設有一組數列定義{ai,j,l},如下: 1. a1,1,1=0 2. ai,j,l規定: (1)除了a1,j,l,a2,j,l,a3,j,l,…,ai-1,j,l的整數不能再出現外的最小非負整數。 (2) 除了ai,1,l,ai,2,l,ai,3,l,…,ai,j-1,l的整數不能再出現外的最小非負整數。本研究首先發現 ai,j,l=aj,i,l,ai,i,l=0,ai,j,l=j-1,a2,j,l=(j-1)-(-1)j。並發現下列現象,並構造Al,r方塊。 Al,1=[0],Al,2=[01 10],Al,3=[0123 1032 2301 3210],設Al,r成立,Al,r=[ai,j,l]2k-lx2k-1xl,A*l,r=[bi,j,l]2k-lx2k-1xl,則bi,j,l=ai,j,l+2r-l Al,r方塊分割成4個方塊,Al,r=[Bl,r-l Cl,r-l Dl,r-l El,r-l] ,則Al,r=[Bl,r-l B*l,r-l B*l,r-l Bl,r-l] 。本研究發現方塊的對稱,主對角線,次對角線的性質,並利用二進位法尋找ai,j,l的一般式1l。本研究並延伸到三維空間,發現三維方塊的構造、三維的軸對稱、三維空間最小步數的奇偶性及以二進位法探討三維空間一般式。
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We investigate the machinery producing successive Simpson’s paradoxical reverse. Taking advantage of algebraic and geometric techniques, we obtain the following results. Take playing baseball for example. In our study, we find that Simpson’s paradox only occurs when the hitter’s hits over 3 times in one game. Set n equal to the times I will hit in one game. If my batting average in each game is at least(n ?1)/2 times higher than the others’; then I am sure that my total batting average would not be invert by the others. In order to find how many the lattice points in the triangle, we use Pick’s formula. But sometimes, the Pick’s formula is not appropriate to triangles whose vertex are not all lattice points. So we develop New Pick’s formula to estimate the number of lattice points in such kind of triangles. Besides, we also find an iterative algorithm to produce successive “Simpson reverse” phenomenon by using C++ language, and we can therefore produce as many “Simpson’s set of four sequences” terms as we like(not beyond the computers’ upper limit).Moreover, if both sequences of ratios converge, then they must have the same limit.我們探討了一般人乍看之下顯得頗弔詭的辛普森詭論。我們配合GSP 作圖,用解析幾何、設立直角座標系和C++ 程式的運算,找出在特殊情況下或一般情況下所產生的辛普森數列組和特殊的性質,並且以棒球場上的打擊率為例子來做印證。通常一場棒球賽中,每個人平均上場3 次~4 次,經過我們的討論,發現要發生逆轉的機會只有在上場達到4 次或以上時才會發生。?了求出在直角座標系中可以滿足的格子點個數,我們用了Pick公式,但?了更準確的估計,我們引進了虛點的概念,重新推導出了新Pick 公式。另外,我們還發現,假設兩個人上場比賽,若打了2 場,且每場最多上場打擊K 次,其中的一個人的打擊率只要是另一個人的(k-1)/2倍以上就保證不會被逆轉。我們又找到了連續產生辛普森逆轉的演算法,利用C++ 寫出程式,經由演算法和遞迴式,製造出項數可任意多(只要電腦能夠承受)的辛普森數列組,且我們發現若兩個比值數列接收斂,則極限趨近於同一個數值。
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突變ras基因造成過度表現在骨髓間質幹細胞啟動氧自由基誘導細胞凋亡
特定基因的表現與不同氧自由基的產生,已知會影響細胞的生長和死亡。我\r 個人有興趣利用間質幹細胞體外培養擴充,以為筋骨組織再生的可能應用。因此\r 利用轉植(transfect)突變ras 基因(Glu61Leu)進入骨髓間質細胞株(HS-5 cells),來\r 控制ras 基因表現的高低,進而研究這些間質細胞隨著Ras 蛋白質表現的高低,\r 對氧自由基引導細胞生長與死亡之影響。結果發現ras 基因高度表現的間質細胞\r 生長減緩;相較於原生株平均減少62.4%。進一步研究其生長減少是否與細胞凋\r 亡有關,發現ras 基因高度表現的間質細胞凋亡確實比原生株高22.6%。探究其\r 凋亡原因,發現與caspase-3 有關但和粒腺體功能無關:因為caspase-3 有活化,\r 但是以粒腺體膜電位螢光追蹤劑JC-1 測得的膜電位卻沒有改變。追蹤ras 基因高\r 度表現的間質細胞其細胞內氧自由基的產量,發現Ras 高度表現株其細胞內氧自\r 由基明顯增加。當細胞外加入超氧根轉化酵素(SOD, 500 U/ml)去清除超氧根時,\r 對Ras 高度表現細胞的凋亡沒有影響;但是外加觸化酵素(catalase, 500u/ml)於培\r 養液中,卻可以抑制ras 基因高度表現的間質細胞內caspase-3 活化和細胞凋亡;\r 並且增加細胞生長循環促進分子Cyclin D1 的表現。從這些研究我們歸結出兩點\r 重要新發現: 1) ras 基因突變造成Ras 高度表現時,會促成細胞內特定氧自由基產\r 生,使得細胞生長減緩並進行細胞凋亡,只有特定抗氧化酵素(catalase)才能恢復\r 其異常; 2) Ras 蛋白高度表現而引導氧自由基產生的細胞凋亡與caspase-3 活化\r 有關,但與粒腺體功能無關。根據這些發現,未來我們或許可以朝調節特定氧化\r 還原反應或使用caspase-3 抑制劑去調控間質幹細胞的生長,以供筋骨組織再生\r 的應用。Certain gene’s expression as well as different species of oxygen radicals can\r affect cell growth and apoptosis. We are interested in amplifying mesenchymal\r progenitor cells for the application of musculoskeletal tissue regeneration. Thus, we\r transfected a mutant ras gene (61Glu/Leu) to change Ras protein expression in the\r mesenchymal progenitor cell line (HS-5 cells) and studied how ras expressing levels\r influenced intracellular oxygen radicals, and its relationship to cell growth and\r apoptosis. Results showed that Ras over-expressing HS-5 cells grew slower than those\r with wild type ras HS-5 cells and revealed a higher apoptosis rate. The higher\r apoptosis in Ras over-expressing cells was not related to mitochondrial dysfunction\r since mitochondrial membrane potential was normal as determined by flow\r cytometric analysis of JC-1 fluorescent staining assay. The higher apoptosis was\r related to higher caspase-3 activation. Further studies showed that Ras\r over-expressing HS-5 cells revealed a higher production of intracellular oxygen\r radicals in comparison to those with wild type ras HS-5 cells. Addition of catalase\r (500 u/ml) but not superoxide dismutase (SOD; 500 u/ml) specifically revived the cell\r growth associated with increase of cyclin D1 expression, but decrease of apoptosis\r associated with lower caspase-3 activation. Results from these studies demonstrated\r two important findings: 1) the ras gene over-expressing in a ras-mutant HS-5 cell line\r triggers a higher production of intracellular oxygen radicals resulting in higher cell\r apoptosis; and 2) the higher oxygen radicals related cell apoptosis is mediated by\r caspase-3 but not mitochondrial dysfunction. Based on these findings, we may\r propose to regulate mesenchymal progenitor cell growth for musculoskeletal tissue\r regeneration via modulation of redox reactions or caspase-3 inhibitors in the future.
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符合畢氏定理X12+X22=X32的正整數解(X1,X2,X3)我們稱為三元畢氏數;符合N元不定方程式X12+X22+⋯+Xn-12=Xn2的正整數解(X1,X2,⋯,Xn-1,Xn)被稱為N元畢氏數。本研究更正陳揚叡同學在台灣2008國際科展中對N元不定方程式X12+X22+⋯+Xn-12=Xn2所提出的N元畢氏數一般解,並利用對圓點方陣的降階分奇偶數組加以探討,其中,奇數組是在(M+1)階方陣中透過一次降一階來探討三元畢氏數中X1=2k+1的情況,而偶數組是在(M+2)階方陣中透過一次降二階來探討三元畢氏數中X1=2k+2的情況。在獲得初步的成果後,又藉著直角三角形的擴充依遞迴定義的方式來進一步來探討N元畢氏數。最後,我得到N元畢氏數(X1,X2,⋯,Xm,⋯,Xn-1,Xn)的關係式(表一)。
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