BERNADETE DE LOURDES LIPHAUS

(Fonte: Lattes)
Índice h a partir de 2011
9
Lattes
ResearcherID
Projetos de Pesquisa
Unidades Organizacionais
Instituto da Criança, Hospital das Clínicas, Faculdade de Medicina - Médico
LIM/36 - Laboratório de Pediatria Clínica, Hospital das Clínicas, Faculdade de Medicina

Filtros

Limpar filtros

Configurações

Indexador: MEDLINE × Tipo de produção: conferenceObject × Tipo de acesso: restrictedAccess ×

Resultados de Busca

Agora exibindo 1 - 4 de 4
  • conferenceObject
    Altered Apoptosis Profile and Associated Soluble Factors In Patients With Juvenile-Onset Systemic Lupus Erythematosus
    (2013) LIPHAUS, Bernadete; KISS, Maria H. B.; CARRASCO, Solange; GOLDENSTEIN-SCHAINBERG, Claudia
  • conferenceObject
    Low Gene Copy Number for C4, C4A and C4B Is a Strong Risk Factor for Developing Systemic Lupus Erythematosus in Childhood
    (2012) ANDRADE, Luis Eduardo C.; PEREIRA, Kaline M. C.; FARIA, Atila G. A.; LIPHAUS, Bernadete; JESUS, Adriana A.; SILVA, Clovis; CARNEIRO-SAMPAIO, Magda
    Background/Purpose: C4 is an important component of the Complement system and plays an essential role in the activation cascade of the classical Complement pathway. Complete C4 deficiency is among the strongest genetic risk factors for systemic lupus erythematosus (SLE). There are two C4 circulating isoforms (C4A and C4B) encoded by C4A and C4B genes, respectively, that differ by only five nucleotides. C4A protein is involved in the clearance of immune complex and apoptotic debris while C4B protein is relevant in the opsonization of microbes. C4A and C4B genes are located at a gene cassette within the MHC class III region and depict gene copy-number variation (CNV). The number of C4A copies may be related to the susceptibility to SLE. This study aimed to investigate the impact of the C4A and C4B gene CNV on juvenile SLE. Methods: We evaluated 90 children and 170 adults with SLE (meeting SLE ACR criteria) sequentially retrieved from the rheumatology outpatient clinic. Two hundred healthy individuals (HI) without evidence of auto-immune diseases were retrieved among blood bank donors. Peripheral blood leukocyte DNA was amplified by quantitative real-time PCR (qPCR) with primers for C4 gene and sequence specific TaqMan® probes for C4A (5FAM-ACCCCTGTCCAGTGTTAG-MGB 3) and C4B (5FAM-ACCTCTCTCCAGTGATAC-MGB 3). Gene copy number (GCN) was determined by the delta-delta cycle threshold (DDCT) method. Results: Children with SLE had lower GCN of total C4 (mean total C4=3.1; 95% CI=2.8–3.4), C4A (mean C4A=1.7; 95% CI=1.5–1.9) and C4B (mean C4B=1.5; 95% CI=1.3–1.6) than HI (C4=4.3 with 95% CI=4.1–4.5, p<0.001; C4A =2.3 with 95% CI=2.2–2.5, p<0.001; C4B=2.0 with 95% CI=1.8–2.1; p<0.001). The frequency of SLE children with total C4 low GCN (<4 copies) was significantly higher than in HI (SLE=59% versus HI=28%; OR=3.68; 95% CI=2.19–6.20; p<0.001). The same was observed for C4A low GCN (2
  • conferenceObject
    SOLUBLE TAM (TYRO3, AXL, MER) RECEPTORS AND GAS6 LIGAND IN PATIENTS WITH JUVENILE SYSTEMIC LUPUS ERYTHEMATOSUS (JSLE)
    (2015) LIPHAUS, B. L.; PALMEIRA, P.; LIMA, L.; SILVA, C. A.; GOLDENSTEIN-SCHAINBERG, C.; CARNEIRO-SAMPAIO, M.
  • conferenceObject
    UP-REGULATED SOLUBLE BCL-2: A UNIQUE PROFILE OF PATIENTS WITH JUVENILE DERMATOMYOSITIS (JDM)
    (2015) LIPHAUS, B. L.; KISS, M. H. B.; SALLUM, A. E.; AIKAWA, N. E.; CARRASCO, S.; PALMEIRA, P.; LIMA, L.; SILVA, C. A.; GOLDENSTEIN-SCHAINBERG, C.; CARNEIRO-SAMPAIO, M.