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國立陽明交通大學 電子物理系所 周苡嘉所指導 周易的 以掃描穿透式電子顯微鏡分析高熵合金與金屬矽化物之原子級微結構 （2021），提出EELS spectrum關鍵因素是什麼，來自於耐退火高熵合金、晶格畸變、短程有序、掃描穿透式電子顯微鏡、金屬矽化物、電子能量損失儀、能量過濾穿透式電子顯微鏡。
而第二篇論文國立中興大學 獸醫學系暨研究所 周濟眾所指導 汪玉祉的 利用醯胺醇類協同作用及組合外排泵抑制劑有效對抗豬胸膜肺炎放線桿菌與敗血性巴氏桿菌 （2021），提出因為有 氟甲磺氯黴素、甲磺氯黴素、外排泵抑制劑、豬胸膜肺炎放線桿菌、與敗血性巴氏桿菌的重點而找出了 EELS spectrum的解答。
以掃描穿透式電子顯微鏡分析高熵合金與金屬矽化物之原子級微結構
為了解決EELS spectrum 的問題，作者周易 這樣論述：
在本實驗中，有兩種高熵合金被製備，分別是NbTaTiV與NbTaTiVZr，其微觀結構在掃描式電子顯微鏡(SEM)之下，呈現的是等軸長且均質的晶粒結構，其晶體結構由X光繞射(XRD)、同步輻射X光繞射(Synchrotron diffraction)與穿透式電子顯微鏡(TEM)分析，呈現單一相的體心立方結構。其機械性質以拉升試驗機(tensile test)進行量測，對應NbTaTiV的降伏強度(yield strength)為1278百萬帕斯卡(MPa)，而NbTaTiVZr的降伏強度為1589百萬帕斯卡，其強度相較其他合金都是非常高的，為了解釋NbTaTiV與NbTaTiVZr的高強度，
由晶格畸變(lattice distortion)所造成的強化也納入機械強度的模擬，結果顯示晶格畸變的強化量，對於NbTaTiVZr為906.81百萬帕斯卡，而NbTaTiV則為431.48百萬帕斯卡，NbTaTiVZr的強化量為NbTaTiV的2.1倍。為了量測晶格畸變係數，理論值與計算值的晶格畸變係數被定義與計算，對於NbTaTiV與NbTaTiVZr其數值分別為0.1186埃(Å)與0.1831埃，但是這個方法使用預設的參數來計算，當預設的狀態不符合時結果會大幅偏離實際值；因此掃描穿透式電子顯微鏡(STEM)的高環角暗場像(HAADF)的特性，如真實空間解析與原子序對比被使用，來直接量測
晶格畸變與高熵合金中元素分布狀況。直接量測的結果顯示，NbTaTiV與NbTaTiVZr的晶格畸變係數分別為0.1140埃與0.1546埃，NbTaTiV的結果與理論計算非常吻合，而且由原子柱的強度分布來判斷，其元素分布相當隨機；而對於NbTaTiVZr，其晶格畸變係數小於理論值15%，由原子隨機分布性的降低推論， NbTaTiVZr中具有短程有序結構，使得晶格畸變程度降低。在室溫與1173 K下11.8%形變的NbTaTiV與4.2%形變的CrMoNbV也由穿透式電子顯微鏡與掃描穿透式電子顯微鏡進行觀察，發現其中大部分的差排(dislocation)屬於刃差排(edge dislocatio
n)，而由此判斷，刃差排是NbTaTiV與CrMoNbV中主要的強化機制來源，其結果與一般預期的結果不同，一般預期體心立方的晶體是以螺旋差排(screw dislocation)來進行強化。二矽化鈷與矽之異質結構特性也被以掃描穿透式電子顯微鏡的高環角暗場像(HAADF-STEM)、能量損失光譜儀(EELS)與近邊精細結構能量損失模擬(ELNES)進行分析，藉由掃描穿透式電子顯微鏡的高環角暗場像之影像，異質結構的模型被建立，此結構用來模擬並解釋矽L2,3的特殊介面峰。
利用醯胺醇類協同作用及組合外排泵抑制劑有效對抗豬胸膜肺炎放線桿菌與敗血性巴氏桿菌
為了解決EELS spectrum 的問題，作者汪玉祉 這樣論述：
Antimicrobial resistance (AMR) not only continues to pose a threat to therapy of infectious disease but also presents a major challenge for global health concerns. To make the matter worse, new antibiotics are not being discovered at a fast enough rate to counter the development of bacterial resist
ance. In veterinary medicine, amphenicols have been extensively used as the drug of choice to treat bacteria associated with porcine respiratory disease complex, namely, Actinobacillus pleruopeumoniae and Pasteurella multocida, thereby leading to varying levels of amphenicol resistance. To re-empowe
r existing antibiotics, using a combination of two commercially available antibiotics in the same class; FF and TAP, or a combination of amphenicols with efflux pump inhibitors (EPIs) as adjuvant therapy were investigated against porcine A. pleruopeumoniae and P. multocida in the current study. In
the first study, the in vitro and in vivo efficacy of FF+TAP combination were evaluated. The in vitro results from the checkerboard assay and reconfirmation with time kill study in the representative isolates illustrated that the synergistic FF-TAP combination was a potential therapeutic option for
treatment of A. pleuropneumoniae and P. multocida infection. In vivo experiments in pigs demonstrated that FF and TAP combination at a ratio correlating to their MIC deductions was equally effective to their original recommended dosage. In the second study, the effects of five EPIs including Carbon
yl Cyanide Chlorophenylhydrazone (CCCP), omeprazole, Phenylalanine-arginine β-naphthylamide (PAβN), reserpine and verapamil, on their ability to enhance the in vitro antimicrobial activity of FF were preliminarily evaluated. The results indicated that CCCP demonstrated promising improvement of FF ac
tivity while PAβN showed some effect but at high concentrations. Both broth microdilution and time kill assay complementarily confirmed the effect of CCCP on the antimicrobial activity of FF. In addition, the beneficial effect between FF and CCCP was initially identified as through the antagonizatio
n of the FloR pump conferred by the floR gene. In the third study, the effect of CCCP on the in vitro FF and TAP antimicrobial activity by a larger number of isolates, the presence of the efflux pump gene, and the intra-bacterial concentration of FF were further investigated. The CCCP, at relatively
low concentrations, could prominently improve FF and TAP antimicrobial activity in a dose-dependent manner, as well as increasing the intracellular concentration of FF, possibly by inhibition of the FloR efflux pump. Collectively, these findings underline the importance of FloR efflux pump in the d
evelopment of amphenicol resistance in A. pleuropneumoniae and P. multocida. Taken together, our studies may provide potential therapeutic options using amphenicols synergism and amphenicols in combination with EPIs against amphenicol-resistant A. pleuropneumoniae and P. multocida.