當急驚風遇上「玻璃片」-以簡單原理研製便宜準確風速計
本專題研究之目的,在於運用簡單的原理自製出準確、廉價、適用於低風速範圍的風速計;方法是藉由將一連接轉軸的玻璃片迎風,探討迎風時,玻璃片偏轉夾角和風速之間的關係。實驗過程中同時發展出可以用馬達旋臂的裝置與v=rω的原理,產生穩定可計算風速的環境。研究結果發現:在低風速的環境下,θ 範圍小時玻璃片與地夾角和風速大略成正比的關係,所以我們可以得到近似式” v≒aθ+b”,參數(a,b)依玻璃片而定。另外θ 範圍大時,我們可以使用二次逼近曲線的方程式與內插法來作角度與風速的對應。藉由控制玻璃片的厚度、質量與形狀,我們可以製造出相對應風速範圍的風速計。The purpose of our research is to use easy theorems to make accurate and inexpensive anemometer which is available in low wind velocity. To make such anemometers, we made a piece of glass, which was connected to a axle, to face wind; then, we could figure out the corresponding relation between wind speed and the angle created by the original and the resulting positions of the piece of glass. While we were experimenting, we found that we could make a steady-wind-speed environment by using motors, sticks, and the theorem ”v=rω”. The research showed that the angle created by the original and the resulting positions of the piece of glass and wind speed are in direct proportion in low wind velocity in small θ range. Consequently, we\r can derive the formula ” v≒aθ+b” , for each piece of glass (a,b) can be different. In addition, when in bigger θ range, we can use quadratic approximate equation and interpolation to describe the corresponding relation between the angle and wind speed. By adjusting the thickness, mass , and the shape of the glass, we can make anemometers corresponding to different wind velocity ranges.
金奈米粒子的合成與其光譜特性
當世界各國正全力朝奈米科技發展,而奈米微粒對環境及人類健康影響與否未明朗之際,有關奈米微粒對人類健康影響之探討是刻不容緩之事。本研究的近程目標是合成金奈米粒子,遠程目標是擬探討金奈米粒子的生物毒性。此份研究主要是描述金奈米粒子的最大表面電漿吸收光譜特性及其最大吸收波長,而金奈米粒子的合成是利用四氯金酸( HAuCl4 )與還原劑—硼氫化鈉( NaBH4 )、聯胺水合物( N2H5OH )或檸檬酸鈉在陽離子界面活性劑的溶液( CH 3(CH2)15N+(CH3)3Br– ,溴化十六烷基三甲基銨,CTAB ) 當保護劑中,利用氧化還原方法直接生成金奈米粒子,並探討四氯金酸的濃度、還原劑的濃度、界面活性劑的濃度及反應溫度,對金奈米粒子生成之影響,另外也探討金奈米粒子的穩定性。有關金奈米粒子的光譜特性則利用UV/Vis 光譜儀測試。研究結果發現在相同的條件下,利用冰浴,以NaBH4 當還原劑所合成出的金奈米粒子之平均粒徑為11.70 nm ,而以N2H5OH 當還原劑所合成出的金奈米粒子之平均粒徑為20.25 nm, 有關金奈米粒子之結構及大小藉由穿透式電子顯微鏡( TEM ) 拍攝出的影像得以驗證。;This study mainly focused on the properties of the maximum surface plasmon absorption of gold nanoparticles and their wavelengths. The synthesis of gold nanoparticles made use of HAuCl4 aqueous solution and reducing agent, through the oxidation reduction method, with reductant, sodium borohydride ( NaBH4 ), hydrazine ( N2H5OH ) or sodium citrate solution in the presence of the cetytrimethylammonium bomide ( C19H42BrN,CTAB ) aqueous solution as protecting agent. The influence of concentration of HAuCl4, reductant, surfactant, and temperature on the synthesis of gold nanoparticles were explored. In addition, the stability of the gold nanoparticles was also explored. Measurements of spectral properties of gold nanoparticles were done by UV/Vis spectrometer.When NaBH4 was used as a reductant, the average diameter of gold nanoparticles was 11.70 nm. When N2H5OH was used as a reductant, the average diameter of the synthesized gold nanoparticles was 20.25 nm. The structures and sizes could be identified by the transmission of electron micrograph (TEM) images.
長期服用安非他命對小鼠腦部紋狀體內蛋白質表
安非他命的濫用在台灣是非常嚴重的公眾健康及社會問題。安非他命會導致一連串的行為異常,包括在中腦紋狀體內釋放多巴胺及阻止多巴胺回收來增加使用者的活動力。由於安非他命會對腦細胞造成傷害,本研究的目的為探討低劑量、無立即毒性之安非他命(類似於人類使用習慣)長期施打下,是否會對C57BL6 小鼠大腦紋狀體內的蛋白質表現有影響。因此利用西方點墨法分析施打低劑量安非他命(2 到6 mg/kg) 約一星期之後,C57BL6 小鼠的大腦紋狀體中一些重要蛋白質(包括腺.酸受體A2A-R、第五亞型腺.酸環化.AC5、caspase-8 及PARP) 的表現是否有改變。實驗結果顯示,低劑量安非他命處理對這些蛋白質的表現並沒有明顯的差異。但利用二維電泳法可看到有少許蛋白質,在經過安非他命處理下有顯著的差別,如KIAA0193 homolog 、GOS-28、gammacrystallin A、malate dehydrogenase 和phosphoglycerate mutase isozyme B (PGAM-B)。這些蛋白質中,malate dehydrogenase 和PGAM-B 與代謝和產生ATP 有關,但前者是增加的,而後者減少,推測安非他命會影響神經細胞的能量代謝,因此長期施打安非他命對紋狀體造成的影響值得進一步探討。;The wide spreading use of amphetamine (AMPH) in Taiwan has become a serious public health and social problem. AMPH evokes a series of behavior abnormality including enhanced locomotor behavior by releasing dopamine and inhibiting dopamine-uptake in the striatum. Since AMPH is known to cause brain damage, the purpose of this study is to investigate the expression of several important proteins in the striatum of C57BL6 mice after chronic treatment with low and non-toxic dosages of AMPH (mimicking the common usage pattern of AMPH addict). C57BL6 mice were daily IP-injected with various dosages of AMPH (0 to 6 mg/kg) for one week. Expression levels of A2A adenosine receptor (A2A-R), adenylyl cyclase type V (AC5), caspase-8 and PARP in the striatum were analyzed by Western blotting analysis. Most proteins examined were not affected by this 1-week AMPH treatment. By the aid of two-dimensional gel electrophoresis, expressions of a few striatal proteins (such as KIAA0193 homolog, GOS-28, gammacrystallin A, malate dehydrogenase and phosphoglycerate mutase isozyme B (PGAM-B) in AMPH-treated mice were altered. Note that malate dehydrogenase and PGAM-B are two enzymes involved in energy metabolism and ATP generation. Interestingly, the former was increased and while the latter was decreased in AMPH-treated mice. Collectively AMPH may affect the energy metabolism in neuronal cells. These results suggest that the injury induced by long-term AMPH exposure warrants our further concerns and investigation.