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Hui-Chung Teng,Huei-Lung Liang,Yih-Huie Lin,Jer-Shyung Huang,Chiung-Yu Chen,Shang-Chieh Lee,Huay-Ben Pan 대한영상의학회 2013 Korean Journal of Radiology Vol.14 No.2
Objective: To evaluate the clinical efficacy as well as long-term clinical outcomes of superselective microcoil embolization for lower gastrointestinal bleeding (LGIB). Materials and Methods: Between 1997 and 2009, 26 patients with intended transcatheter embolotherapy for LGIB were retrospectively reviewed. Embolization was performed only when the catheter could be advanced to or distal to the mesenteric border of the bowel. The main purpose of our study was to assess technical success, recurrent bleeding rate and complications. We also evaluated the long-term clinical outcome, including late recurrent LGIB, bowel ischemia and the survival rate. Results: Twenty-two bleeding sources were in the territory of superior mesenteric artery and four in the inferior mesenteric artery. Technical success was achieved in 22 patients (84.6%). The target vessel of embolization was vasa recta in seventeen patients and marginal artery in the remaining five patients. Early rebleeding occurred in two patients (7.7%) and bowel ischemia in two patients, of whom the embolized points were both at the marginal artery. Delayed recurrent bleeding (> 30 days) occurred in two angiodysplasia patients. Five patients (19.2%) died within the first 30 days of intervention. Long-term follow-up depicted estimated survival rates of 58.2 and 43.1% after one, and five years, respectively. Conclusion: Transcatheter embolotherapy to treat LGIB is effective with low rebleeding and ischemic complications. Considering the advanced age and complex medical problems of these patients, the minimal invasive embolotherapy may be used as both a primary and potentially definitive treatment of LGIB.
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.