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El volumen intracraneal lo integran el volumen de líquido cefalorraquídeo (LCR), el de la sangre y el del parénquima cerebral. La entrada de sangre al cráneo en la sístole incrementa el volumen intracraneal. Según la ley de Monroe-Kellie debe ocurrir una descompensación en los volúmenes restantes para mantener constante el volumen total. Los desequilibrios que se producen en este proceso de la homeostasis cerebral se han asociado tanto a enfermedades neurodegenerativas como a cerebrovasculares. Por tanto, es necesario contar con metodologías adecuadas para analizar la dinámica de los fluidos intracraneales (LCR y sangre). Las secuencias dinámicas de resonancia magnética en contraste de fase (RM-CF) con sincronismo cardíaco permiten cuantificar el flujo de LCR y de sangre durante un ciclo cardíaco. La medición de flujo mediante secuencias de RM-CF es precisa y reproducible siempre que se use un protocolo de adquisición adecuado. La reproducibilidad y exactitud de las medidas dependen también del uso de técnicas adecuadas de posproceso que permitan segmentar las regiones de interés (ROI) independientemente del operador y admitan corregir los errores de fondo introducidos por la supresión imperfecta de las corrientes inducidas y la contribución a la señal de los pequeños movimientos que presenta el mesencéfalo por la transmisión del pulso vascular así como el submuestreo (aliasing), reflejado como un cambio abrupto y opuesto del sentido original del flujo. Estas técnicas de análisis deben también tener en cuenta los errores relacionados con el efecto de volumen parcial (EVP), causado por la presencia de tejido estacionario y de flujo en el interior de los vóxeles de la periferia de la región a estudiar El objetivo principal de esta tesis es desarrollar una metodología reproducible para evaluar cuantitativamente la dinámica de los fluidos intracraneales dentro de espacios de LCR (acueducto de Silvio, cisterna prepontina y espacio perimedular C2C3) y principales va / Flórez Ordóñez, YN. (2009). Intracranial fluids dynamics: a quantitative evaluation by means of phase-contrast magnetic resonance imaging [Tesis doctoral]. Universitat Politècnica de València. https://doi.org/10.4995/Thesis/10251/6029

巴塞爾銀行監督委員會(Basel Committee on Banking Supervision, BCBS) 於2010年發布巴塞爾資本協定三。為強化銀行流動性風險管理，新增兩項流動性風險量化衡量指標：流動性覆蓋比率(Liquidity Coverage Ratio, LCR)以及淨穩定資金比率(Net Stable Funding Ratio, NSFR)。我國於2015年開始將流動性覆蓋比率納入監管要求，亦將於2018年開始導入淨穩定資金比率。然而在提高銀行風險控管及標準的同時，銀行需考量其股東權益報酬。新規範的實施使銀行需要進行調整以符合法規，過往鮮少有研究針對本國銀行探討其資產配置調整與結構調整。本研究除探討個案銀行如何在巴塞爾資本協定三框架下調整其資產負債配置與結構，更進一步探討其各項調整對銀行之獲利能力以及各項法定比率之影響，希望能幫助銀行在未來調整結構之前能更了解其決策所帶來之影響。 本研究發現，在不提高資產負債表規模的情況下，可以透過銀行結構調整達到巴塞爾資本協定三於2019年之標準，同時提高銀行獲利能力；在適度提高資產負債表規模的情況之下，其獲利能力高於不提高資產負債表規模之情況。此外，本研究針對不同情境探討銀行應如何調整資產負債配置與銀行結構。風險趨避情境相較於風險偏好下，應在存放款方面，吸收更多長天期之存款、降低長期放款占比；資產配置方面則應增加政府公債占比。由於巴塞爾資本協定三採階段性實施，本研究針對個案銀行2015到2019 年之資產負債配置與銀行結構做研究，發現個案銀行隨著法規越趨嚴格，應提高公司債占比並同時降低權益類等相對風險較高之資產占比；另一方面為達到淨穩定資金比率要求，銀行應提高其長期存款占比。最後，本研究針對各項結構與資產負債配置調整做更深入的分析，探討其對於各項指標之敏感度，以實際的量化數字表示每項變動的影響，以利銀行在做決策時更了解其決策之利與弊。 / Basel Committee on Banking Supervision (BCBS) released Basel III in 2010. In order to ensure the maintenance and stability of funding and liquidity profiles of banks’ balance sheets, two liquidity standards, Liquidity Coverage Ratio(LCR) and Net Stable Funding Ratio(NSFR), were introduced in Basel III. To in line with international norm, Taiwan government plans to implement LCR and NSFR in 2015 and 2018 respectively. However, there is a trade-off between return and risk. With the implement of new law, how to adjust banks’ asset allocation becomes a critical issue. In this study, we focus on business structure and ways to adjust A bank’s asset allocation. We found that A bank can meet government’s requirements and increase it’s return on equity without increasing balance sheet size by adjusting business structure; In the situation where balance sheet size is increased, A bank can meet the requirements with higher return on equity than where the balance sheet size isn’t increased. In three different scenarios: risk seeking, risk neutral and risk aversion, we found that A bank should increase more long-term deposits and decrease long-term loans in risk aversion scenario than in risk seeking scenario. In risk aversion scenario, A bank should also hold more government bonds than in risk seeking scenario. From 2015 to 2019, the requirements become stricter and stricter, A bank should hold more corporate bonds and less securities. At the same time, A bank should increase more long-term deposits to meet the NSFR requirement. The research also shows how business structure and asset allocation changes can affect A bank’s related required ratio and return on equity. Our findings can help A bank makes more precise decision by knowing actual quantitative influence before they implement the new policies.

This Master’s thesis deals with standard uncertainity determination for electrical quantities measurement. Next, there are proposals of uncertainity calculation procedures for impedance measurement. Impedance is measured by LCR meter Agilent 4263B. Using the proposed procedures, standard uncertainities are then calculated. Furthermore, there is proposal for an improved laboratory exercise for the MEMT subject, implementing the standard measurement uncertainities calculations.

No description available.

L’infection au virus du papillome humain oncogénique (VPH-HR) est associée au développement du cancer du col de l’utérus. L’expression des oncogènes viraux E6 et E7, qui favorisent la progression vers le cancer, est régulée par la région de contrôle longue ou LCR qui contient des sites de liaison pour plusieurs facteurs de transcription cellulaires et pour le répresseur viral E2. L’expression des oncogènes E6 et E7 est souvent dérégulée dans les cancers du col de l’utérus, une résultante de l’intégration du génome viral qui détruit fréquemment le cadre de lecture du gène E2. Plusieurs isolats ou variantes du VPH de type 33 (VPH33) avec une séquence nucléotidique du LCR différente du prototype ont été identifiés dans des spécimens de femmes infectées par le VPH et présentant des lésions intraépithéliales au niveau du col utérin. Deux polymorphismes, une délétion de 79 pb et la transversion C7732G, ont été associés à la persistance de l’infection et à un plus grand risque de développer une lésion intraépithéliale de haut-grade, respectivement. L’effet fonctionnel des polymorphismes du LCR du VPH33 sur l’expression génique virale, en particulier de la délétion de 79 pb et de C7732G, n’a jamais été caractérisé. Dans une première étude, l’activité transcriptionnelle des variantes de LCR du VPH33 a été comparée à celle du prototype dans les lignées cellulaires C33A et HeLa par des études de gènes rapporteurs suite à leur introduction en amont du gène de la Renilla luciférase. Nos résultats indiquent que l’activité transcriptionnelle des variantes du LCR du VPH33 reflète leur classification phylogénétique; les variantes issues de la lignée A2 étant les plus actives dans les C33A que le prototype du groupe A1. Des analyses par mutagenèse dirigée ont établi que l’activité accrue des LCRs de ces variantes est due à plusieurs variations, incluant la délétion de 79 pb et C7732G, et dont leur effet individuel est assez modeste. Dans les cellules HeLa, les niveaux de transcription des variantes de la lignée A2 étaient similaires à ceux observés chez le prototype. Cet effet a été attribué à la variation A7879G qui induit la répression du LCR dans ces cellules. Ces résultats indiquent que la combinaison de plusieurs variations dites faibles altère significativement l’activité transcriptionnelle du LCR du VPH33. D’un autre côté, les résultats rapportés dans notre deuxième étude indiquent que la mutation d’un élément important pour la régulation de la transcription virale peut tout autant altérer l’activité du LCR. La variante rare LCR10 de la lignée B montre une activité transcriptionnelle accrue comparée au prototype. Des analyses par mutagenèse dirigée ont identifié la variation T7791C comme étant responsable de l’activité augmentée du LCR10. L’effet stimulateur de ce polymorphisme est dû au fait qu’un site répresseur pour le facteur cellulaire C/EBPβ est aboli, tel que déterminé par des essais de liaison à l’ADN in vitro et de gène rapporteur. Un deuxième site C/EBPβ a également été identifié, cette fois-ci, agissant comme activateur de l’expression génique. Finalement, dans une troisième étude, nous montrons que C/EBPβ est un régulateur commun de l’expression des gènes chez les VPHs oncogéniques. Effectivement, plusieurs sites C/EBPβ sont retrouvés dans la région amplificatrice du LCR des VPHs à haut-risque tel que déterminé par des prédictions basées sur des matrices d’énergie et de fréquence. Certains de ces éléments sont similaires aux sites répresseurs et activateurs retrouvés dans le VPH33. Dans l’ensemble, nos études démontrent l’importance de caractériser l’effet individuel des polymorphismes du LCR pour mieux comprendre les mécanismes de modulation de la transcription des VPHs. De plus, nous montrons que C/EBPβ joue un rôle central autant dans la répression que dans l’activation de l’expression des gènes viraux. / The infection by the oncogenic human papillomavirus (HR-HPV) is associated with the development of cervical cancer. The expression of the E6 and E7 viral oncogenes favors progression towards cancer and is driven by the long control region (LCR) which contains binding sites for both cellular factors and the viral E2 protein. The expression of these oncogenes is often upregulated in cervical cancer due to the integration of the viral genome which frequently disrupts the open reading frame of the repressor E2 gene. Several isolates or variants of HPV type 33 (HPV33) with a slightly different nucleotide sequence were previously identified in clinical samples from women infected with HPV33 and presenting squamous intraepithelial lesions of the uterus. Two polymorphisms, a 79-bp deletion and the C7732G transversion, were previously associated with an increased risk of persistence of infection and of developing high-grade lesions, respectively. The functional effect of polymorphisms in the HPV33 LCR on viral gene expression has never been assessed in particular for the 79-bp deletion and C7732G. In the first study presented here, the transcriptional activity of the HPV33 LCR variants were compared to that of the prototype in C33A and HeLa cell lines using gene reporter assays following their introduction upstream of the Renilla luciferase. Our results indicate that the LCR activity of the variants reflects their phylogenetic classification. As such, variants from the A2-sublineage were the most active in C33A cells when compared to the A1-sublineage prototype. Mutational analysis showed that the increased in LCR activity was the result of several weakly-acting variations, including the 79-bp deletion and C7732G. In HeLa cells, the lower transcriptional activity of the A2 variants was caused by A7879G which induces repression of the LCR in these cells. These results show that the combination of weakly-acting variations in the LCR significantly alters viral gene expression. In the second study, we show that the mutation of important regulatory elements also significantly enhances the transcriptional activity of the LCR. The rare HPV33 LCR10 variant from the B lineage exhibits increased transcriptional activity compared to the prototype. Mutational analysis shows that the T7791C variation is responsible for this phenotype. The stimulating effect of this variation is caused by the disruption of a repressor C/EBPβ site as determined in an in vitro DNA-binding assay and gene reporter assays. A second site necessary this time for the activation of the LCR was also identified. Finally, in the third study, we show that C/EBPβ is a common regulator of the oncogenic HPV gene expression. Several C/EBPβ sites were found in the enhancer region of the LCR of these HPV types as determined by our prediction using both energy- and frequency-based matrices. Some of these sites were found to be similar to the repressor and activating sites in the HPV33 LCR. Taken together, our studies highlight the importance of characterizing individual variations in the LCR in order to improve our knowledge on the mechanisms involved in the regulation of viral gene expression. We also show that the activating and inhibitory functions of C/EBPβ are important for the modulation of viral transcription.

本文的研究目的為，在一個包含銀行部門的動態隨機一般均衡模型的架構中，探討流動性覆蓋比率限制在利率的信用管道中所扮演的角色以及其對政體經濟的影響為何。在銀行的資產配置決策內生的情形下，加入流動性覆蓋比率的限制，透過放款的勞動成本與抵押品價值來刻畫金融摩擦；本文發現當經濟體系遭受生產與放款的外生衝擊時，流動性覆蓋比率的限制會增強政策利率的信用管道效果，並且相較於無流動性覆蓋比率限制之模型而言，具流動性覆蓋比率限制的模型，其銀行資產配置的變動幅度與金融摩擦的程度皆較大。 / The main purpose of this paper is to explore the role of the liquidity coverage ratio (LCR) in the credit channel and how it influences the overall economy in a dynamic stochastic general equilibrium (DSGE) model with banking sector. Commercial banks endogenously choose their optimal portfolio of assets under the liquidity coverage ratio restriction. On the other hand, we describe the financial friction through the labor cost of making loans and collateral value. We find that when the economy is exposed to exogenous shocks in production and lending, the liquidity coverage ratio will enhance the effect of credit channel. Compared with the model with no LCR restriction, the degree of change of the bank asset allocation and the financial friction are larger in the model with LCR restriction.

This master's thesis describes functionality and principle of the Hefaistos measurement system, which is fully automated and modular. Its purpose is to measure frequency responses of materials and its temperature dependence. The thesis describes all the necessary parts of the modular measurement system. Main part of this system is the control application programmed in LabVIEW software environment. Another necessary parts are impedance analyzers for acquiring frequency dependencies and heating chambers for heating measured materials. The control application ensures hardware synchronization between impedance analyzers and heating chambers. Together they create the Hefaistos system. Modularity of the system means that a user may choose which instrument combination will be used. The system offers choice between three impedance analyzers Agilent 4294A, Wayne Kerr 6520B and HIOKI 3532 LCR Hi-Tester and two heating chambers AOIP GEMINI 700 LRI and AOIP HYPERION. Possibilities of the Hefaistos system are demonstrated on the results of an example measurement.

This thesis aims to contribute to the developments of wireless communication systems. The work generally consists of three parts: the first part is a discussion on general digital communication systems, the second part focuses on wireless channel modelling and fading mitigation techniques, and in the third part we discuss the possible application of advanced digital signal processing, especially time-frequency representation and blind source separation, to wireless communication systems. The first part considers general digital communication systems which will be incorporated in later parts. Today's wireless communication system is a subbranch of a general digital communication system that employs various techniques of A/D (Analog to Digital) conversion, source coding, error correction, coding, modulation, and synchronization, signal detection in noise, channel estimation, and equalization. We study and develop the digital communication algorithms to enhance the performance of wireless communication systems. In the Second Part we focus on wireless channel modelling and fading mitigation techniques. A modified Jakes' method is developed for Rayleigh fading channels. We investigate the level-crossing rate (LCR), the average duration of fades (ADF), the probability density function (PDF), the cumulative distribution function (CDF) and the autocorrelation functions (ACF) of this model. The simulated results are verified against the analytical Clarke's channel model. We also construct frequency-selective geometrical-based hyperbolically distributed scatterers (GBHDS) for a macro-cell mobile environment with the proper statistical characteristics. The modified Clarke's model and the GBHDS model may be readily expanded to a MIMO channel model thus we study the MIMO fading channel, specifically we model the MIMO channel in the angular domain. A detailed analysis of Gauss-Markov approximation of the fading channel is also given. Two fading mitigation techniques are investigated: Orthogonal Frequency Division Multiplexing (OFDM) and spatial diversity. In the Third Part, we devote ourselves to the exciting fields of Time-Frequency Analysis and Blind Source Separation and investigate the application of these powerful Digital Signal Processing (DSP) tools to improve the performance of wireless communication systems.