Collateral circulation affects the prognosis of patients with acute ischemic stroke (AIS) treated by thrombolysis. The present study performed a systematic assessment of the impact of the collateral circulation status on the outcomes of patients receiving thrombolysis treatment. Relevant full-text articles from the Cochrane Library, Ovid, Medline, Embase and PubMed databases published from January 1, 2000 to November 1, 2016 were retrieved. The quality of the studies was assessed and data were extracted by 2 independent investigators. The random-effects model was used to estimate the impact of good vs. poor collateral circulation, as well as baseline characteristics, on the outcome within the series presented as risk ratios. Subgroup analyses explored the potential factors that may interfere with the effects of the collateral circulation status on the outcome. A total of 29 studies comprising 4,053 patients were included in the present meta-analysis. A good collateral circulation status was revealed to have a beneficial effect on favorable functional outcome (modified Rankin scale, 0–3 at 3–6 months; P<0.001) and a higher rate of recanalization (P<0.001) compared with poor collateral circulation. Good collateral circulation was also associated with a lower rate of symptomatic intracranial hemorrhage (P<0.01), a lower rate of mortality (P<0.01) and a smaller infarct size (P<0.01). In conclusion, good collateral circulation was demonstrated to have a favorable prognostic value regarding the outcome for patients with AIS receiving thrombolysis treatment. Assessment of collateral circulation and penumbra area during pre-treatment imaging within an appropriate time-window prior to thrombolytic therapy will therefore improve the identification of AIS patients who may benefit from thrombolysis treatment.
The development of collateral circulation in patients with acute ischemic stroke with ICA occlusion may be influenced by BP. A moderately decreased SBP is associated with good integrity of the collateral circulation in patients with acute ischemic stroke with occlusion of the ICA.
long non-coding (lnc)rnas serve important cellular functions and certain lncrnas have roles in different mechanisms of gene regulation. lncrna-antisense non-coding rna in the INK4 locus (ANRIL) affects cell inflammation; however, the potential genes underlying the inflammatory response regulated by anril remain unclear. in the present study, the potential function of anril in regulating gene expression and alternative splicing was assessed. ANRIL-regulated human umbilical vein endothelial cell (HUVEC) transcriptome was obtained using high-throughput rna sequencing (rna-seq) to evaluate the potential role of ANRIL. Following plasmid transfection, gene expression profile and alternative splicing pattern of HUVECs overexpressing ANRIL were analyzed using rna-seq. anril overexpression affected the transcription levels of genes associated with the inflammatory response, nF-κB signaling pathway, type I interferon-mediated signal transduction pathway and innate immune response. ANRIL regulated the alternative splicing of hundreds of genes with functions such as gene expression, translation, dna repair, rna processing and participation in the nF-κB signaling pathway. Many of these genes serve a key role in the inflammatory response. ANRIL-regulated inflammatory response may be achieved by regulating alternate splicing and transcription. The present study broadened the understanding of anril-mediated gene regulation mechanisms and clarified the role of ANRIL in mediating inflammatory response mechanisms.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.