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@#Objective To investigate the relationship between cerebral microbleeds and cerebral artery stenosis in patients with large atherosclerotic cerebral infarction.Methods We retrospectively enrolled 512 patients with large atherosclerotic cerebral infarction who were the first time admitted to the Department of Neurology of our hospital from October 2018 to June 2021.According to the results from the craniocerebral magnetic sensitive weighted imaging,patients were divided into non-CMBs group and CMBs group.The purpose of this study was to investigate the risk factors and incidence rate of CMBs，the relationship between cerebral microbleeds and cerebral artery stenosis in patients with large atherosclerotic cerebral infarction.Results The incidence rate of CMBs was 39.3% in this study.Factors including age,hypertension,hyperhomocysteinemia,history of antiplatelet drug use,WMH,intracranial and extracranial artery stenosis coexisted independently with CMBs.The degree of CMBs is positively correlated with cerebral artery stenosis.Conclusion Age,hypertension,high-profile cysteinemia,anti-platelet drug application history,WMH and intracranial artery or both of extracranial vessels stenosis are independent risk factors of CMBs.The degree of CMBs is positively correlated with cerebral artery stenosis.Triacylglycerol may be a protective factor for CMBs.
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@#Objective To investigate the relationship between the overall burden of cerebral small vessel disease (CSVD) and cognitive impairment in patients with atrial fibrillation (AF) associated stroke.Methods Patients with acute cerebral infarction related to the cause of atrial fibrillation who were hospitalized in the Department of Neurology,Qingdao University Affiliated Hospital were collected from September 2018 to May 2020.According to the imaging findings of magnetic resonance imaging,the patients were divided into four groups:0,1,2,3~4.Seven days after the onset of stroke,the patients were assessed with the Montreal Cognitive Assessment Scale (MoCA).The patients were divided into cognitive impairment group and non-cognitive impairment group.A total of 168 patients completed the assessment.Results Age,hypertension,smoking history,MOCA score,CHA2DS2-VASC score are related to total CSVD score.Cognitive impairment after atrial fibrillation-related stroke is related to total CSVD score,age,smoking history,drinking history,CHA2DS2-VASc score,frontal lobe and thalamic infarction.Cognitive domain impairment is mainly visual space,executive ability,linguistic ability and delayed recall ability.Conclusion The severity of the overall burden of CSVD is related to cognitive impairment in patients with atrial fibrillation-related stroke.
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Objective To investigate the effects of ischemic postconditioning (IP) on interleukin-1β (IL-1β) and tunor necrosis factor-α (TNF-α) expression in focal cerebral ischenia/reperfusion in rats in order to clarify the rnechanism of neuroprotective effect of IP.Methods One hundred and ten healthy adult male Sprague-Dawley rats were randomized into sham operation (n =10),ischemia/reperfusion and IP groups.The latter two groups were redivided into 6-,12-,24-,48- and 72-hour subgroups (n =10 in each subgroup) according to their reperfusion time.A focal cerebral ischemia/reperfusion model was induced by the middle cerebral artery intraluminal suture method.After middle cerebral artery occlusion for 2 hours,reperfusion for 15 seconds was conducted using the IP method,and this was repeated for 3 times.The neurobehavioral scores of the rats were evaluated in each group.The infarct volume was measured with 2,3,5-triphenyltetrazolium chloride staining.The expression of TNF-α and IL-1β protein in brain tissue was detected by immunohistochemistry assay.The expression of IL-1β and TNF-αmRNA was determined by in situ hybridization.Results Compared with the ischemia/reperfusion group,the neurobehavioral score and and cerebral infarct volume in the IP group decreased significantly (all P ＜0.05).Expressions of IL-1 β,TNF-o protein and mRNA were slight in the frontoparietal cortex in the sham group; however,they were apparent in ischemia/reperfusion group and IP groups,and began to increase at 6 hours and reached the peak at 24 hours (compared to other time points all P ＜0.05),then decreased gradually.There was the same dynamic change trend in the IP group,and the expression at each time point was significantly lower than that in the ischemia/reperfusion group (all P＜0.05).Conclusions IP significantly down-regulates the expressions of IL-1 β and TNF-α and reduces the infarct volume of the ischemia/reperfusion in rats.These findings indicate that IP may play a neuroprotective role by inhibiting the inflammatory response in brain tissue after ischemia/reperfusion.