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        Treatment of Hemodialysis Vascular Access Rupture Irresponsive to Prolonged Balloon Tamponade: Retrospective Evaluation of the Effectiveness of N-Butyl Cyanoacrylate Seal-Off Technique

        Mei-Jui Weng,Matt Chiung-Yu Chen,Huei-Lung Liang,Huay-Ben Pan 대한영상의학회 2013 Korean Journal of Radiology Vol.14 No.1

        Objective: The current study retrospectively evaluated whether the percutaneous N-butyl cyanoacrylate (NBCA) seal-off technique is an effective treatment for controlling the angioplasty-related ruptures, which are irresponsive to prolonged balloon tamponade, during interventions for failed or failing hemodialysis vascular accesses. Materials and Methods: We reviewed 1588 interventions performed during a 2-year period for dysfunction and/or failed hemodialysis vascular access sites in 1569 patients. For the angioplasty-related ruptures, which could not be controlled with repeated prolonged balloon tamponade, the rupture sites were sealed off with an injection of a glue mixture (NBCA and lipiodol), via a needle/needle sheath to the rupture site, under a sonographic guidance. Technical success rate,complications and clinical success rate were reported. The post-seal-off primary and secondary functional patency rates were calculated by a survival analysis with the Kaplan-Meier method. Results: Twenty ruptures irresponsive to prolonged balloon tamponade occurred in 1588 interventions (1.3%). Two technical failures were noted; one was salvaged with a bailout stent-graft insertion and the other was lost after access embolization. Eighteen accesses (90.0%) were salvaged with the seal-off technique; of them, 16 ruptures were completely sealed off, and two lesions were controlled as acute pseudoaneurysms. Acute pseudoaneurysms were corrected with stentgraft insertion in one patient, and access ligation in the other. The most significant complication during the follow-up was delayed pseudoaneurysm, which occurred in 43.8% (7 of 16) of the completely sealed off accesses. Delayed pseudoaneurysms were treated with surgical revision (n = 2), access ligation (n = 2) and observation (n = 3). During the follow-up, despite the presence of pseudoaneurysms (acute = 1, delayed = 7), a high clinical success rate of 94.4% (17 of 18) was achieved, and they were utilized for hemodialysis at the mean of 411.0 days. The post-seal-off primary patency vs. secondary patency at 90, 180 and 360 days were 66.7 ± 11.1% vs. 94.4 ± 5.4%; 33.3 ± 11.1% vs. 83.3 ± 8.8%; and 13.3 ± 8.5% vs. 63.3 ± 12.1%, respectively. Conclusion: Our results suggest that the NBCA seal-off technique is effective for immediate control of a venous rupture irresponsive to prolonged balloon tamponade, during interventions for hemodialysis accesses. Both high technical and clinical success rates can be achieved. However, the treatment is not durable, and about 40% of the completely sealed off accesses are associated with developed delayed pseudoaneurysms in a 2-month of follow-up. Further repair of the vascular tear site, with surgery or stent-graft insertion, is often necessary.

      • KCI등재

        The Usefulness of Fast-Spin-Echo T2-Weighted MR Imaging in Nutcracker Syndrome: a Case Report

        Heong-Leng Wong,Matt Chiung-Yu Chen,Cgek-Siung Wu,Kuo-An Fu,Cheng-Hao Lin,Mei-Jui Weng,Huei-Lung Liang,Huay-Ben Pan 대한영상의학회 2010 Korean Journal of Radiology Vol.11 No.3

        Nutcracker syndrome occurs when the left renal vein (LRV) is compressed between the superior mesenteric artery and the aorta, and this syndrome is often characterized by venous hypertension and related pathologies. However, invasive studies such as phlebography and measuring the reno-caval pressure gradient should be performed to identify venous hypertension. Here we present a case of Nutcracker syndrome where the LRV and intra-renal varicosities appeared homogeneously hyperintense on magnetic resonance (MR) fast-spin-echo T2- weighted imaging, which suggested markedly stagnant intravenous blood flow and the presence of venous hypertension. The patient was diagnosed and treated without obtaining the reno-caval pressure gradient. The discomfort of the patient lessened after treatment. Furthermore, on follow-up evaluation, the LRV displayed a signal void, and this was suggestive of a restoration of the normal LRV flow and a decrease in LRV pressure.

      • KCI등재

        A Neuroprotective Action of Quercetin and Apigenin through Inhibiting Aggregation of Aβ and Activation of TRKB Signaling in a Cellular Experiment

        Chiu Ya-Jen,Teng Yu-Shan,Chen Chiung-Mei,Sun Ying-Chieh,Hsieh-Li Hsiu Mei,Chang Kuo-Hsuan,Lee-Chen Guey-Jen 한국응용약물학회 2023 Biomolecules & Therapeutics(구 응용약물학회지) Vol.31 No.3

        Alzheimer’s disease (AD) is a neurodegenerative disease with progressive memory loss and the cognitive decline. AD is mainly caused by abnormal accumulation of misfolded amyloid β (Aβ), which leads to neurodegeneration via a number of possible mechanisms such as down-regulation of brain-derived neurotrophic factor-tropomyosin-related kinase B (BDNF-TRKB) signaling pathway. 7,8-Dihydroxyflavone (7,8-DHF), a TRKB agonist, has demonstrated potential to enhance BDNF-TRKB pathway in various neurodegenerative diseases. To expand the capacity of flavones as TRKB agonists, two natural flavones quercetin and apigenin, were evaluated. With tryptophan fluorescence quenching assay, we illustrated the direct interaction between quercetin/ apigenin and TRKB extracellular domain. Employing Aβ folding reporter SH-SY5Y cells, we showed that quercetin and apigenin reduced Aβ-aggregation, oxidative stress, caspase-1 and acetylcholinesterase activities, as well as improved the neurite outgrowth. Treatments with quercetin and apigenin increased TRKB Tyr516 and Tyr817 and downstream cAMP-response-element binding protein (CREB) Ser133 to activate transcription of BDNF and BCL2 apoptosis regulator (BCL2), as well as reduced the expression of pro-apoptotic BCL2 associated X protein (BAX). Knockdown of TRKB counteracted the improvement of neurite outgrowth by quercetin and apigenin. Our results demonstrate that quercetin and apigenin are to work likely as a direct agonist on TRKB for their neuroprotective action, strengthening the therapeutic potential of quercetin and apigenin in treating AD.

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