Browsing by Author "Silva, R. F. M."
Now showing 1 - 8 of 8
Results Per Page
Sort Options
- Biological risks for neurological abnormalities associated with hyperbilirubinemiaPublication . Brites, D.; Fernandes, A.; Falcao, A. S.; Gordo, A. C.; Silva, R. F. M.; Brito, M. A.Unconjugated bilirubin (UCB) injury to glial cells leads to the secretion of glutamate and elicits a typical inflammatory response. Release of pro-inflammatory cytokines may influence gliogenesis and neurogenesis, and lead to deficits in learning and memo. - Fundacao para a Ciencia e a Tecnologia (FCT), Lisbon, Portugal. - The authors are grateful to the Fundacao para a Ciencia e a Tecnologia (FCT), Lisbon, Portugal, for their support.
- Exploring Multidrug resistance-associated Protein 1 (MRP1) expression during Neural Stem Cell Proliferation and Diferentiation, Nerve Cell Maturation and Neuro-Glia InteractionsPublication . Falcao, A.; Torrado, E.; Fernandes, A.; Abranches, E.; Bekman, E.; Brito, A.; Silva, R. F. M.; Henrique, D.; Brites, D.
- Implications of nitrosative stress in apoptotic cascades mediated by pro-inflammatory cytokines in immature neuronsPublication . Vaz, A. R.; Leitão Silva, S.; Barateiro, A.; Fernandes, A.; Falcão, A. S.; Silva, R. F. M.; Brito, M. A.; Brites, D.The inflammatory response is essential for survival in response to tissue injury or infection, but it can also cause neuronal damage [1]. In fact, pro-inflammatory cytokines, as well as nitric oxide (NO), are known as mediators of neuronal apoptosis [2,3]. Although apoptosis occurs physiologically in the brain during the period of the growth spurt, an increase in the number of neurons undergoing apoptosis may produce neuropathological sequelae [4]. Therefore, the aim of the present study was to: (i) deepen characterize the mechanisms of neuronal apoptosis upon cytokine exposure in neuronal immature cells; and (ii) investigate the role of NO as a determinant.
- Inhibition of nitric oxide production prevents apoptotic features mediated by inflammation in immature neuronsPublication . Vaz, A. R.; Silva, S. Leitao; Barateiro, A.; Fernandes, A.; Falcao, A. S.; Silva, R. F. M.; Brito, M. A.; Brites, D.
- Microglia acquires a phagocytic or pro-inflammatory phenotype when bilirubin gets into the brainPublication . Leitão Silva, S.; Osório, C.; Vaz, A. R.; Barateiro, A.; Falcão, A. S.; Brito, M. A.; Fernandes, A.; Silva, R. F. M.; Brites, D.
- Nitric Oxide mediates Inflammation-Induced Apoptotic Features and Neuronal Dysfunction at an early stage of NeurodevelopmentPublication . Vaz, A. R.; Silva, Leitao S.; Barateiro, A.; Falcao, A. S.; Fernandes, A.; Silva, R. F. M.; Brito, M. A.; Brites, D.
- PREVENTIVE EFFECTS OF BILE ACIDS ON BILIRUBIN-INDUCED APOPTOSIS OF HUMAN BRAIN MICROVASCULAR ENDOTHELIAL CELLSPublication . Correia, M.; Cardoso, F. L.; Sousa, D.; Pamela, I.; Vaz, A. R.; Silva, S. L.; Falcao, A. S.; Fernandes, A.; Silva, R. F. M.; Kim, K. S.; Brites, D.; Brito, M. A.
- Role of multidrug resistance-associated protein 1 expression in the in vitro susceptibility of rat nerve cell to unconjugated bilirubinPublication . Falcao, A. S.; Bellarosa, C.; Fernandes, A.; Brito, M. A.; Silva, R. F. M.; Tiribelli, C.; Brites, D.Nerve cell injury by unconjugated bilirubin (ILICB) has been implicated in brain damage during neonatal hyperbilirubinemia, particularly in the preterm newborn. Recently, it was shown that UCB is a substrate for the multidrug resistance-associated protein