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Objective To determine clinical features and rupture risk of anterior communicating artery (AComA) aneurysms in different age groups. Methods The clinical data of 519 consecutive patients with AComA aneurysms in the First Affiliated Hospital of Wenzhou Medical University between December 2007 and February 2015 were reviewed and divided into younger group (<65 years) and older group (≥65 years). The clinical characteristics and aneurysm morphologies were compared between the two groups. Results There were 390 aneurysms in younger group, and 129 in older groups. For the younger group, hypertension,the size of the aneurysms, maximum height, perpendicular height, size ratio (SR), aspect ratio (AR), aneurysm angle, A1 segment configuration, morphology showed significantly differences in ruptured aneurysms group compared with those in unruptured aneurysms (P<0.05). The multivariate analysis showed that significant difference between the two groups was aneurysm size ( OR＝1.461,95% CI 1.027-2.079, P＝0.035). For the older group, there were statistically significant differences in hypertension,size of the aneurysms, maximum height, perpendicular height, SR, aneurysm angle, vessel size and the distribution of aneurysm projection between the ruptured aneurysms group and unruptured aneurysms group (P<0.05). The multivariate analysis showed that SR ( OR＝11.516,95% CI 1.782-74.445,P＝0.01) was the only significant predictor of aneurysm rupture. Between the younger and older groups,the distributions of sex, hypertension, smoke, vessel size and SR were statistically significant (P < 0.05). Conclusions For younger people, the males who smoked are more likely to have AcomA aneurysms and the size of the aneurysms is independent risk of aneurysm rupture. For older people, the females with hypertension also more often have AcomA aneurysms and the SR is independently associated with aneurysm rupture.
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Objectives To establish a model of carotid atherosclerotic (AS)stenosis in rabbits and to preliminarily investigate the expression of asparaginyl endopeptidase. Methods Fourteen New Zealand white rabbits were divided into either an model group (n = 8)or a sham operation group (n = 6)according to the random number table. The carotid intima was injured by operation in the model group. The rabbits in both groups were fed with high fat diets containing magnesium for 10 weeks. The rabbits were weighted and their blood lipids were tested every 2 weeks. At the end of the fifth and tenth weeks after procedure,the plaque and vessel stenosis of the rabbits were observed by MRI. At the end of the tenth week after proce-dure,the specimens were collected and sliced. Hematoxylin and eosin (HE)staining was used to observe the pathological changes. Immunohistochemical staining was used to analyze the expression of asparaginyl endopeptidase (AEP). Results One rabbit in the model group died of carotid artery injury. After being fed with high-fat diets,the body quality and the level of blood lipid were increased in the rabbits of both groups compared with those before procedure (all P < 0. 01). At the end of the fifth and tenth weeks after procedure,MRI revealed that the luminal stenosis rates in the operation group were 16 ± 11% and 53 ± 20% respectively. There was significant difference within the group (t = - 4. 83,P < 0. 01). MRI revealed no luminal stenosis twice in the sham operation group. HE staining showed intimal hyperplasia,AS plaque formation,lipid deposition in plaques,macrophage and smooth muscle cells migration and infiltration forming foam cells in the model group. No AS formation was observed in the sham operation group. The expression of AEP was higher in the rabbit carotid artery tissue in the model group,and it expressed rarely in the sham surgery group. The absorbance values were 0. 072 0 ± 0. 028 0 and 0. 002 0 ± 0. 000 9 respectively. There was significant difference (t = 6. 61,P < 0. 01). Conclusions The methods of injuring carotid intima combined with magnesium containing high-fat diet may exactly,reliably,and quickly establish an AS carotid artery stenosis model. AEP may associat with the occurrence of AS plaques.
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Objective To investigate the efficacy of endovascular stenting for aortic arch artery stenosis after nasopharyngeal carcinoma radiotherapy. Methods The clinical data of 8 patients with symptomatic severe aortic arch artery stenosis after nasopharyngeal carcinoma radiotherapy were analyzed retrospectively. The patients were all received endovascular stenting,and their improvement of cerebral ischemic symptoms was observed. They were followed up by cervical color Doppler ultrasound.Results The whole brain vascular DSA confirmed that there were 24 severe arterial stenoses on the aortic arch arteries of extracranial segments in 8 patients,including 11 in internal carotid artery,2 in common carotid artery,10 in vertebral artery and 1 in subclavian artery. The patients were treated with vascular angioplasty and stenting respectively. All the patients were followed up for 1 year;there were no recurrence of cerebral ischemic symptoms.Cervical color Doppler ultrasound did not reveal any obvious restenosis. Conclusion Endovascular stent angioplasty for the treatment of aortic arch artery stenosis after nasopharyngeal carcinoma radiotherapy is relatively safe and feasible.
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Objective To investigate the changes of circulating endothelial progenitor cells (EPCs) in patients with acute cerebral infarction or chronic cerebral ischemia and discuss the related clinical significance.Methods Circulating EPCs were isolated using staining markers of CD34,CD133,and kinase insert domain receptor (KDR).Peripheral venous blood was collected from patients with acute cerebral infarction within 24 hours of onset (infarction group,n =30),with chronic cerebral ischemia (ischemia group,n =20),and without cerebral ischemia (control group,n =10) to quantify circulating level of EPCs using flow cytometry and measure parameters of systolic pressure,glycosylated hemoglobin (HbAlc),total cholesterol (TC),and triglyceride (TG),and low density lipoprotein-cholesterol (LDL-C),and high density lipoprotein-cholesterol (HDL-C).Results CD34-,CD34/CD133-,and CD34/KDR-positive cells counted (14.2 ± 8.1)‰,(7.1 ± 4.1)‰ and (5.0 ± 3.7)‰ in infarction group,(28.5 ± 9.9)‰,(15.2 ± 3.7)‰ and (6.8 ± 2.0)‰ in ischemia group,and (44.8 ± 9.5) ‰,(22.1 ± 6.6) ‰ and (16.7 ± 6.9) ‰ in control group.Taken together,circulating level of EPCs lowered substantially in infarction and ischemia groups compared to control group (P ＜ 0.05) and a far lower level was observed in infarction group (P ＜ 0.05).Circulating level of EPCs in infarction group was in a moderate negative correlation with systolic pressure,TC,TG,and LDL-C (P ＜ 0.05).Conclusions Decreased circulating level of EPCs may be a risk factor to the development of cerebral ischemia in acute cerebral infarction patients.Therefore,level of EPCs is vital for prediction,prevention and treatment of acute cerebral infarction.
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Objective To determine the effect of hypothermia on gene transcription and protein expression of calpain after traumatic brain injury (TBI). Methods Twenty-seven rats were randomly divided into three groups, ie, normal control group, normothermia TBI group and hypothermia TBI group. All rats with TBI were suffered from a lateral fluid percussion injury (FPI) at the right parietal lobe. Hy-pothermia intervention [rectal temperature for (32 ± 0.5) ℃] was performed for four hours immediately after TBI in hypothermia TBI group. Fluorescence PCR and Western blot were utilized to semi-quantify gene transcription and protein expression of ealpain and immunofluorescence used to observe protein dis-tribution of Calpain. Results Compared with normothermia TBi group and normal control group, hypo-thermia TBI group showed increased calpain gene transcription at 12 and 24 hours respectively after FPI (P <0.05). However, the increase of ealpain protein expression in hypothermia TBI group was inhibited more significantly by hypothermia at 6,12,24 and 72 hours after TBI, compared with normothermia TBI group (P < 0.05). Conclusion Neuroproteetion of hypothermia after TBI may somewhat be related to the decrease of calpain protein expression after its gene transcription.