黑擬蛺蝶(Junonia iphita iphita)的幼蟲生存策略
黑擬蛺蝶(Junonia iphita iphita)為台灣地區常見的蛺蝶，其幼蟲具有築巢行為，但文獻中對其幼蟲行為的描述極少，因此本實驗探討黑擬蛺蝶幼蟲在野外的族群變化與環境之關係，並研究幼蟲築巢行為，以探討其適應環境的生存策略。首先於室內及恆溫生長箱中飼養幼蟲，以建立其生活史基本資料，並於野外統計各齡期幼蟲在不同植物上的數量變化及築巢行為的差異，以探討不同環境因素對幼蟲築巢之影響。由實驗結果得知，黑擬蛺蝶生活史短，可取食多種爵床科(Acanthaceae)之植物，其寄主植物除文獻所紀錄之台灣馬藍(Strobilanthes formosanus)及賽山藍(Blechum pyramudatum)等外，也取食大安水蓑衣(Hydrophila pogonocalyx)、無花水蓑衣(Hygrophila violacea)、易生木(Hemigraphis repanda)及翠蘆利(Ruellia brittoniana)等。黑擬蛺蝶幼蟲野外族群波動與溫溼度及雨量等環境因子並無直接關係。黑擬蛺蝶一年發生多世代且有世代重疊情形，世代波動與四季律動關係不明顯，顯示黑擬蛺蝶對環境的適應力大。黑擬蛺蝶幼蟲利用築巢以適應環境變化，應是其幼蟲良好的生存策略。且幼蟲在強風及光線強的環境下築巢率增加，降雨時則減少。Junonia iphita iphita belongs to Nymphalidae（Lepidoptera）. They can be found easily in the wilderness of Taiwan. Its larva shows nest-making behavior. However, there is little literature documenting the behaviors of its larva. Therefore, the purpose of this research is to investigate the relationship between the quantities of Junonia iphita iphita’s larvae and its natural habitat, to research its nesting behaviors, and to investigate its survival strategies to adapt to the environment. I started by raising larvae in a growth chamber under a controlled temperature in order to obtain its initial information regarding its life history. In the field, I documented the numbers and the changes of larvae at each stage on different host plants and recorded the differences in its nest-making behavior in order to find out which environment factors influence the nest-making of Junonia iphita iphita’s larvae. These experiments concluded that the life history of larvae is short. The immature intaking habit showed that the larva takes various plants of the Acanthaceae. In addition to the host plants mentioned in the literature, such as Strobilanthes formosanus, and Blechum pyramidatum, Junonia iphita iphita’s larvae also live by Hydrophila pogonocalyx, Hygrophila violacea, Hemigraphis repanda, and Ruelba brittoniana, which were not listed in the literature. Through experiments, I discovered that there is no direct correlation between the population fluctuations of larvae and it’s enviroment including factors such as temperature, humidity or rainfall. Junonia iphita iphita can produce multi-generations in a year accompanying generation overlapping. There is also no obvious correlation between the generation fluctuations and changing seasons, showing that larvae can easily adapt to the environment. Junonia iphita iphita’s larvae adapt themselves to the different environments by nest-making which should be a good survival strategy. Besides, the rate of nest-making increases when larvae are under strong winds and strong lights and decreases when the rain falls.
阿拉伯芥AtYAK1 基因5'UTR 中的開放讀序框(uORFs)對基因表現調控之探討
在模式植物──阿拉伯芥（Arabidopsis thaliana）中，AtYAK1（Arabidopsis thaliana Yak1-related protein kinase）是目前發現唯一屬於DYRK（Dual specificity Yak1-Related protein Kinase）的蛋白激?。雖然之前研究已證明，不同物種之DYRKs 和細胞的生長與發育過程有關。然而，其在植物中的生理功能卻尚未被明確地研究報導過。在先前的研究中，為瞭解AtYAK1 在阿拉伯芥內作用之位置，前人選取AtYAK1 基因ATG 上游約2.5 kb 的序列（Upstream Element, 2.5KUSE）建構至一含有GUS（β-glucuronidase）報告基因的質體中，並轉形至阿拉伯芥，進行GUS 組織染色分析。但在初步結果中，並沒有在轉殖株觀察到明顯的GUS 表現。進一步分析，我們發現在2.5KUSE 序列末端約0.5 kb 的5’非轉譯區（5’untranslated region, 5’UTR）中，有四組開放讀序框（Upstream Open Reading Frame, uORF）。有趣的是，許多研究也顯示，uORFs 會影響轉譯過程中的再起始（re-initiation）作用而調控該基因的表現。另一方面，前人亦透過構築好的2KUSE 轉殖株（即不含有5’UTR）進行上述GUS 實驗。結果發現，此2KUSE 轉殖株的GUS 表現非常顯著。本實驗即要瞭解AtYAK1 的uORFs 是否也會影響其蛋白質的合成。首先，我們以點突變的方式將四組uORFs 中之ATG 換成TTG，目的為構築不含有uORFs 之5’UTR（mutated uORFs, ΔuORFs）。在進行原生質體短暫表現分析法（protoplast transient assay）及GUS 組織染色分析後，將結果與含有uORFs 的結果作比較：當缺乏uORFs 後，其3’端報告基因的表現量確實比原來顯著。綜合以上，我們認為此uORFs 對於AtYAK1 蛋白質之表現佔有相當重要的影響地位。最後，我們對5’非轉譯區是否存在開放讀序框進行阿拉伯芥全基因組分析，相關結果亦於本研究報告中分析討論。AtYAK1（Arabidopsis thaliana Yak1-related protein kinase）is the first DYRK（Dual specificity Yak1-Related protein Kinase ） family member identified in the model plant ─ Arabidopsis thaliana and exists as one copy gene in Arabidopsis. Previous studies showed that many eukaryotic DYRKs are involved in regulating the growth and development of cells. However, the study of AtYAK1 in Arabidopsis is lacking to date. In order to understand where AtYAK1 expresses and functions in plants, a 2.5 kb fragment which is located upstream from the major ATG of AtYAK1（termed Upstream Element, 2.5KUSE）was previously constructed to drive the expression of a reporter gene, GUS（β-glucuronidase）, in transgenic Arabidopsis. Much to our surprise, no GUS expression signal could be detected in such transgenic plants. When further analyses were performed, we found that there are four upstream open reading frames （uORFs） in the 5’untranslated region ( 5’UTR ) within the 2.5KUSE. Many studies indicating that the uORFs can regulate the translation of downstream ORF encoding the major gene product through the procedure of translation re-initiation. This action represents a mode of translational regulation for gene expression. Indeed, GUS activity could be readily detected in transgenic plants expression 2KUSE::GUS, a construct lacking the 5’UTR of AtYAK1. In this study, I have tried to elucidate whether the uORFs of AtYAK1 can regulate the translation of the downstream major ORF. First, in order to construct a 5’UTR fragment of which uORFs have been mutated（ΔuORFs）, we apply site-directed mutagenesis to substitute ATG with TTG for the four uORFs and examine the expression of GUS driven by this mutated 2.5KUSE. After analyzing the results in both Arabidopsis protoplast transient assay and transgenic Arabidopsis, stronger expression of reporter genes in both systems were observed when the four uORFs were mutated. We have also confirmed that, in transient expression system, the increase of reporter gene activity was not due to the excess accumulation of the corresponding mRNAs. Rather, it is the four uORFs which play an important role in negatively regulating the translation of AtYAK1, possibly via inhibiting the translation re-initiation of major ORF. A genome-wide examination of uORFs in all Arabidopsis genes was also performed to assess the possible contribution of uORF in regulating gene expression.
生生不息-正五邊形的繁衍及算術法則
This study was to explore the nature of two basic constitutes of the regular pentagon,With these two constitutes, the regular pentagon could be multiplied into any times in size. We used four multiplication methodsto show how the regular pentagon enlarge and to verify that the enlarged regular pentagons derived from computer did exist. By integrating these four multiplication rules, we were able to arrange regular pentagon of any length of side, and evidenced the equation was ( If m,n is the number of A,B of a regular pentagon respectively ) When we tried to verify if any regular pentagon could be constituted by other smaller regular pentagons, we found that it was un-dividable only if the length of pentagon side were (the number of A, B were the 2n and 2n-1 item of Lucas Sequence), otherwise, any regular pentagon is able to be constituted by other smaller regular pentagons. The divided forms could be multiple. We also found that any pentagon could be divided by two successive un-dividable pentagons, which is called “standard division rule”. We expected to derive all kinds of division by analysis of two successive un-dividable pentagons in standard division rule.
這個研究起源於一個拼圖玩具：利用兩種黃金三角形排出指定大小的正五邊形。我們的研究動機是：一、 假如無限量供應A 和B，能夠拼出哪些邊長的正五邊形？二、 哪些拼好的正五邊形不能拆成一些較小的正五邊形？我們將研究的主要結果分述如下：
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.
宇宙演化的黑手
We study the effect of dark energy on the evolution of cosmic structure in a scenario where the dark energy is treated as free particles and thus can be localized. By theoretical derivation and numerical simulations, we found that:
1. The dark energy particles gain kinetic energy from a moving dark matter particle through gravitational interaction. Due to energy conservation, the dark matter particle will slow down with time
Ek(t) = Ek0 - 9 × 10-5[|1+3w|ρDE]1.92t where Ek(t) is the kinetic energy of the dark matter particle,Ek0 is its initial kinetic energy, w is the coefficient of equation of state for dark energy, ρDE is the mean energy density of dark energy, and t is the time.
2. The formation history and structure of galaxy clusters are different in the presence of localized dark energy. The more the localized dark energy, the earlier the formation of the cluster core. In addition, the kinetic energy Ek(R) as a function of R will be different if the ρDE is different. Thus we can compare the observed Ek(R) of clusters with our results to deduce the ρDE in our universe. The results here can be applied to the observations in the near future.
我們探討宇宙結構演化受到可局部叢集之黑暗能量粒子的影響。藉由理論推導及電腦模擬，我們發現：
一、黑暗能量粒子會透過重力交互作而從運動中的黑暗物質粒子獲得力學能。因力學能守恆，黑暗物質粒子的速率會減慢，滿足
Ek(t) = Ek0 - 9 × 10-5[|1+3w|ρDE]1.92t
其中Ek(t) 為黑暗物質粒子的動能，Ek0 為其初始動能，w 為狀態方程式係數，ρDE 為黑暗能量的平均密度，t 為時間。
二、星系團的形成過程及結構，會因可局部叢集之黑暗能量的存在而改變。黑暗能量越多時，星系團的核心會越早形成。而且動能 Ek(R) 隨著至星系中心距離R 的變化，會因 ρDE 的不同而不同，因此可以將量測到的 Ek(R) 和這裡的結果比對，推導出宇宙中的 ρDE 。 這些研究成果將可直接應用在未來的觀測結果上。
n x n 方格表中的計數問題
對4 × 4 方格表中計數問題的二個解題方法(1..解方程式的方法， 2.分割圖形的方法)作分析和研究後，首先我推廣分割圖形的方法來証明 : “好的n × n 方格表” 存在若且惟若n 為偶數。同時証明這種“好的n × n 方格表”內所有n2 個數的總和f(n) 為n(n+2)/4。當討論一般的n×m 方格表時，發現分割圖形的方法盲點，無法繼續推廣來証明。再經過深入分析與推廣解方程式的方法，藉由n×m 變數方格表，我們終於找到構造所有“好的n × m方格表”的方法。同時計算“好的n × m 方格表” (n≦m)內所有mn 個數的總和f(n,m), n≦7和証明好的nxm 方格表會有2(n+1)行一個循環的現象。We first studied two solution methods (1.solving equations,2.dissecting diagrams.) for calculations on 4x4 checkboard. Using the method of dissecting diagrams, we proved that``good nxn checkboard'' exists if and only if n is even. Furthermore, the sum f(n) of those n2 numbers in a ``good'' nxn checkboard is equal to n(n+2)/4.In studying the more general nx m checkboards, we found that the method of dissecting diagrams does not work, However, by extending the method of solving equations, and by considering nx m variable checkboards, we obtained a way of obtaining all ``good nxm checkboards.'' By way of computing the sum f(n,m) (n≦7) of those mn numbers in a ``good nxm checkboards,'' periodicity in every 2(n+1) rows is observed.
橡膠鍵鏈結構與自由能的關係
受應力拉伸時，橡膠溫度明顯上升；縮放回原長，橡膠溫度驟降。由文獻得知橡膠內部具有特殊的鍵鍊結構，在一般的情況下，交鏈分子糾結成一團，狀態複雜；受外力拉伸時，交鏈分子依橡膠長度之增加而伸展，排列較為整齊，狀態之複雜度減小。根據熱力學第一定律，當內能變化為零，則外力作功會造成能量變化。在定溫之下，橡膠內能變化為零，當其受應力拉伸，使其內部交鏈分子排列複雜度降低，造成橡膠熵值減小，而有能量（dQ=TdS）的釋出。測量此一能量dQ 變化，即可計算出熵與狀態數之變化The temperature of rubber rises as it is stretched, its temperature comes back again while it restores to its original length. It is known that the rubber is consisted of long-chain molecules, the long-chain molecules strangle each other at normal state, however, they become more order when the rubber is stretched. Based on the 1st law of thermodynamics dU=dQ+dW, The deformation caused by applied force supplies energy to the rubber and reduce its entropy, the heat dQ (=TΔS) released by the reduction of entropy causes the temperature rise of rubber as dU=0. We report the study on the correlation of thermal properties and the molecular network in rubber, from the measurements of temperature change, the changes of entropy and the changes of states’ number were estimated.
停車就是彈硬幣
在這個科展中我們要研究兩個非常有趣的問題：\r 停車場問題 與 彈硬幣遊戲.\r 停車場問題是這樣的：在一條單行道上有n個車位，編號從1到n。現在有n個司機排成一排要進入停車。但是每個司機都有怪癖，各自有最想要停的位子。他們依序將車子開進單行道，如果想要停的位子是空的，當然停在這個位子。但是如果不巧那個位子已經被停了，不得已只好找下一個空位，姑且停之。但是如果往下找都沒有空位，由於是單行道，司機就只好開走不停了。\r 比如說，如果現在有五輛車，司機的喜好分別是(3,1,2,5,2)。則五輛車都可以順利停車。但是司機的喜好如果是(3,1,4,5,4)，有些車就無法停車了。\r 彈硬幣遊戲是這樣的：考慮圓內接正n+1邊形，任意兩點都連線。這正n+1邊形中有一個頂點P是特殊的，每個頂點上一開始都放有一些硬幣(各點硬幣數可以不同)。如果P以外的某個頂點上的硬幣數n個，我們可以對這個頂點進行操作：一次操作是指將這個頂點上的硬幣各分一個給每個其他頂點。點P只在其他點都無法操作時操作。我們不理會頂點P上的錢數，因此這個遊戲可以無限地玩下去。