Zobrazeno 1 - 4
of 4
pro vyhledávání: '"Nelson, J L"'
Autor:
Nelson J. L Aragão, Mauro R. Elkhoury, Henrique J Santos, Wellington da Silva Mendes, Pedro Fernando da Costa Vasconcelos, Elizabeth Salbé Travassos da Rosa, Lourdes Raposo
Publikováno v:
Repositório Digital do Instituto Evandro Chagas (Patuá)
Instituto Evandro Chagas (IEC)
instacron:IEC
Instituto Evandro Chagas (IEC)
instacron:IEC
Universidade Federal do Maranh?o. N?cleo de Patologia Tropical e Medicina Social. S?o Lu?s, MA, Brasil. Secretaria Municipal de Sa?de. Anajatuba, MA, Brasil. Ger?ncia de Qualidade de Vida. Subger?ncia de Vigil?ncia Epidemiol?gica. S?o Lu?s, MA, Brasi
Autor:
Maria de L. Raposo, Cláudio Sérgio Pannuti, Akemi Suzuky, Nelson J. L Aragão, Luíza Teresinha de Sousa, Ivani B. Ferreira, Wellington da Silva Mendes, Luís F.C. Aragão, Mauro R. Elkhoury, Antônio Augusto Moura da Silva
Publikováno v:
Emerging Infectious Diseases
Emerging Infectious Diseases, Vol 10, Iss 8, Pp 1496-1498 (2004)
Emerging Infectious Diseases, Vol 10, Iss 8, Pp 1496-1498 (2004)
In 2000, the first outbreak of hantavirus pulmonary syndrome was recognized in the Brazilian Amazon (Maranhão State). An epidemiologic study identified a 13.3% prevalence of hantavirus-specific immunoglobulin G. The analysis of risk factors suggests
Autor:
Dennis A. Carson, Alex J. MacGregor, E. C. Keystone, W. E. R. Ollier, Charles C. Berry, J. L. Nelson, Salvatore Albani, J. F. Scavulli, A. La Cava, J. C. Thorne
Publikováno v:
The Journal of clinical investigation. 100(3)
Rheumatoid arthritis (RA) is an autoimmune disease associated with HLA- DRbeta1 alleles which contain the QKRAA amino acid sequence in their third hypervariable region(s). The QKRAA sequence is also expressed by several human pathogens. We have shown
Autor:
J. L. Nelson, D. A. Weber, E. C. Keystone, W. E R Ollier, Dennis A. Carson, Alberto Martini, A. C. Montemayor, Carlomaurizio Montecucco, A. La Cava, Salvatore Albani
Publikováno v:
Nature medicine. 1(5)
A novel ‘multistep molecular mimicry’ mechanism for induction of rheumatoid arthritis (RA) by bacterial antigens that activate T lymphocytes previously ‘educated’ by peptides derived from a class of human histocompatibility antigens is report