La maladie de Huntington (MH) est une maladie neurodégénérative fatale, causée par l'expansion des répétitions CAG du gène de Huntingtine. La longueur de l'expansion est instable et proportionnelle à la gravité de la maladie. L'instabilité varie selon les tissus, p.ex. le striatum est très instable et dégénère, alors que le cervelet a une instabilité limitée et est épargné par la maladie. Nous avons étudié le rôle des lésions oxydantes et du mécanisme de réparation par excision de base (BER) dans la sélectivité tissulaire de l'instabilité dans ces deux tissus de souris R6/1. Le niveau des lésions était similaire dans ces tissus, alors que les niveaux et les activités des principales protéines BER étaient globalement diminués dans le striatum. L'efficacité de réparation dépendait de la stoechiométrie de BER, la position de la lésion et la séquence d'ADN. Nos résultats suggèrent une faible coopération entre les activités BER associée à la spécificité tissulaire de l'instabilité de la MH.

L'ultra large bande (UWB) est une nouvelle technologie à fort potentiel pour les futurs réseaux personnels WPAN (wireless personal area networks) à très haut débit et faible portée. L'objectif de cette thèse est de proposer un nouveau système UWB, de type LP-OFDM (linear precoded orthogonal frequency division multiplexing) pour les applications WPAN, visant à améliorer la solution MB-OFDM (multiband OFDM), supportée par l'Alliance WiMedia.<br />Dans un premier temps, une étude analytique est menée sur l'apport de la composante de précodage au système UWB, cette composante se réduisant en pratique à une simple addition d'une matrice d'étalement fréquentiel. La fonction de précodage est ensuite optimisée et différentes stratégies d'allocation dynamique des ressources sont étudiées. En considérant une approche classique tenant compte du taux d'erreur symbole (TES) ainsi qu'une nouvelle approche tenant compte du taux d'erreur binaire (TEB) moyen, différents algorithmes d'allocation dynamique visant à maximiser la portée ou le débit du système, ou à minimiser le TEB moyen du système, sont proposés. Les résultats analytiques montrent l'avantage d'utiliser une composante de précodage pour les applications UWB dont le canal est très sélectif en fréquence.<br />Dans un second temps, une étude système complémentaire à l'étude analytique est réalisée pour le système LP-OFDM UWB. Une composante MIMO est ajoutée au système, d'une part pour augmenter la portée du système à bas et moyen débit, et d'autre part pour augmenter le débit du système qui peut atteindre dans ce cas 1 gigabit/s. Les résultats de simulation sur le système proposé montrent que ce système est plus performant que le système MB-OFDM pour les débits déjà proposés dans la norme, et qu'il offre un débit deux fois plus important que ceux de la norme avec même une meilleure performance en terme de TEB.

L'ultra large bande (UWB) est une nouvelle technologie à fort potentiel pour les futurs réseaux personnels WPAN (wireless personal area networks) à très haut débit et faible portée. L'objectif de cette thèse est de proposer un nouveau système UWB, de type LP-OFDM (linear precoded orthogonal frequency division multiplexing) pour les applications WPAN, visant à améliorer la solution MB-OFDM (multiband OFDM), supportée par l'Alliance WiMedia.<br />Dans un premier temps, une étude analytique est menée sur l'apport de la composante de précodage au système UWB, cette composante se réduisant en pratique à une simple addition d'une matrice d'étalement fréquentiel. La fonction de précodage est ensuite optimisée et différentes stratégies d'allocation dynamique des ressources sont étudiées. En considérant une approche classique tenant compte du taux d'erreur symbole (TES) ainsi qu'une nouvelle approche tenant compte du taux d'erreur binaire (TEB) moyen, différents algorithmes d'allocation dynamique visant à maximiser la portée ou le débit du système, ou à minimiser le TEB moyen du système, sont proposés. Les résultats analytiques montrent l'avantage d'utiliser une composante de précodage pour les applications UWB dont le canal est très sélectif en fréquence.<br />Dans un second temps, une étude système complémentaire à l'étude analytique est réalisée pour le système LP-OFDM UWB. Une composante MIMO est ajoutée au système, d'une part pour augmenter la portée du système à bas et moyen débit, et d'autre part pour augmenter le débit du système qui peut atteindre dans ce cas 1 gigabit/s. Les résultats de simulation sur le système proposé montrent que ce système est plus performant que le système MB-OFDM pour les débits déjà proposés dans la norme, et qu'il offre un débit deux fois plus important que ceux de la norme avec même une meilleure performance en terme de TEB.

Neurodegenerative disorders are heterogenous in nature and include a range of ataxias with oculomotor apraxia, which are characterised by a wide variety of neurological and ophthalmological features. This family includes recessive and dominant disorders. A subfamily of autosomal recessive cerebellar ataxias are characterised by defects in the cellular response to DNA damage. These include the well characterised disorders Ataxia-Telangiectasia (A-T) and Ataxia-Telangiectasia Like Disorder (A-TLD) as well as the recently identified diseases Spinocerebellar ataxia with axonal neuropathy Type 1 (SCAN1), Ataxia with Oculomotor Apraxia Type 2 (AOA2), as well as the subject of this thesis, Ataxia with Oculomotor Apraxia Type 1 (AOA1). AOA1 is caused by mutations in the APTX gene, which is located at chromosomal locus 9p13. This gene codes for the 342 amino acid protein Aprataxin. Mutations in APTX cause destabilization of Aprataxin, thus AOA1 is a result of Aprataxin deficiency. Aprataxin has three functional domains, an N-terminal Forkhead Associated (FHA) phosphoprotein interaction domain, a central Histidine Triad (HIT) nucleotide hydrolase domain and a C-terminal C2H2 zinc finger. Aprataxins FHA domain has homology to FHA domain of the DNA repair protein 5’ polynucleotide kinase 3’ phosphatase (PNKP). PNKP interacts with a range of DNA repair proteins via its FHA domain and plays a critical role in processing damaged DNA termini. The presence of this domain with a nucleotide hydrolase domain and a DNA binding motif implicated that Aprataxin may be involved in DNA repair and that AOA1 may be caused by a DNA repair deficit. This was substantiated by the interaction of Aprataxin with proteins involved in the repair of both single and double strand DNA breaks (XRay Cross-Complementing 1, XRCC4 and Poly-ADP Ribose Polymerase-1) and the hypersensitivity of AOA1 patient cell lines to single and double strand break inducing agents. At the commencement of this study little was known about the in vitro and in vivo properties of Aprataxin. Initially this study focused on generation of recombinant Aprataxin proteins to facilitate examination of the in vitro properties of Aprataxin. Using recombinant Aprataxin proteins I found that Aprataxin binds to double stranded DNA. Consistent with a role for Aprataxin as a DNA repair enzyme, this binding is not sequence specific. I also report that the HIT domain of Aprataxin hydrolyses adenosine derivatives and interestingly found that this activity is competitively inhibited by DNA. This provided initial evidence that DNA binds to the HIT domain of Aprataxin. The interaction of DNA with the nucleotide hydrolase domain of Aprataxin provided initial evidence that Aprataxin may be a DNA-processing factor. Following these studies, Aprataxin was found to hydrolyse 5’adenylated DNA, which can be generated by unscheduled ligation at DNA breaks with non-standard termini. I found that cell extracts from AOA1 patients do not have DNA-adenylate hydrolase activity indicating that Aprataxin is the only DNA-adenylate hydrolase in mammalian cells. I further characterised this activity by examining the contribution of the zinc finger and FHA domains to DNA-adenylate hydrolysis by the HIT domain. I found that deletion of the zinc finger ablated the activity of the HIT domain against adenylated DNA, indicating that the zinc finger may be required for the formation of a stable enzyme-substrate complex. Deletion of the FHA domain stimulated DNA-adenylate hydrolysis, which indicated that the activity of the HIT domain may be regulated by the FHA domain. Given that the FHA domain is involved in protein-protein interactions I propose that the activity of Aprataxins HIT domain may be regulated by proteins which interact with its FHA domain. We examined this possibility by measuring the DNA-adenylate hydrolase activity of extracts from cells deficient for the Aprataxin-interacting DNA repair proteins XRCC1 and PARP-1. XRCC1 deficiency did not affect Aprataxin activity but I found that Aprataxin is destabilized in the absence of PARP-1, resulting in a deficiency of DNA-adenylate hydrolase activity in PARP-1 knockout cells. This implies a critical role for PARP-1 in the stabilization of Aprataxin. Conversely I found that PARP-1 is destabilized in the absence of Aprataxin. PARP-1 is a central player in a number of DNA repair mechanisms and this implies that not only do AOA1 cells lack Aprataxin, they may also have defects in PARP-1 dependant cellular functions. Based on this I identified a defect in a PARP-1 dependant DNA repair mechanism in AOA1 cells. Additionally, I identified elevated levels of oxidized DNA in AOA1 cells, which is indicative of a defect in Base Excision Repair (BER). I attribute this to the reduced level of the BER protein Apurinic Endonuclease 1 (APE1) I identified in Aprataxin deficient cells. This study has identified and characterised multiple DNA repair defects in AOA1 cells, indicating that Aprataxin deficiency has far-reaching cellular consequences. Consistent with the literature, I show that Aprataxin is a nuclear protein with nucleoplasmic and nucleolar distribution. Previous studies have shown that Aprataxin interacts with the nucleolar rRNA processing factor nucleolin and that AOA1 cells appear to have a mild defect in rRNA synthesis. Given the nucleolar localization of Aprataxin I examined the protein-protein interactions of Aprataxin and found that Aprataxin interacts with a number of rRNA transcription and processing factors. Based on this and the nucleolar localization of Aprataxin I proposed that Aprataxin may have an alternative role in the nucleolus. I therefore examined the transcriptional activity of Aprataxin deficient cells using nucleotide analogue incorporation. I found that AOA1 cells do not display a defect in basal levels of RNA synthesis, however they display defective transcriptional responses to DNA damage. In summary, this thesis demonstrates that Aprataxin is a DNA repair enzyme responsible for the repair of adenylated DNA termini and that it is required for stabilization of at least two other DNA repair proteins. Thus not only do AOA1 cells have no Aprataxin protein or activity, they have additional deficiencies in PolyADP Ribose Polymerase-1 and Apurinic Endonuclease 1 dependant DNA repair mechanisms. I additionally demonstrate DNA-damage inducible transcriptional defects in AOA1 cells, indicating that Aprataxin deficiency confers a broad range of cellular defects and highlighting the complexity of the cellular response to DNA damage and the multiple defects which result from Aprataxin deficiency. My detailed characterization of the cellular consequences of Aprataxin deficiency provides an important contribution to our understanding of interlinking DNA repair processes.

Submitted by Automa??o e Estat?stica (sst@bczm.ufrn.br) on 2017-04-17T23:12:49Z No. of bitstreams: 1 AngelicaMariaDeSousaLeal_TESE.pdf: 6582579 bytes, checksum: 5f557c13b6008a7677f62167674670fe (MD5) / Approved for entry into archive by Arlan Eloi Leite Silva (eloihistoriador@yahoo.com.br) on 2017-04-20T22:14:08Z (GMT) No. of bitstreams: 1 AngelicaMariaDeSousaLeal_TESE.pdf: 6582579 bytes, checksum: 5f557c13b6008a7677f62167674670fe (MD5) / Made available in DSpace on 2017-04-20T22:14:08Z (GMT). No. of bitstreams: 1 AngelicaMariaDeSousaLeal_TESE.pdf: 6582579 bytes, checksum: 5f557c13b6008a7677f62167674670fe (MD5) Previous issue date: 2016-09-29 / Coordena??o de Aperfei?oamento de Pessoal de N?vel Superior (CAPES) / No contexto da resposta ao estresse oxidativo, o reparo por excis?o de bases (BER) ? considerado a principal via para o reparo de les?es oxidadas. Entretanto, estudos indicam o papel do reparo por excis?o de nucleot?deos (NER) na corre??o dessas les?es. Al?m disso, fatores do NER j? tiveram fun??es descritas em outros processos biol?gicos, sendo importante que se busque novas fun??es biol?gicas que possam ser associadas aos fen?tipos das s?ndromes causadas por muta??es nos genes da via NER, dentre elas a Xeroderma pigmentoso grupo de complementa??o A, associada a muta??es em XPA, al?m da s?ndrome de Cockayne, ocasionada por muta??es no gene CSB. Nesse contexto, c?lulas deficientes em XPA (XP12RO) ou CSB (CS1AN) foram submetidas ao estresse oxidativo com per?xido de hidrog?nio (H2O2) e apresentaram um perfil de sensibilidade ao agente, indicando que a aus?ncia dessas prote?nas sensibilizou as linhagens a essa condi??o. A an?lise do transcriptoma de c?lulas XP12RO indicou a diminui??o na express?o de genes com papel na resposta ao dano no DNA e que promovem a sobreviv?ncia celular em resposta ao estresse oxidativo. Nesse cen?rio, os resultados indicaram que XPA pode atuar na regula??o da express?o de genes essenciais ? resposta ao dano no DNA e na sobreviv?ncia ao estresse oxidativo (EGR1, GADD45A, GADD45B e XPC). Por outro lado, a an?lise do transcriptoma de c?lulas CS1AN indicaram a diminui??o na express?o de genes-chave nos processos biol?gicos como transcri??o, processamento de mRNA, prote?lise via ubiquitina-proteassoma ou respira??o celular, indicando um poss?vel papel central da prote?na CSB na regula??o desses processos, em resposta ao estresse oxidativo. Al?m disso, dado o fen?tipo de neurodegenera??o associada a s?ndrome de Cockayne, c?lulas progenitoras neurais (NPCs) e neur?nios derivados de c?lulas-tronco pluripotentes induzidas (iPSCs) deficientes em CSB foram utilizados como modelos de estudo de altera??es neuronais in vitro, de modo que os resultados indicaram que assim como observado nos fibroblastos, c?lulas NPCs deficientes em CSB tamb?m apresentaram sensibilidade a agentes oxidantes. Ainda, os resultados mostraram que assim como observado no transcriptoma de fibroblastos CS1AN, dada a diminui??o na express?o de genes com papel na respira??o celular, as an?lises do consumo de oxig?nio em neur?nios deficientes em CSB indicaram uma poss?vel disfun??o mitocondrial, caracterizada pelo decr?scimo na taxa de consumo de oxig?nio basal e pela diminui??o das capacidades respirat?rias m?xima ou de reserva dessas c?lulas, sugerindo o papel de CSB no metabolismo mitocondrial em ambos os modelos celulares utilizados neste estudo. / In oxidative stress response, the base excision repair (BER) is considered the major pathway for repair of oxidative lesions. However, an increasing number of studies have indicated the role of nucleotide excision (NER) in the repair of these lesions. In addition, some NER factors had functions beyond the role in repair already described and it is important to search for new molecular functions that can be associated to the classical phenotypes of the syndromes caused by mutations in NER genes: Xeroderma pigmentosum complementation group A, caused by mutations in XPA and Cockayne syndrome, caused by mutations in CSB. In this context, XPA (XP12RO) or CSB (CS1AN) deficient cells were submitted to oxidative stress induced by Hydrogen peroxide (H2O2) and the results indicated that both cell lines showed sensitivity to this agent. Furthermore, the transcriptome of XP12RO cells revealed the downregulation of genes that play a role in DNA damage response and promote cell survival in response to oxidative stress. In this scenario, the results indicated that XPA regulates the expression of genes that play a key role in DNA damage response and promote survival in response to stress (EGR1, GADD45A, GADD45B and XPC). On the other hand, the transcriptome analysis of CS1AN cells showed the downregulation of genes that play a key role in biological processes such as transcription, mRNA processing, protein degradation by the ubiquitin?proteasome pathway proteolysis or cellular respiration, indicating a possible role for CSB protein in the regulation of these processes, in response to oxidative stress. In adittion, given the neurodegeneration phenotype associated to Cockayne syndrome, neural progenitor cells (NPCs) and neurons derived from CSB deficient induced pluripotent stem cells (iPSCs) were used as cellular models to analyse neuronal changes in vitro. The results showed that, as observed in fibroblasts CS1AN, NPCs also presented sensitivity to oxidizing agents. Furthermore, as indicated in the transcriptome data from CS1AN fibroblasts, given the downregulation of genes that play a pivotal role in cellular respiration, the analysis of oxygen consumption rates in CSB deficient neurons also indicated a mitochondrial dysfunction characterized by the decrease in oxygen consumption basal rate and a lower maximum respiratory and reserve capacities, suggesting that the lack of functional CSB leads to a mitochondrial dysfunction in both cellular models used in this study. / 2017-12-09

El aparato digestivo permite que los alimentos se conviertan en nutrientes y proporcionen al organismo las calorías y los elementos fundamentales para la vida, al mismo tiempo que se expulsan y eliminan los productos residuales de forma adecuada. La motilidad intestinal es muy importante para conseguir la segmentación del quimo y el tránsito intestinal y está determinada por la actividad mioeléctrica de las capas musculares intestinales. Dicha actividad también se le denomina electroenterograma (EEnG). La señal mioeléctrica es el resultado de una componente de baja frecuencia que en condiciones fisiológicas está siempre presente llamada onda lenta (OL) o ritmo eléctrico básico (BER) que constituye el marcapasos intestinal; y una componente de alta frecuencia llamada spike bursts o potenciales rápidos de acción que está asociada a las contracciones intestinales. El análisis del EEnG es un paso clave para monitorizar la actividad intestinal. El estudio del BER intestinal no sólo proporciona información acerca del ritmo básico de las contracciones del intestino, sino que puede ayudar a diagnosticar algunas patologías gastrointestinales. Para ofrecer esta herramienta como aplicación clínica, el registro de la señal del EEnG debe ser no invasivo. El objetivo de la presente Tesis Doctoral es detectar la actividad del marcapasos intestinal y caracterizar el ritmo eléctrico básico en el EEnG externo, comparándolo y estudiando su relación con el EEnG interno. Las señales analizadas fueron obtenidas simultáneamente en la superficie abdominal y en la serosa intestinal de perros Beagle en estado de ayuno. Los métodos de estimación autoregresivo (AR), autoregresivo de media móvil (ARMA), Prony y clasificación de señales múltiples (MUSIC), se emplearon para determinar la distribución espectral de potencia asociada a la actividad de la onda lenta, tanto en los registros internos como externos. Por otro lado, para estudiar la relación entre el espectro de la señal captada en superficie y las señales internas, se estimaron las funciones de coherencia utilizando los modelos autoregresivo multivariante (ARM) y MUSIC. / Moreno Vázquez, JDJ. (2011). Estudio espectral del ritmo eléctrico básico del intestino delgado para la monitorización no invasiva del marcapasos intestinal [Tesis doctoral no publicada]. Universitat Politècnica de València. https://doi.org/10.4995/Thesis/10251/14276 / Palancia

This thesis describes and models wirelesss transmission intereferences in real communication channels. A signal received on a fading channel is subjected to a multiplicative distortion and to the usual additive noise. Real channel adds to the signal noise and fadings. Gaussian noise is a result of channel awgn. Fadings is implicated by multipath propagation of signal in Rayleigh and Rician channels. Main goal of this project is to program BERsolve, which is created in tool GUIDE in Matlab. User program BERsolve makes it possible to analyse bit error rate and symbol error rate for some types of channel models, which are defined by standard COST207. BERsolve offers some other functions i.e. display time behaviour, constellation diagram and spectrum. This program provides us with an overview representation of problem by multipath interferences in communication channels.

Master’s thesis is focused on part of mobile network named LTE. Project is analyzes the LTE physical layer, which is divided into four basic parts: Physical channels and modulation, Multiplexing and channel coding, Physical layer procedures, Physical layer measurements. Every part is described by actual 3GPP standard [1]. To understand the problem is expected a reader basic knowledge of OFDM systems, which the LTE system uses. The next part of this master’s thesis is dedicated to mathematic model physical layer of system LTE, created by program Matlab. This model is designed to measure errors in data transmission.

Disertační práce je zaměřena na měření a modelování kanálu uvnitř a vně vozidla pro komunikaci a lokalizaci. Pro účely vytvoření integrovaného inteligentního dopravního systému ITS (Intelligent transportation system) je důležitý odhad vlastnosti kanálů pro vnitřní a venkovní scénáře. Za tímto účelem je vhodné provést řadu činností, které jsou obsahem disertační práce: Simulace fyzické vrstvy 802.11p, její srovnávání s 802.11a, měření kanálu pro různé scénáře pro 802.11p a pro širokopásmový systém (UWB), vytvoření modelů kanálů pro 802.11p a UWB a výzkum vlastností lokalizace založené na měření v pásmu UWB. Výzkum komunikace vozidla s okolím založená na IEEE 802.11p standardu. Jedním z cílů disertační práce je ukázat rozdíly mezi standardy fyzické vrstvy IEEE 802.11a a IEEE 802.11p prostřednictvím simulace s použitím modelu kanálu HIPERPLAN/2. V práci je uvedena simulace přenosu signálu 802.11p kanálem ITU-R M.1225 s odlišným zpožděním a středním výkonem (pro chodce a vozidla). Vliv kanálu na signál je analyzován za použití simulace v prostředí MATLABu pomocí vyhodnocení chybovosti. Určení vlastností kanálů v kmitočtovém pásmu 5,8 GHz pro standard IEEE 802.11p a UWB. Experimenty byly prováděny pro vnitřní a vnější prostředí vozidla. Bylo zjištěno, že pro protokol 802.11p může být trend (dlouhodobý vývoj) profilu PDP (power delay profile) nejlépe aproximován pomocí modelu obsahujícího dvě klesající exponenciální funkce, na rozdíl od Saleh-Valenzuelova (S-V) modelu, který je více vhodný pro UWB systémy pracující v pásmu 3 až 11 GHz. Vytvoření odpovídající impulzní odezvy (CIR) s využitím trendu PDP. Informace o CIR byla použita pro simulaci 802.11p za účelem vyhodnocení chybovosti při použití Ricianova modelu. Výsledky odhadu BER ukazují vhodnost protokolu pro vnitřní a vnější prostředí bezdrátových aplikací. Výsledky simulací dále ukazují, že se chybovost zásadně nemění a proto je možné určit střední křivku BER pro celou sadu změřených dat. Určení vlivu malé změny polohy antény na vlastnosti kanálu. Práce ukazuje náhodnost parametrů UWB kanálu pro malé změny polohy antény okolo vozidla, zaparkovaného v podzemní garáži. Ztráty šířením jsou monotónně rostoucí se vzdáleností, avšak náhodně se mění v závislosti na úhlu a výšce antén, a proto je vyhodnocení vzdálenosti pomocí síly signálu pro tyto scénáře nevhodné. Na druhé straně může být pro spolehlivé určení vzdálenosti bez ohledu na úhel nebo výšku antény použita doba příchodu prvního svazku. Ověření vlivu změn konfigurace kanálu na parametry S-V modelu. Práce demonstruje závislost parametrů Saleh-Valenzuela modelu v na vzdálenosti a výšce antén, avšak ukazuje, že jejich průměrné hodnoty jsou blízké IEEE 802.15.3 standardu. Ověření možnosti lokalizace pomocí metody TOA (time of arrival). Vzdálenost mezi anténami byla určena z profilu PDP s využitím lineární závislosti vzdálenosti na zpoždění. Souřadnice vysílací antény byly nalezeny pomocí dvou přijímacích antén pomocí 2-D lokalizační techniky TOA. Porovnání vypočtených souřadnic s původními vykazuje chybu menší než 6%, což ukazuje vhodnost navrženého přístupu pro lokalizaci vozidel.

Orthogonal frequency division multiplexing (OFDM) has become a very popular method for high-data-rate communication. However, it is well known that OFDM is plagued by a large peak-to-average power ratio (PAPR) problem. This high PAPR results in overdesigned power amplifiers, which amongst other things leads to inefficient amplifier usage, which is undesirable. Various methods have been recommended to reduce the PAPR of an OFDM transmission; however, all these methods result in a number of drawbacks. In this thesis, a novel method called offset modulation (OM-OFDM) is proposed to control the PAPR of an OFDM signal. The proposed OM-OFDM method does not result in a number of the drawbacks being experienced by current methods in the field. The theoretical bandwidth occupancy and theoretical bit error rate (BER) expression for an OM-OFDM transmission is derived. A newly applied power performance decision metric is also introduced, which can be utilised throughout the PAPR field, in order to compare various methods. The proposed OM-OFDM method appears to be similar to a well-known constant envelope OFDM (CE-OFDM) transmission. The modulation, structural and performance differences between an OM-OFDM and a CE-OFDM method are discussed. By applying the power performance decision metric, the OM-OFDM method is shown to offer significant performance gains when compared to CE-OFDM and traditional OFDM transmissions. In addition, the OM-OFDM method is able to accurately control the PAPR of a transmission for a targeted BER. By applying the power performance decision metric and complementary cumulative distribution function (CCDF), the proposed OM-OFDM method is shown to offer further performance gains when compared to existing PAPR methods, under frequency selective fading conditions. In this thesis, the OM-OFDM method has been combined with an existing active constellation extended (ACE) PAPR reduction method. To introduce a novel method called offset modulation with active constellation extension (OM-ACE), to control the PAPR of an OFDM signal. The theoretical BER expression for an OM-ACE transmission is presented and validated. Thereafter, by applying the decision metric and CCDF, the OM-ACE method is shown to offer performance improvements when compared to various PAPR methods. The use of OM-OFDM for cognitive radio applications is also investigated. Cognitive radio applications require transmissions that are easily detectable. The detection characteristics of an OM-OFDM and OFDM transmission are studied by using receiver operating characteristic curves. A derivation of a simplified theoretical closed-form expression, which relates the probability of a missed detection to the probability of a false alarm, for an unknown deterministic signal, at various signal-to-noise ratio (SNR) values is derived and validated. Previous expressions have been derived, which relate the probability of a missed detection to the probability of a false alarm. However, they have not been presented in such a generic closed-form expression that can be used for any unknown deterministic signal (for instance OFDM and OM-OFDM). Thereafter, an examination of the spectrum characteristics of an OM-OFDM transmission indicates its attractive detection characteristics. The proposed OM-OFDM method is further shown to operate at a significantly lower SNR value than an OFDM transmission, while still offering better detection characteristics than that of an OFDM transmission under Rician, Rayleigh and frequency selective fading channel conditions. In addition to its attractive PAPR properties, OM-OFDM also offers good detection characteristics for cognitive radio applications. These aspects make OM-OFDM a promising candidate for future deployment. / Thesis (PhD)--University of Pretoria, 2012. / Electrical, Electronic and Computer Engineering / unrestricted