隨著大眾對於衛生要求的上升，許多抗菌及消毒成分被廣泛應用於水質處理中，其中次氯酸作為消毒殺菌劑大量使用於泳池及自來水的水質淨化中，然而現行標準方法測定水中有效氯所使用具危害的毒化物且步驟繁雜不利普及民生使用，發展簡便快速且靈敏的偵測方法勢在必行。本研究利用牛血清白蛋白（Bovine serum albumin, BSA）、不同的硫醇分子及金離子合成具螢光特性之硫醇修飾金奈米團簇 （Thiol ligand assists BSA capped gold nanoclusters, BSA/RSH-Au NCs），探討添加不同硫醇分子對所合成之金奈米團簇於不同pH值及常見離子對螢光強度之影響，並利用具有最佳螢光穩定性之2-巰基苯甲酸修飾金奈米團簇（Thiosalicylic acid assists BSA capped gold nanoclusters, BSA/TA-Au NCs），透析後進行次氯酸根檢測，其檢測線性範圍為0.98μM-1000μM，涵蓋法規規定游泳池水及自來水中次氯酸根之容許殘留濃度，最後此方法成功於游泳池水及自來水基質中檢測次氯酸根，分析樣品的回收率介於94.4%-95.6%。此外，在紙上添加金奈米團簇，並加入不同濃度的次氯酸根，觀察其螢光強度的變化，期望此方法未來應用於快篩試紙塗布材料快速檢測水質中次氯酸根濃度。

本研究旨在探討分散式網路爬蟲瀏覽時間及覆蓋率之最佳化問題原理。藉由相異物排列所形成的循環組關係式進行一系列的探討。在n個相異元素的簡單排列中，不存在任意元素個數為k (k≤n)的子集對應到自己本身所成集合，我們稱此型態的排列方式為k-錯排。換言之，假如n個相異元素進行簡單排列，排列後每個元素都不在原來的位置上，此時這樣的排列稱為一般的錯排列，也就是1-錯排。本研究從分散網路爬蟲搜尋網址中進行相關發想，發現它的本質是遍歷完所有的頂點且沒有重複經過，即所謂「哈密頓路徑(Hamiltonian path)問題」中一筆畫的NP-hard問題，即圖遍歷問題的一種。因此本研究由k-錯排遞迴之性質來探討分散式網路爬蟲最佳化問題。最後透過電腦模擬及組合數學分析推導，本研究將提出改善以k-錯排應用至分散網路爬蟲的最佳化方式。

Originally, the Tesla transformer was developed to transmit energy and messages wirelessly. But it did not prove itself for either of these applications, so today it is only used for research purposes. Over time, the Tesla transformer has evolved and improved. Today it is possible with Tesla transformers to generate powerful and highly precise controlled discharges. During operation, impressive high-voltage discharges occur at the transformer. A tesla transformer is basically a high voltage generator that achieves a voltage boost by using two magnetically coupled LC series resonant circuits of the same resonant frequency. The Dual Resonant Solid State Tesla Coil (DRSSTC) built in this work has a high power IGBT half bridge module to excite the primary resonant circuit at the resonant frequency. The IGBTs are driven in such a way that audible pressure waves, and therefore music, are generated by the electrical discharges at the high voltage electrode. Within the scope of this work were the following two questions: - How is a DRSSTC designed and built? The DRSSTC system realized in this work is about 80 cm high and reaches about one-meter-long discharges. The design, development, and construction of the transformer are documented in detail and extensively in this thesis. - How does one measure an electrical voltage of 200,000 V, which changes sign more than 100,000 times per second? Two approaches have been taken to measure the voltages. Derived from the energy balance of an ideal capacitor and an ideal coil, a secondary voltage of about 200 kV was calculated via secondary current measurement. The second approach uses a voltage measurement via an in-house developed measuring electrode and a calculated divider ratio between the measured voltage and the secondary voltage. A relatively unrealistic secondary voltage of about 750 kV was measured since the divider ratio depends on approximate values. Nevertheless, the measuring electrode can be used for investigations of the voltage curve, or the divider ratio can be calibrated via the secondary current measurement. The development of such a transformer laid the foundation for much further research and scientific analysis.

在這篇作品中，研究了在遵守反射定律的情況下，“光點”在x軸和“反射曲線”之間反射時，無限往前彈跳的可能性。 研究分成兩個階段，第一階段沿用了我過去作品中的基本結果，闡述了“入射光線”角度之間的遞迴關係，並用“反射切線”角度寫出第n個入射光線角度的封閉式。 第二階段運用函數值趨近於非零常數（為了研究簡潔，假設趨近於1）的情況下一般可用的“接觸點”估計方式，並使用此結果證明了在特定初始條件下，1+e^(-x)和1+1/x都是“無限反射曲線”，但一開始的接觸點估計方式只適用於反射曲線函數值趨近於非零正數的情況，所以我也針對函數值趨近於零的情況進行了思考，但發現了估計推導上的困難，這將是我未來繼續研究的方向。

強化學習為當前AI領域的熱門話題，其特點是在環境的獎勵與懲罰下，進行學習。強化學習雖然較為困難，但其成功的項目都非常有名，其中最著名的例子有: AlphoGo、AlphaZero等等。 深度強化學習(DRL)是深度學習與強化學習的結合體，本專題透過DRL實現近端優化策略演算法，來使BipedalWalker環境中的二足模型學會行走，並調適超參數與神經網路來讓模型訓練擁有更好的結果。 經過實驗後發現，適當的降低獎勵折扣衰減率能有效的提升學習速度以及學習上限，同時可以避免分數落差過大導致的Dead relu問題。最終的結果能讓平均分數達到302分，成功達成了BipedalWalker環境要求(平均分數>=300分)。 為了使智能體擁有更好的探索能力，本專題加入了ICM(Intrinsic Curiosity Module)，成功提升了最終的平均分數至316分，將不摔倒的機率提升至99%，最高分數則到了320分，使得雙足模型能以更快的速度向前移動並保持穩定。

Coronavirus Disease 2019 (COVID-19) is a newly emerged infectious disease caused by the new severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV-2). In less than one year, the virus has spread around the entire world, killing millions of people and disrupting travel and business worldwide. During infection, the virus uses its Spike protein to dock onto the Ace2 protein on the surface of its human host cell. Spike is 1273 amino acids long and only a short fragment of Spike (319-541) is sufficient to bind Ace2. We hypothesized that the remaining protein sequences of Spike might have functions for viral replication beyond the binding of Ace2. We have performed Split-Ubiquitin protein-protein interaction screens to isolate human proteins by their ability to bind to Spike, and we have identified Annexin2A2 and Cytochrome b as novel human protein interaction partners of Spike. Annexin2A2 is involved in both endocytosis and exocytosis, and the protein interaction with Spike might help the virus to enter and exit its host cell. The presence of the mitochondrial Cytochrome b protein inside the cytosol promotes apoptosis, and the protein interaction with Spike could speed up sapoptosis of the infected human cell. The Nub cDNA libraries that we have generated also allowed us to screen for synthetic peptides that interact with Spike. We have isolated two synthetic peptides, FL1a and FL7a, derived from the non-coding parts of human mRNAs by their ability to interact with Spike. We found that both FL1a and FL7a interact with the C-terminal half of the Spike protein. We also found that FL7a is able to block the Spike-Spike self-interaction at the C-terminal half of the Spike protein and we think that this could block the reassembly of the Spike protein in the host cell during viral reassembly. We hope that those synthetic peptides could be used as drugs due to their ability to block protein-protein interactions of Spike with human host proteins that are essential for viral replication.

幹細胞會進行不對稱分裂以維持組織恆定，一個子細胞分化為有特定功能的細胞，而另一個則維持其細胞潛能。粒線體能進行分裂和融合並維持動平衡。現今的研究已經了解，誘導型多能幹細胞(iPSC)的粒線體動平衡變化會促使其直接分化 (Seo BJ, et al., 2018)。然而，果蠅卵巢生殖幹細胞(GSC)內粒線體動平衡與幹細胞分化的關聯仍不清楚。本研究利用容易辨認的果蠅卵巢生殖幹細胞來探討這個問題，並使用Gal4-UAS系統與RNAi操縱粒線體動平衡，並發現粒線體融合蛋白被抑制會導致油滴堆積及幹細胞損失。另外，使用左旋肉鹼(L-carnatine)增進脂肪酸代謝，發現增進代謝會導致油滴減少及幹細胞回復。本研究著重於探討粒線體動平衡對GSC維持與脂肪酸代謝的影響，並對粒線體脂肪酸代謝與幹細胞分化的潛在關係提出觀點與佐證，盼未來能有更進一步的研究與醫療方面的應用。

Money drives the world and in times of crisis, money is more important than ever. Most political, economic and, as we have seen recently, health crises are accompanied by pressure on the economy. With such pressure, ordinary citizens are worried about their money, which is at risk either from inflation or from an uncertain economic outlook. In such times, some people resort to appreciating their money by investing. It is wise investments that can protect savings from inflation, or at least mitigate the effects of inflation. Investing in the stock market is among the most popular ways of investing. During the global coronavirus crisis, the number of small investors more than doubled (Galik and Brody [2022]), and in 2021, Covid (new) investors accounted for 15 % of investors in the U.S. market (Schwab [2021]). It is this phenomenon that inspired the author to write this paper. Investing in the stock market is one of the riskiest forms of investment, which means that there is a high probability of losing the originally invested capital. Some companies that allow retail investors to invest state that more than 90 % of their users lose their capital when investing in the stock market. On the other hand, investing in the stock market has one of the greatest potentials for profit. In the case of a long-term investment in index funds, for example, an average annual appreciation of between 8 % and 12 % can be expected (the average appreciation of the S&P 500, the most famous US index). However, it is necessary to wait several years for stable results. To see appreciation in a long-term portfolio, it is recommended to wait at least 12 years. This is because if a recession or a simple market correction comes, said portfolio can lose up to 50 % of its value in a year. But as history shows, markets do rise over the long term, and that is what long-term investors bet on, waiting for their capital to appreciate over time. But the market does not grow all the time. The market often changes price trends, and in some rare cases a long-term trend can reverse for up to several tens of months. This phenomenon, volatility, is attempted to be exploited by so-called speculators. A speculator is an investor who sells and buys in short periods of time and thus speculates on price movements. The speculator therefore needs a way to determine the likely behaviour of the price in the foreseeable future in order to make their trades profitable. The two main ways of analysing price behaviour are fundamental and technical analysis. And since fundamental analysis incorporates a large amount of diverse information into its predictions, this paper concentrates on working with technical analysis.

Coronavirus Disease 2019 (COVID-19) is a newly emerged infectious disease caused by the new severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV-2). In less than one year, the virus has spread around the entire world, killing millions of people and disrupting travel and business worldwide. During infection, the virus uses its Spike protein to dock onto the Ace2 protein on the surface of its human host cell. Spike is 1273 amino acids long and only a short fragment of Spike (319-541) is sufficient to bind Ace2. We hypothesized that the remaining protein sequences of Spike might have functions for viral replication beyond the binding of Ace2. We have performed Split-Ubiquitin protein-protein interaction screens to isolate human proteins by their ability to bind to Spike, and we have identified Annexin2A2 and Cytochrome b as novel human protein interaction partners of Spike. Annexin2A2 is involved in both endocytosis and exocytosis, and the protein interaction with Spike might help the virus to enter and exit its host cell. The presence of the mitochondrial Cytochrome b protein inside the cytosol promotes apoptosis, and the protein interaction with Spike could speed up sapoptosis of the infected human cell. The Nub cDNA libraries that we have generated also allowed us to screen for synthetic peptides that interact with Spike. We have isolated two synthetic peptides, FL1a and FL7a, derived from the non-coding parts of human mRNAs by their ability to interact with Spike. We found that both FL1a and FL7a interact with the C-terminal half of the Spike protein. We also found that FL7a is able to block the Spike-Spike self-interaction at the C-terminal half of the Spike protein and we think that this could block the reassembly of the Spike protein in the host cell during viral reassembly. We hope that those synthetic peptides could be used as drugs due to their ability to block protein-protein interactions of Spike with human host proteins that are essential for viral replication.

肺癌是目前全世界首要致死的癌症。雖然現有的標靶治療與免疫療法已經改善某些病患的情況，但有許多病患仍無有效治療方法。因此，我們急需探求新的藥物治療方法來改善肺癌治療的成效。 在此我們選擇一個新標靶藥物Palbociclib來進行研究，Palbociclib 是剛核准的乳癌藥物，主要是藉由抑制CDK4/6來延緩乳癌生長。我們發現Palbociclib能有效地抑制肺癌細胞株的生長和死亡。特別的是，Palbociclib不僅誘發肺癌細胞凋亡(apoptosis)，亦誘發肺癌細胞自噬死亡(Autophagy)。因為AMPK能同時影響細胞凋亡與自噬死亡，我們進一步研究AMPK在Palbociclib誘發癌細胞死亡中的角色，發現Palbociclib主要是藉由抑制去磷酸酶PP5的活性，來增加AMPK的磷酸化，進而活化AMPK，誘發肺癌細胞產生凋亡與自噬。這些藥效原非抑制CDK4/6會產生的作用，我們發現Palbociclib藉由調控PP5-AMPK路徑以誘發細胞死亡。希望這些研究結果能幫助肺癌的臨床研究，以造福病患。