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To investigate the clinical characteristics and angio-architecture features of patients with dural arteriovenous fistulas (DAVF).The clinical data of 48 patients with DAVF were analyzed retrospectively.All patients were diagnosed by digital subtract angiography and 43 cases were also examined by MRI.Patients were divided into the bleeding group and non-bleeding group,whose clinical features and angio-architecture were compared.Of 48 cases,13 patients demonstrated intracranial bleeding,and men were more common in bleeding group (M/F:10/3) than in non-bleeding group (M/F:15/20) (P =0.036).The Cognard scores of bleeding group and nou-bleeding group were 3.77 ±0.28 and 2.49 ±0.21,respectively (P =0.002) ; however,there was no significant difference in age and the number of feeding artery between two groups.The results indicate that male patients with high Cognard scores tend to intracranial bleeding.
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Objective To investigate the possible roles of serum bilirubin and uric acid in the course of carotid artery intima thicken/plaque formation. Methods Patients with ischemic cerebral vascular disease were divided into the control group, intima thicken group and plaque formation group according to the carotid artery intimamedia thickness (IMT) examination by B-mode ultrasound. The serum bilirubin and uric acid were detected by Automatic Chemistry Analyzer. Results The serum level of uric acid of (391.22 ± 27.52) μmol/L in intima thicken group was significantly higher than that in the control group and plaque formation group((307.32 ± 13.68)μmol/L and (327.84 ± 17.96)μmol/L, P ＜ 0.05). The serum level of indirect bilirubin and total bilirubin in plaque formation group was (10.96 ± 0.58) μmol/L and (15.91 ± 0.71) μmol/L respecitively, which were significantly lower than those in the control group ((15.09 ± 2.21) μmol/L and (20.59 ± 2.43) μmol/L,respectively) and the intima thicken group((15.09 ± 2.21) μmol/L and (20.59 ± 2.43) μmol/L, respectively) (Psignificantly lower than that of (5.70 ± 0.28) μmol/L in the control group(P ＜ 0.05). Conclusions Bilirubin and uric acid play different roles in carotid artery plaque formation during different stage.
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Objective To investigate whether N-methyl-D-aspartate(NMDA) signal pathway is involved in platelet-activating factor(PAF)-induced apoptosis in neurons.Methods Mice cortex neurons were treated by PAF in different dose for 24 hours or pretreated by a PAF receptor antagonist BN52021, an NMDA receptor antagonist MK801 and a nitric oxide synthase(NOS) inhibitor L-NAME for 30 min. Then the neurons were stained by propidium iodide(PI)/calcein AM and the images were taken by a digital camera on a fluorescent microscope. Neuron death ratio(%) was calculated. In the mean time, neuron NOS(nNOS) expression of the cells was detected by Western Blot method, as well as nNOS activity was measured by 3H radioimmunoassay.Results (1)Neuronal death increased after neurons were treated with 0.01, 0.1, 0.3 and 0.6 ?mol/L PAF 24 h. There were signifitantly changed in 0.3 ?mol/L and 0.6?mol/L comparing control. (2)PAF-induced neurotoxicity was prevented not only by BN5021, but also by MK-801 or L-NAME. (3)PAF enhanced nNOS expression and activity in neurons.Conclusion NMDA signal pathway is involved in platelet-activating factor-induced neurotoxicity.
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Objective To investigate whether PSD 93 reduce neurotoxity induced by platelet activating factor (PAF) and study on the mechanism of cell molecularbiology.Methods PAF treated the cultural cortex neurons in wild type and PSD 93 knockout mice and the cells were stained with PI/Calcein AM for apoptosis; neuronal viability was measured by MTT. The expression of PSD93 and PSD95 protein in neurons was tested by Western Blot.Results PSD 93 and PSD 95 expressed in wild type neurons and only PSD 95 expressed in PSD 93 knockout. Cortex neuronal apoptosis in PSD 93 knockout mice was lower then that in wild type ( P