費氏蛇
At the website “MathLinks EveryOne,” we found a problem “Snakes on a chessboard,” which was raised by Prof. Richard Stanley. The following is the problem. A snake on the m n chessboard is a nonempty subset S of the squares of the board with the following property: Start at one of the squares and continue walking one step up or to the right, stopping at any time. The squares visited are the squares of the snake. Prove that the total number of ways to cover an m × n chessboard with disjoint snakes is a product of Fibonacci numbers. We call the total number of ways to cover a chessboard with disjoint snakes “the snake-covering number.” This problem hasn’t been solved since it was posted on September 18, 2004, so it aroused our interest to study it. First, we used the way in which we added each block to the chessboard, and therefore we discovered some regulations about the snake-covering number of the1 × n , 2 × n and 3 × n chessboard. Through “recursive relation” and “mathematical induction”, we proved the general term of the snake-covering number of the1 × n , 2 × n and 3 × n chessboard. In the following study, we found a key method in which we added a group of blocks to the chessboard. Finally, we proved the general term of the snake-covering number of the m × n chessboard. Also, we discovered the way to figure out the snake-covering number of the nonrectangular chessboard.在網站“ MathLinks EveryOne ”中，我們找到了一個有趣的問題“棋然上的蛇” ( Snakes on a chessboard ) ，這個問題是由教授 Richard Stanley 所提出。問題如下：在m x n棋盤形格子上，蛇由任意一格出發，但蛇的走法只能往右 → ，往上↑，或停住 ‧ 若此蛇已停住，將由另一條蛇來走，且不同蛇走過的格子不可重疊”證明：將 m × n 棋盤形格子完全覆蓋的總方法數為費氐（ Fibonacci ）數列某些項的乘積。我們將把棋盤形格子完全覆蓋的所有方法數稱之為“蛇填充數” 由於這個問題自從 2004年 9 月 18 日被登在網站上後，還沒有人提出解答，於是引發了我們研究的興趣。首先，我們使用了將一個一個格子加到棋盤上的方法，並發現了 l × n 、 2 x n、 3 × n 棋盤形格子蛇填充數的一些規律。我們使用遞迴關係及數學歸納法來證明 l x n 、 2 x n ， 3 × n 棋盤形格子蛇填充數的一般項。在接下來的研究中我們發現一個特別的方法，一次增加數個方塊 ‧ 最後我們證明了，m x n, ，棋然形格子的蛇填充數的一般項 ‧ 而且，我們也找到如何求出不規則棋盤形格子的蛇填充數。
幽靈雷劈數的推廣及其性質研究
在2003 年台灣國際科展之作品說明書「Concatenating Squares」中【9】與2004第三屆旺宏科學獎「SA3-119 ：與特殊型質數之倒數關聯的兩平方總和的整數分解」成果報告書中【10】，就已有令人驚訝的結果。在2005 第四屆旺宏科學獎「SA4-298 ：分和累乘再現數產生的方法及其性質探討之推廣與應用」成果報告書中【11】，更是以逆向思維進行研究推廣，創造出許多新穎且引人注意的美麗數式，由原創性的觀點來進行逆向思維的研究。正由於這些再現數充滿奇巧，且與不定方程（代數）、簡單的數整除性分析（數論）以及同餘式理論都有所關聯，我們要發展前所未有的同步關聯與研究分歧， 且是最新的發現，更以豐富的想像力、創造力與推理能力提出令人耳目一新的重要結果，得到許多從未見過世面的美麗數式，回眸觀賞時內心充滿了數學之美！;Number which when chopped into two（three）parts, added / subtracted and squared（cubed） result in the same number. Consider an n -digit number k , square it and add / subtract the right n or n .1 digits. If the resultant sum is k , then k is called a Kaprekar number. The set of n -Kaprekar integers is in one-to-one correspondence with the set of unitary divisors of 10 n m1. If instead we work in binary, it turns out that every even perfect number is n - Kaprekar for some n . We wish to find a general pattern for numbers these numbers cubed or 3-D Kaprekar. We also investigate some 3-D Kaprekar of special forms. In addition, some results relating to the properties of the Kaprekar numbers also presented. This study indicates the “interesting” and “pragmatic” natures of the research project. We have developed the original results based upon his initiatives and has thus created a new horizon through the research project. This is the proudest achievement for this study. Generalization of Some Curiously Fascinating Integer Sequences：Various Recurrent Numbers！
台灣兒科病人罹患神經母細胞瘤者可檢測到微小病毒B19的存在
罹患神經母細胞瘤的兒科病人，尤其是罹患stage IVs 神經母細胞瘤者，他們有些伴隨著非常嚴重的貧血，但卻檢測不出神經母細胞瘤已經侵犯骨髓；有時病情來勢洶洶，尤其是腫瘤細胞中已可偵測到N-myc 基因增幅者，診斷時腫瘤細胞可能已在腹腔四處擴散並已侵犯大部分的肝臟。但是，某些這種病患，特別是腫瘤細胞中N-myc 基因沒增幅者，即使在沒有治療的狀況下卻可能有自然恢復的現象，也就是腫瘤細胞會自動消退，但原因仍待進一步的證實與探討。可是，這些病人在其病情最嚴重的時候，骨髓內紅血球母細胞形態上的改變顯示可能與病毒感染有關。但是關於病毒來源的研究，現有的資訊仍然十分有限，其中最重要的是，病毒感染與引發其後天之免疫作用是否有關，更需要深層的研究。因此，為更進一步了解罹患神經母細胞瘤之兒科病人的病毒感染及病毒蛋白表現的作用，我們這次研究的目的在檢驗罹患神經母細胞瘤及貧血之兒科病人與微小病毒B19 (PVB19)、Epstein-Barr Virus (EBV)、腸病毒71 型(EV 71)和巨細胞病毒(CMV)的關係，以及病毒蛋白表現對這些病人的作用與臨床意義。In pediatric patients with neuroblastoma, in particular, those with stage IVs neuroblastoma, sometimes the disease was combined with severe anemia. However, no tumor involvement was detected in the bone marrow. Although some of these patients may have N-myc gene amplification, and the disease could have invaded many abdominal organs, especially liver, interestingly, the disease might regress spontaneously in some of these patients. The medical reason of the spontaneous regression, nonetheless, remains to be determined. It is worth noting that morphological changes of erythroid progenitor cells in the bone marrow have suggested virus infection in these pediatric patients. However, the available information of viral origin is limited. Furthermore, it is possible that the virus infection in these patients could be associated with the revocation of immune responses related to the spontaneous regression of the tumor. In this study we will investigate the relationship of parvovirus B19 (PVB19), Epstein-Barr virus (EBV), enterovirus 71 (EV71) and cytomegalovirus (CMV) with neuroblastoma by PCR in Taiwanese pediatric patients. Moreover, we will study the effect and the clinical significance of viral gene expression as well as N-myc gene amplification in these patients.
完美長方形
正方形和長方形是每一個人都非常熟悉的圖形，但其中卻隱藏了非常多奇妙的“數學之謎”。 所謂「完美長方形」是：在一個長方形中 (長、寬不等)，能否分割出最少大小相異的正方形。 這個研究中，首先用「草圖」的解題方法研究完美長方形，接下來利用「平面圖形」的解題方法可簡化計算的過程，最後利用「對偶關係」證明出：完美長方形的最少階數為 9 階。 進而，我們將這個問題擴展至三維空間，思索在一個長方體中（長、寬、高都不等長） ，能否仿照二維空間，分割出最少大小相異的正方體，而完成這個研究。 Square and the rectangle are figures that everyone knows well very much, but what a wonderful " mystery of mathematics " is hidden among them. What is called the perfect rectangle is whether in a rectangle (its length and width is different ) could cut apart two squares as the least difference in size . In this research, the solution approach of "the sketch map" is used to study the perfect rectangle at first, then the solution approach of "the level figure" to simplify the complicatied calculation of the solving course , and "the dual relation" is finally used to prove 9 orders are the least orders for a perfect rectangle . And then, we expand this question to three-dimensional space, considering in a cuboid (its length, width, and height is different) whether could follow the two-dimensional space model to cut apart two squares as the least difference in size, and finish this research.
Mechanism of the subcellular localization of the actin binding protein adducin
Adducin蛋白在細胞骨架的調節上扮演著重要的角色。然而，近來有許多研究指出，骨架蛋白也會出現在細胞核並參與轉錄調控，因此本研究的目的即在探討adducin蛋白是否會進入細胞核中，並參與轉錄調控或具有其他功能。在本研究中，我們將綠色螢光蛋白(GFP)標示的adducin質體DNA，利用轉染技術送入老鼠纖維母細胞株NIH3T3中表現。NIH3T3細胞原本並無adducin蛋白的表現，在共軛焦顯微鏡下觀察，野生型的GFP-adducin蛋白會表現於細胞核與細胞質中。由於adducin蛋白尾端序列攜有可能往核內運輸的訊號，於是將位在此一訊號中的離胺酸718及離胺酸719進行突變，結果發現此一突變株只能在細胞質中表現。此外，蛋白磷酸脢C(protein kinase C)已知能磷酸化adducin蛋白在絲胺酸716及絲胺酸726的位置，於是假設其磷酸化是否與其在細胞內的分布有關。將adducin的絲胺酸726置換成丙胺酸，並不影響其在細胞內的分布。然而將絲胺酸716置換成丙胺酸後，則完全只在細胞核中表現。由於adducin可分布於細胞核，因此我們懷疑adducin蛋白可能與細胞分裂有關，於是本研究利用流式細胞儀分析adducin轉染後NIH3T3細胞的細胞週期。流式細胞儀的分析結果顯示，攜有GFP-adducin或其突變株的細胞與未經轉染的NIH3T3細胞的細胞週期並沒有顯著差異。其次，為了避免因轉染的效率不高而造成統計上的誤差，我們利用顯微鏡追蹤技術觀察攜有GFP-adducin的細胞株，結果顯示攜有adducin突變株的NIH3T3細胞株仍能正常分裂。再者，因為adducin能與細胞骨架中的肌動蛋白結合，所以adducin不同的分布位置可能影響細胞附著與細胞展延的效率。細胞展延試驗的結果顯示，adducin及其突變株對細胞附著與細胞展延的效率並無明顯的影響。本研究的結果證明，adducin的確帶有往核內運輸的訊號，其在細胞質中的分布可能也同時受到絲胺酸716磷酸化的影響。然而adducin的功用似乎與纖維母細胞的分裂與展延無明顯的關聯性。Adducin, an actin binding protein, is known to play an important role in the regulation of the membrane cortical cytoskeleton. More and more evidence indicates that proteins involved in the cytoskeletal regulation could also reside in the nucleus and participate in gene regulation. Thus, the goal of this study is to examine whether adducin is expressed in the nucleus and involved in certain nuclear events. In this study, adducin and its various mutants were fused with green fluorescent protein (GFP) and transfected into mouse NIH3T3 fibroblasts which do not have endogenous adducin for monitoring their subcellular distribution under a laser scanning confocal microscope. The wild-type GFP-adducin was found to be present both in the nucleus and in the cytoplasm. The COOH-tail of adducin contains a motif analogous to the nuclear localization signal (NLS). Mutation of two lysine residues (lysine 718 and lysine 719) located within this motif abolished the nuclear localization of adducin. Moreover, adducin is known to be phosphorylated by protein kinase C at serine 716 and 726. Substitution of adducin serine 726 with alanine had no effect on its subcellular localization. In contrast, substitution of adducin serine 716 with alanine led to only nuclear expression. Nuclear localization of adducin renders it possible that adducin may be involved in the regulation of cell division cycle. For cell cycle analysis, flow cytometry was applied. The results of flow cytometry indicated that expression of adducin and its mutants in NIH3T3 fibroblasts did not affect their cell cycle progression. To further examine the effect of adducin on cell division, NIH3T3 cells transiently transfected by adducin were monitored by time lapse video microscopy. The video clearly showed that the cells with GFP-adducin underwent cell division to generate two daughter cells. Since adducin is well known to bind to actin and thereby regulate microfilaments, we wondered that expression of adducin in NIH3T3 cells might affect their adhesion and spreading onto extracellular matrix proteins. The results of cell spreading assays showed that adducin appeared not to affect cell spreading. In conclusion, our results demonstrate that the subcellular distribution of adducin is likely regulated by two signals, one is the nuclear localization signal and the other is the phosphorylation status of the serine 716. However, enforced expression of exogenous adducin in fibroblasts such as NIH3T3 cells does not alter their cell cycle or cell spreading on fibronectin.