Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
Add more filters











Database
Language
Publication year range
1.
Int J Neurosci ; 132(1): 95-99, 2022 Jan.
Article in English | MEDLINE | ID: mdl-32700627

ABSTRACT

Purpose/aim of the study: Posterior circulation stroke (PCS) accounts for 20% of ischemic stroke, and vertebrobasilar stenosis is an important cause of PCS. Notably, not all patients with artery stenosis progress to ischemic stroke, and one of the important reason is that collateral circulation construction plays important protection role in this process.Clinical presentation: Here, we present the case of a 71-year-old male who presented with lightheadedness and three episodes of loss of consciousness after bilateral subclavian artery stenting. Digital subtraction angiography (DSA) demonstrated severe stenosis of the left vertebral artery, and the bilateral subclavian artery was kept open. The patient was then given the left vertebral artery stenting in an effort to resolve the vascular stenosis. As expected, he achieved a complete remission after stenting. However, 6 months later the patient suffered from loss of consciousness again. Repeat DSA confirmed restenosis of the left vertebral artery, and revealed a collateral flow to the left vertebral artery which fed by external carotid collateral branches. Then DSA was performed after 12 months, and another collateral circulation involving thyrocervical trunk was also found supplying flow to the left vertebral artery. In this process, the frequency of loss of consciousness gradually decreased as the collateral circulation construction. Conclusion: Through this case, we observe the whole process of the collateral circulation construction. Moreover, this case serves as a testament to the variability and complexity of vertebrobasilar arteriopathies, suggesting promotion of collateral flow offers the opportunity for outcome improvement.


Subject(s)
Collateral Circulation/physiology , Stents , Vertebrobasilar Insufficiency/diagnosis , Vertebrobasilar Insufficiency/physiopathology , Vertebrobasilar Insufficiency/therapy , Aged , Constriction, Pathologic/therapy , Humans , Male
2.
Neurosci Lett ; 388(1): 17-20, 2005 Nov 04.
Article in English | MEDLINE | ID: mdl-16043284

ABSTRACT

There is a compelling body of evidence indicating an association between cholesterol and Alzheimer's disease (AD). Acyl-coenzyme A: cholesterol acyltransferase 1 (ACAT1), an endoplasmic-reticulum-resident enzyme that catalyses the formation of cholesteryl esters (CEs) from cholesterol and long-chain fatty acids, modulates the generation of beta amyloid peptide (Abeta). A single nucleotide polymorphism rs1044925 in the sterol O-acyltransferase 1 (SOAT1), the gene encoding ACAT1, has been reported to be association with an increased risk for sporadic AD (SAD) in European population. In the present study, we examined the association of the SOAT1 rs1044925 polymorphism with SAD in our northern Han-Chinese (107 cases, 118 age and gender-matched controls) sample using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis. There was no genotypic (chi(2)=0.030, OR 0.942, 95% CI=0.478-1.857) or allelic (chi(2)=0.021, OR 0.955, 95% CI=0.508-1.794) association between SAD and controls, even when the data were stratified by APOEvarepsilon4 carrier status. Our results indicate that the polymorphism rs1044925 in the 3'UTR of SOAT1 gene does not affect the risk of SAD in the northern Han-Chinese.


Subject(s)
Alzheimer Disease/enzymology , Alzheimer Disease/genetics , Brain/enzymology , Genetic Predisposition to Disease/genetics , Polymorphism, Genetic/genetics , Sterol O-Acyltransferase/genetics , 3' Untranslated Regions/genetics , Aged , Alzheimer Disease/ethnology , Amyloid beta-Peptides/metabolism , Apolipoprotein E4 , Apolipoproteins E/genetics , Asian People/genetics , Brain/physiopathology , China/ethnology , Cholesterol/metabolism , Cohort Studies , DNA Mutational Analysis , Female , Gene Frequency , Genetic Testing , Genotype , Humans , Longitudinal Studies , Male , Mutation/genetics
SELECTION OF CITATIONS
SEARCH DETAIL