• Title/Summary/Keyword: National Taiwan Normal University

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Novel Phosphors for UV Excitable White Light Emitting Diodes

  • Liu, Ru-Shi;Lin, Chun-Che;Tang, Yu-Sheng;Hu, Shu-Fen
    • 한국정보디스플레이학회:학술대회논문집
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    • 2008.10a
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    • pp.1343-1346
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    • 2008
  • $KSrPO_4$ and $Sr_3(Al_2O_5)Cl_2$ phosphors doped with $Eu^{2+}$ emit a blue and orange-yellow luminescence under ultraviolet (UV) excitation at ~ 400 nm, respectivel, which can be used for making white light emitting diodes.

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Fusion of Library, Archive, Museum, Publisher (LAMP): the NTNU Library Experience

  • Ke, Hao-Ren
    • Journal of Information Science Theory and Practice
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    • v.4 no.2
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    • pp.66-74
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    • 2016
  • The convergence of libraries, archives, and museums (LAMs) has garnered attention in recent years. Extending the tendency further, National Taiwan Normal University (NTNU) fuses the library, archive, museum, and publisher (LAMP) functionality together in its library. This article elaborates on the LAMP practices of the NTNU Library, which indicates that without creating new units in a university, its library can play a good role of curating invaluable university assets.

Comparison of the trometamol-balanced solution with two other crystalloid solutions for fluid resuscitation of a rat hemorrhagic model

  • Ting, Wen-Ting;Chang, Ru-Wen;Wang, Chih-Hsien;Chen, Yih-Sharng;Lee, Jih-Jong
    • Journal of Veterinary Science
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    • v.21 no.1
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    • pp.6.1-6.12
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    • 2020
  • Currently, the optimal resuscitation fluid remains debatable. Therefore, in the present study, we designed a trometamol-balanced solution (TBS) for use as a resuscitation fluid for hemorrhagic shock. Hemorrhagic shock was induced in 18 male Wistar-Kyoto rats, which were assigned to normal saline (NS), Ringer's solution (RS), and TBS groups. During the hemorrhagic state, their hemodynamic parameters were recorded using an Abbott i-STAT analyzer with the CG4+ cartridge (for pH, pressure of carbon dioxide, pressure of oxygen, total carbon dioxide, bicarbonate, base excess, oxygen saturation, and lactate), the CG6+ cartridge (for sodium, potassium, chloride, blood glucose, blood urea nitrogen, hematocrit, and hemoglobin), and enzyme-linked immunosorbent assay kits (calcium, magnesium, creatinine, aspartate aminotransferase, alanine aminotransferase, bilirubin, and albumin). Similar trends were found for the parameters of biochemistries, electrolytes, and blood gas, and they revealed no significant changes after blood withdrawal-induced hemorrhagic shock. However, the TBS group showed more effective ability to correct metabolic acidosis than the NS and RS groups. TBS was a feasible and safe resuscitation solution in this study and may be an alternative to NS and RS for resuscitation in hemorrhagic shock patients without liver damage.

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

  • Ya-Jen Chiu;Yu-Shan Teng;Chiung-Mei Chen;Ying-Chieh Sun;Hsiu Mei Hsieh-Li;Kuo-Hsuan Chang;Guey-Jen Lee-Chen
    • Biomolecules & Therapeutics
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    • v.31 no.3
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    • pp.285-297
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    • 2023
  • 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.