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Objective To study the cerebral vascular anomalies in patients with posterior circulation infarction and their risk factors.Methods The clinical data of 337 consecutive patients with first-onset of posterior circulation infarction,extracted from Nanjing Stroke Registry Program from January 2007 to June 2010,were collected.Computerized tomography angiography(CTA),magnetic resonance imaging angiography(MRA)and digital subtraction angiography(DSA)were performed in all the patients to clarify the site of vascular anomalies and their mechanisms; and their relation with their risk factors were analyzed.Results One hundred and ninety-five patients with posterior circulation infarction(57.9％)had vascular anomalies with 394 lesions.There were 115 lesions in the ostial vertebral artery,81 lesions in the V4 of vertebral artery,49 lesions in the basilar artery and 47 lesions in the posterior cerebral artery.Hypertension(64.9％)was the most common risk factors in patients with posterior circulation infarction smoking,followed by diabetes mellitus,drinking,and hyperhomocysteinemia.In patients with vascular anomalies,patients with hypertension enjoyed significantly higher incidence of vascular anomalies than those without hypertension,while those with cardiac disease were not(P＜0.05).Conclusion The incidence of posterior circular anomalies in patients with posterior circulation infarction is high,especially in the patients with hypertension and diabetes mellitus.
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Objective To evaluate the neuronal injury induced by organophosphorus(OP) compound exposurein rats andinvestigate andthepossible mechanisms. Methods Eighteen SD rats were randomly divided into OP groups(n=12)and the control group(n=6).SD rats were given intramuscular sarin inection followed 1 min later by intraperitoneal injection of atropine sulphate and pralidoxime,and the rats with typical toxic reactions were used for subsequent experiment.The rats in the control group received normal saline injections in identical manners.Twenty-four hours later,the brain tissue of the rats were taken for HE staining and neuronal nuclei antigen(NeuN)immunohistochemistry to quantitatively assess the neuronal damages in the pyriform cortex,hippocampus CAl and striatum.Results HE staining showed massive degeneration of the neurons in the pyriform cortex,hippocampus CAland striatum of rats with satin injection.Compared to the rats with saline injections,the rats exposed to satin presented with significantly decreased number of NeuN-positive neurons(P<0.05).Conclusion OP Can induce acute neuronal death in rat brain and cause a series of symptoms in the central nervous system,probably by such noncholinergic mechanisms as glutamic acid-induced eytotoxieity and oxidative stress.
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Objective To study the effect of intranasal(IN)delivery of nerve growth factor(NGF) on pyriform cortex of satin-poisoned rats.Methods Sprague-Dawley rats were treated with satin and atropine sulphate, pralidoxime to establish satin-poisoned rat model.Then NGF or saline was administered via the olfactory pathway.24 hours later, damaged and residual healthy neurons were estimated and quantified on pyriform cortex using hematoxylin-eosin(HE)staining and neuronal nuclei antigen(NeuN) immunohistochemistry.Results A massive quantity of degenerating neurons were seen in the pyriform cortex of rats with intranasal saline.And compared to the normal rats, the number of neurons of rats with intranasal saline was significantly reduced by 39.44% [(404.75?25.17)/mm~2].But the number of neurons in rats with intranasal NGF [(651.94?36.02)/mm~2] didn't change significantly compared to the normal rats.Conclusion Intranasal delivery of NGF, reducing the degenerating neurons on pyriform cortex of satin-exposure rats, is a potential treatment for satin intoxication.