Navegando por Assunto "Fisiopatologia"

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Acesso aberto (Open Access)
Polimorfismos gênicos do tipo indel: o papel da vulnerabilidade genética no desenvolvimento da neuroinflamação e na fisiopatologia do Transtorno Depressivo Maior
(Universidade Federal do Pará, 2017-07-26) REIS, Deyvson Diego de Lima; BURBANO, Rommel Mario Rodriguéz; http://lattes.cnpq.br/4362051219348099; YAMADA, Elizabeth Sumi; http://lattes.cnpq.br/7240314827308306
The pathophysiology of depression still remains not fully understood. And despite the contributions of the monoaminergic hypothesis to the understanding of neurobiological aspects of this disorder, studies have been carried out to investigate the role of neuroinflammation, polymorphisms in genes that influence inflammatory activity and monoaminergic receptor functions in the development of major depressive disorder (MDD). However, few studies have analyzed the role of upstream inflammatory pathways (such as the role of NFKB1 and PAR1 genes, which are capable of influencing transcription of proinflammatory cytokines) and of the alpha 2 adrenergic receptor encoding gene's polymorphism (ADRA2B gene) in individuals diagnosed with depression. Therefore, the objective of this study was to analyze the role of the INDEL type polymorphisms of NFKB1 (rs28362491), PAR1 (rs11267092) e ADRA2B (rs34667759) genes in the development of major depressive disorder. Twelve patients diagnosed with MDD and 145 healthy controls had blood samples collected and the INDEL polymorphisms of these 3 genes were genotyped by a single multiplex reaction. The multiplex PCR products were separated by capillary electrophoresis and the data analyzed in GeneMapper 3.7 software (Applied Biosystems). This research found a statistically significant association between depression and Del/Del genotype of the ADRA2B gene (p = 0.002): these individuals presented a 6.41 times greater chance of developing depression when compared to Del/Ins and Ins/Ins genotypes. There was no statistical significance between the INDEL polymorphisms of NFKB1 and PAR1 genes and depressive phenotype. Our results suggest that the INDEL marker of the ADRA2B gene (rs34667759), specifically the deletion allele, is a possible genetic biomarker of vulnerability for the development of MDD.
Acesso aberto (Open Access)
Ruptura do tendão calcâneo induz alterações bioquímicas e histológicas na medula espinhal de camundongos
(Universidade Federal do Pará, 2019-07-08) FRANÇA, Martha de Souza; SILVA, Anderson Manoel Herculano Oliveira da; http://lattes.cnpq.br/8407177208423247
The pathophysiology of the tendons involves release of neuronal mediators that play an active role in regulating tendon pain, inflammation and homeostasis. New directions have pointed out that injury is not restricted to tissue structural changes but indicates a possible involvement of the CNS in the regulation of the lesion. In this way, it is still unknown if the tendon injury affects the CNS, so the present study aims to investigate possible histological and biochemical changes in the spinal cord (L5) caused by the total rupture of the Achilles tendon in murine model. For this, the animals were submitted to tenotomy of the Achilles tendon, and separated in three groups (n = 36): Control; Rupture and Rupture+Suture. The total number cells of the spinal cord gray matter in the L5 vertebral segment was assessed by DAPI labeling. Glial reactivity was assessed by immunohistochemistry for microglia (IBA-1) and astrocytes (GFAP) at 7, 14 and 21 days after tendon rupture. The participation of the nitrergic system was investigated by the quantification of tissue levels of nitrite in lumbar intumescence at 7, 14 and 21 days post-injury and by iNOS (NOS2) immunostaining in L5. Statistical analyzes were performed using the ANOVA-1way test and post-test tukey, considering a significant p <0.05. The results were expressed as mean ± SD. The analysis of the number of cells showed that the Rupture group had a lower number of cells in 7 (1408.33 ± 58.59, p <0.05), 14 (1402.7 ± 72.7, p <0.05) and 21 (1374.5 ± 74.2, p <0.01) days post-injury in relation to the Control group (1668 ± 52.3) and in relation to the Rupture + Suture group on days 7 (1655 ± 66.5 , p <0.05) and 21 (1668.3 ± 14.1, p <0.01). The Suture group did not differ from the Control group. The results of glial reactivity showed that at 14 days after injury the microglia were activated at L5 and that astrocytes were activated at 7, 14 and 21 days after injury. The nitrite quantification showed higher levels of nitrite in the group Rupture in 7 (0.0004 ± 10.8x10-5, p <0.01) and 14 days (0.0006 ± 1.06 x10-5, p <0.01) post-injury in relation to the control group (0.0002 ± 3.45x10-5). Immunostaining for iNOS was identified at 14 days after injury in the Rupture group. Our results showed that the rupture of the Achilles tendon induces changes in the spinal cord in terms of total cell number, activation of glial cells and participation of the nitrergic system in a murine experimental model. In this way, it points to possible degenerative, oxidative, inflammatory and neural plasticity events in the spinal cord resulting from the Achilles tendon injury, highlighting the CNS participation in the repair process of this lesion.