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1.
Genet Mol Res ; 14(3): 10281-7, 2015 Aug 28.
Artigo em Inglês | MEDLINE | ID: mdl-26345966

RESUMO

We investigated single nucleotide polymorphisms (SNP) at 87 sites of the phosphodiesterase 4D (PDE4D) gene in Mongol and Han patients with ischemic stroke in Inner Mongolia. SNPs in 226 patients with ischemic stroke (case group, 110 Mongol patients, 116 Han patients) and 220 patients without neurological disease (control group, 102 Mongol patients, 118 Han patients) were detected by polymerase chain reaction-restriction fragment length polymorphism and gene sequencing. The genotype and allele frequencies of all groups were compared. There were no statistically significant differences in genotypes in the PDE4D gene at 87 sites between the case and control groups (P > 0.05). The C allele frequency in the case group was significantly higher than that in the control group (P < 0.05). The CC genotype and C allele frequencies in the Mongol case subgroup were higher than those in the Mongol control subgroup (P < 0.05). The CC genotype and C allele frequencies in the Han case subgroup were higher than those in the Han control subgroup (P < 0.05). In the case group, there were no significant differences at 87 sites for genotypes and allele frequencies between the Mongol and Han subgroups. In the control group, there were no significant differences at 87 site genotypes and allele frequencies between the Mongol and Han subgroups. The increase in the C allele frequency at 87 SNP sites in PDE4D may increase ischemic stroke risk. We found no differences in the risk between Mongol and Han populations in Inner Mongolia.


Assuntos
Povo Asiático/genética , Isquemia Encefálica/genética , Nucleotídeo Cíclico Fosfodiesterase do Tipo 4/genética , Etnicidade/genética , Predisposição Genética para Doença , Polimorfismo de Nucleotídeo Único/genética , Acidente Vascular Cerebral/genética , Adulto , Idoso , Idoso de 80 Anos ou mais , Sequência de Bases , Isquemia Encefálica/complicações , Isquemia Encefálica/enzimologia , Estudos de Casos e Controles , China , Feminino , Frequência do Gene , Humanos , Masculino , Pessoa de Meia-Idade , Dados de Sequência Molecular , Reação em Cadeia da Polimerase , Acidente Vascular Cerebral/complicações , Acidente Vascular Cerebral/enzimologia
2.
Genet Mol Res ; 13(4): 8080-8, 2014 Oct 07.
Artigo em Inglês | MEDLINE | ID: mdl-25299192

RESUMO

The aim of this study was to determine whether monocyte/macrophage ß2-AR could act as the therapeutic target of antisympathetic excitation-induced atherosclerotic progression. Cultivated human THP-1 cells were divided into different groups and incubated with isoprenaline, metoprolol, propranolol or ß2-AR blocker for 24 h, together with oxidized low-density lipoprotein (ox-LDL). Afterwards, each group was analyzed for C-C chemokine receptor type 2 (CCR2) expression, monocyte chemotactic protein 1 (MCP-1) release into medium and cell migration ability. In the isoprenaline group, CCR2 protein level was increased, as well as the secretion of MCP-1, and cell motility was enhanced, in a concentration-dependent manner. Propranolol and ICI 118,551 significantly reversed the stimulatory effect of isoprenaline on THP-1 cells induced by ox-LDL, but only high concentrations of metoprolol interfered significantly with the action of isoprenaline (P < 0.05). Isoprenaline or a ß-AR blocker could mediate through ß2-AR, affecting MCP-1 secretion, CCR2 protein expression and cell migration capacity of THP-1 cells. Therefore, monocyte-macrophage ß2-AR may act as a target of antisympathetic excitation-induced atherosclerotic progression.


Assuntos
Antagonistas de Receptores Adrenérgicos beta 2/farmacologia , Aterosclerose/etiologia , Aterosclerose/metabolismo , Macrófagos/metabolismo , Monócitos/metabolismo , Receptores Adrenérgicos beta 2/metabolismo , Simpatolíticos/farmacologia , Antagonistas de Receptores Adrenérgicos beta 1/farmacologia , Aterosclerose/patologia , Linhagem Celular , Movimento Celular/efeitos dos fármacos , Células Cultivadas , Quimiocina CCL2/metabolismo , Progressão da Doença , Humanos , Receptores CCR2/metabolismo
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