Made available in DSpace on 2014-12-17T15:03:27Z (GMT). No. of bitstreams: 1 WelitonFBF_DISSERT.pdf: 2010897 bytes, checksum: 9145c54f00922f08967d3beb644f5f73 (MD5) Previous issue date: 2011-07-28 / Coordena??o de Aperfei?oamento de Pessoal de N?vel Superior / The improper disposal of nitrogen in receiving water courses causes problems such as toxicity to living beings through the consumption of oxygen to meet the nitrogen demand, eutrophication and nitrate contamination of aquifers. For this reason it is often necessary to be carried out complementary treatment of wastewater to eliminate or reduce the concentration of this compound in the wastewater. The objective of this study is to evaluate the biological removal of nitrogen compounds using submerged aerated and anoxic filters as post-treatment of an anaerobic system, with low cost and innovative technology, which in previous studies has shown high removal efficiency of organic matter and great potential biological nitrogen compounds removal. The simple design with perforated hoses for air distribution and filling with plastic parts proved to be very efficient in relation to organic matter removal and nitrification. The system presented, in the best stage, efficiency in converting ammonia to nitrate by 71%, and produced a final effluent concentration below 10 mg / L of NH3-N. In addition, carbon concentration was removed by 77%, producing final effluent with 24 mg/L COD. However, denitrification in anoxic filter was not effective even with the addition of an external carbon source. There was a reduction of up to 56% of nitrogen caused by the process of simultaneous nitrification and denitrification (SND). The high voids space presented by this type of support material coupled with direct aeration of the sludge, allows the respiration of biomass retained between the endogenous phase, increased cell retention time and sludge retention capacity, producing a final effluent with turbidity less than 5 UT and total suspended solids around 5.0 mg/L / A disposi??o inadequada do nitrog?nio em corpos receptores gera problemas como: toxicidade para seres vivos; consumo de oxig?nio do meio para atender a demanda nitrogenada; eutrofiza??o; e contamina??o dos aqu?feros por nitrato. Por esta raz?o ? muitas vezes necess?rio que seja realizado tratamento complementar dos esgotos para eliminar, ou reduzir, a concentra??o deste composto nas ?guas residu?rias. O objetivo deste trabalho ? avaliar a remo??o biol?gica dos compostos nitrogenados utilizando filtros aerados submersos como p?s-tratamento de um sistema anaer?bio, com tecnologia inovadora, de baixo custo, que em estudos anteriores demonstrou grande efici?ncia na remo??o de mat?ria org?nica carbon?cea e grande potencial na remo??o biol?gica de compostos nitrogenados. A forma simples como o sistema foi concebido, com mangueiras perfuradas para distribui??o do ar e preenchimento com pe?as pl?sticas - condu?te cortado - mostrou-se bastante eficiente em rela??o ? remo??o de mat?ria org?nica e na nitrifica??o. O sistema apresentou, na melhor fase, efici?ncia na convers?o de nitrog?nio amoniacal em nitrato de 71%, e produziu efluente final com concentra??o de N-NH3 inferior a 10 mg/L. Al?m disso, observou-se uma redu??o de 77% na concentra??o de carbono, produzindo efluente final com 24 mg/L de DQO. Contudo a desnitrifica??o no filtro an?xico n?o se mostrou eficiente mesmo com a adi??o de uma fonte externa de carbono. Mesmo assim observou-se redu??o de at? 56% do nitrog?nio causado pelo processo de Nitrifica??o e Desnitrifica??o Simult?neas (SND). O grande ?ndice de vazios apresentado por este tipo de material suporte aliado ? aera??o direta do lodo, permite que a respira??o da biomassa retida entre na fase end?gena, aumentado o tempo de reten??o celular e a capacidade de reten??o de lodo, produzindo um efluente final com turbidez inferior a 5 UT e SST em torno de 5,0 mg/L

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