RESUMEN
Carotid duplex sonography is a useful method for evaluation of dural arteriovenous fistulas. The resistance index of the external carotid artery has been reported to correlate with the efficacy of treatment and recurrence or aggravation of dural arteriovenous fistulas. Herein, we describe a case of dural arteriovenous fistulas mainly supplied by the occipital artery and show that the resistance index of the occipital artery was more sensitive than that of the external carotid artery. To the best of our knowledge, this is the first report to describe the feasibility of occipital artery detection by carotid duplex sonography and clinical application of the resistance index of the occipital artery for dural arteriovenous fistulas.
RESUMEN
BACKGROUND AND PURPOSE: Sorbin and SH3-domain-containing-1 (SORBS1) is an important adaptor protein in insulin-signalling pathway, and its genetic polymorphism may regulate the activity of insulin resistance. We investigated the association between the SORBS1 T228A polymorphism and ischaemic stroke. METHODS: Genotyping was achieved by a rapid-cycle PCR and melting curve analysis using fluorescent probes in 1049 incident cases of ischaemic stroke and 1049 age- and sex-matched control subjects recruited from the Hisayama study. RESULTS: The allele distributions of the SORBS1 T228A polymorphism were similar amongst cases and controls. The multivariate-adjusted odds ratio (OR) of the AA genotype for ischaemic stroke was 2.897 (95% CI, 0.907-8.018) compared with the TT genotype. In terms of stroke subtype, there was a trend toward a difference in the AA genotypes for lacunar infarction, compared with the TT genotype (OR = 8.740, P = 0.0510), and combined TT and TA genotypes (OR = 8.768, P = 0.0505). The other polymorphisms genotyped were not associated with any subtypes of ischaemic stroke. T228A polymorphism of SORBS1 was not associated with the prevalence of diabetes. CONCLUSIONS: The AA genotype of SORBS1 T228A polymorphism may play a role in lacunar infarction in the Japanese population.
Asunto(s)
Infarto Encefálico/epidemiología , Infarto Encefálico/genética , Predisposición Genética a la Enfermedad , Proteínas de Microfilamentos/genética , Polimorfismo Genético , Anciano , Infarto Encefálico/clasificación , Estudios de Casos y Controles , Estudios de Cohortes , Femenino , Frecuencia de los Genes , Genotipo , Humanos , Japón/epidemiología , Japón/etnología , Masculino , Persona de Mediana Edad , Oportunidad Relativa , Sistema de Registros , Estudios Retrospectivos , Riesgo , Factores de RiesgoRESUMEN
The C242T polymorphism of p22phox, a component of NAD(P)H oxidase, may have an impact on cardiovascular diseases; however, the association between this polymorphism and brain infarction is not fully understood. Here, we investigate the relationship between the C242T polymorphism and brain infarction in Japan. We recruited 1055 patients with brain infarction and 1055 control subjects. A chi-squared test revealed that the T-allele frequency was lower in patients with cardioembolic infarction (5.6%) than in control subjects (11.0%, P < 0.001); however, allele frequencies in patients with lacunar and atherothrombotic infarction (11.2%) were not significantly different from those in control subjects (11.0%). A multivariate-adjusted conditional logistic regression analysis also revealed no association between CT + TT genotype, and lacunar and atherothrombotic infarction (odds ratio = 0.97, 95% confidence interval: 0.72-1.32). To investigate the functional effects of the C242T polymorphism, we examined superoxide production in COS-7 cells cotransfected with Nox4 and p22phox of each genotype. The superoxide-producing activity in those cells expressing p22phox with the T allele was not significantly different from that in cells expressing p22phox with the C allele. The present results suggest that the p22phox C242T polymorphism may have a protective effect against cardioembolic infarction, but is not related to lacunar and atherothrombotic infarction in Japan.
Asunto(s)
Isquemia Encefálica/enzimología , Isquemia Encefálica/genética , NADPH Oxidasas/genética , Polimorfismo Genético/genética , Sistema de Registros , Accidente Cerebrovascular/enzimología , Accidente Cerebrovascular/genética , Anciano , Anciano de 80 o más Años , Animales , Isquemia Encefálica/epidemiología , Células COS , Infarto Cerebral/enzimología , Infarto Cerebral/epidemiología , Infarto Cerebral/genética , Chlorocebus aethiops , Femenino , Frecuencia de los Genes/genética , Humanos , Japón/epidemiología , Masculino , Persona de Mediana Edad , Accidente Cerebrovascular/epidemiologíaRESUMEN
To investigate the role of tumor necrosis factor-alpha (TNF-alpha) in the brain in nociception, we injected recombinant human TNF-alpha (rhTNF-alpha; 1 pg-10 ng/rat) into the lateral cerebroventricle (LVC) in rats and observed the changes in paw withdrawal latency to radiant heat by using the plantar test for 90 min after injection. LCV injections of TNF-alpha at doses of 10 pg, 100 pg and 1 ng reduced paw withdrawal latency, showing a maximal response at a dose of 10 pg which peaked 60 min after injection. TNF-alpha at doses of 1 pg and 10 ng had no effect on nociception during the test period. The TNF-alpha (10 pg)-induced reduction in paw withdrawal latency was blocked by simultaneous injection of diclofenac (1 ng), a cyclooxygenase inhibitor, or interleukin-1 receptor antagonist (IL-1 ra, 10 ng). LCV injection of neither diclofenac (1 ng) nor IL-1 ra (10 ng) had any effect on nociception by itself. The results suggest that TNF-alpha in the brain induces thermal hyperalgesia and that the brain TNF-alpha-induced hyperalgesia is mediated by the central action of interleukin-1 and activation of the cyclooxygenase pathway of the arachidonate.
