de populações celulares envolvidas na resposta imunológica. Os objetivos desta tese foram estudar a desestruturação da polpa branca do baço na leishmaniose visceral canina e quais as células e citocinas envolvidas nesse processo. Para isso, amostras de baços de cães de uma área endêmica para LV foram agrupadas em três categorias: TIPO1-CONT ou TIPO1-SIA (cães não infectados ou sem infecção ativa e com polpa branca organizada), TIPO1-INF (cães infectados com polpa branca organizada) e TIPO3-INF (cães infectados com polpa branca desorganizada). No capítulo 2 e 3, as secções de baço foram marcadas através de imunoistoquímica com anticorpos anti-CD3 (linfócitos T), anti-CD79-α (linfócitos B), anti-S100 (célula dendrítica folicular), anti-Ki-67 (células em proliferação), anti-IgG e anti-IgM (plasmócitos secretores de IgA, IgG e IgM). Foram estimadas as densidades de todas as populações celulares através de morfometria. As expressões de citocinas e quimiocinas foram avaliadas através de RT-PCR em tempo real. A ativação policlonal de células B e hipergamaglobulinemia foram avaliadas por ELISA e eletroforese de proteínas séricas. No capítulo 2, foi visto que a densidade de linfócitos B foi maior nos folículos e na zona marginal dos animais com baço TIPO1 do que nos dos animais com baço TIPO3 (teste de Mann-Whitney P < 0,02). Os números de células proliferantes, células B e células dendríticas foliculares foram menores em animais de baço TIPO3. A expressão da quimiocina CXCL13 foi maior nos animais com baço TIPO 1 (teste de Mann-Whitney, P < 0,02). No capítulo 3, foi visto que a plasmocitose foi maior em animais de baço TIPO3 do que nos animais com baço TIPO1 (Teste qui-quadrado, P < 0,04). A densidade de plasmócitos secretores de imunoglobulina do isotipo IgG foi maior na polpa vermelha de animais com baço TIPO3 (Teste Man-Whitney, P <0,05). Em geral, observou-se uma tendência de maior densidade de plasmócitos secretores de imunoglobulinas dos isotipos IgM e IgG nos animais de baço TIPO3 em comparação com animais do baço TIPO1. Animais de baço TIPO3 apresentam maiores níveis séricos de proteína gamaglobulina e também uma maior expressão das citocinas BAFF e APRIL e da quimiocina CXCL12, que estão envolvidas no processo de ativação e homing de plasmócitos. No capítulo 4 foi visto que uma região de aproximadamente 1.28Mb do cromossomo 8 canino foi encontrada com os segmentos gênicos VH, DH e JH. As principais conclusões obtidas nesse estudo foram que a redistribuição de populações celulares do baço, especialmente de linfócitos B, células dendríticas foliculares e plasmócitos estão relacionada com a desorganização do tecido esplênico e com a expressão anômala de CXCL13, CXCL12, BAFF e APRIL, que são citocinas e quimiocinas envolvida com a organização do tecido esplênico, ativação e homing de plasmócitos. A ativação policlonal, a hipergamaglobulinemia e a diglobulinemia são também relacionadas com a desorganização do baço. As regiões variáveis (VH), diversidade (DH) e de junção (JH) da cadeia pesada de imunoglobulina são compostos de noventa e dois, dez e nove genes obtidos na linha germinativa canina, respectivamente.
Visceral leishmaniasis is associated with splenic architectural changes and redistribution of cell populations involved in the immune response. The objectives of this thesis was to study the disruption of the white pulp of the spleen in canine visceral leishmaniasis and which cells and cytokines are involved in this process. For this, samples of spleens of dogs from an endemic area for VL were grouped into three categories: TYPE1-CONT or TYPE1-NIF (non-infected dogs or without active infection with organized white pulp), TYPE1-INF (infected dogs with pulp organized white) and TYPE3-INF (infected animals with disorganized white pulp). In Chapter 2 and 3 the spleens sections were stained by immunohistochemistry with anti-CD3 (T lymphocytes), anti-CD79 (B lymphocytes), anti-S100 (follicular dendritic cells), anti-Ki-67 (cells proliferation), anti-IgG and anti-IgM (plasma cells). The number and distribution of all cell populations were estimated by morphometry. The expressions of cytokines and chemokines were assessed by real time RT-PCR. The polyclonal B cell activation and hypergammaglobulinemia were evaluated by ELISA and serum protein electrophoresis. In chapter 2, it was seen that the density of B lymphocytes was higher in the marginal zone and follicles of animals with spleen TYPE1-INF than animals with the spleen TYPE3-INF (Mann -Whitney test P < 0.02). The numbers of proliferating cells, B cells and follicular dendritic cells was lower in animals of TYPE3-INF. The expression of the chemokine CXCL13 was higher in the spleen of animal with the spleen TYPE 1 (Mann-Whitney, P < 0.02). No difference was observed in the expression of other cytokines compared between the two groups of animals. In chapter 3, it was seen that the plasma cells was higher in animals with spleen TYPE 3 than in animals with spleen TYPE1 (Chi-square test, P < 0.04). The density of plasma cells secreting the isotype IgG was higher in the red pulp of spleen of animals TYPE3 (Man-Whitney test, P < 0.05). In general, there was a trend toward higher density of plasma cells secreting the immunoglobulin of isotype IgM and IgG in the spleen of animals with spleen TYPE3-INF in comparison to animal’s spleen TYPE1. Animals with spleen TYPE3 have higher levels of serum gamma globulin protein as well as increased expression of citokines, BAFF and APRIL and the chemokine CXCL12 that are involved in the activation and homing plasma cells. The main conclusions of this study were that the redistribution of cell populations of the spleen, especially B lymphocytes, follicular dendritic cells and plasma cells (characterized by intense plasmacytosis) are related to the disorganization of the splenic tissue and aberrant expression of CXCL13, CXCL12, BAFF and APRIL, which are cytokines and chemokines involved in the organization of the splenic tissue, activation of B cells and plasma cell homing. The polyclonal activation, hypergammaglobulinemia and diglobulinemia are also related to the structural disorganization of the splenic lymphoid tissue. In addition, it was concluded that the variable regions (VH), the diversity (DH) and junction (JH) immunoglobulin heavy chain are composed of ninety-two, ten and nine genes that have been obtained in canine germline.
Chamond, Nathalie. „Quand un mitogène est une enzyme. .“ Paris 6, 2003. http://www.theses.fr/2003PA066048.
Der volle Inhalt der QuelleLeclercq, Lise. „Analyse du mode d'action du lymphocyte T "helper" : son rôle dans les phases précoces de l'activation de la cellule B et sa contribution à la régulation isotypique“. Paris 7, 1985. http://www.theses.fr/1985PA077058.
Der volle Inhalt der QuelleBücher zum Thema "Activation polyclonal"
Carlino, Joseph A. Pregnancy-associated growth factor (PAGF): A T-dependent polyclonal activator of human lymphocytes. 1986.
Den vollen Inhalt der Quelle findenBuchteile zum Thema "Activation polyclonal"
Azim, T., J. Golay, K. Lam und D. H. Crawford. „Polyclonal Activation of B Lymphocytes after EB Virus Infection“. In Epstein-Barr Virus and Human Disease, 331–32. Totowa, NJ: Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4590-2_72.
Der volle Inhalt der QuelleSultzer, Barnet M. „Polyclonal Lymphocyte Activation by M. tuberculosis and Its Products“. In Infectious Agents and Pathogenesis, 277–304. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5418-5_13.
Der volle Inhalt der QuelleTzioufas, A. G., N. Talal und H. M. Moutsopoulos. „Sjögren’s Syndrome: From Polyclonal B Cell Activation to Monoclonal B Cell Proliferation“. In Immunology of the Connective Tissue Diseases, 335–53. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1432-5_16.
Der volle Inhalt der QuelleGreco, Raffaella, und Dominique Farge. „CART Cells and Other Cell Therapies (ie MSC, Tregs) in Autoimmune Diseases“. In The EBMT Handbook, 837–48. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-44080-9_93.
Der volle Inhalt der QuelleKlinman, Dennis M., Akira Shirai und Yoshiaki Ishigatsubo. „Polyclonal B Cell Activation and B Cell Cross-Reactivity During Autoantibody Production in Systemic Lupus Erythematosus“. In Advances in Experimental Medicine and Biology, 115–23. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2427-4_12.
Der volle Inhalt der QuelleMayer, Lloyd. „Factors Generated by Human T-Cell Hybridomas Regulate B-Cell Activation, Polyclonal Differentiation, and Isotype Expression“. In Human Hybridomas and Monoclonal Antibodies, 401–18. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4949-5_24.
Der volle Inhalt der QuelleKarulin, Alexey Y., Melinda Katona, Zoltán Megyesi, Greg A. Kirchenbaum und Paul V. Lehmann. „Artificial Intelligence-Based Counting Algorithm Enables Accurate and Detailed Analysis of the Broad Spectrum of Spot Morphologies Observed in Antigen-Specific B-Cell ELISPOT and FluoroSpot Assays“. In Methods in Molecular Biology, 59–85. New York, NY: Springer US, 2024. http://dx.doi.org/10.1007/978-1-0716-3690-9_5.
Der volle Inhalt der QuellePlagemann, Peter G. W., Quentin A. Jones und William A. Cafruny. „Polyclonal Activation of B Cells by Lactate Dehydrogenase-Elevating Virus is Mediated by N-Glycans on the Short Ectodomain of the Primary Envelope Glycoprotein“. In Advances in Experimental Medicine and Biology, 375–84. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1325-4_56.
Der volle Inhalt der QuelleBeris, Photis, und Francis A. Waldvogel. „Hematologic Alterations in Infectious Disease Patients“. In Clinical Infectious Diseases, 121–32. Oxford University PressNew York, NY, 1998. http://dx.doi.org/10.1093/oso/9780195081039.003.0013.
Der volle Inhalt der QuelleSilman, Alan J., und Marc C. Hochberg. „Systemic lupus erythematosus*“. In Epidemiology of the Rheumatic Diseases, 163–91. Oxford University PressNew York, NY, 1993. http://dx.doi.org/10.1093/oso/9780192623560.003.0007.
Der volle Inhalt der QuelleKonferenzberichte zum Thema "Activation polyclonal"
Kazama, M., H. Ishii, J. Tsubouchi, M. Nakano, N. Hiramoto, T. Abe und P. W. Majerus. „PREPARATION OF ANTI-HUMAN THROMBOMODULIN ANTIBODIES AND THEIR APPLICATION FOR STUDY ON PLASMA THROMBOMODULIN“. In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643962.
Der volle Inhalt der QuelleRickles, F. R., W. W. Hancock, K. Kobzik, N. Hogg und C. O’Hara. „THE DISTRIBUTION OF CROSS-LINKED FIBRIN IN HUMAN LUNG CARCINOMA PARALLELS THAT OF ACTIVATED HOST MONONUCLEAR LEUKOCYTES: IMMUNO-HISTOLOGIC STUDIES WITH MONOCLONAL ANTIBODIES“. In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643669.
Der volle Inhalt der QuelleGordon, Stuart, Bonnie Sloane, Phil Cavanugh, Barbara Cross, Kenneth Honn und Mohanathasan Chelladurai. „PURIFICATION AND CHARACTERIZATION OF TWO PROCOAGULANTS FROM WALKER 256 CARCINOSARCOMA TUMORS“,. In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643666.
Der volle Inhalt der QuelleVeloso, D., M. Shapira, F. Kueppers und R. W. Colman. „MONOCLONAL ANTIBODY 13G11 RECOGNIZES PREKALLIKREIN, KALLIKREIN AND COMPLEXES OF KALLIKREIN WITH,C1-INHIBITOR AND. α2-MACR0GL0BULIN“. In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642901.
Der volle Inhalt der QuelleOft, Martin, Aung Naing, Jeffrey R. Infante, Kyriakos P. Papadopoulos, Ivan H. Chan, Cong Shen, Navneet P. Ratti et al. „Abstract A016: PEGylated IL-10 (pegilodecakin) induces systemic immune activation, CD8+ T-cell invigoration and polyclonal T-cell expansion in cancer patients“. In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-a016.
Der volle Inhalt der QuellePiotrowicz, Randolph S., Kenneth M. Yamada und Kunicki J. Kunicki. „HUMAN PLATELET GLYCOPROTEIN Ic-IIa IS AN ACTIVATION-INDEPENDENT FIBRONECTIN RECEPTOR“. In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643911.
Der volle Inhalt der QuelleLindon, J. N., L. Kushner, E. Shiba und E. W. Salzman. „PLATELET ADHESION ON SYNTHETIC SURFACES PRETREATED WITH DILUTED PLASMA IS DETERMINED BY THE SURFACE CONCENTRATION OF "NATIVE" FIBRINOGEN“. In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643551.
Der volle Inhalt der QuelleBartsch, P., A. Haeberli und P. W. Straub. „NORMAL FIBRINOPEPTTDE A (FPA) AND ELEVATED FIBRINOGEN DEGRADATION PRODUCTS AFTER LONG DISTANCE RUNNING“. In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643132.
Der volle Inhalt der QuelleGralnick, H. R., L. M. Magurder, K. Hansmann, M. Vail, G. Marti, R. McEver und S. Williams. „THE SURFACE EXPRESSION OF ALPHA GRANULE PROTEINS FOLLOWING THROMBIN STIMULATION“. In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643859.
Der volle Inhalt der QuellePalabrica, Theresa M., Barbara C. Furie, Marvin A. Konatam, Barbara Brockway, Mart Aronovitz und Bruce Furie. „IMAGING OF THROMBI USING ANTI-PADGEM ANTIBODIES SPECIFIC FOR ACTIVATED PLATELETS“. In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643955.
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