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Literatura académica sobre el tema "Anticorps Hu"
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Artículos de revistas sobre el tema "Anticorps Hu"
Guilloton, L., A. Drouet, F. Pasquet, C. Camarasa, A. Didelot, O. Bruneau y D. Felten. "Pandysautonomie paranéoplasique avec anticorps anti Hu". Revue Neurologique 168 (abril de 2012): A153. http://dx.doi.org/10.1016/j.neurol.2012.01.392.
Texto completoLeroy, T., H. Porte, C. Rousselot, S. Taieb, O. Outteryck y É. Dansin. "Syndrome des anticorps anti-Hu : difficultés diagnostiques et thérapeutiques". Revue des Maladies Respiratoires 30, n.º 7 (septiembre de 2013): 563–66. http://dx.doi.org/10.1016/j.rmr.2013.03.004.
Texto completoPrim, N., B. Mennecier, C. Behr, P. Fraisse, A. Echaniz-Laguna, C. Tranchant y É. Quoix. "Cancer bronchique à petites cellules et syndrome des anticorps anti-Hu". Revue des Maladies Respiratoires 27, n.º 3 (marzo de 2010): 261–65. http://dx.doi.org/10.1016/j.rmr.2010.02.006.
Texto completoLevenes, H., É. Monlun, Ch Berton, F. Sellal, D. Di Vincenzo y A. Jaeger. "Anticorps anti-Hu révélateurs d'un cancer pulmonaire anaplasique à petites cellules". La Revue de Médecine Interne 13, n.º 7 (diciembre de 1992): S520. http://dx.doi.org/10.1016/s0248-8663(05)81099-9.
Texto completoPujol, J. L., J. P. Di Mercurio y B. Carlander. "Anticorps anti-Hu : un phénotype immunologique singulier pour des syndromes paranéoplasiques multiples". Revue des Maladies Respiratoires 30, n.º 7 (septiembre de 2013): 521–23. http://dx.doi.org/10.1016/j.rmr.2013.05.006.
Texto completoGuilloton, L., D. Rabar, J. Honnorat, A. Drouet, M. Pavic y D. Felten. "Pandysautonomie paranéoplasique avec anticorps anti-Hu : révélation d’un adénocarcinome bronchique par le PET scan". Revue Neurologique 160, n.º 4 (abril de 2004): 465–67. http://dx.doi.org/10.1016/s0035-3787(04)70932-7.
Texto completoMontaut, S., M. Mallaret, O. Lagha-Boukbiza, A. Echaniz-Laguna, N. Entz Werlé, M. Anheim y C. Tranchant. "Une encéphalopathie avec anticorps anti-HU associée à un ganglioneuroblastome chez une jeune adulte". Revue Neurologique 170 (abril de 2014): A69. http://dx.doi.org/10.1016/j.neurol.2014.01.199.
Texto completoMirouse, A., D. Gobert, J. M. Chamouard, L. Iordache, A. Mekinian y O. Fain. "Mort subite au cours d’une dégénérescence cérébelleuse subaiguë paranéoplasique avec dysautonomie associée aux anticorps anti-Hu révélant un cancer bronchique à petites cellules". La Revue de Médecine Interne 35, n.º 11 (noviembre de 2014): 757–59. http://dx.doi.org/10.1016/j.revmed.2013.12.007.
Texto completoGonçalves Fukuda, Thiago. "Múltiplos anticorpos paraneoplásicos (Anti-Sox, Anti-HU e Antianfifisina) detectados em um paciente com encefalite límbica e câncer de pulmão". Revista Científica Hospital Santa Izabel 2, n.º 4 (14 de mayo de 2020): 43–45. http://dx.doi.org/10.35753/rchsi.v2i4.122.
Texto completoGarcia, Marcina, Domingos Da Silva Leite, Tomomasa Yano, Antonio Fernando Pestana de Castro y Maria Aparecida Moreira Shenk. "Avaliação de uma vacina oleosa contra a colibacilose bovina utilizando os antígenos K99-F41 semipurificados". Brazilian Journal of Veterinary Research and Animal Science 31, n.º 3-4 (3 de diciembre de 1994): 225. http://dx.doi.org/10.11606/issn.1678-4456.bjvras.1994.52070.
Texto completoTesis sobre el tema "Anticorps Hu"
Villagrán-García, Macarena. "Clinical-immunological characterization and immune tolerance breakdown in paraneoplastic neurological syndromes associated with Hu antibodies". Electronic Thesis or Diss., Lyon 1, 2024. http://www.theses.fr/2024LYO10259.
Texto completoHu antibodies, the most common in paraneoplastic neurological syndromes (PNS), strongly indicate small-cell lung cancer (SCLC). The clinical spectrum of Hu-PNS is diverse, most patients develop multifocal central, peripheral, and/or autonomic nervous system dysfunction. Despite extensive research, questions remain, namely regarding the immunological basis of clinical heterogeneity and why only a minority of SCLC patients develop Hu-PNS. Our PhD project aims to phenotype Hu-PNS patients, explore the immunogenetics and humoral responses underlying neurological phenotypes, and the genomic and transcriptomic features of their SCLC. First, we described 466 Hu-PNS patients. Hierarchical clustering identified three groups: patients with central nervous system (CNS) involvement; isolated neuropathy; and mixed CNS/peripheral phenotypes. Overall survival was similar across groups, primarily determined by cancer, but dysautonomia, present in 26% of patients, significantly influenced neurological mortality. Prominent CNS dysfunction led to fatal cardiovascular dysautonomia or central hypoventilation, while peripheral involvement was associated with gastrointestinal or secretomotor alterations, without increased mortality risk. We also characterized patients who developed neurological syndromes with Hu antibodies after immune checkpoint inhibitor (ICI) treatment. These patients were clinically indistinguishable from spontaneous cases and shared a strong association with SCLC, suggesting ICIs may induce Hu-PNS. Second, we immunologically investigated neurological phenotypes using two approaches. HLA genotyping of 100 patients confirmed an association with the DR3~DQ2 haplotype, particularly in patients with sensory neuropathy, and absent in those with only CNS involvement. Phage immunoprecipitation sequencing was used to evaluate Hu antibody epitope reactivity and other autoantibodies in serum and/or CSF of 210 patients. We found no direct clinical association with the Hu dominant epitope, but epitope reactivity differed between serum and CSF in 75% of patients with paired samples. This variation correlated with sample timing and phenotype: CSF from patients with differing serum/CSF epitopes was collected later after PNS onset, while patients with serum/CSF consistent epitope reactivity always had CNS phenotypes. In addition, we identified reactivities to other proteins, some more specific to serum or CSF, and a subset linked to specific phenotypes. Third, we examined SCLC molecular features of Hu-, GABAbR-PNS and control patients. Next-generation sequencing, copy number variation analysis, and bulk-RNA sequencing revealed no mutations, gains, deletions, or overexpression in the Hu gene family of Hu-PNS SCLC. However, a distinct transcriptomic profile with upregulated genes largely related to immune system processes characterized these tumors. We also identified specific genes upregulated in the SCLC of patients with sensory neuropathy, some of which were linked to axonogenesis and neuropathy development. Our findings suggest multiple factors contribute to Hu-PNS clinical variability, particularly a broad range of additional autoantigens. These may be partly driven by gene expression patterns in SCLC, as some upregulated genes in patients with sensory neuropathy were linked to axonogenesis. Genetic predisposition may also favor specific phenotypes, as the DR3~DQ2 haplotype was associated with sensory neuropathy. Compartmentalization within the nervous system could further contribute, as most patients targeted different Hu epitopes in serum and CSF, and some autoantigens were more specific to CSF. Finally, Hu genes alterations in SCLC are unlikely causes of neoantigenicity, while a distinct immune-related gene profile and ICIs could contribute to immune tolerance breakdown. This work advances understanding of Hu-PNS complexity and paves the way for further studies into the immunological and molecular drivers of paraneoplastic immunity