RESUMO
Ischemic stroke is a significant health condition, whose frequency in childhood is increasing day by day. Although many factors are effective in development of the stroke, it has been showed that individuals having risk factors have a genetic predisposition. The aim of the study is to determine whether distinct genetic mutations are risk factors for children with history of ischemic stroke. Our sample data is taken from 58 patients (29 male and 29 female) who applied our hospital between 2012 and 2016 with diagnosis of acute or chronic arterial stroke and from 70 healthy children (32 male and 38 female) with similar particularities in the sense of age and sex, who have not any chronical disease. Blood samples are taken from each child participated in the study to conduct genetic analysis. It has been examined whether a mutation exists in gene locations of CDKN2B-AS1 (Rs2383206), HDAC9 (Rs11984041), NINJ2 (Rs12425791), NAA25 (Rs17696736). Moreover, whether there are significant difference between patient and control group has been investigated. In the genetic analysis of patients and control groups, no significant difference has been found for any of the genes. Mutations in gene locations of CDKN2B-AS1 (Rs2383206), HDAC9 (Rs11984041), NINJ2 (Rs12425791), NAA25 (Rs17696736) are not risk factors for ischemic stroke in childhood. However this study showed us, the patients who inherit CDKN2B-AS1 and HDCA9 gene mutations had poor prognosis. However, this study should be replicated for a wider sample of patient population.
Assuntos
Isquemia Encefálica/genética , Moléculas de Adesão Celular Neuronais/genética , Inibidor de Quinase Dependente de Ciclina p15/genética , Predisposição Genética para Doença , Histona Desacetilases/genética , Mutação , Acetiltransferase N-Terminal B/genética , Proteínas Repressoras/genética , Acidente Vascular Cerebral/genética , Criança , Feminino , Humanos , Masculino , Fatores de RiscoRESUMO
Sleep is essential for memory consolidation that stabilizes a memory trace. Memory consolidation includes waves of new gene expression and protein synthesis. Recently, microRNAs (miRNAs) have emerged as critical regulators of memory processes. Previous studies demonstrated that rapid eye movement (REM) sleep deprivation (REM SD) during specific time windows after training in the Morris water maze (MWM) task impairs memory consolidation. Here, we showed that the post-learning REM sleep, extending from 3 to 6 h after last training, is critical for spatial learning in the MWM task. Further, we found that the REM SD after training significantly changes the hippocampal expression of brain-derived neurotrophic factor (BDNF) mRNA; however, it causes minimal difference in the hippocampal expressions of calcium-calmodulin-dependent protein kinase II (CAMKII) and cAMP response-element-binding (CREB). In addition, it considerably affected the hippocampal expressions of miR-132, miR-182, and miR-124. In conclusion, after the MWM task, the post-learning REM sleep during specific time windows can modulate spatial memory consolidation, and its deprivation can impact the hippocampal transcriptional processes including memory-related miRNAs and mRNAs.
Assuntos
Aprendizagem/fisiologia , Plasticidade Neuronal/genética , Privação do Sono/fisiopatologia , Animais , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Proteína Quinase Tipo 2 Dependente de Cálcio-Calmodulina/metabolismo , Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo , Hipocampo/metabolismo , Masculino , Aprendizagem em Labirinto/efeitos dos fármacos , Memória/fisiologia , Consolidação da Memória/fisiologia , Camundongos , Camundongos Endogâmicos BALB C , MicroRNAs/genética , Plasticidade Neuronal/fisiologia , Sono , Privação do Sono/metabolismo , Sono REM/fisiologiaRESUMO
BACKGROUND: Acute appendicitis (AA) is a momentous, emergency, surgical pathology that has still been investigated for both etiopathogenetic unknowns and challenges in diagnosis. Presently, there is little information about the role of microRNAs (miRNAs), which have basic biological functions in the cell, can be a marker, and are associated with various pathologies, in patients with AA. The aim of this study was to investigate the expressions of some miRNAs in AA. METHODS: Overall, 41 miRNAs were screened in 48 individuals comprising 24 patients with AA and 24 healthy controls at Erciyes University Genome and Stem Cell Center (GENKOK). The obtained data were analyzed using appropriate statistical methods. RESULTS: miR-29c-3p was found to be increased 2-fold during the first 4-6 h in AA, and this increase was revealed to be statistically significant compared with healthy individuals. Similarly, expressions of let-7b-5p, let-7i-5p, miR-30a-5p, miR-29b-3p, and miR-23a-3p also increased approximately 2-fold in AA, although not statistically significant. No significant differences were found in the screening of the remaining 35 miRNAs in patients with AA. CONCLUSION: Although there is little information about the relationship between AA and miRNAs currently, miR-29c-3p was reported to increase in the acute period of AA in this study. With the current results, it can be argued that miR-29c-3p bears the potential to be a marker in patients with AA. The present study may also be a basic research for more extensive and necessary miRNAs screening in this field.