Renewable energy sources normally require power converters to convert their energy into standardized regulated ac output. The motivation for this thesis is to design and control power converters for renewable energy systems to ensure very good power quality, efficiency and reliability. The renewable energy sources considered are low voltage dc sources such as photovoltaic (PV) modules. Two transformer-isolated power circuit topologies with input voltage of less than 50V are designed and developed for low and medium power applications. Various design and control issues of these converters are identified and new solutions are proposed. For low power rating of a few hundred watts, a line-frequency transformer interfaced inverter is developed. In the grid connected operation, it is observed that this topology injects considerable lower order odd and even harmonics in the grid current. The reasons for this are identified. A new current control method using adaptive harmonic compensation technique and a proportional-resonant-integral (PRI) controller is proposed. The proposed current controller is designed to ensure that the grid current harmonics are within the limits set by the IEEE 1547-2003 standard. Phase-locked loops (PLLs) are used for grid synchronization of power converters in grid-tied operation and for closed-loop control reference generation. Analysis and design of synchronous reference frame PLL (SRF-PLL) and second-order generalized integrator (SOGI) based PLLs considering unit vector distortion under the possible non-ideal grid conditions of harmonics, unbalance, dc offsets and frequency deviations are proposed and validated. Both SRF-PLL and SOGI-PLL are low-complexity PLLs. The proposed designs achieve fastest settling time for these PLLs for a given worst-case input condition. The harmonic distortion and dc offsets in the resulting unit vectors are limited to be well within the limits set by the IEEE 1547-2003 standard. The proposed designs can be used to achieve very good performance using conventional low-complexity PLLs without the requirement of advanced PLLs which can be computationally intensive. A high-frequency (HF) transformer interfaced ac link inverter with a lossless snubber is developed medium power level in the order of few kilowatts. The HF transformer makes the topology compact and economical compared to an equally rated line frequency transformer. A new synchronized modulation method is proposed to suppress the possible over-voltages due to current commutation in the leakage inductance of the HF transformer. The effect of circuit non-ideality of turn-on delay time is analyzed. The proposed modulation mitigates the problem of spurious turn-on that can occur due to the turn-on delay time. The HF inverter, rectifier and snubber devices have soft switching with this modulation. A new reliable start-up method is proposed for this inverter topology without any additional start- up circuitry. This solves the problems of over-voltages and inrush currents during start-up. The overall research work reported in the thesis shows that it is possible to have compact, reliable and high performance power converters for renewable energy conversion systems. It is also shown that high control performance and power quality can be achieved using the proposed control techniques of low implementation complexity.

The interest in renewables for energy has increased in the last 2-3 decades because of the negative environmental impact caused by the burning of fossil fuels, the raising prices of traditional fuels, the dependence on foreign oil, and the decrease in fossil fuels resources. Biomass energy represents one of the most promising alternatives. Many studies worldwide were devoted to investigate growth and yield of short rotation forestry plantations for energetic use and several empirical and process-based models were developed to predict the potential production of biomass. The current work was concentrated on modelling site productivity (potential of biomass production) of specific poplar clones planted on arable Saxon land under different stocking densities. Empirical data collected from several experimental areas were used. Site productivity has been predicted depending on stand age and site variables using a two-step model. In step one age and site variables were used to model stand dominant height and in step two the constructed dominant height was involved with stocking density to predict stand oven dried biomass. Depending on data availability the model was parameterized for four different groups of poplar clones: Androscoggin (clone Androscoggin), Matrix (Matrix and hybrid 275), Max (Max 1 …Max 5) and Münden (clone Münden). Both stand dominant height and stand dry biomass were modelled for ages 2 – 9 years for clone groups: Matrix and Max and for ages 2 – 7 years for clone groups: Androscoggin and Münden. The model has been tested and validated using several statistical and graphical methods. The relative bias (ē %) in the dominant height estimates ranged between 0.5 % > ē % > - 0.5 % in all clone groups and had a maximum bias of 10.41 % in stand biomass estimates. Model accuracy (mx %) in the dominant height estimates ranged between 12.25 and 17.56 % and between 8.05 and 27.32 % in stand biomass estimates. Two different scenarios were presented to show the potential of biomass that can be produced from poplar plantations on arable and former fallow Saxon lands at different stocking densities. ArcGIS has been used to visualize model application results. In order to produce a mean annual increment ≥ 8 [dry t/ha/a] from poplar plantations (Max group) for more than 50 % of arable or former fallow lands in the first rotation at least 9 years are required under stocking density of 4000 stems/ha and 7 years for both stocking densities 8333 and 10,000 stems/ha. / Die Nachfrage nach Holz für energetische Zwecke nimmt in Deutschland und ganz Europa zu. Um diesen Bedarf künftig besser befriedigen zu können, müssen verstärkt Ressourcen aus verschiedenen Quellen wie z. B. Holz aus Niederwäldern oder Durchforstungsreserven im Hochwald mobilisiert und ergänzend Holz in Kurzumtriebsflächen produziert werden (Guericke, M. 2006). Ziel dieser Arbeit war es, das Ertragspotential von Pappelklonen in Kurzumtriebsplantagen unterschiedlicher Baumdichte auf sächsischen Ackerflächen zu untersuchen. Hierzu wurden die potentiellen Erträge anhand empirischer, auf verschiedenen Versuchsflächen erhobener Daten modelliert. Zur Schätzung des Ertragspotentials wurde ein zweistufiges Modell entwickelt: Im ersten Schritt erfolgte die Modellierung der Oberhöhe eines Bestandes (ho, m) in Abhängigkeit von Bestandesalter und Standortfaktoren unter Verwendung einer multiplen linearen Regressionsanalyse, dabei wurden Bestimmtheitsmaße (R²) von 0,975 bis 0,989 erreicht. In einem zweiten Schritt lässt sich dann der Biomassevorrat [tatro/ha/a] mittels nichtlinearer Regressionsanalyse durch die Bestandesoberhöhe schätzen. Das Bestimmtheitsmaß von R² ≥ 0,933 weist auch hier auf eine hohe Anpassungsgüte hin. Die Modellparametrisierung erfolgte für folgende vier Gruppen von Pappelklonen: • Max-Gruppe: Klone Max 1, Max 2, Max 3, Max 4 und Max 5, Altersbereich 2 – 9 Jahre, Baumdichten von 1150 – 13000 Stämmen/ha; • Matrix-Gruppe: Klon Matrix und Hybride 275, Altersbereich 2 – 9 Jahre, Baumdichte 1550 Stämme/ha; • Androscoggin-Gruppe: Klon Androscoggin, Altersbereich 2 – 7 Jahre, Baumdichte 1550 Stämme/ha; und • Münden-Gruppe: Klon Münden, Altersbereich 2 – 7 Jahre, Baumdichte 1550 Stämme/ha. Die Güte des Modells wurde mit Hilfe verschiedener statistischer Verfahren überprüft. Bei der Validierung anhand des Datensatzes, welcher für die Modellkonstruktion Verwendung fand, zeigte das Modell eine Verzerrung bzw. einen Bias von 0,5 % > ē % > - 0,5 % bei der Bestandesoberhöhenschätzung und einen maximalen Bias von 10,41 % bei der Schätzung der Bestandesbiomasse. Die Treffgenauigkeit (mx %) des Modells hingegen variierte zwischen 12,25 % und 17,56 % bzw. 8,05 und 27,32 % (bei Schätzung der Bestandesoberhöhe bzw. der Bestandesbiomasse). Zudem wies das Modell keinen systematischen Fehler zwischen den geschätzten und den realen Werten auf. Bei der Validierung mit einem unabhängigen Datensatz betrug die Treffgenauigkeit (mx %) für die Schätzung der Bestandsoberhöhe und des Biomassevorrates 15,72 bzw. 26,68 %. Um das Ertragspotenzial von Pappelplantagen für die gesamte sächsische Ackerfläche bzw. die gesamte ehemalige Stilllegungsfläche zu bestimmen, wurden die zu Schätzung erforderlichen Standortvariablen auf Gemeindebasis kalkuliert, mittels ArcGIS dargestellt sowie Simulationsrechungen für verschiedene Bestandsdichten vorgenommen und ebenfalls visualisiert. Den Ergebnissen der Simulationsrechnungen zufolge wäre bei einer Stammzahl von 4000 N/ha eine Rotationslänge von 9 Jahren, bei 8333 bis 10.000 N/ha von 7 Jahren erforderlich, um einen durchschnittlichen Gesamtzuwachs (dGz) von ≥ 8 [tatro/ha/a] auf mehr als 50 % der sächsischen Ackerflächen bzw. ehemaligen Stilllegungsflächen in erster Rotation zu erreichen. Würde die gesamte ehemalige sächsische Stilllegungsfläche mit einer Baumdichte von 10.000 Stämmen/ha bepflanzt werden, könnten Pappelplantagen im Alter 9 einen dGz von 520.000 [tatro/a] (entsprechend 250.000 Kubikmeter Diesel) erreichen. Bei Bestockung aller sächsischen Ackerflächen würde sich der Ertrag auf bis zu 9.087.000 [tatro/a] (entsprechend 4.367.000 Kubikmeter Diesel) erhöhen.

神經系統裡，神經滋養因子在調控細胞分化與生存作用中扮演非常重要的角色，近年來的研究顯示 BDNF 的神經保護效果是透過細胞外訊息調控激酶 (extracellular signal-regulated kinase, ERK) 及磷脂酰肌醇3-激酶 (phosphatidylinositol-3 kinase, PI3K) 訊息傳遞路徑調控，然而，還有許多其他的細胞信號傳遞路徑可能參與 BDNF 的保護作用機制中。而蛋白激酶 CK2 (casein kinase 2) 是一種普遍存在於細胞且具有高度保留序列的絲胺酸/蘇胺酸蛋白質激酶，在細胞中具有非常重要的地位。近來研究有非常多證據支持 CK2 是細胞凋亡的抑制者。此外，血清反應因子 (serum response factor, SRF) 是一種轉錄因子，會與保留序列 SRE (即 CArG box) 相結合，而此段序列過去曾在早期即時表現基因 (如 c-fos、Egr ) ，或是抗細胞凋亡基因－Mcl-1－上的啟動子被發現， SRF 調控著基因的活化，進而與細胞增生、存活、突觸活性相關聯，然而調節 SRE 調控之基因的作用機制尚未十分明瞭。因此，本論文研究主要探討在 PC12 細胞中， BDNF調節 SRE 調控轉錄作用機轉 CK2 是否參與其中? 由冷光酶活性試驗結果顯示 BDNF 會顯著地促進 SRE 的轉錄活性，並且當 CK2α 過度表現亦會促進 SRE 調控的轉錄活性，而利用小干擾 RNA 抑制內生性 CK2α 生成，則會降低 SRE 的轉錄活性，更進一步證明 CK2α siRNA 會降低 BDNF 促進 SRE 調控的轉錄活性。此外，將 CK2α 與 SRF S99A 質體一同轉染至細胞中，會減緩 CK2 促進的 SRE 啟動子轉錄活性。為了探討 CK2 調控 SRE 的轉錄活性在神經保護作用裡扮演的角色，因此，將 CK2 蛋白表現量增加是否會保護 PC12 細胞對抗Rotenone所誘發的細胞凋亡傷害?結果顯示 CK2 表現量增加會保護細胞對抗Rotenone誘導的細胞凋亡，並減緩 Rotenone 對 SRE 調控的轉錄活性降低，但是，突變型 SRF S99A 蛋白會降低 CK2α 的影響作用。這些結果顯示 BDNF 促進 SRE 調控的基因表現是會透過 CK2 訊息傳遞路徑。 / The neurotrophins play an important role in cell differentiation and survival of the nervous system. Among them, the neuroprotective effects of brain-derived neurotrophic factor (BDNF) is showed to be mediated by extracellular signal-regulated kinase (ERK) and phosphatidylinositol-3 kinase (PI3K) signaling pathway in the recent studies. However, other cellular signaling pathways might be involved in these effects of BDNF. Protein kinase CK2 (casein kinase 2) is a ubiquitous and highly conserved serine/threonine protein kinase and is indicated as a vital cellular role. In recent years, evidences have been mounted in support of the importance of CK2 in the suppression of apoptosis. Serum response factor (SRF) is a transcription factor binding to a consensus DNA sequence SRE (known as a CArG box) which was found in the promoters of some immediately early genes (such as c-fos, Egr) and anti-apoptotic Mcl-1 gene. The activations of SRF-regulated genes were associated with cell proliferation, cell survival and perception of synaptic activity. However, the regulatory mechanism of SRE-mediated genes is not well studied. The SRE-mediated transcription activity through CK2 signaling by BDNF treatment was studied in the PC12 cells in the present study. Results revealed that BDNF significantly increased the SRE promoter activity by luciferase report assay. The SRE-mediated transcription activity was increased by overexpression of CK2α, and the inhibition of endogenous CK2α by small interfering RNA was also shown to reduce this transcription activity. Furthermore, CK2α siRNA treatment antagonized the up-regulation effects of BDNF on SRE-mediated transcription activity. The co-transfection of CK2 and mutant SRF S99A plasmids significantly diminished up-regulatory effects of CK2 on SRE promoter activity. To test this CK2 induction in SRE-mediated transcription plays a role in neuroprotecion, we determined whether over-expression CK2 protects PC12 cells against rotenone-induced apoptosis. The results revealed that the over-expression of CK2α protected cells against rotenone-induced apoptosis and rescued the SRE-mediated transcription activity. Further, these effects of CK2α were blocked by co-transfection of mutant SRF S99A. These above results demonstrate that the up-regulation of BDNF on SRE-mediated genes is through CK2 signaling pathway.

蛋白質激酶 CK2 是一種多功能的絲胺酸／蘇胺酸蛋白激酶，且普遍存在於哺乳類動物細胞中，CK2 受質眾多，對於細胞週期的發展、轉錄作用以及抗細胞凋亡等過程中扮演很重要的角色。SRF 是一種哺乳類動物的轉錄因子，它會結合到血清反應元素 SRE 上進而調控一些促進細胞存活的基因轉錄作用。Mcl-1歸類於抗細胞凋亡 Bcl-2 家族，具有促進細胞存活的能力。過去研究顯示 SRF 的 DNA 結合活性會受到蛋白激酶 CK2 的磷酸化而增加，且 SRF 對 Mcl-1 的活性調控作用也被描述在其他的研究中，然而，對於細胞的訊息目前還沒有更詳細的研究。在本實驗中，我們探討是否可以藉由 CK2 調控 SRF 的路徑來影響 Mcl-1 的表現以作為抗細胞凋亡的機制。利用 CK2 抑制劑 TBB 處理的結果顯示，在 4 hr 後，phospho-SRF 蛋白質表現的降低具有劑量相關性。而相似的降低也可以從 Mcl-1 的 mRNA 和蛋白質表現量觀察到。處理 24 hr 後，phospho-SRF 的蛋白質表現量有顯著降低，而 Mcl-1 的 mRNA 表現量相較 Mcl-1 的蛋白質影響層面微弱。另一方面，轉染野生型 CK2α 會增加 phospho-SRF，相反的，轉染抑制催化活性的突變型 CK2αA156 則會顯著降低 phospho-SRF 的表現。更進一步，野生型 CK2α 同時增加 Mcl-1 的 mRNA 及蛋白質層級，而 CK2αA156 則會降低 Mcl-1 的表現。突變型的 SRF99A 轉染作用降低 Mcl-1 的 mRNA 及蛋白質，並經由共同轉染的實驗顯示具有抵抗上游野生型CK2α 對 Mcl-1 蛋白質的影響。綜合這些結果我們認為 CK2α對 SRF 的訊息調控影響包括對 Mcl-1 的表現。且這條訊息路徑所促進的 Mcl-1 蛋白質表現可能對魚藤酮處理所引發的細胞凋亡作用具有保護的效果。 / Protein kinase CK2 is a multifunctional serine/threonine protein kinase with many protein substrates and is ubiquitously expressed in mammalian cells to play an important role in cell cycle progression, transcription, and anti-apoptosis. The serum response factor (SRF) is a mammalian transcription factor which binds to serum response element (SRE) and mediates some gene transcriptions relevent to promote the cell survival. The Myeloid cell leukemia 1 (Mcl-1) belongs to the anti-apoptotic Bcl-2 family and its effect are involved in promoting cell viability. Previous studies have revealed that the DNA-binding activity of SRF is enhanced when it is phosphorylated by protein kinase CK2. The activation regulation of Mcl-1 by SRF has also been reported in other studies. However, the detailed cellular signaling has not been studied well. In the present study, we investigate whether the regulation of Mcl-1 expression through CK2-mediated SRF pathway is involved in its anti-apoptotic effects. The results from CK2 inhibitor TBB revealed that the phosphorylated SRF were reduced in a dose-dependent manner after 4 hr of TBB treatments in PC12 cells. The similar decreases were also observed in the mRNA and protein levels of Mcl-1. After a 24 hr exposure of PC12 cells to TBB, a decreased in phosphorylated SRF and Mcl-1 mRNA were observed; a decreased in Mcl-1 protein level was also detected, albeit to a lesser extent. On the other hand, transfection of the wildtype CK2α increased, whereas transfection of the catalytically inactive CK2αA156 mutant decreased phosphorylated SRF. Further, wildtype CK2α increased, whereas CK2αA156 mutant decreased the mRNA and protein levels of Mcl-1. Furthermore, the mutant SRF99A transfection decreased, the mRNA and protein levels of Mcl-1 and antagonized the up-regulatory effects of wildtype CK2α on Mcl-1 protein level in the co-transfection experiments. These results together suggest that CK2α-mediated SRF signaling is involved in the regulation of Mcl-1 expression, and this signaling pathway may involves the anti-apoptotic effects of Mcl-1 against rotenone treatment.

L'activació sostinguda de Hog1 porta a una inhibició del creixement cel·lular. En aquest treball, hem observat que el fenotip de letalitat causat per l'activació sostinguda de Hog1 és parcialment inhibida per la mutació del complexe SCFCDC4. La inhibició de la mort causada per l'activació sostinguda de Hog1 depèn de la via d'extensió de la vida. Quan Hog1 s'activa de manera sostinguda, la mutació al complexe SCFCDC4 fa que augmenti l'expressió gènica depenent de Msn2 i Msn4 que condueix a una sobreexpressió del gen PNC1 i a una hiperactivació de la deacetilassa Sir2. La hiperactivació de Sir2 és capaç d'inhibir la mort causada per l'activació sostinguda de Hog1. També hem observat que la mort cel·lular causada per l'activació sostinguda de Hog1 és deguda a una inducció d'apoptosi. L'apoptosi induïda per Hog1 és inhibida per la mutació al complexe SCFCDC4. Per tant, la via d'extensió de la vida és capaç de prevenir l'apoptosi a través d'un mecanisme desconegut. / Sustained Hog1 activation leads to an inhibition of cell growth. In this work, we have observed that the lethal phenotype caused by sustained Hog1 activation is prevented by SCFCDC4 mutants. The prevention of Hog1-induced cell death by SCFCDC4 mutation depends on the lifespan extension pathway. Upon sustained Hog1 activation, SCFCDC4 mutation increases Msn2 and Msn4 dependent gene expression that leads to a PNC1 overexpression and a Sir2 deacetylase hyperactivation. Then, hyperactivation of Sir2 is able to prevent cell death caused by sustained Hog1 activation. We have also observed that cell death upon sustained Hog1 activation is due to an induction of apoptosis. The apoptosis induced by Hog1 is decreased by SCFCDC4 mutation. Therefore, lifespan extension pathway is able to prevent apoptosis by an unknown mechanism.