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Laser diode based free-space, underwater, and white-lighting visible light communication
No full text可見光(波長範圍350~750 nm)通訊可將全球高速網路延伸至特定空間，是未來銜接人類社會所有通訊網路的必要發展，藉由使用具有比發光二極體更高調變頻寬與更低發散角的藍光雷射二極體，不但能提高可見光通訊之傳輸速率，也能以低衰減係數有效進行水下通訊，同時若搭配黃色螢光片或混合以紅光與綠光雷射二極體，更可在通訊外添加白光照明功能。 首先，在最佳化操作參數後，所使用之藍光雷射二極體可實現10.8-Gbps/16-m之點對點自由空間傳輸性能，接著以藍光雷射二極體搭配Lu3Al5O12:Ce3+ 與 CaAlSiN3:Eu2+ 共摻雜之螢光玻璃為基礎建構白光照明可見光通訊系統。當螢光玻璃之厚度為0.85-mm時，其所產生之白光色溫、色座標與最大照度分別為7856 K、(0.29, 0.3)和1337 lux。同時，照明白光內之殘留藍光成分對人眼可能造成之危害藉由計算其曝露限制來分析。在不對人眼造成危害前提下，可達1-m/2.8-Gbps 之傳輸性能。 接著，利用藍光雷射二極體建構以自來水與純海水為傳輸介質之水下光通訊系統。在以自來水為基礎時，其不同傳輸距離所對應的最大傳輸速率分別為12.4-Gbps/1.7-m、12-Gbps/3.4-m、9.6-Gbps/6.8-m與5.2-Gbps/10.2-m，同時可得傳輸容量隨距離之衰減率為0.847 Gbps/m。接著將自來水更換為純海水，由於海水內雜質引起的散射會導致藍光光束在傳輸中功率被衰減。因此，其傳輸容量對距離之衰減率會增加至0.941 Gbps/m，同時其在不同傳輸距離下所對應的最大傳輸速率分別為7.2-Gbps/6.8-m與4-Gbps/10.2-m。 最後，利用紅、藍及綠光雷射二極體來建構室內照明與通訊系統，並提供分波多工訊號傳輸。藉由此方式產生之白光色座標、色溫與最大照度分別為(0.2928, 0.2981)、8382 K與7520 lux。為了減少藍光對人眼之傷害，光學密度為0.3之光衰減片被使用使產生白光之色座標與色溫分別被改變至(0.2938, 0.3513)與7275 K。在尚未混成白光前，其紅、藍及綠光雷射二極體輸出光在1公尺自由空間傳輸後分別展現10.8、10.4與8 Gbps之最大傳輸速率。而在混成白光後，在0.5公尺自由空間傳輸下，可達總傳輸速率為5.2 Gbps。Since visible light (wavelength ranging from 350 to 750 nm) communication (VLC) can extend the global high-speed network to specific space, its development of connecting all communication networks in human society is necessary. Using blue laser diode (LD) with higher modulation bandwidth and lower divergence than light emitting diode (LED) can not only enhance the VLC transmission performance but also further perform underwater communication. By further adhering phosphorous glass upon blue LD or mixing the red/green/blue (RGB) LDs, white-lighting source can also be provided. In this thesis, laser diode based free-space, underwater, and white-lighting visible light communication is proposed. Firstly, a 450-nm blue LD is used to perform 10.8-Gbps/16-m point-to-point VLC. Furthermore, the white-lighting VLC is constructed by adhering Lu3Al5O12:Ce3+ and CaAlSiN3:Eu2+ co-doped phosphorous glass upon 450-nm blue LD. The correlated color temperature (CCT), Commission International de l’Eclairage (CIE) and maximal illuminance value of white light generated by 0.85-mm phosphorous glass is 7856 K, (0.29, 0.3) and 1337 lux, respectively. In addition, the blue light damage of human eye is discussed by measuring the exposure limit. In addition, the white-lighting VLC with transmission data rate of 2.8 Gbps and free-space distance of 1 m is demonstrated without endangering human eyes. Moreover, the blue LD is also used to demonstrate the tap and pure ocean water based underwater optical wireless communication (UOWC) systems. For the tap water based UOWC system, the maximal allowable transmission capacities with corresponding underwater distances of 12.4-Gbps/1.7-m, 12-Gbps/3.4-m, 9.6-Gbps/6.8-m and 5.2-Gbps/10.2-m are demonstrated, which exhibits a distance related decay rate on capacity of 0.847 Gbps/m. When using the pure ocean water to replace the tap water, it inside impurities induced scattering would attenuate the blue laser power during underwater transmission. Therefore, a slightly high decay rate of 0.941 Gbps/m is observed for the pure ocean water based UOWC system, which achieves 7.2 Gbps for 6.8-m and 4 Gbps for 10.2-m. Finally, RGB LDs based indoor white-lighting communication is demonstrated for wavelength-division multiplexing (WDM) transmission. Before mixing the RGB LDs, the individual RGB LDs carried 16-QAM OFDM data exhibit maximal transmission data rate of 10.8, 10.4 and 8 Gbps at 1-m free-space transmission distance, respectively. After mixing the RGB laser light, the generated white light with CIE coordinate of (0.2928, 0.2981) and CCT of 8382 K exhibits a maximal illuminance of 7540 lux. To reduce the blue light hazard of human eyes, a filter with 0.3 optical density (OD) is adhered on the blue LD, and the CIE coordinate and CCT of RGB LDs generated white light are (0.2938, 0.3513) and 7275 K, respectively. Moreover, the indoor white-lighting WDM system reveals a total allowable transmission data rate of 5.2 Gbps with transmission distance of 0.5 m
Silicon Based Photonic Crystal biosensors for Glucose Concentration Analysis
No full text近年來，物聯網逐漸興起，穿戴式裝置及各式建置物聯網所需的感測器需求使的這個領域具有龐大的市場需求。物聯網應用於生物感測器上如食品安全、醫學檢測、藥品測試上，能夠以低成本、高性價比製作而成的感測器相當吸引人。生物感測器如二維光子晶體生物感測器，其量測極限已能到達相當低的物質濃度。唯其使用之量測設備諸如光源及偵測器之價格仍相當高昂，使用低解析度及低成本光源又能維持相當的量測精度為普及生物感測器之重要課題。 本篇論文主要研究於二維光子晶體利用能帶分布圖檢測待測物的折射率。 在第一部分的研究中，我們在矽基板上製作二維光子晶體，以三種不同顏色的色光進行0.002到0.5莫耳濃度區間的葡萄糖水溶液折射率量測。我們將元件置於載台上並且將入射光以固定角度經由光纖照射於光子晶體生物感測器之區域。並以低成本光譜儀收集其反射訊號，以傳統方式量測其反射光譜之角度隨濃度變化、反射光譜之波長隨濃度變化之訊號。 其結果發現我們的二維光子晶體生物感測器以傳統方式之量測分析，在低解析度之光譜儀下其結果並無法反映待測物葡萄糖溶液之折射率。 在第二部分的研究中，我們一樣製做了二維光子晶體在矽基板上，由於二維光子晶體在橫截面上可視為多種不同周期之一維光子晶體，為此我們延續第一部分的實驗，將三種不同顏色的色光照射於裝載0.002到0.5莫耳濃度葡萄糖水溶液的光子晶體生物感測器上，並且將光子晶體生物感測器置於可旋轉之載台上調整其載台角度使入射光照射於不同的一維光子晶體周期上。並延續第一部分的實驗以傳統的角度變化、波長變化以及本篇的研究主題-能帶分布圖進行葡萄糖水溶液的折射率分析。結果發現在低解析度下的傳統方式量測分析，其結果受外在環境干擾嚴重。而光子晶體能帶分布圖則受惠於正規化的數據處理技巧，能不受外在環境影響並且以自校準的方式顯示出個別葡萄糖水溶液的折射率值，我們同時定義出感測器的敏感度和其量測極限，並且得到敏感度和量測之光子晶體周期成正比，量測極限會受到入射光波長影響及待測物本身光吸收率的影響。Recent years, Iot (internet of things) has become a very popular topic in consumer electronics. Wearable device and various of sensors which construct the Iot makes the market have tremendous demand. Iot biosensing application such as food safety, medical and drug testing. It is attractive article of sensor product with cost-effective price. Biosensing technology such as 2 D PhC (photonic crystal) biosensor. The detection limit can reach to watery concentration. Although the high detection limit it reached, the measurement facility such as light source and monochromatic meter are still in high cost. Usage of low resolution detector and low cost light source but sill remain the sufficient precision is an important issue to promote the biosensor to consumer. In this thesis, the anatyle detection via 2 D PhC band diagram is studied. In the first part, we fabricated the 2 D PhC structure on silicon wafer. Three kinds of LED (light emitting diode) are used to measuring refractive index of glucose solution which the concentration range are 0.002 mole/L to 0.5 mole/L. The device is putting on the stage and fixing the angle of incident light. The LED illuminated the PhC biosensor sensing area via fiber. The reflect signal was collected by the cost-effective spectral meter. The traditional analysis method including angular spectra and spectral analysis was executed. The results found that our 2 D PhC biosensor cannot measure the glucose solution reflective index under the low resolution spectral meter with traditional analysis. In second part, the same 2 D PhC structure is fabricate on silicon wafer. Multi period grating can be measured by changing the incident direction on 2 D photonic crystal. Thus we extend the experiment in the first part. Measuring the 3 kinds LEDs and changing the glucose solution range from 0.002 mole/L to 0.5mole/L on the PhC biosensor. Changing the grating period by rotating the stage. Also, traditional measurement method employed and the main method in this thesis – band diagram analysis to analyze the reflective index of glucose concentration. Results shows that the traditional measurement method still interfered by noise. The PhC band diagram analysis benefits from the normalize process which can control the noise and presenting the refractive index with self-align rather than water reference. The sensor’s detection limit and sensitivity are also defined. The sensitivity is proportional to PhC period. The detection limit is effected by incident spectral and absorption of analyte
Electromagnetic Analysis of Grating Reflectors: The Relation between Quality Factors and Structural Parameters
No full text本篇論文利用平板介質波導的物理特性配合電磁理論去估算出光柵反射器的品質因子，其中平板波導邊界電場受到介電質差異的擾動(perturbation)對於分析光柵反射器的品質因子有重要的影響，使用數值軟體計算各種結構參數光柵反射器的品質因子並驗證理論估算的品質因子，證明我們能藉由理論估算出光柵反射器的品質因子以省去數值軟體大量的計算時間。 藉由模態耦合理論(Coupled-Mode Theory, CMT)去分析光柵反射器的頻率響應，再由全波模擬的結果驗證光柵反射器的頻率響應頻譜，經由模態耦合理論可以省去模擬軟體大量的計算時間，也能獲得高準確度的頻率響應頻譜。In this work, we estimate the quality factor of grating reflectors with properties and theories of the planar dielectric waveguide. The scattered electric field due to perturbation of dielectric difference at the waveguide’s boundary is a huge factor to estimate the quality factor of grating reflectors. Then, we use simulation software COMSOL Multiphysics to calculate the quality factor with different structure parameters to clarify and prove we can reduce the time of simulation. We analyze the frequency response of grating reflectors with Couple-Mode Theory and use the full-wave simulation to verify the frequency response. We can save lots of time on the simulation and obtain much more accurate frequency responses
Study on the Immune Regulatory Mechanisms of Single Allergen-Induced Oral Tolerance Inhibits Airway Inflammation in Conjugated Allergen Immunized Mice
No full text口服耐受性被認為由數種機制達成，包含特異性T細胞凋亡、特異性T細胞無應性、特異性調節性T細胞生成，然而詳細完整的機制尚未了解透徹。本研究目的為探討在多種過敏原致敏的個體，透過餵食單一過敏原而誘發單一特異性口服耐受性，是否具調節不同特異性過敏反應的功能。本實驗利用化學鍵結兩種實驗常用抗原—卵清蛋白 (ovalbumin) 和 β-乳球蛋白 (β-lactoglobulin)，以此鍵結抗原 (BLG-conjugated OVA，B-O) 致敏小鼠，探究餵食其中一種抗原，是否能保護小鼠免於另一抗原誘發的呼吸道發炎反應。實驗發現餵食卵清蛋白有效避免β-乳球蛋白誘發的抗原特異性反應，包含血清中特異性免疫球蛋白E (BLG-specific IgE)、呼吸道過度反應 (airway hyperresponsiveness)、肺部細胞浸潤、呼吸道發炎反應。餵食β-乳球蛋白也可減緩卵清蛋白誘發的過敏反應。利用帶有單一T細胞受體小鼠 (DO11.10 mouse)，發現餵食卵清蛋白可增進CD4+CD25+ T細胞的非抗原特異性抑制功能。轉送帶有卵清蛋白短鏈 (OVA323-339 peptide) 的B細胞到DO11.10小鼠，可促使脾臟細胞和脾臟CD4+ T細胞對卵清蛋白短鏈產生無應性，暗示脾臟B細胞可能呈獻卵清蛋白短鏈誘發調節性T細胞生成，而參與口服耐受性。口服抗原活化的CD4+CD25+ T細胞與B細胞誘發的調節性T細胞 (Treg-of-B cells) 具數個相似處，包含兩者皆表達誘導T細胞共刺激分子 (inducible T-cell co-stimulator，ICOS) 和程序性細胞死亡蛋白質1 (programmed cell death 1，PD1)、分泌介白素10 (interleukin-10，IL-10) 和轉化生長因子β (transforming growth factor-β，TGF-β)、具有非抗原特異性抑制功能。此結果暗示脾臟B細胞誘發之調節性T細胞，有可能參與在口服耐受性複雜的非特異性抑制機制中。單一過敏原產生的口服耐受性具潛力調節相關性過敏原的不當反應，此效果可見於調節性T細胞與不當反應的特異性T細胞共同存在的環境中，在鍵結抗原誘發的過敏性氣喘模式中，此非特異性調節潛力可更清楚呈現。 另外，我們探究重複給予呈獻抗原的B細胞，對B細胞誘發的調節性T細胞 (Treg-of-B cells) 生成的影響。我們發現在第三輪B細胞誘發的調節性T細胞 (Treg-of-B3rd cells) 中，表現介白素10 (IL-10) 的細胞比例增加，介白素的表達量也有增加。同時，介白素10也在第三輪B細胞誘發的調節性T細胞的抑制功能中扮演角色。第三輪B細胞誘發的調節性T細胞和B細胞誘發的調節性T細胞相比，仍然維持表達誘導T細胞共刺激分子 (ICOS)、程序性細胞死亡蛋白質1 (PD1)、毒殺T淋巴球相關抗原4 (cytotoxic T-lymphocyte associated antigen 4, CTLA4) 和抑制功能。我們也發現主要表達介白素10的細胞群，大多侷限在表達肌肉腱膜纖維肉瘤癌基因同源物 (avian musculo-aponeurotic fibrosarcoma oncogene homolog, c-Maf) 的細胞群中。在培養過程中，介白素10、、介白素4、轉化生長因子β、介白素27都有逐漸增加的趨勢。此結果顯示，多次給予呈獻抗原的B細胞具有能力誘發T細胞成為介白素10表達的細胞，可能透過可能透過介白素27與和轉化生長因子β的調控。 總結地說，我們的研究成果顯示B細胞誘發的調節性T細胞，具有非抗原特異性抑制功能，而且可能參與在複雜的口服耐受性機制中。另一部分，多次給予呈獻抗原的B細胞具有能力，透過活化肌肉腱膜纖維肉瘤癌基因同源物使T細胞成為表達介白素10的細胞。在未來研究，會著重在肌肉腱膜纖維肉瘤癌基因同源物的表達與否和B細胞誘發的調節性T細胞的抑制能力是否有關，以及肌肉腱膜纖維肉瘤癌基因同源物是否有協同其他蛋白共同調控介白素10的基因表現 。Although oral tolerance has been considered the result of a number of protective mechanisms, the real mechanisms of oral tolerance are yet to be defined. The present study was aimed to determine whether a single allergen-induced oral tolerance would affect the immune responses to other related allergens that were primed together with the orally treated allergen. We investigated whether oral administration of a single antigen would protect the conjugated antigen-sensitized mice from the other antigen induced airway inflammation. We found that oral administration of ovalbumin (OVA) was able to prevent the immune responses to β-lactoglobulin (BLG) in BLG-conjugated OVA (B-O) sensitized mice and vice versa. Oral administration of antigen enhanced the suppressive potential of CD4+CD25+ T cells to inhibit non-antigen-specific T cell proliferation. The B cell-induced regulatory T (referred to as Treg-of-B) cells showed several similarities with orally treated CD4+CD25+ T cells, including the expression of inducible T-cell co-stimulator (ICOS) and programmed cell death 1 (PD1), the production of interleukin (IL)-10 and transforming growth factor (TGF)-β, and the non-antigen-specific suppressive ability, and therefore might play a role in the sophisticated mechanism of oral tolerance. The results suggested that single allergen induced oral tolerance had the ability to modulate the immune responses to other related allergens and was able to be more clearly detected in our conjugated antigen-induced asthmatic model. In addition, we investigated the effect of re-encounter the antigen-presenting B cells on the generation of Treg-of-B cells. We found that the IL-10-producing population and production of IL-10 increased in Treg-of-B3rd cells. IL-10 also played a role in the suppressive function of Treg-of-B3rd cells. Treg-of-B3rd cells maintained expressions of ICOS, PD1, and cytotoxic T-lymphocyte associated antigen 4 (CTLA4) and the suppressive abilities as that of Treg-of-B1st cells. The major population of IL-10-producing Treg-of-B3rd cells was confined to the avian musculo-aponeurotic fibrosarcoma oncogene homolog (c-Maf)-expressing population. The levels of IL-10, IL-4, IL-27, and TGF-β increased gradually during the generation of Treg-of-B3rd cells. These results suggested that re-encounter the antigen-presenting B cells converted CD4+CD25- T cells into IL-10-producing Treg-of-B3rd cells and the pathway of IL-27/TGF-β-c-Maf might be involved. In summary, our results suggested that Treg-of-B cells had a non-antigen-specific suppressive function and might play a role in the sophisticated mechanism of oral tolerance. Moreover, re-encounter the antigen-presenting B cells induced IL-10-producing CD4+ Treg-of-B3rd cells via activation of c-Maf. In the future, the upstream signaling activated generation of IL-10-producing Treg-of-B cells, the relationship between c-Maf and the suppressive function of Treg-of-B cells required further research and the binding proteins of c-Maf in the regulation of IL-10 or other genes required more investigations as well
Role of TRAIL in inflammatory bowel disease
No full textTRAIL(TNF-related apoptosis-inducing ligand)是一個屬於TNF家族的第二型胯膜蛋白 (type II transmembrane protein)，可藉由與TRAIL受體(TRAIL-R)作用而引發細胞凋亡。在免疫系統中，TRAIL表現在多數已活化的免疫細胞上，包含自然殺手細胞、 NKT細胞、單核細胞 (monocytes)、樹突狀細胞 (DCs), 巨噬細胞(macrophage), T細胞和B 細胞。 除了引發細胞凋亡，研究也發現TRAIL可能參與自體免疫的調控。在一些自體免疫疾病的動物模式，如實驗性自體免疫腦炎 (EAE )和鏈脲佐菌素誘導糖尿病(Streptozotocin-induced diabetes)中，TRAIL-/-小鼠有更嚴重的發炎。除此之外，我們實驗室的初步研究發現，在膠原蛋白誘發類風濕性關節炎 (collagen induced arthritis；CIA)的中，注射TRAIL重組蛋白能顯著降低發炎症狀，並能夠抑制T細胞的活化。基於這些發現，我們想研究TRAIL在其他自體免疫疾病中的角色。 發炎性大腸疾病(Inflammatory bowel disease；IBD) 是一個由於免疫變化，導致了患者對失去對腸道內共生菌的免疫耐受性(immune tolerance)，或是影響腸道的功能而造成的大腸發炎之自體免疫疾病。雖然TRAIL在IBD致病機轉中的角色仍不明確，但有研究指出TRAIL-R-/-小鼠在DSS誘發腸炎的動物模式中，表現出更嚴重的腸炎，而且T細胞在此模型中的重要性也有被探討過。因此我們使用DSS誘發腸炎的模型來研究TRAIL在腸道發炎中的角色。 在這篇研究中，我們發現注射TRAIL到DSS誘發大腸炎小鼠體內，會顯著降低體重下降、大腸長度減短、腸道發炎和腸道上皮層損傷的程度，這些結果暗示TRAIL可能有抑制發炎反應的功能。然而，分析腸道內細胞之促發炎細胞激素和抗發炎細胞激素的表現量，卻發現兩者都被顯著抑制，因此TRAIL有可能是作用在抑制T細胞的活化，因為它們是IBD中細胞激素的重要來源。 另一方面，利用TRAIL-R-/-小鼠，我們發現TRAIL無法在TRAIL-R-/-小鼠中 呈現腸道發炎的保護作用，顯示出TRAIL的保護功能必須透過和TRAIL-R作用。進一步的研究發現，TRAIL和TRAIL-R結合並不會誘導小鼠的T細胞或是大腸組織中其他細胞的凋亡，反而具有抑制T細胞活化的效用。此研究不但發現在IBD致病機轉中TRAIL抑制T細胞活化之重要性，同時也助於發展新的IBD治療方式。TRAIL (TNF-related apoptosis-inducing ligand) is a type II transmembrane protein that belongs to TNF family, and it can induce apoptosis through binding with TRAIL receptor (TRAIL-R). TRAIL is widely expressed on activated immune cells, including NK cells, NKT, monocytes, DCs, T cells and B cells. Apart from inducing cell apoptosis, reports have suggested that TRAIL may play a role in regulation of autoimmunity. In autoimmune disease animal models such as EAE (experimental autoimmune encephalomyelitis) and streptozotocin (STZ) -induced diabetes, TRAIL-/- mice suffered more severe inflammation and accelerated pathogenesis. Moreover, our preliminary results showed that injection of recombinant TRAIL significantly reduced the severity of inflammation and may suppress the activation of T cell in CIA (collagen induced arthritis) mice. Based on these findings, we would like to investigate the role of TRAIL on other autoimmune disease. Inflammatory bowel disease (IBD) is an autoimmune disease caused by immune dysregulation, which leads to defective host immune tolerance toward commensal intestinal microbiota, and effects on intestinal epithelial barrier function. Although the role of TRAIL in IBD pathogenesis remained unclear, it has been reported that TRAIL-R-/- mice suffered more severe colitis in DSS-induced colitis, a widely use experimental IBD model. In addition, the importance of T cell in the pathogenesis of DSS-induced colitis has been well addressed. Therefore, we applied DSS-induced colitis to investigate the role of TRAIL in inflammatory colitis. Injection of recombinant TRAIL into DSS colitis mice significantly reduced DSS-induced weight loss, colon inflammation and epithelial damage. These result implied that TRAIL may promote anti-inflammatory response. However, the expression of both pro-inflammatory and anti-inflammatory cytokines are significantly down-regulated in colon tissue, suggesting that TRAIL may have direct effects on T cells. On the other hand, we found that the protective function of TRAIL was abolished in TRAIL-R-/- mice, indicating the therapeutic effect of TRAIL is dependent on the interaction with TRAIL-R. Further studies showed that TRAIL/TRAIL-R did not trigger apoptosis of either T cells or other cells in the colonic tissue, but suppressed the activation of T cells instead. Here we found that TRAIL plays an important role in IBD pathogenesis through suppressing the activation of T cells, and it may also provide a new potential therapeutic strategy for IBD
Regulation of osteoclast activation and inflammation signal transduction in inflammatory arthritis
No full text蝕骨細胞是多核並具有蝕骨功能的細胞，屬於腫瘤壞死因子家族成員可與其接受體互相作用而促進蝕骨細胞分化，有許多研究已廣泛地指出RANKL的訊息機制可促進蝕骨細胞生成。RANKL活化蝕骨細胞分化中，TRAF6訊息路徑是不可或缺的，在之前的研究當中，我們的研究結果顯示TRAIL透過TRAF6訊息路徑活化蝕骨細胞分化，有趣的是，我們的結果也顯示TRAIL具有抑制RANKL以及M-CSF促進蝕骨細胞分化的現象。然而，TRAIL在RANKL或是其他腫瘤壞死因子中有無共同刺激，影響促進以及抑制蝕骨細胞分化，認為TRAIL可能在調控骨免疫學中蝕骨細胞分化中扮演重要的角色，很有可能是透過影響脂質閥以及TRAF6相關訊息，脂質閥對於聚集或排除接受器之特定訊息物質而活化免疫細胞中扮演重要的角色，我們的結果指出RANKL對於脂質閥之訊息分子傳遞而影響蝕骨細胞的功能，而TRAIL會干擾脂質閥中RANK訊息傳遞影響蝕骨細胞的分化。更進一步使用大鼠實驗性關節炎的動物模式，TRAIL不但可以改善骨密度以及骨侵蝕，更可以減少關節腫脹及發炎，然而，TRAIL抑制發炎的功能是透過抑制T細胞的活化而不是影響細胞凋亡，因此TRAIL有效地抑制實驗性關節炎的發炎以及關節炎的進展，TRAIL提供了關節炎具有潛力以及新的治療方針。 PSTPIP2參與巨噬細胞活化、噬中性白血球移動性以及蝕骨細胞分化，然而，PSTPIP2對於自體發炎以及蝕骨細胞生成的角色並不是很清楚。在我們的研究中，我們建立PSTPIP2基因剔除老鼠探討表型以及自體發炎疾病的角色，所有PSTPIP2基因剔除老鼠具有腳掌腫脹、滑膜炎、骨肥厚以及骨髓炎，類似SAPHO症候群（滑膜炎、痤瘡、膿皰病、骨肥厚、骨髓炎），發生在骨頭、皮膚以及關節的發炎疾病，多病灶性骨髓炎在發炎性腳掌中有較多的巨嗜細胞以及噬中性白血球浸潤在骨頭、關節以及皮膚，顯著性骨侵蝕的病灶部位腳掌以及肢體也發現明顯降低骨密度，在發炎的組織中也發現顯著增加趨化噬中性白血球的趨化素以及介白素-1β。我們的研究認為PSTPIP2在自體發炎骨疾病中，先天性免疫以及蝕骨細胞生成的發展扮演重要的角色，並且可能跟人類SAPHO症候群的病理具有相關性。 總而言之，我們指出TRAIL以及PSTPIP2參與蝕骨細胞活化以及發炎，認為與蝕骨細胞活化的訊息傳導路徑具有相關性，了解發炎性關節炎以及骨破壞的傳導路徑，對於骨免疫學是重要的並且可發展新的治療方式。Osteoclasts are bone resorbing multinucleated cells involves interactions between tumor necrosis factor (TNF) ligand superfamily members and their receptors. Accumulated evidences indicate that the signaling mechanism of RANKL in promoting osteoclasteogenesis has been extensively studied. RANKL activates TRAF6 signaling pathways, which are indispensable for the induction and activation of osteoclast differentiation. In previous study, our results have demonstrated that TRAIL induces osteoclast differentiation via a TRAF-6-dependent signaling pathway. Interestingly, our results also demonstrated that TRAIL suppressed osteoclastic differentiation induced by RANKL plus M-CSF. Therefore, TRAIL can both promote and suppress osteoclast differentiation, depending on the presence of RANKL or other TNF superfamily molecules, suggesting that TRAIL may play a role in regulating osteoclast differentiation in osteoimmunology. It is possible that the regulation is at the lipid raft and TRAF6 associated signaling. Membrane lipid rafts play a key role in immune cell activation by recruiting and excluding specific signaling components of immune cell surface receptors upon the receptor engagement. We demonstrated that rafts in osteoclasts may function as the platform for a network of signaling molecules that assemble in response to RANKL. TRAIL blocked osteoclastic differentiation was accompanied by interference the RANK signaling required the function of raft membrane microdomains. Furthermore, in collagen-induced arthritis rat animal model, treatment with TRAIL not only the improved the bone density and inhibited bone erosion, but also reduced the joint swelling and inflammation. However, the anti-inflammation effects of TRAIL inhibited T cell activation instead of increased apoptosis in T cells. Therefore, TRAIL administration is an effective anti-inflammatory treatment that prevents the development and progression of experimental arthritis. It may provide a potential and new therapeutic strategy of treatment in arthritis. PSTPIP2 is involved in macrophage activation, neutrophil motility, and osteoclast differentiation. However, the role of PSTPIP2 in autoinflammation and osteoclastogenesis is still not clear. In our study, we generated PSTPIP2 knockout (Pstpip2-/-) mice to investigate its phenotype and role in autoinflammatory diseases. All Pstpip2-/- mice developed paw swelling, synovitis, hyperostosis, and osteitis, resembling SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, osteitis), an inflammatory disorder of the bone, skin, and joints. Multifocal osteomyelitis was found in inflamed paws with increased macrophage and marked neutrophil infiltrations in the bone, joint, and skin. Profound osteolytic lesions with marked decreased bone volume density developed in paws and limbs. Neutrophil-attracting chemokines and IL-1s were markedly elevated in inflamed tissues. Our study suggests that PSTPIP2 could play a role in innate immunity and development of osteoclastogenesis in autoinflammatory bone disorders, and may associate with the pathogenesis of human SAPHO syndrome. Taken together, we demonstrated that both TRAIL and PSTPIP2 is involved in osteoclast activation and inflammation, suggesting the cross-talk between signaling transduction pathways in osteoclast activation and inflammation. Understanding of the regulation of these pathways is important to explore the critical steps in oseoimmunology, and help to development of new therapeutic approach in inflammatory arthritis and bone destruction
Study on the Molecular Mechanism of Deltex1 in T cell Anergy
No full textE3泛素連接酶對於誘發及維持T細胞去活化 (T cell anergy) 扮演重要的角色。誘發T細胞去活化過程中，去活化相關的E3泛素連接酶如Cbl-b, Itch和GRAIL的蛋白質表達量會上升，並透過降解T細胞活化訊息傳遞分子PKCθ和PLCγ1而抑制T細胞再活化。然而這些去活化相關的E3泛素連接酶如何彼此協同，進而維持T細胞去活化卻未完全清楚。 本篇研究中，我們探討Notch相關E3泛素連接酶deltex1 (DTX1) 在維持T細胞去活化的扮演的角色。我們發現，DTX1會結合PKCθ和PLCγ1並抑制其蛋白質表現。進一步的研究顯示，相似Cbl-b和Itch的作用，DTX1催化PKCθ單體泛素化，使得單體泛素化的PKCθ經由核內體-溶小體 (endosome-lysosome) 途徑而分解，處理蛋白酶體抑制劑並不會降低DTX1所調控PKCθ降解。此外，我們也觀察到DTX1會與Cbl-b結合並促進Cbl-b的表現。進一步的實驗證實，DTX1抑制PKCθ主導的Cbl-b降解並增加Cbl-b的蛋白質穩定。本篇的研究闡述了去活化相關的E3泛素連接酶在T細胞去活化中的協同作用：DTX1泛素化PKCθ並經由核內體-溶小體 (endosome-lysosome) 途徑調控PKCθ降解；DTX1透過調控PKCθ降解促進Cbl-b蛋白質穩定；DTX1與Cbl-b共同作用確保PKCθ的活性完全抑制。Ubiquitin E3 ligases are associated with induction and maintance of T cell anergy. These E3 ligases, including Cbl-b, Itch, and GRAIL, attenuate T cell activation by targeting to signaling molecules such as PKCθ and PLCγ1 for degradetion. How these anergy-associated E3 ligases coordinate during T cell anergy remains incompletely understood. In this study, we found that Notch-related E3 ligase deltex1 (DTX1) also regulated the expression of PKCθ and PLCγ1. DTX1 interacted with PKCθ and PLCγ1 and promoted the degradation of PKCθ and PLCγ1. T cell anergy-induced downregulation of PKCθ was prevented in Dtx1-/- T cells, supporting the essential role of DTX1 in PKCθ downregulation. DTX1 promoted monoubiquitination of PKCθ, similar to Cbl-b and Itch. DTX1-directed PKCθ degradation was not prevented by proteasome inhibitor, but instead DTX1 directed the re-localization of PKCθ into the lysosomal pathway. In addition, DTX1 interacted with Cbl-b and increased the protein levels of Cbl-b. We further demonstrated that, through the downregulation of PKCθ, DTX1 prevented PKCθ-induced Cbl-b degradation and increased Cbl-b protein stability. Our results illustrate the coordination between E3 ligases during T cell anergy; DTX1-mediated PKCθ degradation further stabilizes Cbl-b and DTX1 acts with Cbl-b to assure a more completely silencing of PKCθ
Development of High Efficiency Perovskite Solar Cell Module and Related Prototype Product
No full text鈣鈦礦太陽能電池由於其優異的光電轉換效率在近幾年受到各方的關注和研究；除此之外由於其能夠以濕式製程製備元件，非常適合低成本、卷對卷方式進行量產，因此被認為具有相當大的潛力商業化。在本研究中我們著手於未來量產上會遭遇的其中兩項挑戰:一是元件的製備環境，我們無法將一間廠房維持如手套箱般的超低濕超低氧，所以開發在相對濕度較高的環境中製作元件的技術是必須的；二是如何製備高效率的模組元件。 首先我們嘗試在正常氧值、溼度控制在2~3%的乾燥箱中製備元件。透過增加二甲基亞碸與碘化鉛在鈣鈦礦前驅溶液中的莫耳數比(1:1到3:1)，我們能夠獲得更好的薄膜品質使短路電流由14.3mA/cm2上升至16.4 mA/cm2。接著我們以NiOx取代導電高分子PEDOT:PSS作為電洞傳導層，將轉換效率進一步由11.3%提升至12.9%，並且與在手套箱中製備之元件效率相同。 而在模組製作上，我們在一般環境下以波長為532nm的奈秒脈衝雷射在原件上製備模組的P1、P2和P3線。透過調整脈衝雷射的入射方向、脈衝能量以及脈衝重疊率，成功以單一波長雷射完成所有線的切割。我們嘗試在面積為4cm2與25cm2的基材上製作分別串聯兩顆、八顆的模組，在考慮有效面積下光電轉換效率分別達到12.82%與11.76% ，是目前以全雷射切割製作模組的最高值。 最後，我們成功以鈣鈦礦模組驅動信標與溫濕感應器，證實其應用於日常生活中的可能性。Recently, perovskite solar cell draws lots of attention due to its outstanding performance. Besides, because it can be manufactured by solution processing, it is very suitable for mass production in a low cost, roll-to-roll way. Thus, perovskite solar cell is believed to have potential to be commercialized in near future. In this research, we focus on two challenges that will meet when the device is in mass production. First, we cannot make the atmosphere of factory the same as in the glove box. Therefore, it is essential to develop an ambient process of cell fabrication. The second challenge is how to make a high efficiency solar module. For the first challenge, we build a dry air box with relative humidity controlled at 2~3%. The quality of film becomes better when the molar ratio of dimethyl sulfoxide to perovskite precursor is increased from 1:1 to 3:1. The short circuit current density of devices is increased from 14.3mA/cm2 to16.4 mA/cm2. Next, we substitute NiOx for PEDOT:PSS as hole transport layer and further raise the performance of devices from 11.3% to 12.9% and is the same as the performance of cells fabricated in glove box. For the second challenge, we use nanosecond pulse laser with a wavelength of 532nm to scribe P1, P2 and P3 line on the devices to make solar module. By changing the inject direction, pulse energy and pulse overlap ratio, we successfully scribe P1, P2 and P3 line using the single wavelength laser. And then, we fabricate perovskite solar module with 2 and 8 sub-cells on 4cm2 and 25cm2 substrate, respectively. The performance of each module is 12.82% and 11.76% calculated under active area. Both are the highest performance reported for perovskite module scribed with a single wavelength pulse laser based on our knowledge. Finally, we successfully use our perovskite solar module to drive beacon and senor which demonstrate the usage of perovskite solar cell
Recombinant Coat Protein Suppress Whitefly Transmission of Tomato yellow leaf curl Thailand virus
No full text粉蝨不僅藉由取食造成植株的危害，更做為媒介昆蟲傳播植物病毒。菸草粉蝨傳播的 begomoviruses 威脅世界上許多作物的栽培。番茄黃化捲葉泰國病毒 (Tomato yellow leaf curl Thailand virus, TYLCTHV) 及番茄捲葉台灣病毒 (Tomato leaf curl Taiwan virus, ToLCTWV) 是臺灣番茄田間最常見的兩種病毒。鞘蛋白 (coat protein, CP) 是 begomoviruses 唯一的結構蛋白，CP 被推測與菸草粉蝨中腸推定的受體 (receptor) 有交互作用。In vivo binding assay 結果顯示 recombinant TYLCTHV CP與菸草粉蝨 (Bemisia tabaci) 的中腸細胞有專一性的結合。本研究的目的是探討菸草粉蝨獲得病毒前先餵食 recombinant TYLCTHV CP 是否會競爭粉蝨中腸推定的受體，進而降低其獲得 TYLCTHV 病毒量與粉蝨傳播TYLCTHV的能力。實驗結果顯示先餵食 recombinant TYLCTHV CP 會降低 TYLCTHV 在粉蝨中腸細胞內的累積程度，但是卻沒有降低粉蝨體內的 TYLCTHV 病毒量。此外，先餵食 recombinant TYLCTHV CP會抑制粉蝨傳播TYLCTHV。本研究也利用相似的實驗來探討先餵食 recombinant TYLCTHV CP (homologous to ToLCTWV CP) 是否也會降低粉蝨中腸細胞內 ToLCTWV 的累積程度與粉蝨體內的病毒量，以及抑制粉蝨傳播 ToLCTWV。實驗結果指出先餵食 recombinant TYLCTHV CP不會降低 ToLCTWV 在菸草粉蝨中腸細胞內的累積程度與粉蝨體內的 ToLCTWV 病毒量。此外，先餵食 recombinant TYLCTHV CP也不會抑制菸草粉蝨傳播ToLCTWV。本研究證實 TYLCTHV CP 做為 attachment protein的功能並且能抑制菸草粉蝨傳播 TYLCTHV。此外，餵食 recombinant TYLCTHV CP 無法有效降低菸草粉蝨傳播 ToLCTWV 的結果也顯示 TYLCTHV CP與菸草粉蝨中腸的 receptor 具有專一性。了解 CP 與菸草粉蝨中腸的交互作用不僅可以揭開菸草粉蝨傳播 begomoviruses 的機制，日後進一步的研究更能幫助我們發展對抗病害的防治策略。Whiteflies not only damage plants through feeding but also serve as vectors transmitting plant viruses. Whitefly-transmitted begomoviruses threaten a wide range of crops worldwide. Tomato yellow leaf curl Thailand virus (TYLCTHV) and Tomato leaf curl Taiwan virus (ToLCTWV) are two most prevalent viruses in tomato fields in Taiwan. Coat protein (CP), the only structural protein of begomoviruses, is hypothesized to interact with a putative receptor in the midgut of Bemisia tabaci. In vivo binding assay demonstrated recombinant TYLCTHV CP specifically bound to the midgut cells of B. tabaci. The objective of this study was to determine if preacquisition of TYLCTHV CP competes the putative receptor in the midgut of B. tabaci hence suppresses the acquisition and vector transmission of TYLCTHV. Preacquisition of recombinant TYLCTHV CP decreased the accumulation level of TYLCTHV in the midgut cells of B. tabaci but did not reduce the acquisition of TYLCTHV in B. tabaci. Further, preacquisition of recombinant TYLCTHV CP suppressed the whitefly transmission of TYLCTHV. Similar experiments were conducted to investigate if preacquisition of TYLCTHV CP (homologous to ToLCTWV CP) would reduce virus accumulation and acquisition in B. tabaci, and the whitefly transmission of ToLCTWV. The results demonstrated that preacquisition of recombinant TYLCTHV CP did not influence the accumulation and acquisition of ToLCTWV in B. tabaci and did neither reduce the whitefly transmission of ToLCTWV. In conclusion, TYLCTHV CP functioned as an attachment protein and preacquisition of TYLCTHV CP reduced the whitefly transmission of TYLCTHV. The failure that using TYLCTHV CP to inhibit the whitefly transmission of ToLCTWV suggested that the interaction between TYLCTHV CP and the putative receptor in the midgut of B. tabaci is specific. Understanding the CP-midgut interaction would unveil the mechanism of whitefly transmission of begomoviruses and warrant further study to develop strategies for disease control
Effect of Carbohydrates in Hemipteran Honeydew on Invasion Success of Red Imported Fire Ant (Solenopsis invicta)
No full text近來許多研究已證實，在螞蟻與半翅目昆蟲共生關係中，半翅目昆蟲之蜜露對於螞蟻而言不僅是食物來源，且為影響其拓殖成功的重要因素，尤其於入侵蟻種更為顯著。蜜露為成分複雜之複合醣類，過去研究多直接使用蜜露作為試驗材料，因此影響螞蟻入侵成功之關鍵成分至今仍未明。為初步釐清此問題，本研究以入侵紅火蟻 (Solenopsis invicta, 簡稱火蟻) 為材料，並供給半翅目昆蟲蜜露中主要八種醣類成分 (總稱使用｢醣｣字，別稱使用｢糖｣字)，分別是蔗糖、果糖、麥芽糖、松三糖、葡萄糖、海藻糖、木糖和棉仔糖，來測試 1) 蜜露中何種醣類最為火蟻偏好，2) 火蟻偏好之醣類是否影響蟻巢成長，3) 受偏好之醣類是否影響火蟻種內與種間 (與黑棘蟻 Polyrhachis dives 作競爭) 競爭表現。試驗結果顯示，火蟻對蜜露中的蔗糖 (sucrose)、松三糖 (melezitose) 與棉仔糖 (raffinose) 等三種主要醣類成分具偏好性，尤其以蔗糖和松三糖更為顯著。在族群成長試驗中額外添加蔗糖之蟻巢較餵食正常餌料之蟻巢產生更多幼體，但添加棉仔糖及松三糖之蟻巢幼體增加較不明顯。而添加蔗糖之蟻巢工蟻的減少數目最少，棉仔糖和松三糖則較不明顯。競爭試驗結果顯示，無論種內或種間層級，餵食添加蔗糖餌料的火蟻巢競爭優勢明顯高於餵食棉仔糖和松三糖的蟻巢，而在群體競爭的試驗中，餵食蔗糖的蟻巢擊敗競爭蟻巢的時間也較餵食棉仔糖和松三糖的蟻巢來的短。歸納三項試驗結果，蜜露中的蔗糖可能為促進蟻巢成長及競爭優勢的主要成分，而火蟻具強烈偏好性的松三糖則在族群成長及競爭表現上沒有蔗糖來的顯著，棉仔糖在此兩樣項目上為影響最低的醣類。由於族群成長和競爭表現是使火蟻順利入侵並定殖的眾多要素之一，故推測環境中穩定蔗糖供應源與火蟻入侵成功有極密切的關連。此外，松三糖可能作為蜜露中的誘引成分，使火蟻得知蜜露的所在，棉仔糖則同樣可能是誘引火蟻的成分之一，但作用沒有很明顯。本研究並使用木瓜秀粉介殼蟲 (Paracoccus marginatus Williams and Granara de Willink) 與火蟻作連接，來檢測半翅目昆蟲蜜露對火蟻的實際影響。結果指出與介殼蟲連接的火蟻比未連接介殼蟲之蟻巢具較高的幼體和工蟻增加量，在種內和種間競爭中先攻擊的比率也有所提升。由此試驗結果可知實際的半翅目昆蟲蜜露對火蟻族群成長和競爭表現的重要性與帶來的正向影響。本研究得知蜜露本身與其中的蔗糖成分是火蟻族群成長和競爭的關鍵要素，而此兩項要素的正向影響也是紅火蟻得以入侵成功的基石。並期待此研究成果能應用於擬定入侵螞蟻和半翅目害蟲之整合蟲害管理策略或是火蟻餌劑的開發