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1.
Genet Mol Res ; 16(1)2017 Feb 08.
Artigo em Inglês | MEDLINE | ID: mdl-28198501

RESUMO

Congenital deafness is a serious and irreversible condition in humans. The GJB2 gene is implicated in the pathogenesis of autosomal recessive nonsyndromic hearing loss. Its 235delC and 30-35delG polymorphisms are reported to be associated with risk of hereditary deafness. However, the effect of the interaction between GJB2 235delC and 30-35delG and environmental factors on congenital deafness has not been described. Therefore, we performed a case-control study to investigate the influence of these polymorphisms on congenital deafness risk, and their interaction with maternal and other environmental factors in the development of this disease. Between March 2014 and May 2015, 118 patients with congenital deafness and 242 healthy controls were enrolled into our study. Compared with the GG genotype, the adjusted odds ratios (ORs) [and 95% confidence intervals (CIs)] for the 235delC GC and CC genotypes were 4.66 (1.77-13.07) and 8.28 (2.06-47.52), respectively. Individuals harboring the GC+CC genotypes were at a greatly increased risk of congenital deafness compared to those with the GG genotype (OR = 5.65, 95%CI = 2.54-13.18). However, no significant relationship was established between the 30-35delG variant and this disease. The 235delC polymorphism exhibited an interaction with use of aminoglycoside antibiotics during pregnancy in conferring susceptibility to congenital deafness (chi-square = 8.76, P = 0.003). In conclusion, our study suggests that the GJB2 235delC polymorphism, but not the 30-35delG variant, contributes to congenital deafness susceptibility in the Chinese population examined, and demonstrates an interaction with consumption of aminoglycoside antibiotics during pregnancy in exerting this effect.


Assuntos
Povo Asiático/genética , Conexinas/genética , Surdez/congênito , Surdez/genética , Polimorfismo Genético , Deleção de Sequência , Alelos , Estudos de Casos e Controles , China/epidemiologia , Conexina 26 , Surdez/epidemiologia , Feminino , Genótipo , Humanos , Razão de Chances , Gravidez , Risco
2.
Genet Mol Res ; 13(4): 10769-78, 2014 Dec 18.
Artigo em Inglês | MEDLINE | ID: mdl-25526197

RESUMO

Previous studies have found that children with multiple exposures to anesthesia at an early age are at increased risk of learning and memory impairment. Sevoflurane is the most commonly used inhalational anesthetic for general anesthesia in children. Multiple exposures to sevoflurane have been shown to induce neuroinflammation, inhibit neurogenesis, and cause subsequent learning and memory impairments in fetal mice. Histone-tail acetylation has been implicated in memory formation. In this study, we employed suberanilohydroxamic acid (SAHA), an inhibitor of histone deacetylases, to treat sevoflurane-induced learning and memory impairments. Six-day-old C57BL/6 mice were exposed to sevoflurane for 2 h daily for 3 days. Morris water maze test performed to evaluate learning and memory impairments and the expression of genes related in to synaptic remodeling/plasticity, or regulated by neuronal activity or the cell cycle were detected by real-time PCR. We found that SAHA attenuated sevoflurane-induced learning and memory impairments in fetal mice. Our findings suggest that SAHA may have potential as a therapeutic agent for preventing or treating the neurotoxicity associated with anesthesia.


Assuntos
Anestésicos Inalatórios/metabolismo , Anestésicos Inalatórios/farmacologia , Inibidores de Histona Desacetilases/uso terapêutico , Ácidos Hidroxâmicos/uso terapêutico , Aprendizagem em Labirinto/efeitos dos fármacos , Transtornos da Memória/tratamento farmacológico , Éteres Metílicos/farmacologia , Animais , Animais Recém-Nascidos , Transtornos da Memória/patologia , Camundongos Endogâmicos C57BL , Plasticidade Neuronal/efeitos dos fármacos , Plasticidade Neuronal/genética , Sevoflurano , Vorinostat
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