溫變性轉(孵化條件對宮廷雞性別的影響)
目前生物學知識認為雉科鳥類的性別，在卵受精後即決定(WZ型)，不受環境的影響，但是在本組一連串的實驗中發現，雉科鳥類的性別與孵化的溫度變化有非常大的影響，一般宮廷雞的孵化條件在濕度55％RH及溫度98℉～99℉，在此孵化條件下宮廷雞的子代♀：♂=1：1，若溫度降為97℉的孵化條件下所得子代♀性佔93％，倘若溫度升高為100℉的孵化條件下所得子代♂性佔92％，可見在比正常孵化溫度高的環境下宮廷雞的受精卵會轉變為♂性，而比正常孵化溫度低的環境下孵化的宮廷雞受精卵卻會轉變為♀性，本實驗續做了六代，結果大致相似，由此可以證明控制孵化溫度可以改變宮廷雞的性別，這一行為，可能與Z染色體上一個溫度依賴型的連鎖基因(DMRT1)之表現有關。 ;The temperature of hatching can affect Chinese silkys's sex It is now established that the sex of Pheasants is determined when the egg is impregnated, rather than by environmental factors. However, in a series of experiments, we find that the sex of Pheasants is strongly related to the temperature of hatching. In the normal hatching condition (humidity:55% RH ,temperature: 98.5℉), the ratio of female and male offspring of Chinese silkys is 1:1. If the temperature is lowered to 97℉, the female offspring occupies a proportion of 93%. If the temperature is raised to 100℉, the male proportion will reach 92%. We can thus derive the conclusion: the impregnated eggs of Chinese silkys will be transformed to male at a temperature higher than the normal one, while a lower temperature than the normal one will cause the impregnated eggs to be female. The experiments have been conducted through six generations of Chinese silkys, and the results are practically the same. This indicates that temperature changes can affect gender, This may be related to a Z-linked of DMRT1 gene on the DNA, which is temperature-dependent.
樂器聲波之探討(The Study of A Sound Wave on Musical Instruments)
演奏樂器時，是使發聲體產生駐波而發出各式各樣悠揚的聲音及音調；樂器主要分成振動體(發聲體)及共鳴器兩部分，依發音方式分為弦樂器(使弦振動產生駐波)、管樂器(利用空氣柱振動產生駐波) 及打擊樂器(利用板、膜或磚等彈性材料的固有頻率振動產生駐波)。聲音有三要素：振幅、頻率及波型，響度取決於振幅大小、音調與頻率有關、波型則由不同的頻率及響度組成。樂音多變的主因是音色及音調。音色是發聲體的發音特性，取決於該發聲體的聲波波型。音調即聲音的高低，與發聲體的振動頻率材質息息相關，頻率愈高，其音調愈高，而樂曲中的音階高低則是由音調高低所構成。樂曲的製作及演奏必涉及到律制，從駐波的產生、律制的探討、頻率的測量和琴鍵的振動模型建立與波形的觀察，我們使用計頻器、示波器及有限元素ANSYS 軟體、數學計算Mathematica 軟體，我們設計一系列實驗，企圖對樂器聲波操作技巧有更進一步的認知。從實地走訪樂器製造廠，了解到設計與改良仍是樂器工藝家重要課題，本文的實驗方法可提供大型演奏會現場調音、樂器調音師或樂器工藝家設計製造樂器時參考用，對於發展文化產業期待提供更經濟與實用的建議。;Playing musical instrument is to make sounding part produce stationary wave so as to give off various gentle sounds and tones. According to different modes of sound producing, musical instruments which comprise vibrator (sounding part) and resonator can be divided into stringed instruments (which vibrate the strings to produce stationary wave), wind instruments (which produce stationary wave with vibration of the air column) and percussion instruments (which produce stationary wave with natural frequency of boards, films or bricks). Three Essentials of sound include amplitude, frequency and waveform, in which the amplitude decides the volume, tones are related to frequency and the waveforms are composed of different frequency and volume. Various musical sounds are mainly due to different timbres and tones. Timbres, sounding characteristics of sounding part, is decided by waveform of the sounding part. Tone means pitch of the sound and is closely related to vibrating frequency of sounding part. Higher frequency makes higher tones and pitch of a musical scale is decided by different tones. Music composing and playing is necessarily connected with music temperament including producing of stationary wave, discussion of temperament, measurement of frequency, establishment of vibrating mode of keys and observation of waveform. We adopted frequency counter, wave inspector, ANSYS software and Mathematica software and designed a series of experiment to get further knowledge of technique of handling musical instrument wave. After visiting musical instrument manufacturers, we learnt that design and improvement are still the essential subjects for instrument craftsmen. Experimental method in his article can provide reference for on-the-spot tuning of large concert, musical instrument tuner and musical instrument designing and manufacturing by craftsmen, and more economic and practical suggestion for cultural industry development.
Poly(ADP-ribose)polymerase-1 對細胞內DNA damage修補的調控
Poly(ADP-ribose) polymerase-1 (PARP-1)是一個細胞核內的酵素，它可以被因DNA damage\r 而形成的DNA片段活化，並將NAD(+)上的ADP-ribose轉載到結合蛋白質。這些結合蛋白質對\r 於DNA的合成、DNA的修補、以及細胞週期的調控都有關係。因此，PARP-1被認為是維持基\r 因完整性的重要角色。根據初步的研究，抑制PARP-1的活性對許多疾病的治療都可能有效，\r 其中包括癌症、心臟病、中風、糖尿病、發炎以及反轉錄病毒的感染。然而，以藥物抑制一\r 個對DNA修補這麼重要的酵素會有什麼潛在的問題呢？為了要得到解答，我們需要進一步了\r 解PARP-1在DNA damage反應的機能。在這一份報告中，我製造了一個失去活性的PARP-1突變\r 種，即E988K。經過對E988K詳細的研究，我將比較及分析PARP-1野生型與E988K之間不一樣\r 的互動蛋白質，希望能對PARP-1所控制的DNA修補有更進一步的了解。\r \r \r Poly(ADP-ribose) polymerase-1 (PARP-1) is a nuclear enzyme activated by DNA strand breaks\r during DNA damage response and catalyzes the transfer of ADP-ribose units from the substrate NAD(+)\r to acceptor proteins. These acceptor proteins involve in modulation of chromatin structure, DNA\r synthesis, DNA repair, transcription, and cell cycle control. Thus, PARP-1 is believed to play an\r important role in maintaining genome integrity through modulation of protein-protein and protein-DNA\r interactions. PARP-1 has been the target for design of inhibitors for over twenty-five years. Inhibitors of\r the activity of PARP-1 have been claimed to have applications in the treatment of many disease states,\r including cancer, cardiac infarct, stroke, diabetes, inflammation and retroviral infection. However, are\r there potential problems associated with inhibition of this DNA-repair enzyme? To answer this question,\r we need to further understand the biological function of PARP-1 during DNA damage response. In this\r report, an enzyme dead mutant (E988K) of PARP-1 was generated. Detailed studies of E988K show that\r E988K could be used in the following studies. Compare and identify the different associated proteins of\r PARP-1 wild-type and E988K will shed light into the molecular mechanism of PARP-1-mediated DNA\r repair.
口琴簧片振動與氣流的影響
本研究主題在測量口琴簧片受到各種氣流因子影響後，所產生音色、音頻等變化之探討。在過去我們認為，一片簧片不論如何吹奏，其發出的頻率皆相同。但是事實上，演奏家控制氣流的強弱、方向、渦流等，便可吹奏出多樣的音頻。探討形狀因子對簧片頻率的影響，如：長度、寬度、厚度對頻率所造成的影響。自製口琴，利用變壓器控制送風機風速。探討氣流因子對簧片主頻之影響，利用各種不同的自製吹嘴，改變風速、角度、渦流…等，找出可能使簧片改變頻率的氣流因素。實驗結果發現改變風速會影響簧片主頻的變化，風速越大，頻率越大，為一條平滑線。但並非一直都會上升，當簧片頻率上升至某一極限，便無法再利用風速使頻率上升。例如實驗四吸音標準狀態下，風速大於8 Kt 後，頻率一直停在429Hz。在外加障礙物時(模擬吹奏舌頭時隆起)和標準狀態(正常零度入射)下頻率比較吹音和吸音有明顯的差異。吹音時，同風速下，其頻率比標準狀態高，發生音升；吸音時，同風速下，其頻率比標準狀態低，發生音降，具應用性。我們發現在頻率改變時，簧片的振動型態會有所不同，所以利用高畫素像機拍攝和電腦相位差算出簧片之曲折點至尾端的距離，發現頻率和簧片之曲折點至尾端的距離成正向關係。如實驗五中頻率從414 至419Hz，簧片的曲折點到振動端距離也明顯變大。我們發現吹嘴和口琴只要稍有一點空隙(大約在0.2cm 左右)，便會和完全吻合時有顯著的頻率差距(吻合後大約比有空隙低20Hz 左右)，此實驗頻率變化現象和現實壓音頻率變化極為相近。實驗過程中發現，改變簧片吹嘴的吻合程度，吹入口琴的風速相近，但頻率變化卻也有壓音的音頻變化。在實驗三加入各種氣流因子發現入射角度和標準情形差異不明顯，因此推論壓音的頻率變化和風力強度、入射角度關係不大，壓音主要為渦流所造成的現象。簧片振動模式改變，導致簧片振動頻率發生變化，且簧片的自然頻率不變。當壓音產生時，氣流在振動面造成妨礙簧片振動的抗力，但琴格內部同時也給簧片的風壓，使簧片產生一種非自然振動的頻率。The theme of the research is to explore the changes on its timbre and frequency after the harmonica reed is influenced by each kind of air current factor .In the past ,most people think no matter how to play the reed ,the frequency it produced was supposed to be the same. But in fact the frequency will be changeable under different direction, turbulent flow and air intension by the perform. First to explore the basic feature of harmonica reed, for example: The length, the width, thickness cause the influence on the frequency. To make the self-made harmonica, using the transformer control air feeder wind speed. To discussion the influenced caused by air current factors,and use each kind of different self-restraint to boast, change the wind speed, angle, turbulent flow ,in order to discover possible factors the reed causes to change the frequency of the air current factor. The experimental result discovered the change of wind speed can affect the change of basic frequency , the stronger speed cause the bigger frequency, It will be a curve. But it will not be rising continuously, when the reed frequency rise to some limit, it is unable to cause the frequency rise again by using the wind speed. For example experiment four sound absorption standard conditions, after the wind speed is higher than 8 Kt, the frequency continuously stops in 429Hz. To compare obstacle (simulation plays when tongue sticks out) and the standard condition (normal zero degree incidence) , comparison blows the sound agreement sound absorption to have the obvious difference. When blows the sound, under the same wind speed, its frequency is higher than the standard condition, has the sound to rise; When sound absorption, under the same wind speed, its frequency is lower than the standard condition, has the sound to fall. The harmonica terminology for presses the sound, extremely has the application. We discovered when frequency change, the reed vibration condition have differently, therefore use the camera photography and the computer phase different figures out the reed winding point to the end distance, discovered the frequency and the reed winding point relate to end distance is being connected. If tests five medium frequencies from 414 to 419Hz, the reed winding point is away from to the vibration end also obviously changes . The different reed vibration condition cause the frequency to change. Natural frequency is constant. When cause “bending” (the frequency is lower than the standard condition), the airflow make a force keep from reed vibration. But the chamber air pressure still drive reed. therefore cause the reed to give off not natural frequency sound
重金屬錯影響細胞生理功能的研究
儘管鍺在電子工業上被廣泛運用，但對於暴露在鍺化合物所產生的毒害則尚未被詳細的探討。在探討鍺對細胞所產生的生理影響中，我們使用了二氧化鍺 ( GeO2）和有機鍺（ Ge-132 ）。由實驗結果顯示， GeO2，會造成人類子宮上皮癌細胞（ A 431 ) 及巨噬細胞株（ Raw264.7 ）死亡，而 Ge -132 對細胞生長則不造成任何影響，為了進一步了解鍺引起細胞死亡是否是經過細胞凋亡（apoptosis ) ，我們將鍺處理過的細胞進行染色體 D NA 的分析，結果發現細胞中 DNA 染色體沒有斷裂。由先前 Huang 等人於 1999 年的研究結果顯示，砷對細胞所造成的毒性是經由有絲分裂活化酵素（ MAPK ）傳導路徑，所以為了解鍺誘導細胞死亡的路徑，我們亦分析 MAPK 傳導路徑是否亦參與其中，我們發現 GeO2加入 A431 細胞後，會活化有絲分裂活化酵素中的 ERK ，但對JNK 及 p38 皆無影響，在對蛋白質表現方面，轉錄因子 c-Jun 的蛋白質表現也是隨著GeO2加入的時間增加而上升。 GeO2加入 Raw 264 . 7cell 後，會造成 JNK 、 ERK 的活化，同樣的轉錄因子 c- Jun 也會增加，由此一結果得知鍺對細胞的影響會因細胞的不同而有所差異，為了分析自由基是否參與砷及鍺所造成細胞死亡的過程，我們分析在 A431 細胞中可產生的 NO 的可誘導性 nitric oxide synthase ( iNOS ）的表現，我們發現氧化鍺及砷都會誘導 iNOS 的表現量增加。綜合以上結果，可能顯示氧化錯可能會經由 M A PK 訊息傳遞路徑來促使細胞的死亡，並且 iNOS 亦可能參與此過程。就我們所知，這是第一個提出重金屬所造成的毒害可能會經由 iNOS 來誘導產生的研究。
Despite the extensive use of germanium (Ge) in the electronic industry and optical devices, the potential risks of exposure to germanium compounds have not been evaluated. The effects of germanium on cell physiological functions were studied. We first asked if germanium oxide (GeO2) or carboxyethylgermanium (Ge-l32) could affect cell viability. We found that GeO2, but not Ge-l32, reduced cell viability in a dose-dependent manner in epidermoid carcinoma A43 I and macrophage Raw 264.7 cells. In order to test whether apoptosis contributes to germanium cytotoxicity, DNA fragmentation was evaluated in A43 1 and Raw 264.7 cells treated with GeO2 or Ge-132, respectively. We found that neither GeO2 nor Ge- 132 had effect on chromosomal DNA fragmentation. Previous studies by Huang (1999) et al indicated that sodium arsenite (NaAsO2) cytotoxicity is mediated through mitogen-activated protein kinase (MAPK) pathways. In order to study the mechanism(s) by which GeO2 mediates cell death, we analyzed the signal transduction pathways triggered by GeO2 We found that GeO2 stimulated the extracellular signal-regulated kinase (ERK) activity and transcription factor c-Jun in a time-dependent manner, but not c-Jun amino-terminal kinasc (JNK), or p38 MAPK in A431 cells. Treatment of the Raw 264.7 cells with GeO2, induced activities of ERK, JNK and c-Jun in a time-dependent manner. Collectively, these results suggested that GeO2 effects might be cell type specific. To test whether free radicals were involved in NaAsO2 or GeO2 mediated cell death, the expression of inducible nitric oxide synthase (iNOS), which produced the NO free radical, was determined in A431 cells treated with NaAsO2 or GeO2. We found that expression of iNOS was induced in a time-dependent manner in NaAsO2 or GeO2-treted A431 cells. Taken together, our results indicated that GeO2-induccd cell death may be mediated through MAPK signal pathways and that iNOS may contribute to NaAsO2 or GeO2 mediated cell death. To our knowledge, this is the first report that iNOS may contribute to heavy metal mediated cytotoxicity.