Browsing by Author "Leite, Luís"
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- Antonímia e organização lexical em rede no 1.º CEB: proposta didática com recurso a narrativas bimodais e à realidade aumentadaPublication . Baptista, Adriana; Morgado, Celda; Costa, José António; Azevedo, João; Querido, Joana; Oliveira, Inês; Leite, Luís; Ribeiro, IolandaNeste artigo, apresentamosuma proposta didática para o ensino das relações semânticas múltiplas entre palavras, para o 1.º CEB, com o auxílio da Realidade Aumentada.Propõe-se que a aprendizagem das relações semânticas entre palavras não se fundamente em relações antonímicas binárias, sob pena de se instalar nas crianças o pensamento dicotómico. Através de trêsnarrativas bimodais, são questionadas as possibilidades de organização lexical,colocando pares de palavras aparentemente dicotómicos em contextos textuais diversos, que criam relações de gradação ou sinonímia, comprometendo a inevitabilidade de organização/interpretação antonímica binária, assim como as negativasconsequências do seu ensino a crianças em idades precoces.
- IL-10 overexpression predisposes to invasive aspergillosis by suppressing antifungal immunityPublication . Cunha, Cristina; Gonçalves, Samuel M.; Duarte-Oliveira, Cláudio; Leite, Luís; Lagrou, Katrien; Marques, António; Lupiañez, Carmen B.; Mesquita, Inês; Gaifem, Joana; Barbosa, Ana Margarida; Pinho Vaz, Carlos; Branca, Rosa; Campilho, Fernando; Freitas, Fátima; Ligeiro, Dário; Lass-Flörl, Cornelia; Löffler, Jürgen; Jurado, Manuel; Saraiva, Margarida; Kurzai, Oliver; Rodrigues, Fernando; Castro, António G.; Silvestre, Ricardo; Sainz, Juan; Maertens, Johan A.; Torrado, Egídio; Jacobsen, Ilse D.; Lacerda, João; Campos, Jr, António; Carvalho, AgostinhoProinflammatory immune responses are critically required for antimicrobial host defenses; however, excessive inflammation has the potential to damage host tissues thereby paradoxically contributing to the progression of infection. A central negative regulator of inflammatory responses is IL-10, an immunosuppressive cytokine with a wide variety of functions across multiple cell types. Although the role of IL-10 during infection appears to vary for different microorganisms, a largely detrimental role has been attributed to this cytokine during fungal disease. Given the variable risk of infection and its outcome among patients with comparable predisposing factors, susceptibility to invasive aspergillosis (IA) is thought to rely largely on genetic predisposition. The initial investigation of genetic variability at the IL10 locus led to the identification of single nucleotide polymorphisms (SNPs) influencing its transcriptional activity; thus, IL-10 may be a reasonable candidate for the genetic regulation of susceptibility to IA in high-risk patients.
- PTX3 polymorphisms influence cytomegalovirus reactivation after stem-cell transplantationPublication . Campos, Cláudia F.; Leite, Luís; Pereira, Paulo; Vaz, Carlos Pinho; Branca, Rosa; Campilho, Fernando; Freitas, Fátima; Ligeiro, Dário; Marques, António; Torrado, Egídio; Silvestre, Ricardo; Lacerda, João; Campos Jr., António; Cunha, Cristina; Carvalho, AgostinhoBackground: Reactivation of latent human cytomegalovirus (CMV) in patients undergoing allogeneic stem-cell transplantation (HSCT) predisposes to several clinical complications and is therefore a major cause of morbidity and mortality. Although pentraxin-3 (PTX3) has been previously described to bind both human and murine CMV and mediate several host antiviral mechanisms, whether genetic variation in the PTX3 locus influences the risk of CMV infection is currently unknown. Methods: To dissect the contribution of genetic variation within PTX3 to the development of CMV infection, we analyzed described loss-of-function variants at the PTX3 locus in 394 recipients of HSCT and their corresponding donors and assessed the associated risk of CMV reactivation. Results: We report that the donor, but not recipient, h2/h2 haplotype in PTX3 increased the risk of CMV reactivation after 24 months following transplantation, with a significant effect on survival. Among recipients with h2/h2 donors, CMV seropositive patients as well as those receiving grafts from unrelated donors, regardless of the CMV serostatus, were more prone to develop viral reactivation after transplantation. Most importantly, the h2/h2 haplotype was demonstrated to display an influence toward risk of CMV reactivation comparable to that conferred by the unrelated status of the donor alone. Conclusions: Our findings demonstrate the important contribution of genetic variation in donor PTX3 to the risk of CMV reactivation in patients undergoing HSCT, highlighting a promising prognostic value of donor PTX3 to predict risk of CMV reactivation in this clinical setting.
