ABSTRACT
BACKGROUND: Stenting appears to be a safe means of treatment for vertebral artery ostium stenosis with low complication rates and positive long-term effects, but the incidence of in-stent restenosis (ISR) after stenting is high. Different treatment strategies are applied for the revascularization of ISR; however, currently the optional approach is not recommended. The study was designed to investigate the feasibility, safety, and effectiveness of balloon-assisted angioplasty for the treatment of ISR after vertebral artery ostium stenosis. METHODS: In this study, we included patients from the Department of Neurology, Lishui Hospital of Zhejiang University, who were treated with balloon-assisted angioplasty as a result of suffering from ISR after previously undergoing vertebral artery ostium stenting. We retrospectively analyzed the clinical and functional outcomes of the patients. RESULTS: From January 2015 to December 2019, 11 patients were included in the study. The technical success rate reached 100% and the average operation time was 73 minutes. The Thrombolysis in Cerebral Infarction Score 2b-3 was acquired in all patients except 1 patient, who was presented with symptoms of hypoperfusion syndrome. The remaining 10 patients did not experience any intraoperative or postoperative complications. No restenosis, new cerebral infarction or transient ischemic attack were reported within 6 months of follow-up. CONCLUSION: Balloon-assisted angioplasty could be feasible for the treatment of ISR after vertebral artery ostium stenting, however, more research is needed to confirm this.
Subject(s)
Angioplasty, Balloon , Coronary Restenosis , Vertebrobasilar Insufficiency , Angioplasty, Balloon/adverse effects , Cerebral Infarction/etiology , Constriction, Pathologic/etiology , Follow-Up Studies , Humans , Retrospective Studies , Stents/adverse effects , Treatment Outcome , Vertebral Artery/surgery , Vertebrobasilar Insufficiency/surgeryABSTRACT
BACKGROUND/AIMS: Long noncoding RNAs (lncRNAs) have recently emerged as novel and potentially promising therapeutic targets in various cancers. However, the expression pattern and biological function of lncRNAs in glioma remain largely elusive. In the present study, we investigated the functional role of an lncRNA, small nucleolar RNA host gene 16 (SNHG16), in glioma. METHODS: The expression levels of SNHG16 and miR-4518 were measured using qRT-PCR. The relationship between the levels of SNHG16 and clinicopathologic features were statically analyzed. The levels of proteins were detected using western blot. Bioinformatics analysis and luciferase reporter assays were applied to the analysis of the relationship between SNHG16, miR-4518 and PRMT5. Cell viability and apoptosis were measured using MTT and apoptosis ELISA assay, respectively. RESULTS: SNHG16 was highly expressed in glioma tissues and cell lines, which was related to poorer clinicopathologic features and shorter survival time. Knockdown of SNHG16 inhibits the viability and induces apoptosis of glioma cells. Further investigation revealed that SNHG16 could up-regulate the expression of miR-4518 targeted gene PRMT5 via acting as an endogenous sponge of miR-4518. Moreover, SNHG16 also affects the expression of Bcl-2 family proteins and the activation of PI3K/Akt signaling pathway. CONCLUSION: Our study revealed a novel SNHG16-miR-4518-PRMT5 pathway regulatory axis in glioma pathogenesis. SNHG16 could be used as a potential therapeutic target in the treatment of glioma.
Subject(s)
Brain Neoplasms/pathology , Glioma/pathology , MicroRNAs/metabolism , Protein-Arginine N-Methyltransferases/metabolism , RNA, Long Noncoding/metabolism , 3' Untranslated Regions , Aged , Antagomirs/metabolism , Apoptosis , Base Sequence , Brain Neoplasms/genetics , Brain Neoplasms/mortality , Cell Line, Tumor , Cell Proliferation , Disease-Free Survival , Female , Glioma/genetics , Glioma/mortality , Humans , Kaplan-Meier Estimate , Male , MicroRNAs/antagonists & inhibitors , MicroRNAs/genetics , Middle Aged , Phosphatidylinositol 3-Kinases/metabolism , Protein-Arginine N-Methyltransferases/antagonists & inhibitors , Protein-Arginine N-Methyltransferases/genetics , Proto-Oncogene Proteins c-akt/metabolism , Proto-Oncogene Proteins c-bcl-2/metabolism , RNA Interference , RNA, Long Noncoding/antagonists & inhibitors , RNA, Long Noncoding/genetics , RNA, Small Interfering/metabolism , Sequence Alignment , Signal Transduction , Up-RegulationABSTRACT
Free radical toxicity due to poorly maintained cellular redox levels is crucial events that have been associated with the pathogenesis of Guillain-Barre syndrome (GBS) patients. Uric acid (UA) and albumin correlate with oxidative stress in some degree. We aimed to evaluate the relationship between GBS and serum levels of UA and albumin in the present study.The serum levels of UA and albumin were determined in 203 individuals including 88 patients with GBS and 153 healthy controls (HC).We found that serum levels of UA and albumin in patients with GBS were significantly lower than those in HC group. Besides, similar phenomenon was observed when the male and female subgroups were estimated, respectively. Additionally, we found that there is no statistic difference among subgroups of GBS regarding UA and albumin. The univariate analysis revealed that both the high UA and high albumin were protective factors for patients with GBS (odds ratio [OR] 0.140; 95% confidence interval [CI]: 0.074-0.264; Pâ<â.001 and OR 0.016; 95% CI: 0.006-0.038; Pâ<â.001, respectively). It was further confirmed by the multivariable logistic regression analysis after adjusting for other potential confounding factors (OR 0.168; 95% CI: 0.055-0.514; Pâ=â.002 and OR 0.027; 95% CI: 0.011-0.071; Pâ<â.001, respectively).In conclusion, we found that patients with GBS had significantly low serum UA and albumin levels. Moreover, we demonstrated that both the high UA and high albumin were protective factors for patients with GBS.