National Taiwan University Repository
Not a member yet
222849 research outputs found
Sort by
Determination of silicate in natural waters based on the formation of the yellow α-silicomolybdenum using a step flow analysis
No full text本研究探討以鉬酸銨測定水中矽酸鹽方法中黃色矽鉬複合物之反應動力學，本文改變了矽鉬黃複合物呈色條件，測定靈敏度較低的α-矽鉬黃複合物為主。其優點為：α-矽鉬黃複合物呈色穩定且受溫、鹽度影響與磷酸鹽干擾較小。但在應用至自動分析前，則必須改善其反應在常溫下較慢的缺點。當要求靈敏度時可採用較長的光徑或在較低的波長測定。因不使用漂白劑，此法所測出之訊號應為矽酸鹽與磷酸鹽其合併吸光值： 〖Abs〗_(Si+P)^λ ={[P]×ε_p^λ +[Si]×ε_Si^λ }×b×Q_s/Q_f ×10-6+RB 其中ε_Si^λ 及ε_p^λ 為矽鉬黃及磷鉬黃複合物在波長400 nm下的摩爾吸光係數，單位為(M-1cm-1)；b為光徑，單位為(cm)；[Si]及[P]分別為樣品的矽酸鹽與磷酸鹽濃度，單位為(M)；Qs 、Qf分別為原樣與加藥後的體積比，RB為試劑空白值，因此可算出矽酸鹽濃度，單位為(μM)： [Si](μM)=(〖Abs〗_(Si+P)^λ-[P]×ε_p^λ×b×Q_s/Q_f )/(ε_Si^λ×b×Q_s/Q_f )×106 本研究發現溫度(T,oC)、鹽度(S)對於其摩爾吸光係數有些許影響，在波長400 nm測定，可用下列經驗公式修正之： ε_Si^400(T,S)(M-1cm-1) = 1166+T×(4.4-0.1532×S+0.00154×S2) 溫度(T)適用範圍20-40oC、鹽度(S)適用範圍0-35 至於磷鉬黃的摩爾吸光係數值在上述條件下，在波長400 nm測定為： ε_p^400(M-1cm-1) = 390 本研究使用醋酸鈉緩衝溶液將以上反應控制在pH=4.2-4.3之間，在常溫之下反應大約需4分鐘以上，加溫至40oC情況之下可縮短至2分鐘，其速率足以因應自動分析之要求。本文比較了兩種自動分析系統，分別為傳統連續式測定及間歇式上樣測定，後者的原理為將樣水加入試劑後，送入恆溫的流動光槽中停止幫浦運作使樣水停滯在光槽中靜待反應完成。結果發現間歇式流動分析系統較為精密準確。使用一公分長光徑測量矽酸鹽的最小解析度為1 μM，線性範圍為0-200 μM，在100 μM的濃度下的相對誤差在0.5%以下，即使在船上顛簸海況下也可操作，不但可測定外洋水柱同批不同溫度的樣品，也可適用於在河口測定同批不同溫度鹽度的樣品，分析速率可達每小時20個樣品。This study focuses on the reaction kinetics of the yellow α-silicomolybdenum complex for the determination of silicate in natural waters. The less sensitive yellow α-silicomolybdenum reaction has several advantages: the α-silicomolybdenum color is stable; it has less salt effect and phosphate interference. However, it is still unfavorable to be employed on automated analysis due to the slow reaction rate. To solve this problem the pH of the reaction is adjusted to 4.2-4.4 by a buffer system so as to enhance the reaction completeness to less than 4 minutes under room temperature, and can be further shortened to less than 2 min by moderate heating. Since the adding of bleaching reagent is avoided, the final absorbance may contain some signals attributed to phosphate: 〖Abs〗_(Si+P)^λ ={[P]×ε_p^λ +[Si]×ε_Si^λ }×b×Q_s/Q_f ×10-6+RB Where ε_Si^λ and ε_p^λ are molar extinction coefficients of silicomolybdic acid and phosphomolybdic acid(M-1cm-1), respectively, at a wavelength of 400(nm), b the path length(cm), [Si] and [P] the concentrations for silicate and phosphate(M),Qs and Qf represent the sample and final volume ratios and RB the reagent blank. The silicate concentration should be corrected for the phosphate interference for which the phosphate concentration has been identified by a separate channel: [Si](μM)=(〖Abs〗_(Si+P)^λ-[P]×ε_p^λ×b×Q_s/Q_f )/(ε_Si^λ×b×Q_s/Q_f )×106 The molar extinction coefficient for silicate(ε_Si^λ) was formed to be functions of temperature and salinity, but that for phosphate(ε_p^λ) is not. At the wavelength of 400 nm: ε_Si^400(T,S)(M-1cm-1)= 1166+T×(4.4-0.1532×S+0.00154×S2) ε_p^400(T,S) (M-1cm-1) = 390 20 oC < T <40oC, 0< S <35 A new automated analysis system for the determination of silicate has been proposed and it has been compared with the traditional flow injection analysis. The system uptakes samples and add reagents in a quick flow manner to fill a thermostat cuvette, then the flow is stopped so that the sample is allowed to stay in the cuvette for complete reaction. Since the determination is static and the color is fully developed, it has a higher sensitivity and better precision than do conventional methods. The minimum resolution (Abs=0.001) is 1 μM Si with 1 cm cuvette and can be lowered to 0.2 μM Si if a 5 cm long cuvette is used. The linear range is up to 200 μM Si. The precision at 100 μM Si is less than 0.5%
Chirp Sonar Images on Liquefaction and Their Implications on Seafloor Stability Offshore SW Taiwan
No full text臺灣西南海域因海底重力流極端事件導致一系列的海底電纜斷裂，並造成嚴重的經濟損失，本研究結合地球物理與地球化學方法，探討導致海床不穩定的可能原因，並針對臺灣西南海域陸棚、陸坡區，評估易發生海底重力流之敏感區分布。本論文以2006年12月26日屏東地震於枋寮峽谷引發重力流之事件為例，利用高解析水深、海床底質回聲剖面以及反射震測資料，藉由比對事件前後地形與地層特徵之變化，先確認該事件所引發之塊體運動發生區域，再探討為何地震後會在該處誘發海床崩塌。研究結果顯示，崩塌區域海床下之地層並未有明顯的斷層、褶皺或貫入體構造，進而可直接引發海床崩塌；反而在海床底質回聲剖面資料中發現崩塌區域淺部地層中，廣泛存在一層聲波反白透明層，再搭配高解析三維海床底質回聲影像的分析，發現該透明層與沉積物發生崩塌有所關連。藉由該透明層之地物特徵以及箱型岩心分析結果，透明層之發生應與地層液化有關，而地層液化則是導致海床不穩定之關鍵因素。因此本研究提出一套由淺部沉積層中液化地層引發海床崩塌發生的機制：海床下的某特定沉積層在流體的充填下，使得該層的孔隙水壓逐漸上升，同時有效應力下降，當上覆沉積物給予的荷重較少時，此沉積層容易形成不穩定的狀態，最後在一定規模地震的擾動下，使其有效應力歸零，造成沉積層發生液化。而由於液化地層可藉由底質回聲剖面中的透明層辨識，所以檢視整個高屏棚坡區域回聲剖面中的透明層分布，顯示發現顯示除了枋寮峽谷頭部東側區域外，高屏峽谷與枋寮峽谷之間的陸棚區域也有不少潛在發生液化的海床不穩定區域，其中又以枋寮峽谷頭部西北側分布最為密集。本研究認為這些富含流體的沉積層，在有適當的誘發機制情況下，例如2006年的屏東地震事件，容易使得這些含有流體且處於不穩定狀態的沉積層受到擾動而發生液化，導致海床崩塌而引發重力流。Large scale submarine cable breakages often occur along the submarine canyons offshore southwest Taiwan after some extreme gravity flow events caused significant economic losses. This study analyzes both marine geophysical and geological/geochemical data to investigate the possibly causes of seafloor instability, and identify the regions prone to submarine landslides that trigger submarine gravity flows in the area off southwest Taiwan. Taking Pingtung Earthquake as an example, this earthquake occurred on 26 December 2006, which triggered gravity flow in the Fangliao Submarine Canyon. By analyzing high-resolution bathymetry, chirp sonar, and reflection seismic data to search for the locations of seafloor failures that caused an extreme gravity flow event, and to investigate why this event occurred in that region. Our study shows that there are not obvious active faults, folds, and diapers to trigger the seafloor failures in our study region. However, from chirp sonar profiles, an acoustic transparent layer is widely distributed in the shallow substrata in the study region. We also construct a 3D chirp sonar image to reveal the distribution of this layer, which we think is closely linked to the seafloor failures. Based on the analyses results of box core data and geophysical characteristics of the transparent layer, we suggest that sediment liquefaction caused the transparent layer, and liquefaction is the major factor of seafloor instability in our study area. We establish a model to show how the liquefied layer affects the shallow substrata and causes seafloor failures: when a layer is supplied with large amount of fluid in the shallow substrata, pore water pressure increases and effective stress decreases in the sediments. With inadequate loading pressure from the sediments above, the fluid saturated layer is easy to become unstable. When a large earthquake hits the region with unstable seafloor strata, the effective stress in the fluid over-saturated substrata will decrease to zero, and cause the liquefaction. Because the liquefied strata can be identified on chirp sonar profiles as a transparent layer, we examine all the chirp sonar profiles in the Gaoping shelf and slope region to map this layer. Our investigation results show that there are many potential liquefaction regions between the Gaoping and Fangliao Submarine Canyons in the shelf, and the area near the northwestern side of the Fangliao Submarine Canyon is the most unstable region. In conclusion, we suggest that the layer with fluid could be easily liquefied when an appropriate events happen, such as 2006 Pingtung Earthquake
The topography, morphology and sedimentation patterns in Sun Moon Lake
No full text日月潭是台灣最重要的觀光湖泊及重要的電力調節設施，但由其東側引水口而來之溪水每天不斷將含泥的濁水溪渾水引入，造成從引水隧道口往外形成淤泥淤積，在水庫內堆積成沖積扇，除降低水庫有效之庫容空間，也嚴重導致潭水在淤泥處的生態受衝擊使得環境改變。此外日月潭是個70年前因抽續發電目的而改變形貌的盆地，由於水力的開發迫使邵族原來在日月潭畔的舊部落，現今被淹在水中。本研究利用日月潭水庫為實驗場所，利用多音束測深系統、側掃聲納及震測系統取得水下資料，觀察此區域的水下地形及地貌，討論和水下考古有關的水下特徵，並說明潭底沖積扇在過去十年來生長的狀態，間接預測水庫內沉積變化的趨勢，或許可提供為水庫維護的重要參考依據。 結果顯示日月潭西側月潭多年來幾乎無沉積物的產生，拉魯島之水下形貌幾乎一致；而西側日潭則會受東側引水口所帶來之泥砂淤積所影響地形高程。地形資料顯由潭深處漸往淺水域(721-748公尺)，高程位置的變化趨勢分為三個段落，斜率最大的為728m~739m這段，為2006-2014年來淤積的主要區域位置，也是沖積扇主要生長的範圍。新武界隧道在2006年啟用後，可以由2006-2012年變異圖上看到兩個淤積中心，顯示了新舊武界出水口所送出的淤泥推積在不同的位置上，且新武界送出的淤泥量比較多，並往正西方向推移，有向依達邵侵襲的趨勢；側掃聲納影像資料對比，可以找到相對應之地貌特徵如梯田構造、道路、古河道等，表示這117餘年來水下樣貌幾乎沒有改變，且在水下發現和古地圖上相似之古建物樣貌，但其真正結果下一步需要經由水下攝影機來佐證；震測資料可以發現地層間有壓密現象的發生，且日潭東側大於西側。此壓密現象是連續性的，沉積物會因為壓密作用於層間產生氣體。並且可以在震測剖面上看到基盤有下陷的情形，此現象或許和構造有關，並不完全是由壓密現象所引起。 Sun Moon Lake is a famous attraction and an important electricity generation facility in Taiwan. But the underground tunnel’s outlets in the east side of the lake which bring water to the lake will bring water mixed with a large number of muds continuously and accumulate near tunnel outlets, resulting in an alluvial delta in the reservoir. The accumulation will not only reduce the water capacity but also make serious ecological impact to the lake. In addition, the Lake is a basin which changed its appearance to reservoir 70 years ago due to conducting pumping storage project. The development of the project caused the village of Ita Thao near the lake been submerged in the water In this study, we use multi-beam echo sounders, side scan sonar and sub-bottom profiler to collect bathymetric data to observe the underwater terrain and topography of this area, in order to discuss the archeology features under the water and descript the growth of the alluvial over the past decade. We expect to predict the changes of accumulation within the reservoir, perhaps it can provide an important reference for reservoir maintenance. The results show that the west side of Sun Moon Lake has almost no deposit over the years, the Lalu Island which is in the middle of the lake appears almost the same underwater topography like 117 years ago ; But the west side of the lake is controlled by the sand and mud brought from the tunnel outlet.Bathymetry data shows the topographic elevation change is been dividing into three parts, the part which has the the maximum slope (728m ~ 739m) is the main area that the alluvial grew the most since 2006. The new Wu Jie tunnel was enabled to use after 2006, we can clearly see two deposition centers between 2006 to 2012 in deviation topographic map, showing that new Wu Jie tunnel sent the silt out in a different direction from old Wu Jie tunnel. Also, the new Wu Jie sent more silt than the old one, and there is a tendency that the alluvial extends west, and has the tendency to invade toward Ida village; Compared the side scan sonar image to the maps which was 117 years ago, we can find the corresponding structure features underwater such as terraces, roads, rivers and other ancient building remains, indicating that the underwater appearance has very little changed in this 117 years. We also found ancient buildings which the shapes are very similar to the ones on ancient map, but it needs to be confirm via underwater cameras, and that’s our next step. Chirp sonar data indicates the phenomenon of compaction can be found between the stratum layers, and the east side is more notable than the west side. This phenomenon is continuous, and the sediment in the stratum layer will generate gas. We can also see the ancient base plate sunk, perhaps this phenomenon was related to geological structure, not entirely caused by the compaction phenomenon
Atmospheric Cycling and Air-Sea Exchange of Mercury in the South China Sea
No full text本研究主要研究南海海域汞的大氣循環及海氣交換，於2003至2007年間，共有十六次航次，搭乘海研一號至南海時序 (Southeast Asian Time-Series Station, SEATS) 測站進行採樣及分析。航次中進行現場測定，觀測大氣中元素汞(GEM, Gaseous elemental mercury, Hg0)及表水中元素汞(DEM, Dissolved elemental mercury) 濃度。在大氣汞方面，各季節平均分別3.2 ± 0.6 ng m-3、2.8 ± 0.4 ng m-3、3.6 ± 0.6 ng m-3、4.5 ± 1.5 ng m-3，其中夏季最低，冬季為最高。在水氣汞方面，各季節平均分別為70 ± 40 fM、160 ± 40 fM、120 ± 30 fM、60 ± 30 fM，呈現一個夏季高、冬季低的趨勢，與大氣汞的趨勢相反。大氣汞與水氣汞濃度的趨勢並不相同，顯示主要影響二者濃度的原因並不相同。本研究使用HYSPLYT模式追蹤當時氣團軌跡發現，冬季盛行東北季風，帶來歐亞大陸的陸緣物質及人為活動汙染物，使得大氣元素汞濃度升高。夏天盛行西南季風和季風交替期間，帶來中南半島和印度洋和西太平洋上方汙染較少的氣團，故大氣元素汞濃度較低。夏季水氣汞濃度較高，冬季則較低，此一現象同溫度變化趨勢一致。利用水氣汞濃度及表水溫度計算溫度係數Q10，結果推測此一季節性變化主要由非生物因素主導。根據海氣交換通量公式估算，汞的海氣交換通量在春天 (60 ± 160 pmol m-2 d-1)、夏天 (580 ± 120 pmol m-2 d-1) 及秋天 (730 ± 210 pmol m-2 d-1) ，由海洋逸散至大氣（源），而冬天則有一個相反的方向(-180 ± 110 pmolm-2d-1)，由大氣傳輸至海洋（匯）。冬季南海元素汞由大氣傳輸至海洋，係因較低的海表面溫度及較高的風速，造成水團的垂直混合較強，並且大氣汞濃度較高的關係，使得元素汞的海氣交換在冬季有此一特殊匯的現象，與其他低緯度海域觀測結果不同。Atmospheric cycling and air-sea exchange of mercury in the northern South China Sea (SCS) were investigated during 16 cruises of the SEATS (Southeast Asian Time-series Study) station between 2003 and 2007. The GEM (Gaseous elemental mercury, Hg0) and DEM (Dissolved elemental mercury) were measured all together on board ship during the cruise period. The GEM concentrations in spring, summer, autumn and winter averaged ca. 3.2 ± 0.6 ng m-3, 2.8 ± 0.4, 3.6 ± 0.6, and 4.5 ± 1.5, respectively. Additionally, seasonal DEM concentrations were 70 ± 40 fM, 160 ± 40, 120 ± 30, and 60 ± 30, respectively. Unlike the annual GEM pattern, the DEM concentrations were high in summer and low in winter. The opposite temporal trends between the GEM and DEM implied different controlling factors on those concentration variations. Source tracking through backward air trajectory of The HYSPLYT model demonstrated that the GEM concentrations were strongly influenced by seasonal monsoons. In winter, the prevailing northeast monsoon with terrigenous and anthropogenic pollutants resulted in high GEM concentrations. Instead, the summer southwest monsoon and inter-monsoon with less polluted air masses from the Indochina Peninsula and Indian Ocean and west Pacific Ocean resulted in low GEM levels. The DEM concentrations were highly correlated with sea water temperature (SST), showing high in summer and low in winter. The Q10 temperature coefficient calculation of DEM suggested that a seasonal change in DEM was mostly abiologically driven. Annually, the air-sea Hg0 exchange fluxes were estimated ca. 60 ± 160 pmol m-2 d-1, 580 ± 120, and 730 ± 210 in spring, summer and autumn, respectively, indicating that the SCS could be the source of Hg0 to the atmosphere in warm seasons. In winter, the SCS acted as a sink of atmospheric Hg0 (-180 ± 110 pmol m-2 d-1) due to low SST and high wind of the year, enhanced vertical mixing and elevated atmospheric Hg0. This is the first time we observed that ocean behaves as a sink of atmospheric Hg0 in low latitude marginal seas. Key words: South China Sea (SCS), Atmospheric cycling, Air-sea exchange, Gaseous elemental mercury (GEM) and Dissolved elemental mercury (DEM
Trace Metal Composition of Marine Micro Phytoplankton in East China Sea.
No full text本研究藉由ORII-2023航次於東海海域利用多層次粒徑收集器(Catnet Sequential Filtration，Catnet)採集10~60um浮游植物，以了解表層海水及次表層海水的浮游植物體內基礎生長元素(C、N、P、Si)及微量金屬(Fe、Zn、Cu、Ni、Cd、Mn)組成比例。 研究發現表層海水及次表層海水中的較大之微型浮游植物(10~60um)約百分之九十的浮游植物細胞大小介於10~12um之間。浮游植物個體數量於各測站間差異大，整體而言表層海水的浮游植物個體數量高於次表層海水。近岸區域主要以矽藻、渦鞭毛藻、定鞭藻為優勢族群，近太平洋的區域則以綠藻、隱藻為主要族群。 浮游植物體內基礎元素C、N、P組成比值大致穩定，整體而言，表層海水的浮游植物C:N:P=145:21:1，次表層海水之浮游植物基礎元素C、N、P比值為121:18:1。微量金屬元素組成於表層海水及次表層海水之平均比值分別為(Fe1082Zn39Cu6.0Ni1.6Cd0.02Mn1.4)P1000 與 (Fe267Zn43Cu3.6Ni5.7 Cd0.09 Mn1.6)P1000。金屬元素在浮游植物體內的含量會因浮游植物的生長環境(光照強度)及浮游植物種類而異。整體來說，於東海海域，生長於表層海水的浮游植物體內金屬含量高於次表層海水的浮游植物
Identification of FN1-FGFR1 Fusion Gene in Phosphaturic Mesenchymal Tumor with Next-generation Sequencing and Insights into the Plausible Tumorigenesis Mechanism and Translational Relevance
No full text高磷尿性間質腫瘤（phosphaturic mesenchymal tumor, PMT）是一種特殊的軟組織及骨骼腫瘤，其特色為藉由分泌包括纖維母細胞生長因子-23（FGF23）在內的抑磷素而造成低磷血症及腫瘤誘導骨軟化症（tumor-induced osteomalacia, TIO）。FGF23主要作用在腎小管，促進磷酸根排出，進而造成低磷血症，而阻礙類骨質之礦化，致使骨質脆弱、易於骨折，亦即骨軟化症。TIO之成因，以往認為可由多種不同腫瘤造成，但依照目前的認知，絕大部分TIO皆由一種具有特定組織型態之腫瘤類型所引發，亦即PMT；而此概念也獲得最新版之世界衛生組織認可，後者認定PMT為一種特定腫瘤類型。但是，PMT之腫瘤形成分子機制則仍屬未知。 本研究基於「PMT可能為一類基因轉位所造成之腫瘤」的假設，採用次世代核醣核酸(RNA)定序之方法，在4個PMT發現其中三個具有FN1-FGFR1融合基因之RNA表達。此發現經由反轉錄聚合酶連鎖反應證實，且西方墨點法亦證實此融合蛋白之表達。螢光原位雜合進一步在另外11個PMT中發現6個案例有FN1-FGFR1融合基因。整體上，15個PMT中有9個（60%）有此融合基因。本研究進一步納入第二批腫瘤，並使用涵蓋5’端FN1、5’端FGFR1、及3’端FGFR1之三色探針進行螢光原位雜合分析，兩批總共29例得到可判讀之結果，其中17例有5’端FN1與3’端FGFR1之融合；加上RNA定序之結果，仍然有60%（18/30）之腫瘤具有此融合基因。值得注意的是，這17例中有10例其三種顏色之探針訊號重疊或緊鄰，而非FGFR1基因之5’與3’分離之樣態，此現象一方面可能反映出此兩基因之染色體相對位置關係之特殊性，另一方面也警示了使用FGFR1探針進行PMT之分子診斷時必須注意的實務上考量。 本研究之發現，對於PMT之腫瘤形成機制，產生了相當直觀的啟發。FN1基因可能藉由提供其活躍之促進子來過度表達FN1-FGFR1融合蛋白，而其所編碼之蛋白（fibronectin）之寡聚合區域可能有助於C’端之FGFR1酪氨酸激酶區域之交互磷酸化與活化。至於FGFR1則是一個已知的原致癌蛋白，在腫瘤中可經由基因突變、放大、以及轉位融合的方式而活化。不同於FGFR1基因轉位之腫瘤原型（某類血液腫瘤，其FGFR1融合基因皆丟失配體結合區域、且其活化不需要配體），在PMT所發現的FN1-FGFR1融合基因皆保留至少部分之配體結合區域，暗示著其配體（例如PMT大量分泌之FGF23）之存在可能對於FN1-FGFR1融合蛋白之活化具有促進、甚至必要之作用，由此形成一個自分泌或旁分泌的迴圈，此為一個可能且直觀的腫瘤形成機制。此外，證據顯示FGFR1的訊息傳遞可導致FGF23表現量上升，因此此融合蛋白之活化，或可解釋PMT分泌FGF23導致臨床上TIO之表現的機制。 最後，本研究的發現，也可能具有臨床治療上的意義。新發展的FGFR1抑制劑以及FGF23抗體或可藉由阻斷FN1-FGFR1融合蛋白所主導之自分泌迴圈，而被用於治療無法以手術切除之PMT，發揮抑制腫瘤生長及減輕FGF23所致TIO的作用。上述假說皆需進一步實驗證實，並將以回歸於病人之治療作為最終目標。Phosphaturic mesenchymal tumors (PMT) are distinctive soft tissue and bone tumors that typically cause hypophosphatemia and tumor-induced osteomalacia (TIO) through secretion of phosphatonins such as fibroblast growth factor 23 (FGF23). FGF23 acts on renal tubules and promotes renal wasting of phosphate. The resultant hypophosphatemia then hinders osteoid mineralization and renders the skeletal system fragile and prone to fracture, hence osteomalacia. Although TIO was previously thought to be caused by a variety of different tumor types, it is now understood that PMT underlie the overwhelming majority of cases of TIO. As such, PMT has recently been accepted by the World Health Organization as a formal tumor entity. However, the genetic basis and oncogenic pathways underlying its tumorigenesis remain obscure. In this study, we employed the next-generation RNA sequencing technique and identified a novel FN1-FGFR1 fusion gene in 3 out of 4 PMTs. The fusion transcripts and proteins were subsequently confirmed with RT-PCR and western blotting analyses, respectively. Fluorescence in situ hybridization (FISH) analysis showed 6 cases with FN1-FGFR1 fusion, out of an additional group of 11 PMTs studied. Overall, 9 out of 15 PMTs (60%) were positive for this fusion. An expanded group of 30 cases were then analyzed with a tri-color 5’-FN1/5’-FGFR1/3’-FGFR1 probe set. Again, 60% (18/30) of PMT harbored FN1-FGFR1 fusion. Of note, 10 of the 17 cases with FISH-confirmed FN1-FGFR1 fusion had the three probes fused together instead of break-apart of the 5’ and 3’ ends of FGFR1, a phenomenon that likely reflected the unusual relative chromosomal orientation of the fusion partners, with practical relevance in molecular diagnosis. The current findings provide immediate insights into the tumorigenesis of PMT. The FN1 gene probably provides its constitutively active promoter to over-express the FN1-FGFR1 fusion protein, while the oligomerization domains of the encoded protein (fibronectin) may facilitate the activation of the FGFR1 kinase domain. Fibroblast growth factor receptor 1 (FGFR1) is a well-known proto-oncoprotein, which is activated in tumors through mutations, amplifications, and translocations. Interestingly, unlike the prototypical leukemia-inducing FGFR1 fusion genes which are ligand-independent, the FN1-FGFR1 chimeric protein was predicted to preserve its ligand-binding domains, suggesting a requirement for, or an advantage of, the presence of its ligands (such as FGF23 highly secreted by the tumor cells) in the activation of the chimeric receptor tyrosine kinase, thus effecting an autocrine or paracrine mechanism of tumorigenesis. Furthermore, as FGFR1 signaling has been shown to lead to the upregulation of FGF23, the fusion gene may also account for the over-expression of FGF23, hence the clinical manifestation of TIO. Finally, the current findings may also have therapeutic relevance. Emerging fibroblast growth factor receptor inhibitors and anti-FGF23 antibody may serve to block the FN1-FGFR1 autocrine loop and ameliorate the FGF23-mediated TIO in cases with inoperable PMT. Further studies are warranted to confirm our hypotheses, with an ultimate goal to benefit the patients
Investigation of the Wnt5a function in lung cancer and the correlation between Wnt5a and TKI-resistance
No full text肺癌是癌症死亡排行榜的首位。研究報告顯示表皮生長因子受體 (epidermal growth factor receptor, EGFR) 的突變在東方人的肺癌細胞有較高比例。EGFR是一個酪胺酸激酶受體 (receptor tyrosine kinase)，與肺癌細胞的分化、增生、轉移及存活有關。目前國內的肺癌病患若是檢測出具有EGFR mutations (exon 19 deletion or/and L858R)，將以表皮生長因子受體激酶抑制劑 (EGFR-TKI) 作為標靶治療的藥物。目前可以使用的EGFR-TKI包括有 Gefitinib (Iressa) 與 Erlotinib (Tarceva) 以及 Afatinib (Gilotrif)。然而EGFR突變的病患平均在標靶治療後的8到12個月就會出現抗藥性，因此仍須尋找EGFR-TKI產生抗藥性的相關基因。目前此實驗初步的研究結果顯示在gefitinib-resistant cell line (PC9/gef) and sensitive cell line (PC9) 透過cDNA microarray分析中找到與EGFR-TKI抗藥性相關的Wnt5a基因。Wnt5a是Wnt家族19個成員的其中之一，Wnt配體由高保守性的醣蛋白組成，能夠調節各種細胞功能，包括增殖、存活以及遷移。有研究報告指出Wnt5a與癌症病患的預後不佳有關係。根據本研究結果表示相較於EGFR-TKI-sensitive PC9 細胞株，Wnt5a在EGFR-TKI-resistant PC9/gef的細胞株表現有明顯的上升。當我們在PC9/gef細胞株抑制了Wnt5a的表現時將可以觀察到細胞對於EGFR-TKI的抗藥性、細胞生長、遷移以及入侵能力受到抑制。這可能暗示著Wnt5a在肺癌細胞的功能與EGFR-TKI抗藥性過程中扮演重要的角色。Lung cancer is the leading cause of cancer death. Some studies indicate that epidermal growth factor receptor (EGFR) mutation in Asian lung cancer cell of a substantial percentage. EGFR is a receptor tyrosine kinase that correlates with cell proliferation, growth, metastasis and survival in lung cancer. Currently, EGFR-TKI target therapy is specific for patients with exon 19 deletion or/and L858R mutations. EGFR-TKIs include the drugs Gefitinib (Iressa), Erlotinib (Tarceva) and Afatinib (Gilotrif). Gefitinib and Erlotinib are the first-generation reversible EGFR TKIs. Afatinib is the second-generation irreversible EGFR TKI. Despite of high response rate in these patients, the resistance to EGFR-TKIs occurs on average between 8-12 months. Therefore, we tried to find genes capable of conferring EGFR-TKI resistance. In our studies, we performed cDNA microarrays comparing gefitinib-resistant cell line (PC9/gef) and parental sensitive cell line (PC9) to identify the resistance-related genes, which may be involved in the EGFR-TKI resistance. The candidate gene Wnt5a (Wingless-type MMTV integration site family, member 5A) is a component of Wnt signaling, and we are interested in studying the role of Wnt5a in EGFR-TKI resistance. Wnt ligands consist of 19 highly conserved secreted glycoproteins that regulate various of cell functions including proliferation, survival, and migration. Although some studies indicate that Wnt5a correlates with poor overall survival in patients with lung cancer, the role of Wnt5a in relation to EGFR-TKIs resistance remains unclear. In our results, significant up-regulation of Wnt5a mRNA and protein in EGFR-TKI resistant PC9/gef as compared to its expression in EGFR-TKI sensitive PC9 cell line. We found that EGFR-TKI resistance decreased by the knockdown of Wnt5a in EGFR-TKI resistant cells. At the same time we also found that cell proliferation, migration and invasion ability were decreased by the knockdown of Wnt5a in EGFR-TKI resistant cells. These results implied that Wnt5a played a critical role in EGFR-TKI resistance and the functions of lung cancer
Molecular Genetic Alterations in Ovarian Clear Cell Carcinoma
No full textAT-rich interactive domain 1A (ARID1A)是switch/sucrose non-fermentable (SWI/SNF)複合體的一個次單元。近年來，ARID1A gene, phosphatidylinositol 3-kinase-protein kinase B (PI3K-Akt) pathway，以及zinc finger protein 217 (ZNF217) gene被發現是常見於卵巢亮細胞癌的基因變化。E-cadherin表現以及telomerase reverse transcriptase (TERT) promoter突變也可以發生在部份的卵巢亮細胞癌。本研究的目的是找出這些分子基因變化的關連性，以及這些分子基因變化對於臨床預後以及治療的影響。我們發現ARID1A失去表現與年紀較輕、PI3K-Akt pathway變化、以及ZNF217 amplification有關。Chromosome 20q13.2 ZNF217 locus amplification與E-cadherin表現量下降相關。帶有activating PI3k-Akt pathway的卵巢亮細胞癌病人，E-cadherin表現量下降與FIGO stage晚期以及較短的overall survival相關。我們也發現對於早期卵巢亮細胞癌病人(FIGO stage I and II)，TERT promoter突變與較短的disease-free survival和overall survival相關。若早期病人出現復發，帶有TERT promoter突變的病人，通常會於化療後六個月內復發。 我們的結果顯示：ARID1A失去表現與PI3K-Akt pathway活化以及ZNF217 amplification對於卵巢亮細胞癌形成可能有加成的效果。ZNF217可降低E-cadherin的表現，是未來可能的治療標的目標。對於帶有activating PI3K-Akt pathway的卵巢亮細胞癌病人，E-cadherin表現可做為預後因子。對於早期卵巢亮細胞癌的病人，TERT promoter突變是可能的治療標的。AT-rich interactive domain 1A (ARID1A) is a subunit of switch/sucrose non-fermentable (SWI/SNF) complex. Recently, alterations of ARID1A gene, phosphatidylinositol 3-kinase-protein kinase B (PI3K-Akt) pathway and zinc finger protein 217 (ZNF217) gene have been identified as frequent molecular genetic changes in ovarian clear cell carcinoma. E-cadherin and mutations of telomerase reverse transcriptase (TERT) promoter were found in some ovarian clear cell carcinomas. The present study was aimed at determining the correlation between these molecular events and other clinicopathological factors, including the prognostic impacts of these clinicopathological factors. We found that loss of ARID1A expression was significantly related to younger patient age, PI3K-Akt pathway activation and ZNF217 amplification. Chromosome 20q13.2 ZNF217 locus amplification was significantly associated with decreased E-cadherin expression. In ovarian clear cell carcinoma patients with activating PI3k-Akt pathway, decreased E-cadherin expression and advanced FIGO stage predicted shorter overall survival. We also found that in ovarian clear cell carcinoma patients with early FIGO stage (stage I and II), TERT promoter mutation was an independent prognostic factor and correlated with a shorter disease-free survival and overall survival. In recurrent ovarian clear cell carcinoma patients with early FIGO stage, TERT promoter mutations were associated with early relapse within 6 months. Our results showed that synergic effects of loss of ARID1A and PI3K-Akt pathway activation as well as ZNF217 amplification may be related to the development of ovarian clear cell carcinoma. ZNF217 plays a role in downregulating E-cadherin expression and is a potential therapeutic target for ovarian clear cell carcinoma patients. E-cadherin expression is a prognostic marker for ovarian clear cell carcinoma patients with activating PI3K-Akt pathway. In ovarian clear cell carcinoma of early FIGO stage, TERT promoter mutation is a potential therapeutic target
The Future of Retail Banking Industry in Bank 3.0
No full text隨著高科技的發展，在新一代消費者的認知中，銀行已經由一個場域的觀念，轉化為無處不在的服務。無論是家中、辦公室，或是通勤途中，只要有網路的地方，交易無時無刻都在進行。以科技為核心策略的銀行3.0時代的來臨，不只是消費者購買金融產品的地方和方式的改變，更是銀行面臨非傳統金融機構蓬勃發展的一大挑戰。 傳統的商業銀行需要確保，新的策略可以反映新的市場特性。客戶能掌握的資訊越多，忠誠度當然也日益下降。在這個「分行消失中」的時代，商業銀行勢必透過個性化、客製化的金融服務與異業高手競爭。 然而，在這波轉型下，必定有部門，或是分行遭到裁撤，並伴隨人員的淘汰。銀行的轉型、成本的降低是我們所樂見的，但如何降低轉型過程中的傷痛，便是本文欲探討的課題。本文將探討銀行轉型與分行員工的溝通及輔導，在這數位化時代的今日，持續互榮互惠。 本研究透過問卷分析法及深度訪談法，分析台灣商業銀行轉型過程中，本土零售銀行員工的心態及期待，並深入訪談高階主管未來的決策方向，並整理台灣商業銀行不同角度推展數位化金融之過程。財富管理仍不脫離「人」的本身，因此未來在結合科技發展上，雖然有可能將服務過程科技化，但只有人才能了解人的問題，並不會仰賴機器來解決人的問題。期盼透過本研究發現之成果，將可成為提供銀行在職人員在銀行3.0時代，自身因應策略之重要參考。With the advanced technology development, banks are no longer physical and fixed locations. With the network, people can do transactions every time and everywhere. In the new era of Bank 3.0, not only consumers need to change their consumption habits, but banks need to change their strategies to deal with more challenges. However, the more information customers can receive, the more the loyalty declines. Traditional banks should ensure their innovative strategies could grasp the new market trends. Banks must be equipped with customized financial services so to stand out other competitors and to avoid elimination. However, some branches and departments must be eliminated under this trend, and so do some employees. We would like to see the banking transformation and the cost reduction. But at the same time, we still need to figure out how to reduce the pain during process, which is the subject of this thesis. This article will explore the communication and counseling between banking management and executives -- how they continue bringing prosperity to each other in this era. Through questionnaire analysis and in-depth interviews, this study analyzes the attitudes and expectations of local retail banking staffs, and the future strategies of executives. Wealth management is still not out of ""people"" things. That is to say, even though the whole transaction system might be digitalized, banks still need people, rather than robotics, to solve human’s problems. Therefore, this study suggests business model and strategies as an example for banking executives in the era of Banking 3.0
The Development of Electronic Payment Business in the Banking Industry after the Enactment of “The Act Governing Electronic Payment Institutions”
No full text第三方支付議題持續延燒數年，終於在2015年5月邁入法制化；在此之前，對於銀行業等金融機構及非金融機構以網路虛擬帳戶方式儲值，暨非金融機構辦理非基於實質交易之資金移轉等業務，尚乏適當之法律依據。政府為協助金流服務發展，在各界殷切期盼下，「電子支付機構管理條例」(以下稱「本條例」)遂完成制定。 本條例所規範之主體包括專營電子支付機構，與兼營之電子支付機構。而兼營電子支付機構中之銀行，長期以來都扮演金流提供者角色，惟本條例施行後，金融支付不再是銀行專利，各種新興網路支付工具挾著龐大電子商務商機挑戰銀行，這將對一向保守經營之國內銀行業產生巨大之衝擊。 本研究以美國PayPal及中國支付寶作為國際主要第三方支付機構之代表，探討其等之經營模式，並借鏡中國支付寶，論述其與銀行之競合關係及對銀行業務經營之影響，藉以分析未來我國專營電子支付機構與銀行二者間之競合關係及對銀行業務經營可能產生之影響；同時觀察我國第三方支付發展，及透過本條例及其相關授權法規命令之介紹，瞭解政府對電子支付機構之監理，進而歸納出銀行經營電子支付業務之未來發展趨勢。 藉由本條例開始施行，日後各類電子支付機構將推出各項創新之支付服務，來吸引使用者使用意願，有助於台灣電子支付產業快速翻轉，以迎頭趕上國際發展之腳步，甚而發展出在地化之電子支付服務，使我國電子商務產業更加繁盛。 對銀行而言，本條例允許非金融機構進入支付市場，勢將降低銀行在支付業務上之獲利。惟如從創新之角度觀之，第三方支付歷經多年發展，已衍生出多種業務模式，可為銀行帶來創新之金融服務；加之，以支付作為媒介，支付背後連結的是消費者之生活，以及因生活所產生之大數據，使銀行有機會接觸到新的消費客群，創造絶佳商機。 歸納本研究針對銀行因應本條例之施行所採取之策略，如：組織調整、人才建構及異業結合；電子支付業務未來發展趨勢，如：發展境內O2O、合作境外O2O、跨業整合互補優勢、銀行同業競爭激烈大者恆大等。Third-party payment has been a popular topic in recent years, and the regulations for third payment are finally implemented in May 2015. Before the enactment, banking institutions and non-financial institutions devoting in internet virtual account for online deposit along with non-financial institution conducting funds transfer service based on non-real transactions lacked legal basis. Eventually, under ardent expectations, and for the better off in payment services, “The Act Governing Electronic Payment Institutions” (hereby called, “the Act”) has finally been formulated. The main subject of the Act includes specialized electronic payment institutions and dual-status electronic payment institutions. Banking industry had always taken a part as dual-status electronic payment institutions offering payment services. However, as the Act is implemented, the payment services will no longer be banking institutions’ specialty. The institutions offering new e-payment tools with many e-commerce opportunities will inevitably impact the banking institutions. This study will discuss the representative third-party payment institutions, United States’ PayPal and China’s Alipay, by inquiring into their business models, and using China’s Alipay as reference to discourse its coopetition relationship with the banking industry. Thereby the future impact of third-party payment model to banking industry in Taiwan and their coopetition relationship could be examined as well. Reviewing on the Act and related law is to understand the government’s supervision on electronic payment institution. Finally, the banking industry’s future developments for electronic payment services are summed up. With the enactment of the Act, various electronic payment institutes will introduce different newly developed electronic payment services to attract consumers. The development could help strengthen Taiwan’s electronic payment industry instantly to catch up with the globalize progress, nurture Taiwan’s localization e-payment services, and flourish the e-commerce industry. As for the banking industry, the newly enacted Act allows non-financial institutions to enter the payment market, which certainly will cut down the banking industry’s profit in the payment service performances. However this new policy could also bring out new variety of business models, introducing innovative financial services. In addition, every payment connects the consumer’s lifestyle with the big data developed that makes the banking industry maximize the potential of data value behind each transaction, innovating commercial opportunities. To sum up, this study aims to analyze the banking industry’s development strategies after the enactment of the Act— e.g., organizational restructuring, talent construction, and horizontal alliances. Electronic payment service’s upcoming development trends— e.g., developing local O2O market, cross-border O2O market, convergence business models for complementary strengths, banking industry’s intense competition that makes the big ones get bigger, etc