Dissertations / Theses: 'Electron transport Complex I'

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Lemma-Gray, Patrizia. "Structure-function relationships within cytochrome C oxidase and complex I a dissertation /." San Antonio : UTHSC, 2008. http://proquest.umi.com.libproxy.uthscsa.edu/pqdweb?did=1594481111&sid=12&Fmt=2&clientId=70986&RQT=309&VName=PQD.

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Au, Harry C. "Molecular genetics of complex II of the mammalian mitochondrial electron transport chain /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1997. http://wwwlib.umi.com/cr/ucsd/fullcit?p9735265.

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Mohsin, Ahmed Abdul Hussein. "Modulation of electron transport by Metformin in cardiac protection: role of complex I." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5554.

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Modulation of mitochondrial complex I during reperfusion reduces cardiac injury. Complex I exists in two structural states: active (A) and deactive (D) with transition from A→D during ischemia. Reperfusion reactivates D→A with an increase in ROS production. Metformin preserves the D-Form. Our aim was to study the contribution of maintenance of deactivation of complex I during early reperfusion by metformin to protect against ischemia reperfusion injury. Our results showed that metformin decreased H9c2 cardiomyoblast apoptosis and total cell death following simulated ischemia for six hours followed by reoxygenation for twenty four hours compared to untreated cells. Reactive oxygen species (ROS) generation was reduced at the onset of reoxygenation with metformin treatment. Metformin also prevented the acute reactivation of complex I during reoxygenation following 10 minutes of hypoxia accompanied by decreased ROS generation. In addition, the content of C/EBP homologous protein was decreased in metformin treated cells, suggesting that metformin treatment decreased endoplasmic reticulum stress. 5' adenosine monophosphate-activated protein kinase was activated in our model independent of metformin treatment. Intriguingly, metformin protects in 5' adenosine monophosphate-activated protein kinase knock down system. Surprisingly, we found that metformin successfully downregulated p53 compared to untreated simulated ischemia reoxygenation. We sought potential metformin related impact on anti-apoptotic protein B-cell lymphoma 2. Our results showed the expression of the anti-apoptotic protein B-cell lymphoma 2 was markedly decreased in SI6/RO24 and metformin increased expression of B-cell lymphoma 2. Metformin, likely by partial inhibition of complex I with decreased ROS generation, resulted in less sulfhydryl modification and decreased modification of thiol groups by nitrosylation. We propose that the slowing down of activation of complex I at early stage of reperfusion by acute use of high dose metformin would be protective in cells and hearts against ischemia reperfusion injury. This potential new mechanism of protection is relevant at the onset of reperfusion to directly modulate electron transport to achieve cardiac protection and to decrease cardiac cell injury. Modulation of mitochondrial complex I during reperfusion reduces cardiac injury. Complex I exists in two structural states: active (A) and deactive (D) with transition from A→D during ischemia. Reperfusion reactivates D→A with an increase in ROS production. Metformin preserves the D-Form. Our aim was to study the contribution of maintenance of deactivation of complex I during early reperfusion by metformin to protect against ischemia reperfusion injury. Our results showed that metformin decreased H9c2 cardiomyoblast apoptosis and total cell death following simulated ischemia for six hours followed by reoxygenation for twenty four hours compared to untreated cells. Reactive oxygen species (ROS) generation was reduced at the onset of reoxygenation with metformin treatment. Metformin also prevented the acute reactivation of complex I during reoxygenation following 10 minutes of hypoxia accompanied by decreased ROS generation. In addition, the content of C/EBP homologous protein was decreased in metformin treated cells, suggesting that metformin treatment decreased endoplasmic reticulum stress. 5' adenosine monophosphate-activated protein kinase was activated in our model independent of metformin treatment. Intriguingly, metformin protects in 5' adenosine monophosphate-activated protein kinase knock down system. Surprisingly, we found that metformin successfully downregulated p53 compared to untreated simulated ischemia reoxygenation. We sought potential metformin related impact on anti-apoptotic protein B-cell lymphoma 2. Our results showed the expression of the anti-apoptotic protein B-cell lymphoma 2 was markedly decreased in SI6/RO24 and metformin increased expression of B-cell lymphoma 2. Metformin, likely by partial inhibition of complex I with decreased ROS generation, resulted in less sulfhydryl modification and decreased modification of thiol groups by nitrosylation. We propose that the slowing down of activation of complex I at early stage of reperfusion by acute use of high dose metformin would be protective in cells and hearts against ischemia reperfusion injury. This potential new mechanism of protection is relevant at the onset of reperfusion to directly modulate electron transport to achieve cardiac protection and to decrease cardiac cell injury.

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Bassalo, Marcelo Colika 1989. "Estudo do metabolismo aeróbico da bactéria anaeróbica facultativa Propionibacterium acidipropionici." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/316761.

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Orientador: Gonçalo Amarante Guimarães Pereira
Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: A sociedade atual é fundamentalmente dependente do petróleo, recurso natural inserido na grande maioria dos setores da economia. Entretanto, fatores como a limitada disponibilidade deste recurso, sua instabilidade no mercado devido a problemas de natureza geopolítica e a emissão de dióxido de carbono ocasionada pela utilização deste combustível, acentuaram as iniciativas para substituir o petróleo por fontes alternativas e renováveis de matéria prima. A bactéria Propionibacterium acidipropionici surge como uma excelente candidata para a substituição de compostos petroquímicos, através da produção do ácido propiônico. No entanto, antes de transformar esta bactéria em uma plataforma industrial, é necessário aprofundar a compreensão do metabolismo deste microrganismo e desenvolver ferramentas de manipulação genética. No que diz respeito à compreensão do metabolismo, poucos estudos avaliaram o perfil aeróbico desta bactéria, considerada anaeróbica estrita até recentemente. No presente trabalho, foi identificada nesta bactéria a presença de todos os componentes de uma cadeia transportadora de elétrons. No entanto, a citocromo c oxidase identificada apresenta-se mutada e os testes realizados confirmaram a não funcionalidade deste complexo. A existência de uma oxidase alternativa, a citocromo bd oxidase, caracterizada pela alta afinidade ao oxigênio, surge então como uma hipótese promissora acerca da microaerofilia desta bactéria. O trabalho também avaliou o perfil fermentativo dessa bactéria em condições aeróbicas com diferentes fontes de carbono, o que ressaltou a enorme flexibilidade metabólica apresentada por P. acidipropionici, capaz de redirecionar o fluxo de carbono para diferentes produtos finais a depender da necessidade de manutenção do balanço redox. Este estudo também revelou uma propriedade bastante peculiar e industrialmente relevante do xarope de cana-de-açúcar. A fermentação aeróbica com este substrato, ao contrário de todas as outras fontes de carbono, apresentou um crescimento superior ao das condições anaeróbicas e, adicionalmente, exibiu um perfil fermentativo próximo ao observado em ausência de oxigênio. A identificação do composto presente no xarope de cana-de-açúcar, responsável por simular o metabolismo anaeróbico, poderia viabilizar a produção do ácido propiônico em dornas de fermentação aeróbicas, o que traria enormes benefícios para a produção economicamente viável do ácido propiônico e na implementação de P. acidipropionici como uma plataforma industrial
Abstract: The dependence of contemporary society on petroleum is axiomatic, and this natural resource could be found intrinsically embedded in the vast majority of economic sectors. Nonetheless, the limited availability of this natural resource, the instability in the stock market due to geopolitical problems, and also the carbon dioxide emissions associated with the use of fossil fuels have highlighted the need to search for renewable energy sources. The bacteria Propionibacterium acidipropionici arises as an excellent strategy for the substitution of petrochemical compounds, through the production of propionic acid. Before we could implement this bacterium as an industrial platform, however, it becomes necessary to enhance the knowledge regarding the metabolism of P. acidipropionici, and thus create a backbone for the development of genetic manipulation tools. Regarding the metabolism of this bacterium, there aren't comprehensive studies about its aerobic metabolism, thus being considered strict anaerobes until recently. In the present work, it was identified that P. acidipropionici has all required components for a functional electron transport chain. However, the cytochrome c oxidase of this bacterium has a frameshift mutation, and the functional studies proved that this complex is not operative. The presence of an alternative oxidase of high oxygen affinity, called cytochrome bd oxidase, is then suggested as a hypothesis to explain the microaerofilic habit of this bacterium. This work has also shed light into the fermentative profile showed by this bacterium under aerobic cultivation with different carbon sources, bringing attention to the highly flexible metabolism of P. acidipropionici. This bacterium has shown to be capable of completely changing its carbon flux to different end products, as a strategy to maintain the redox balance. In addition, this work has also unveiled an interesting and industrially-relevant property of the sugar cane syrup. It was demonstrated that the aerobic cultivation of P. acidipropionici with sugar cane syrup increased the culture growth, as well as it changed the fermentation end products in a way more similar to the anaerobic cultivation. It was hypothesized that this unusual property found in the sugar cane syrup was due to the presence of a mineral compound that could be used as a final electron acceptor by P. acidipropionici. The identification of this specific compound would allow the aerobic production of propionic acid in industrial conditions, and thus could be a major breakthrough to turn its industrial production into an economically viable process
Mestrado
Genetica de Microorganismos
Mestre em Genética e Biologia Molecular

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Ädelroth, Pia. "Mechanisms and pathways for proton transfer in cytochrome-c oxidase." Göteborg : Göteborg University, 1998. http://catalog.hathitrust.org/api/volumes/oclc/68945135.html.

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Walker, Glen William, and not available. "Electron Transfer Reactivity, Synthesis, Surface Chemistry and Liquid-Membrane Transport of Sarcophagine-Type Poly-Aza Cage Complexes." The Australian National University, 1997. http://thesis.anu.edu.au./public/adt-ANU20010702.124104.

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[Formulae and special characters can only be approximated here. Please see the pdf version of the Abstract for an accurate reproduction.] The kinetics for outer-sphere electron transfer between a series of cobalt(II) poly-aza cage ligand complexes and the iron(III) sarcophagine-type hexa-aza cage complex, [Fe(sar)]3+ (sar = 3,6,10,13,16,19-hexaazabicyclo[6.6.6]icosane), in aqueous solution have been investigated and the Marcus correlation is used to deduce the electron self-exchange rate constant for the [Fe(sar)]3+/2+ couple from these cross-reactions. The deduced electron self-exchange rate constant is in relatively good agreement with the experimentally determined rate constant (k ex calc = 4 ´ 10 5 M -1 s -1 ; k ex obs = 8 ´ 10 5 M -1 s -1 ). The successful application of the Marcus correlation to the electron transfer reactions of the Fe cage complex is consistent with the trend for the Co, Mn, Ni and Ru cage complexes which all follow the pattern of outer-sphere electron transfer reactivity expected from the Marcus-Hush formalism. A comparison of predictions based on the Marcus correlation with the experimentally determined kinetics of an extended series of cross reactions involving cobalt cage complexes with low-spin-high-spin cobalt(III)/(II) couples shows that electron transfer reactions involving large spin changes at the metal centre are not necessarily anomalous in the context of the adiabatic Marcus-Hush formalism. The results of this study also show that for suitable systems, the Marcus correlation can be used to reliably calculate the rates of outer-sphere electron transfer cross-reactions, with reaction free-energy changes spanning the range -6 to -41 kJ mol -1 and many different combinations of initial electronic configurations. Together, these results provide a coherent and internally consistent set of experimental data in support of the Marcus-Hush formalism for outer-sphere electron transfer. The results with the caged metal-ion systems also highlight the special nature of the mechanism of electron transfer in reactions of metal-aqua ions. ¶ A new range of symmetrically disubstituted hexa-aza sarcophagine-type cage ligand complexes are prepared in this study by the base-catalysed co-condensation of formaldehyde and a-methylene aliphatic aldehydes with cobalt(III) tris(1,2-diamine) precursors in acetonitrile solution. Encapsulation reactions based on the condensation of the weak carbon di-acids propanal and decanal with formaldehyde and the cobalt(III) tris(1,2-diamine) precursors, [Co(en)3 ] 3+ (en = 1,2-ethanediamine) and D-lel3 -[Co((R, R)-chxn)3 ] 3+ (chxn = 1,2-cyclohexanediamine), yield unsaturated cobalt(III) cage complexes with an endo-cyclic imine function in each cap. The Co III -coordinated endo-cyclic imine units of the cage ligands are reactive electrophiles that are readily reduced by the BH4 - ion to give the corresponding symmetrically di-substituted hexaamine macrobicyclic cage ligands. The nitromethane carbanion is also shown to add at the endo-cyclic imine function to yield a novel nitromethylated cage ligand complex. The latter reaction introduces a new method for the regioselective functionalisation of cage ligands at sites removed from the more commonly substituted bridgehead positions. The capping of cobalt(III) tris(1,2-diamine)-type complexes with weak CH-acids developed in this study introduces a new and more direct route to symmetrically di-substituted cage ligand complexes. ¶ A new range of cobalt(III) surfactant cage complexes, with linear octyl, dodecyl and hexadecyl hydrocarbon chains built directly into the bridgehead structure of the cage ligand, have been prepared by the base catalysed co-condensation of formaldehyde and long chain aliphatic aldehydes with the tripodal cobalt(III) hexaamine complex, [Co(sen)]3+ (sen = 4,4',4''-ethylidynetris(3-azabutan-1-amine)), in acetonitrile solution. Chiral surfactant cage complexes are obtained by capping reactions beginning with the optically pure L-[Co(sen)]3+ precursor complex. The cobalt(III) cage complexes with octyl to hexadecyl substituents are surface active and reduce the surface tension of water to levels approaching those of organic solvents. The dodecyl substituted cage complex forms micelles in aqueous solution when the concentration of cage complex is > 1 ´ 10 -3 mol dm -3 at 25 °C. The cobalt(III) cage head-group of these surfactants undergoes an electrochemically reversible one-electron reduction to the corresponding cobalt(II) cage complex. The reduction potential of the surfactant head group can be tuned to more positive potentials by replacing the bridgehead hydrocarbon chain substituent with an ether linked hydrocarbon chain. The cobalt(III) surfactant-cage complexes are biologically active and are lethal to the tapeworm Hymenolepis diminuta, and the vaginal parasites, Trichomonas vaginalis and Tritrichomonas foetus. The surfactant cage complexes also cause lysis in red-blood cell membranes at concentrations as low 10 -5 mol dm -3 . Their biological activity is linked to the high head-group charge (3+) and size which cause distortions in biological membranes when the membrane is treated with these molecules. The combination of the chemically reversible outer-sphere redox properties of the cobalt cage head-groups and the chirality of the head group introduces a new and possibly unique series of chiral surfactant coordination complexes which are also redox active. ¶ The chiral carboxylic-acid ionophore, lasalocid A, has been used to promote the selective supramolecular transport and extraction of cobalt(III) hexa-aza cage cations and related tripodal cobalt(III) complexes. The conjugate base anion of lasalocid A forms stoichiometric outer-sphere complexes with the cobalt(III) cage and tripod complexes. These outer-sphere complexes are highly lipophilic and partition strongly from water into a chloroform phase. The extraction of the dissymmetric cobalt(III) complexes by the chiral polyether anion is enantioselective for many systems and results in the partial resolution of initially racemic complexes in the aqueous phase. A strong structural preference was demonstrated by the ionophore for symmetrically disubstituted cobalt(III) hexa-aza cage cations with a D-absolute configuration of the ligand about the metal-ion and an R configuration of the coordinated secondary amine N-H groups. The lasalocid A anion was also shown to promote the transport of the complexes, intact, across a chloroform bulk-liquid membrane against an NH4 + concentration gradient. The transport of the cobalt(III) complexes was also enantioselective and resulted in partial resolution of the initially racemic aqueous phase. The most efficiently transported enantiomer of each complex was also the most efficiently extracted isomer in all systems examined, consistent with a transport process limited by interfacial diffusion. The magnitude of the enantiomer separation obtained in some systems was sufficient to indicate that lasalocid A mediated extraction and transport may become a practical method for the resolution of particular types of kinetically-inert chiral metal-amine complexes.

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Halavaty, Andrei Stepanovich. "The "shuttle" mechanism of the electron transport by the ruthenium(II) bipyridyl complex-modified bovine adrenodoxin in the steroid hydroxylase crystal structure and intramolecular electron transfer /." [S.l.] : [s.n.], 2005. http://www.diss.fu-berlin.de/2005/340/index.html.

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Silva, Thiago Miranda da 1985. "Funcionalidade do complexo I da cadeia respiratoria de Trypanosoma Cruzi." [s.n.], 2010. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314220.

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Orientador: Fernanda Ramos Gadelha
Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: O Trypanosoma cruzi é o agente etiológico da doença de Chagas (DC), cujo tratamento é feito através do uso do nifurtimox e benzonidazol. Esses medicamentos não são efetivos tornando a busca para novos alvos para o desenvolvimento de uma terapia mais específica uma prioridade. O alto grau de heterogeneidade existente entre as cepas representa um desafio para o desenvolvimento desta terapia, tornando a compreensão da biologia do parasita essencial nessa busca. O objetivo deste trabalho foi avaliar a funcionalidade do complexo I da cadeia respiratória de epimastigotas de T. cruzi ao longo da curva de proliferação (fases log, estacionária e estacionária tardia). Deste modo foi avaliado em duas cepas (Tulahuen 2 e Y) o consumo de oxigênio, potencial de membrana mitocondrial (??) e a atividade da enzima succinato desidrogenase (SDH), utilizando-se diferentes substratos respiratórios (malato/piruvato (M/P) malato/piruvato + malonato (MPM) ou succinato (SUC)). De um modo geral, em ambas as cepas o consumo de oxigênio foi maior na fase estacionária tardia em relação à log. A utilização de diferentes substratos não resultou em diferenças significativas nas taxas de respiração em ambas as cepas. Tulahuen 2 exibiu maiores taxas de consumo de oxigênio em relação à Y. Não foram observadas diferenças significativas nos valores de controle respiratório (-1,7) nas duas cepas, nas diferentes fases de proliferação. Na presença de um desacoplador da fosforilação oxidativa, as taxas não variaram na cepa Y, enquanto na Tulahuen 2 ocorreu um aumento em direção à fase estacionária tardia. A administração de malonato, inibidor competitivo da SDH, rendeu padrões diferenciados de inibição com a respiração sustentada por diferentes substratos que não variaram quando as células foram submetidas a um "jejum" (incubadas em PBS / 1 raM MgCb) por 3 horas. A atividade da SDH diminuiu em ambas as cepas na fase estacionária em relação à log, justificando a queda das taxas de inibição pelo malonato. Não foram registradas diferenças significativas com o aumento da concentração deste inibidor. A adição de cianeto de potássio não inibiu completamente a respiração, não importando o substrato utilizado ou a fase de proliferação, indicando que outras fontes além da cadeia respiratória estão consumindo oxigênio. Interessantemente, o ?? não variou entre as cepas em nenhuma fase de proliferação. Estes resultados fornecem novos dados sobre a cadeia respiratória do parasita, além de indicarem que não foi possível estabelecer a funcionalidade do complexo I, uma vez que o malonato não é um inibidor eficiente do complexo II.
Abstract: Trypanosoma cruzi is the etiological agent of Chagas' disease, where nifurtimox and benznidazole are used in treatment. These drugs are not efficient turning the search for new targets to be used in the development of a more effective therapy a priority. The high degree of heterogeneity among strains represents a challenge for the development of this therapy, and the comprehension of the parasite biology becomes essential in this search. The aim of this work was to evaluate the functionality of the respiratory chain complex I along the growth curve in T. cruzi epimastigotes. In this way it was analyzed in two strains (Tulahuen 2 and Y) the oxygen consumption, mitochondrial membrane potential (??) and succinate dehydrogenase (SDH) activity, using different respiratory chain substrates (Malate/Pyruvate, Malate/Piruvate + Malonate or Succinate). Generally, in both strains oxygen consumption was higher in the late stationary phase in relation to the log phase. The use of different substrates for the respiratory chain did not lead to significant variations in the respiratory rates in both strains. Tulahuen 2 showed higher oxygen consumption rates than the Y strain. No significant differences were observed in the respiratory control rates (~1,7) in both strains along the growth curve. In the presence of an uncoupler, the respiration rates did not vary in the Y strain while in Tulahuen 2 an increase towards the late stationary phase was observed. Addition of malonate, a SDH competitive inhibitor, resulted in distinct inhibition patterns when respiration was sustained by different substrates and did not change when cells were "starved" (incubated in PBS / 1 mM MgCb) for 3 hours. SDH activity decreased in both strains in the stationary phase in relation to log phase that could explain the decrease in the inhibition rates induced by malonate. No significant differences were observed with higher inhibitor concentration. Addition of potassium cyanide did not completely inhibit respiration in both strains regardless the substrate or growth phase, suggesting that other sources beyond the respiratory chain consume oxygen. Interestingly, ?? were similar between strains in all growth phases. These results provide new data about the parasite's respiratory chain indicating that complex I functionality was not possible to determine, once malonate is not a good inhibitor of complex II.
Mestrado
Bioquimica
Mestre em Biologia Funcional e Molecular

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Sato, Motoaki. "Investigation of the essential amino acid residues of respiratory complex I in Escherichia coli for proton translocation." Kyoto University, 2015. http://hdl.handle.net/2433/200319.

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Ebert, C. Edward. "Effects of mutations of the iron-sulfur protein on the function and structure of the cytochrome bc₁ complex of yeast mitochondria." Morgantown, W. Va. : [West Virginia University Libraries], 2003. https://etd.wvu.edu/etd/controller.jsp?moduleName=documentdata&jsp%5FetdId=3.

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Thesis (Ph. D.)--West Virginia University, 2003.
Title from document title page. Document formatted into pages; contains viii, 144 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 129-144).

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Worgan, Lisa Catherine Women &amp Children's Health UNSW. "The role of nuclear-encoded subunit genes in mitochondrial complex 1 deficiency." Awarded by:University of New South Wales. Women and Children's Health, 2005. http://handle.unsw.edu.au/1959.4/22307.

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BACKGROUND: Mitochondrial complex I deficiency often leads to a devastating neurodegenerative disorder of childhood. In most cases, the underlying genetic defect is unknown. Recessive nuclear gene mutations, rather than mitochondrial DNA mutations, account for the majority of cases. AIM: Our aim was to identify the genetic basis of complex I deficiency in 34 patients with isolated complex I deficiency, by studying six of the 39 nuclear encoded complex I subunit genes (NDUFV1, NDUFS1, NDUFS2, NDUFS4, NDUFS7 and NDUFS8). These genes have been conserved throughout evolution and carry out essential aspects of complex I function. METHODS: RNA was extracted from patient fibroblasts and cDNA made by reverse transcription. Overlapping amplicons that together spanned the entire coding area of each gene were amplified by PCR. The genes were screened for mutations using denaturing High Performance Liquid Chromatography (dHPLC). Patient samples with abnormal dHPLC profiles underwent direct DNA sequencing. RESULTS: Novel mutations were identified in six of 34 (18%) patients with isolated complex I deficiency. Five patients had two mutations identified and one patient had a single mutation in NDUFS4 identified. All patients with mutations had a progressive encephalopathy and five out of six had Leigh syndrome or Leigh like syndrome. Mutations were found in three nuclear encoded subunit genes, NDUFV1, NDUFS2 and NDUFS4. Three novel NDUFV1 mutations were identified (R386H, K111E and P252R). The R386H mutation was found in two apparently unrelated patients. Four novel NDUFS2 mutations were identified (R221X, M292T, R333Q and IVS9+4A<G). The novel NDUFS4 mutation c.221delC was found in two patients - one in homozygous form and the other heterozygous. Specific genotype and phenotype correlations were not identified. CONCLUSIONS: Nuclear encoded complex I subunit gene mutations are an important contributor to the aetiology of isolated complex I deficiency in childhood. Screening of these genes is an essential part of the investigation of complex I deficiency.

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Su, Yang Ph D. Massachusetts Institute of Technology. "Disassembly of electron transport chain complexes drives macrophage TLR responses by reprogramming metabolism and translation." Thesis, Massachusetts Institute of Technology, 2020. https://hdl.handle.net/1721.1/127139.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, May, 2020
Cataloged from the official PDF of thesis.
Includes bibliographical references.
Metabolic switch from oxidative phosphorylation (OxPhos) to glycolysis is a key feature of inflammatory response in macrophages, but how this switch occurs in response to inflammatory signals and how it precisely contributes to macrophage function is still obscure. Here we show that stimulation of macrophages through Toll-like receptors (TLR) disrupts the assembly of mitochondrial electron transfer chain (ETC) complexes I-V, leading to the metabolic switch by inhibiting OxPhos and activating HIF-1[alpha]-dependent glycolysis. Disassembly of ETC complexes influences the global metabolic status of macrophages not only by inducing glycolysis but also largely by inducing the reprogramming of cellular translational capacity via mTORC1 and ATF4, leading to enhanced global translation rate, cell growth, and production of inflammatory cytokines. Inhibition of OxPhos via myeloid-specific knockout of OPA1, which stimulates ETC complex assembly, exacerbates sepsis in mice while inhibition of mTORC1 reverses this effect. These findings reveal that disassembly of ETC complexes underlies macrophage metabolic switch and inflammatory responses and may be a conserved pathway to reprogram cellular anabolism and function.
by Yang Su.
Ph. D.
Ph.D. Massachusetts Institute of Technology, Department of Biology

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Michelini, Luiz Guilherme Bueno 1983. "Caracterização do estímulo da produção mitocondrial de H2O2 por inibição parcial do Complexo I da cadeia respiratória = Stimulatory effects of a partial respiratory Complex I inhibition on mitochondrial H2O2 generation." [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/313031.

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Orientador: Roger Frigério Castilho
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: A inibição parcial do Complexo I da cadeia respiratória mitocondrial em ratos tratados cronicamente com rotenona está associada com o desenvolvimento de características neuroquímicas, comportamentais e neuropatológicas da doença de Parkinson. Os objetivos deste trabalho foram (i) caracterizar os efeitos de uma inibição parcial do Complexo I por rotenona na produção de peróxido de hidrogênio (H2O2) por mitocôndrias de cérebro de ratos (MCR) em diferentes estados respiratórios e (ii) avaliar a suscetibilidade de MCR velhos (24 meses) à inibição do consumo de oxigênio (O2) e ao estímulo da produção de H2O2 por rotenona em comparação a MCR adultos (3-4 meses). A análise do potencial de membrana por citometria de fluxo em mitocôndrias isoladas indicou que a adição de rotenona promoveu uma inibição uniforme da respiração mitocondrial nestas organelas. Quando mitocôndrias foram incubadas na presença de uma baixa concentração de rotenona (10 nM) e de substratos geradores de NADH, o consumo de O2 foi reduzido de 45,9±1,0 para 26,4±2,6 nmol O2.mg-1.min-1 e de 7,8±0,3 para 6,3±0,3 nmol O2.mg-1.min-1 nos estados respiratórios 3 (respiração estimulada por ADP) e 4 (respiração de repouso), respectivamente. Nessas condições, a produção mitocondrial de H2O2 foi estimulada de 12,2±1,1 para 21,0±1,2 pmol H2O2.mg-1.min-1 e de 56,5±4,7 para 95,0±11,1 pmol H2O2.mg-1.min-1 nos estados respiratórios 3 e 4, respectivamente. Resultados similares foram observados ao comparar preparações mitocondriais enriquecidas com organelas sinápticas e não-sinápticas ou quando o íon 1-metil-4-fenilpiridina (MPP+) foi utilizado como inibidor de Complexo I mitocondrial. O estímulo da produção de H2O2 por rotenona nos estados respiratórios 3 e 4 foi associado a um aumento do estado reduzido de nucleotídeos de nicotinamida endógenos. Na respiração mitocondrial com succinato, onde a maior parte da produção de H2O2 se origina do fluxo reverso de elétrons do Complexo II para o I, baixas concentrações de rotenona inibiram a produção de H2O2. Rotenona não exerceu efeito sobre a eliminação mitocondrial de concentrações micromolares de H2O2. Em sinaptossomas intactos, observamos que rotenona 10 nM estimulou a liberação de H2O2 em 20,2±3,3% no estado respiratório basal. Ao compararmos MCR adultos e velhos, verificamos que o consumo de O2 no estado respiratório 3 e a atividade da citrato sintase foram 21,0±3,3% e 17,0±5,4% mais baixos em MCR velhos. Experimentos conduzidos na presença de diferentes concentrações de rotenona (5, 10 e 100 nM) demonstraram sensibilidade similar à inibição do consumo de O2 por rotenona no estado respiratório 3, com IC50 de 7,8±0,4 e 6,5±0,5 nM para MCR adultos e velhos, respectivamente. De acordo com esses resultados, o estímulo da produção de H2O2 observado foi similar em MCR adultos e velhos, tratadas com diferentes concentrações de rotenona. Concluímos que, uma inibição parcial do Complexo I pode resultar em uma crise energética e/ou estresse oxidativo mitocondrial, enquanto o primeiro evento predominaria numa situação de alta demanda de fosforilação oxidativa, o segundo ocorreria em condições de respiração de repouso. Em adição, os experimentos com ratos velhos indicaram que rotenona exerce efeitos similares no consumo de O2 e na produção de H2O2 em MCR adultos e velhos
Abstract: Partial inhibition of mitochondrial Complex I is associated with the development of neurochemical, behavioral, and neuropathological features of Parkinson's disease in rats chronically and systemically treated with rotenone. The aims of this work were (i) to characterize the effects of partial inhibition of respiratory Complex I by rotenone on H2O2 production by rat brain mitochondria in different respiratory states and (ii) to evaluate the susceptibility of brain mitochondria from old rats (24 month-old) to rotenone-induced inhibition of oxygen consumption and increased generation of H2O2 when compared with organelles from adult rats (3-4 month-old). Flow cytometric analysis of membrane potential in isolated mitochondria indicated that rotenone leads to uniform respiratory inhibition when added to a suspension of these organelles. When mitochondria were incubated in the presence of a low concentration of rotenone (10 nM) and NADH-linked substrates, oxygen consumption was reduced from 45.9±1.0 to 26.4±2.6 nmol O2.mg-1.min-1 and from 7.8±0.3 to 6.3±0.3 nmol O2.mg-1.min-1 in respiratory states 3 (ADP-stimulated respiration) and 4 (resting respiration), respectively. Under these conditions, mitochondrial H2O2 production was stimulated from 12.2±1.1 to 21.0±1.2 pmol H2O2.mg-1.min-1 and 56.5±4.7 to 95.0±11.1 pmol H2O2.mg-1.min-1 in respiratory states 3 and 4, respectively. Similar results were observed when comparing mitochondrial preparations enriched with synaptic or nonsynaptic organelles or when 1-methyl-4-phenylpyridinium (MPP+) ion was used as a respiratory Complex I inhibitor. Rotenone-stimulated H2O2 production in respiratory states 3 and 4 was associated with a high reduction state of endogenous nicotinamide nucleotides. In succinate-supported mitochondrial respiration, where most of the mitochondrial H2O2 production relies on electron backflow from Complex II to Complex I, low rotenone concentrations inhibited H2O2 production. Rotenone had no effect on mitochondrial elimination of micromolar concentrations of H2O2. In intact synaptosomes, we observed that 10 nM rotenone stimulated H2O2 release by 20.2 ± 3.3% under basal respiratory state. When comparing isolated brain mitochondria from adult and old rats we observed that oxygen consumption under respiratory state 3 and citrate synthase activity were 21.0±3.3% and 17.0±5.4% lower in mitochondria from old rats. Experiments conducted in the presence of different rotenone concentrations (5, 10 and 100 nM) showed that brain mitochondria from adult and old rats have similar sensitive to rotenone-induced inhibition of oxygen consumption in respiratory state 3, with IC50 of 7.8±0.4 and 6.5±0.5 nM for adult and old rats, respectively. In line with these results, similar stimulations in H2O2 production were observed in mitochondria from adult and old rats treated with different concentrations of rotenone. We conclude that partial Complex I inhibition may result in mitochondrial energy crisis and oxidative stress, the former being predominant under oxidative phosphorylation and the latter under resting respiration conditions. Rotenone exerts similar effects on oxygen consumption and H2O2 production by isolated brain mitochondria from adult and old rats
Mestrado
Biologia Estrutural, Celular, Molecular e do Desenvolvimento
Mestre em Ciências

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14

Jones, Torrie Turner. "Age-Related Deficits in Electron Transport Chain Complexes in Rat Neurons and 3xTg-AD Mouse Neurons." Available to subscribers only, 2009. http://proquest.umi.com/pqdweb?did=1797219571&sid=1&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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Thesis (Ph. D.)--Southern Illinois University Carbondale, 2009.
"Department of Molecular Biology, Microbiology, and Biochemistry." Keywords: Aging, Cytochrome c oxidase, Electron transport chains, Estrogen, Mitochondria, Neurons. Includes bibliographical references (p. 102-137). Also available online.

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15

Choi, Wookjin. "Development of complex permittivity analysis techniques for evaluation of charge transport and trapping on 2D electronic systems." Kyoto University, 2018. http://hdl.handle.net/2433/231018.

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16

Herman, Leslie. "Ru(II) under illumination: a study of charge and energy transfer elementary processes." Doctoral thesis, Universite Libre de Bruxelles, 2008. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210399.

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Une compréhension sans cesse plus pointue des processus élémentaires de transferts de charges et d’énergie, qui sont à la base même de nombreux processus biologiques, permet non seulement l’élaboration mais aussi l’amélioration de la mise au point de molécules photoactives utiles dans différentes applications. C'est le cas (i) de systèmes moléculaires et supramoléculaires destinés à mimer efficacement la photosynthèse, ou encore (ii) de molécules photoactives capables d’interagir avec des macromolécules biologiques et d’induire une transformation de ces biomolécules. C’est dans ce cadre général que s’inscrit l’élaboration de nouveaux complexes polyazaaromatiques de Ru(II) capables d’interagir avec la double hélice d’ADN et de photoréagir avec sa base la plus réductrice, la guanine, par transfert d’électron photoinduit. C’est sur la base de ces processus que des nouveaux agents antitumoraux photoactivables ont pu être développés. L’utilisation de complexes de Ru(II) dans le design d’entités supramoléculaires polymétalliques destinées à jouer le rôle de collecteurs de lumière et permettant ainsi de mimer les systèmes d’antennes naturels s’intègre également dans cette démarche.

L’ensemble de notre travail s’est concentré sur ces deux domaines d’applications. Par l’étude de différents processus de transfert de charges/d’énergie au sein des complexes seuls (processus intramoléculaires) ou en interaction avec un environnement spécifique (processus intermoléculaires), nous avons souhaité mettre en évidence l’intérêt de l’utilisation d’un nouveau ligand plan étendu, le tpac, au sein de complexes du Ru(II). Un tel ligand permet en effet de conférer d’une part une affinité élevée des complexes résultants pour l’ADN, et d’autre part, de par sa nature pontante, de connecter des unités métalliques entre elles au sein d’entités supramoléculaires de taille importante.

Les propriétés photophysiques de quatre complexes basés sur le ligand plan étendu tpac, le [Ru(phen)2tpac]2+ (P) et son homologue dinucléaire le [(phen)2Ru tpac Ru(phen)2]4+ (PP) (à base de ligands ancillaires phen), ainsi que le [Ru(tap)2tpac]2+ (T) et son homologue dinucléaire le [(tap)2Ru tpac Ru(tap)2]4+ (TT) (à base de ligands ancillaires tap), ont été étudiées et comparées entre elles.

L’examen de ces propriétés, d’abord pour les complexes seuls en solution, en parallèle avec celles de complexes dinucléaires contenant un ligand pontant PHEHAT, a permis de mettre en évidence l’importance de la nature du ligand pontant utilisé. Ces résultats ont ainsi révélé qu’un choix judicieux du ligand pontant permet de construire des entités de grande taille capables de transférer l’énergie lumineuse vers un centre (cas du ligand PHEHAT), ou, au contraire, de relier entre elles des entités ne s’influençant pas l’une l’autre d’un point de vue photophysique (cas du ligand tpac).

Les propriétés des complexes du tpac, étudiés cette fois en présence de matériel génétique (mononucléotide GMP, ADN ou polynucléotides synthétiques), se sont révélées très différentes selon que le complexe portait des ligands ancillaires phen (P, PP) ou tap (T, TT). Seuls les complexes à base de tap sont en effet photoréactifs envers les résidus guanine. Nous avons dès lors focalisé cette partie de notre travail sur les deux complexes T et TT. Cette photoréaction, ainsi que le transfert d’électron photoinduit entre ces complexes excités et la guanine, ont pu être mis en évidence par différentes techniques de spectroscopie d’émission tant stationnaire que résolue dans le temps, ainsi que par des mesures d’absorption transitoire dans des échelles de temps de la nano à la femto/picoseconde. L’étude du comportement photophysique des complexes en fonction du pH a en outre révélé de manière très intéressante que, pour des études en présence d’ADN, la protonation des états excités des complexes devait être considérée. Les résultats de cette étude nous ont fourni des pistes quant à l’attribution des processus observés en absorption transitoire.

Le transfert d’électron a également fait l’objet d’une étude par des méthodes théoriques. Ces calculs ab initio ont permis de mettre en évidence une faible influence de l’énergie de réorganisation sur la vitesse de transfert d’électron, qui semble dépendre plus sensiblement de la non-adiabaticité du processus, mais surtout de l’énergie libre de la réaction et d’un éventuel couplage à un transfert de proton.

L’ensemble des résultats obtenus avec les complexes T et TT en présence de matériel génétique, qui, de manière assez inattendue, sont très semblables, indiquent que ces complexes présentent tous deux un grand intérêt pour le développement de nouvelles drogues antitumorales photoactivables.

Doctorat en Sciences
info:eu-repo/semantics/nonPublished

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Dornan, Thomas Joseph. "Calcium Transport Inhibition, Stimulation, and Light Dependent Modulation of the Skeletal Calcium Release Channel (RyR1) by the Prototropic Forms of Pelargonidin." PDXScholar, 2014. https://pdxscholar.library.pdx.edu/open_access_etds/1931.

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The principle calcium regulator in the muscle cell is the calcium ion release channel (RyR). Improper calcium homeostasis in the muscle cell is the foundation of many pathological states and has been targeted as a contributing factor to ventricular tachycardia, which is known to precede sudden cardiac arrest. Numerous endogenous and exogenous compounds can affect the way RyR regulates calcium. In this study the anthocyanidin Pelargonidin (Pg), an important natural colorant and dietary antioxidant, is evaluated for its effect on regulating the transport of calcium through the RyR1 of skeletal muscle sarcoplasmic reticulum. Pelargonidin undergoes time dependent structural changes in aqueous solutions at physiological pH and a mixture of up to seven forms of Pelargonidin are present in solution simultaneously. Pelargonidin is a unique RyR1 modulator. It can both stimulate and inhibit the RyR1 depending on the experimental conditions. In addition, when Pelargonidin is irradiated with white light, its inhibition properties on the RyR1 are essentially nullified. Proposed mechanisms include excited state charge shift within RyR1-Pg complexes.

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Pashkovskaia, Natalia. "ROS generated by mitochondrial electron transport chain complexes I and III regulate differentiation of the pluripotent cell line P19." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2018. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-233704.

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Mitochondria are essential for the viability of mammalian cells and provide a compartment for specific chemical reactions. Cellular respiration -- the main mitochondrial function -- is tightly connected with ROS production: the mitochondrial electron transport chain complexes I and III are the main ROS sources in mammalian cells. It has been reported that complex I and complex III activities are essential for cell cycle, apoptosis and stem cell differentiation (Spitkovsky et al., 2004; Varum et al., 2009; Lee et al., 2011; Ma et al., 2011; Tormos et al., 2012). In our work, we aimed to investigate the role of mitochondrial electron transport chain activity in the regulation of the differentiation potential and to unravel signaling pathways that could participate in this regulation. As a model, we used the P19 pluripotent stem cell line that can be easily differentiated into trophoblasts, expressing intermediate filaments cytokeratin 8/18, and neurons, which express cytoskeleton protein beta-III-tubulin. We first showed that both trophoblast and neural differentiation of P19 cells were accompanied by activation of cellular respiration. The analysis of respiratory chain complexes and supercomplexes, however, showed that undifferentiated P19 cells, as well as their differentiated derivatives did not differ in their respiratory machinery, including functional respirasomes. While undifferentiated cells did not use respiration as the main energy source, cellular respiration was activated during differentiation, indicating that oxidative metabolism was important for efficient differentiation. To investigate the potential role of mitochondrial electron transport chain activity we monitored the influence of a disrupted electron flow on the differentiation of P19 cells. We found that the activity of complex I and complex III influenced the differentiation potential of the pluripotent P19 cell line: the presence of complex I and complex III inhibitors rotenone, antimycin A, or myxothiazol increased the amount of cytokeratin 8/18+ cells during trophoblast differentiation, but almost completely prevented the formation of neuron-like beta-III-tubulin+ cells during neuron differentiation. Moreover, a low oxygen level (1 % O2 vs 21 % O2 in atmosphere) - the final electron acceptor - had the same effect on differentiation. These data suggest that mitochondrial electron transport chain activity contributes to the regulation of differentiation. The presence of complex I and complex III inhibitors, as well as oxygen scarcity, increase ROS production. We suggested that increased ROS level could explain the observed effects. By visualizing mitochondrial superoxide production with a specific dye – MitoSox - we confirmed that rotenone, antimycin A, myxothiazol, as well as low oxygen conditions, increased the superoxide level. These results suggest that the observed changes of the differentiation potential of P19 cells are associated with ROS production. To prove this idea, we differentiated P19 cells in presence of paraquat – a known ROS inducer. In line with our hypothesis paraquat promoted trophoblast differentiation. The received results suggest that the mitochondrial electron transport chain activity regulates differentiation through the ROS level. ROS are secondary messengers that participate in numerous processes including cell proliferation and differentiation. We aimed to predict the signal pathway that connects ROS level in stem cells and their differentiation potential. For this purpose, we performed a microarray analysis and compared the gene expression profiles of cells grown under hypoxia or in the presence of the complex III inhibitor myxothiazol with untreated control cells. The expression analysis revealed p53 as a transcriptional factor that impacts the differentiation potential in treated cells. p53 is a known redox-sensing molecule (Bigarella et al., 2014) that influences the differentiation potential through cell cycle control (Maimets et al., 2008). This observation is in line with our results and suggests that p53 may regulate the differentiation potential of P19 cells. We are planning to investigate the role of p53 signaling in the regulation of cell cycle and differentiation potential of P19 cell line.

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19

Temirov, Ruslan [Verfasser]. "Studying complex metal-molecule interface with low temperature scanning tunneling microscope : from electronic structure to charge transport / Ruslan Temirov." Bremen : IRC-Library, Information Resource Center der Jacobs University Bremen, 2008. http://d-nb.info/1034984187/34.

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20

Chan, Yiu Him. "Effect of dopants and gate dielectrics on charge transport and performance of organic thin film transistor." HKBU Institutional Repository, 2012. https://repository.hkbu.edu.hk/etd_ra/1450.

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21

Hjelm, Johan. "Conducting Polymers Containing In-Chain Metal Centres : Electropolymerisation and Charge Transport." Doctoral thesis, Uppsala University, Department of Physical Chemistry, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3789.

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Conjugated polymers that exhibit high electronic conductivities play key roles in the emerging field of molecular electronics. In particular, linking metal centres with useful electrochemical, photophysical, or catalytic properties to the backbone, or within the polymer chain itself, is a topic which has attracted a significant amount of interest lately. Structurally rigid monomers that can be electropolymerised to form highly conducting molecular wires may provide new insights into conduction mechanisms, e.g., exploiting resonant superexchange (electron-hopping) by tuning the energies of redox centre and bridge states. The focus of this thesis lies on the electrochemical investigation of preparation, growth dynamics, and charge transport dynamics of oligothiophene/transition metal hybrid materials. The incorporation of ruthenium(II) and osmium(II) terpyridine complexes into such polymeric assemblies was accomplished by an electropolymerisation procedure, to produce rod-like oligothienyl-bridged metallopolymers. The properties of the monomers used were characterised by optical spectroscopy and electrochemical techniques. Charge transport was studied in detail for some of the materials created, and it was found that the electron transport rate and dc conductivity was enhanced by up to two orders of magnitude compared to relevant non-conjugated polymers, demonstrating the usefulness of this approach for optimization of charge transport in metallopolymers. The charge transport diffusion coefficent was determined to (2.6 ± 0.5) x 10^-6 cm² s^-1 for a quaterthienyl-bridged {Os(tpy)₂} polymer by use of an electrochemical steady-state method carried out using a transistor-like experimental geometry. It was found that charge transport in these materials is concentration-gradient driven. The rate limiting step of the charge transport process was investigated using electrochemical impedance spectroscopy. The electropolymerisation dynamics of one of the monomers was studied using microelectrodes, and the results obtained shows that electropolymerisation is highly efficient, and indicate that mass transport controls this process. Through a combination of controlled potential deposition and SEM imaging it was demonstrated that it is possible to exploit the edge effect of microelectrodes to promote film growth in a direction co-planar with the electrode surface.

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22

Dyck, Richard Henry. "Cytochrome oxidase histopathology in the central nervous system of developing rats displaying methylmercury-induced movement and postural disorders." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/27873.

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Sprague-Dawley rats were administered daily, subcutaneous injections of methylmercuric chloride at a dose of 5 mg/Hg/kg beginning on postnatal day 5. By their fourth postnatal week, animals exhibited a constellation of neurological signs of motor impairment which resembled the cerebral palsy syndrome of humans perinatally exposed to methylmercury. Routine histological examination of the brain revealed no gross differences between methylmercury-treated (MeHg), normal control (NC) or weight-matched littermates. The histochemical localization of the mitochondrial enzyme cytochrome oxidase (CO) was utilized in Experiment I to examine possible alterations in the metabolic activity of motor nuclei which might contribute to the observed movement and postural disorders. A population of intensely-staining cytochrome oxidase neurons (ICONs) in the magnocellular portion of the red nucleus (RMC) and interrubral mesencephalon (IRM) were conspicuously present in all MeHg animals at the onset of motor impairment. These morphologically, histochemically, and anatomically distinct neurons did not exhibit intense CO staining in control animals. Conversely, a significant decrease was demonstrated in the oxidative metabolic activity of many neurons in the substantia nigra, zona reticulata of MeHg animals. In Experiment II, the postnatal appearance of ICONs was morphometrically quantified in MeHg animals sacrificed at PND 14, 16, 18, 20, 22, or 25. The histochemically-defined onset of increased metabolic activity in ICONs was first observed on PND 16, at least one week before the onset of clinical signs of neurological impairment. This was the earliest manifestation of methylmercury neurotoxicity yet described in this animal model. A subsequent four-fold increase in the total number of ICONs at PND 18 was followed by a gradual decrease in number to PND 25. Significantly more of the ICONs were found in the IRM than in the RMC at PND 18 & 20. The possibility that the increased activity of ICONs may result from disinhibition of specific afferents to the red nucleus was addressed by introducing either hemidecortication or hemicerebellectomy on PND 10 and then morphometrically determining the deviation from symmetry in the bilateral distribution of the total number of ICONs in the RMC and IRM at PND 22. The distribution of ICONs was symmetrical and not different in either hemidecorticate or unoperated controls. A significant (36%) decrease in the total number of ICONs was observed in both the RMC and IRM contralateral to hemicerebellectomy. The identical ipsilateral regions did not differ from control or hemidecorticate MeHg animals. In Experiment III, the anatomical distribution of major histocompatability complex antigens (MHC) in the brain of MeHg animals was examined using immunohistochemical methods. MHC immunoreactivity was widely distributed throughout the brain of MeHg animals. Areas with low immunoreactivity, or lack of it, stand out and include all of the hippocampus, thalamus, pyriform and entorhinal cortex, and lateral cerebellar hemispheres. Moderate staining intensity was observed in neocortical areas, basal forebrain, caudate-putamen and cerebellar vermis. Strong immunoreactivity was found in red nucleus, substantia nigra, cingulate cortex, retrosplenial cortex, presubiculum, parasubiculum and vestibular nuclei. It was suggested that the increased activity of ICONs likely contributes to the movement and postural disorders resulting from methylmercury intoxication. The increased activity in ICONs was determined to be, at least partially, dependent upon cerebellar input. The results are discussed with reference to the toxic effects of methylmercury and specifically to the susceptibility of GABAergic interneurons in perinatal trauma. Possible analogies are drawn between the mechanisms of methylmercury-induced cerebral palsy syndrome and those of other developmental movement and postural disorders.
Medicine, Faculty of
Graduate

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23

Aitken, Gillian Roxburgh. "Investigation of UV-induced reactive oxygen and nitrogen species in human skin cells and its association with the individual complexes of the mitochondrial electron transport chain." Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424156.

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24

Bergdoll, Lucie. "Purification et caractérisation d'un super-complexe respiratoire." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066310/document.

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Les membranes impliquées dans les processus bioénergétiques arborent une très grande densité de protéines, paramètre déterminant pour leur organisation supra-moléculaire. Dans ce travail, nous avons utilisé la bactérie thermophile Geobacillus stearothermophilus comme modèle pour étudier la formation de super-complexes de protéines membranaires, en vue d'une étude structurale. Nous avons purifié et caractérisé un super-complexe comprenant une menaquinol: cytochrome c oxydoréductase (b6c), un cytochrome c550 et une cytochrome c oxydase caa3. En combinant des titrations par spectroscopie optique et résonance paramagnétique électronique, nous avons pu déterminer les potentiels d'oxydo-réduction de la plupart des cofacteurs et combler ainsi une lacune dans l'étude des chaînes de transfert d'électrons utilisant des quinones à bas potentiel redox, les ménaquinones. Nous avons ainsi montré que les potentiels redox des cofacteurs du cytochrome b6c terminés par celui des quinones. Ce travail va à l'encontre de données partielles antérieures publiées, mais est en parfait accord avec les modèles du Q-cycle de Peter Mitchell. Les résultats obtenus ont des répercussions sur les rendements bioénergétiques des différents maillons de la chaîne de transfert
Bioenergetic membranes present a high protein density - a crucial factor for their organizationinto super-complexes. This project uses the thermophilic bacteria Geobacillus stearothermophilusas a model to study the formation of membrane protein super-complexes with the aim of structuralstudies. We purified and characterized a super-complex between a menaquinone : cytochromec oxidoreductase (b6c), a cytochrome c550, and a cytochrome c oxidase caa3. Using both opticaland EPR spectroscopy methods, we performed the redox titrations of most of the redox cofactorsof the super-complex. Thus, these results enable a new understanding of menaquinone-usingelectron transport chains, showing that quinones’ redox potential determines the redox potentialof the cytochrome b6c’s cofactors. The conclusions differ from previous partial data, althoughthey fit perfectly with Peter Mitchell’s model of the Q-cycle. These unexpected redox potentialsimpact bioenergetic yields at different levels of the electron transfer chain

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Mori, Mateus Prates. "Novo papel da proteína XPC na regulação dos complexos da cadeia de transporte de elétrons e desequilíbrio redox." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-20072015-105008/.

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Espécies reativas de oxigênio (EROs) são normalmente e continuamente geradas em mitocôndrias, majoritariamente na cadeia de transporte de elétrons (CTE). Harman (1956, 1972 e 1992) teorizou que os radicais livres gerados nas mitocôndrias seriam a principal causa do envelhecimento. De fato, durante o envelhecimento é observado um desequilíbrio entre formação e remoção de EROs, que resulta em estresse redox. Essa condição favorece a formação de lesões oxidadas no DNA, acarretando em mutagênese ou morte celular. Diversos mecanismos moleculares cooperam para o reparo de DNA. Duas vias de reparo de DNA lidam com a maioria das lesões: o reparo por excisão de base (BER) e o reparo por excisão de nucleotídeos (NER). A via BER corrige pequenas modificações de bases que surgem de reações de desaminação, alquilação e oxidação. A via NER é mais versátil, reconhecendo lesões que distorcem a dupla hélice de DNA, como danos induzidos por luz UV e adutos volumos. Pacientes xeroderma pigmentoso (XP-A a XP-G) herdam mutações em um de sete genes que codificam proteínas envolvidas na via NER, ou em um gene que codifica uma polimerase translesão (XP-V). A doença é caracterizada por fotosensibilidade e incidência elevada de neoplasias cutâneas. A proteína XPC atua na etapa de reconhecimento da lesão de DNA na subvia de reparo global do genoma (GG-NER), e sua mutação dá origem aos sintomas clássicos de XP. Novas funções de XPC foram recentemente descritas: i) atuando como cofator na via BER auxiliando as DNA glicosilases OGG1, TDG e SMUG; ii) atuando como cofator transcricional de elementos responsivos a Oct4/Sox2, RXR e PPARα; e iii) na adaptação metabólica na transformação de queratinócitos. Então, propusemo-nos a investigar as relações entre XPC e a manutenção da integridade do DNA mitocondrial, a sensibilidade celular a estresse redox mitocondrial e possíveis alterações bioenergéticas e redox. Para tal, padronizamos um ensaio in vitro de cinética de incisão em DNA plasmidial a fim de investigarmos o possível papel de XPC no reparo de lesões oxidadas em mtDNA. Porém, nossos dados revelaram que XPC não se encontra em mitocôndrias. Apesar disso, células XP-C são mais sensíveis ao tratamento com azul de metileno (AM), antimicina A (AA) e rotenona (ROT), que geram estresse redox mitocondrial. A sensibilidade à AA foi completamente revertida em células corrigidas. Células XP-C apresentaram alterações quanto ao uso dos complexos mitocondriais, com diminuição da taxa de consumo de oxigênio (OCR) via complexo I e um aumento da OCR via complexo II, dependente da presença de XPC. Ademais, a linhagem XP-C apresentou um desequilíbrio redox mitocondrial com maior produção de EROs e menor atividade de GPx. O DNA mitocondrial de células XP-C apresentou níveis elevados de lesão e deleção, que no entanto não retornaram aos níveis encontrados em células selvagens na linhagem XP-C corrigida. Observamos uma acentuada diminuição da expressão de PPARGC1A, um importante regulador de biogênese mitocondrial. Contudo, não foi possível determinar o mecanismo de supressão da expressão de PPARGC1A. Por fim, identificamos que o tipo de mutação em XPC pode estar associado a expressão de PPARGC1A. Esse estudo abre novas possibilidade na investigação do papel de proteína XPC, à parte da instabilidade genômica, na adaptação metabólica e desequilíbrio redox em direção da progressão tumoral.
Mitochondria continuously produce reactive oxygen species (ROS), mainly at the electron transport chain. Harman (1956, 1972 e 1992) proposed that normal aging is driven by increased mitochondrially generated free radicals. Indeed, during the course of aging there is an increased imbalance between formation and removal of ROS, leading to redox stress. This condition favours the formation of oxidized DNA lesions, given rise to mutations and cell death. Several molecular mechanisms cooperates to repair the DNA. Two DNA repair pathways deal with the majority of lesions: base excision repair (BER) and nucleotide excision repair (NER). The BER pathway corrects small base modifications that arise from deamination, alkylation and oxidation reactions. The NER pathway is more versitile, recognizing helix-distorting lesions, such as UV-induced damage and bulky adducts. Xeroderma pigmentosum (XP-A to XP-G) patients inherit mutations in one of seven protein-coding genes involved in NER pathway, or in a gene coding a translesion DNA polymerase (XP-V). Photosensitivity and a thousand-fold increased in the risk of developing cutaneous neoplasms are the main clinical features of XP. XPC protein functions in the recognition step of global genome NER (GG-NER) sub-pathway, and mutations in this gene lead to classical XP symptoms. Recently, it has been described that XPC acts: i) as a cofactor in BER pathway through functional interaction with DNA glycosylases OGG1, TDG and SMUG1; ii) as coactivator in transcription at Oct4/Sox2, RXR and PPARα responsive elements; iii) in metabolic shift during keratinocytes transformation. Thus, we sought to investigate a possible role for XPC in the maintenance of mtDNA integrity, cellular sensitivity to mitochondrial redox stress and eventual bioenergetic and redox changes. For this purpose, we established an in vitro plasmid incision assay to investigate the possible role of XPC in the repair of oxidized lesions in mitochondrial DNA. However, our data revealed that XPC did not localized in mitochondria. Nonetheless, XP-C cells are more sensitive to methylene blue, antimycin A (AA) and rotenone treatment, which induce mitochondrial redox stress. The XP-C sensitivity to AA was completely reverted in XPC-corrected cells. XP-C cells presented altered usage of mitochondrial complexes, with decreased oxygen consumption rate (OCR) via complex I and increased OCR through complex II, an XPC-dependent phenomenon. Furthermore, the XP-C cell line showed mitochondrial redox imbalance with increased ROS production and decrease GPx activity. MtDNA from XP-C cells accumulate lesions and deletions, which, however, were found at similar levels in the corrected cell line. We identified a sharp decrease in the expression of PPARGC1A, a master regulator of mitochondrial biogenesis. Nevertheless, it was not possible to determine the mechanism of suppression of PPARGC1A expression. Finally, our results suggest a possible link between the type of XPC mutation and PPARGC1A expression. This study unfolds new possible roles for XPC, aside from its established roles in genomic instability, in metabolic adaptation and redox imbalance towards tumour progression.

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Pashkovskaia, Natalia [Verfasser], Gerhard [Akademischer Betreuer] Rödel, Gerhard [Gutachter] Rödel, and Ben [Gutachter] Wielockx. "ROS generated by mitochondrial electron transport chain complexes I and III regulate differentiation of the pluripotent cell line P19 / Natalia Pashkovskaia ; Gutachter: Gerhard Rödel, Ben Wielockx ; Betreuer: Gerhard Rödel." Dresden : Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2018. http://d-nb.info/1154680363/34.

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Sousa, Rafael Augusto Teixeira de. "Fisiopatologia do Transtorno de Humor Bipolar e efeito do tratamento com lítio: enfoque em neuroproteção e função mitocondrial." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5142/tde-05052014-142705/.

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Introdução: Diversas evidências apontam para um papel da disfunção mitocondrial no Transtorno de Humor Bipolar (THB), mas pouco se sabe sobre isso no THB de início recente. Na mitocôndria a atividade da cadeia transportadora de elétrons (CTE) atua juntamente com o ciclo do ácido cítrico na produção de energia, mas não está claro se estão alteradas no THB. O DNA mitocondrial (DNAmt) codifica diversas proteínas da CTE e está associado ao estresse oxidativo, mas nunca foi avaliado em pacientes no THB in vivo. O estresse oxidativo está associado ao THB e à disfunção mitocondrial, mas não se sabe muito das atividades das enzimas antioxidantes no THB de início recente. O óxido nítrico (NO) é uma molécula com efeitos neuromoduladores, mas com um papel no THB ainda não elucidado. O lítio é um tratamento padrão-ouro no THB, tendo mostrado efeitos neuroprotetores. Apesar disso, pouco se conhece do efeito do lítio na CTE, nas enzimas do ciclo do ácido cítrico, no conteúdo de DNAmt e na regulação de NO em humanos. Também não está claro o papel antioxidante do lítio no THB. Metódos: Pacientes com THB em depressão (n=31), não medicados em sua maioria (84%), foram tratados por 6 semanas com lítio. Antes e depois do tratamento, verificaram-se em leucócitos as atividades dos complexos I-IV da CTE, atividades das enzimas citrato sintase, succinato desidrogenase e malato desidrogenase e também o conteúdo de DNAmt; em plasma foram analisados os níveis de NO, substâncias reativas ao ácido tiobarbitúrico (TBARS) e as atividades de catalase (CAT), glutationa peroxidase (GPx), superóxido dismutase (SOD) e razão de SOD/CAT. Os pacientes com depressão bipolar foram comparados com 28 controles saudáveis. Resultados: Em comparação com controles, os pacientes com THB tiveram um aumento de GPx (p < 0,001) e CAT (p=0,005) e uma diminuição de SOD/CAT (p=0,001), sem outras diferenças nos demais biomarcadores. Pacientes com THB I mostraram uma diminuição de citrato sintase (p=0,02) e uma discreta diminuição do conteúdo de DNAmt (p=0,05) em comparação com o THB II; o conteúdo de DNAmt esteve ligeiramente diminuído no THB I comparado com controles (p=0,05). Do início ao fim do tratamento com lítio houve aumento da atividade do complexo I da CTE (p=0,02), diminuição de TBARS (p=0,02) e SOD (p=0,03) e aumento de NO (p=0,02), sem haver alteração de outros parâmetros. Depois do tratamento, o TBARS se mostrou diminuído em respondedores comparados a não respondedores (p=0,02) e diminuído no THB II em comparação com o THB I (p=0,04). Discussão: No THB de início recente, houve poucas alterações em biomarcadores. Os achados sugerem aumento de CAT e GPx na depressão bipolar de início recente e uma diminuição de conteúdo mitocondrial no THB I comparado com o THB II, que devem ser confirmadas por outros estudos. Os resultados reforçam um papel neuroprotetor do lítio, sugerindo que a droga aumente a atividade do complexo I da CTE mitocondrial e aumente os níveis de NO na depressão bipolar. Além disso, o lítio reforçou o seu papel antioxidante e modulador das enzimas antioxidantes no THB
Background: Several evidences point to a role for mitochondrial dysfunction in Bipolar Disorder (BD), but few is known about it on short-term BD. In mitochondria the electron transport chain (ETC) acts jointly with citric acid cycle to produce energy, but it is not clear if they are altered in BD. Mitochondrial DNA (mtDNA) encodes several ETC proteins and is associated with oxidative stress, but it was never evaluated in BD in vivo. Oxidative stress is associated with BD and with mitochondrial dysfunction, but few is known about the activities of antioxidant enzymes in short-term BD. Nitric oxide (NO) is a molecule with neuromodulatory effects, but with an unclear role in BD. Lithium is a gold-standard treatment for BD, which has shown neuroprotective effects. However, few is known about lithium effect on ETC, citric acid cycle, mtDNA content, and NO regulation in humans. Also, lithium\'s antioxidant role in BD is unclear. Methods: Patients with BD depression (n=31) unmedicated in majority (84%) received lithium treatment for 6 weeks. Before and after treatment, in leukocytes the activities of ETC complex I-IV, citrate synthase, succinate dehydrogenase, and malate dehydrogenase, and mtDNA content were evaluated; in plasma, NO levels, thiobarbituric acid reactive substances (TBARS), the activities of catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD), and SOD/CAT ratio were evaluated. Bipolar depression patients were compared with 28 healthy controls. Results: When compared with controls, BD patients showed an increase in GPx (p < 0.001) and CAT (p=0.005) and a decrease in SOD/CAT (p=0.001), but showed no difference for other biomarkers. Patients with BD I showed a decrease in citrate synthase (p=0.02) and a slight decrease in mtDNA content (p=0.05) when compared to BD II; mtDNA content was slightly decreased in BD I compared to controls (p=0.05). From baseline to endpoint, there was an increase in ETC complex I activity (p=0.02), a decrease in TBARS (p=0.02) and SOD (p=0.03) and an increase in NO (p=0.02), without change in other parameters. After treatment, TBARS was decreased in responders compared to non-responders (p=0.02) and decreased in BD II compared to BD I (p=0.04). Discussion: In short-term BD few alterations were observed on biomarkers. The findings suggest increase on CAT and GPX in short-term bipolar depression and mitochondrial content decrease in BD I when compared to BD II, which deserve other studies for confirmation. The results reinforce a lithium\'s neuroprotective role and suggest that lithium increases ETC complex I activity and NO levels in bipolar depression. Moreover, lithium reinforced its role as antioxidant and as a modulator of antioxidant enzymes in BD

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Pisanty, Alatorre Emilio. "Electron dynamics in complex time and complex space." Thesis, Imperial College London, 2016. http://hdl.handle.net/10044/1/43538.

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This thesis investigates the dynamics of electrons ionized by strong low frequency laser fields, from a semiclassical perspective, developing a trajectory-based formalism to describe the interactions of the outgoing electron with the remaining ion. Trajectory models for photoionization generally arise in the regime known as optical tunnelling, where the atom is subjected to a strong, slow field, which tilts the potential landscape around the ion, forming a potential energy barrier that electrons can then tunnel through. There are multiple approaches that enable the description of the ionized electron, but they are generally limited or models derived by analogy, and the status of the trajectories is unclear. This thesis analyses this trajectory language in the context of the Analytical R-Matrix theory of photoionization, deriving a trajectory model from the fundamentals, and showing that this requires both the time and the position of the trajectory to be complex. I analyse this complex component of the position and I show that it requires careful handling: of the potentials where it appears, and of the paths in the complex plane that the trajectory is taken through. In this connection, I show that the Coulomb potential of the ion induces branch cuts in the complex time plane that the integration path needs to avoid, and I show how to navigate these branch cuts. I then use this formalism to uncover a kinematic mechanism for the recently discovered (Near-)Zero Energy Structures of above-threshold ionization. In addition, I analyse the generation of high-order harmonics of the driving laser that are emitted when the photoelectron recollides with the ion, using a pair of counter-rotating circularly polarized pulses to drive the emission, both in the context of the conservation of spin angular momentum and as a probe of the long-wavelength breakdown of the dipole approximation.

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Levett, Philip Charles. "New electron transport inhibitors." Thesis, University of Nottingham, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.357948.

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Wilson, Emma Katherine. "Electron transfer in and complex assembly of the trimethylamine dehydrogenase-electron transfer flavoprotein complex." Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627132.

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Restivo, Rick A. "Free electron laser weapons and electron beam transport." Monterey, Calif. : Springfield, Va. : Naval Postgraduate School ; Available from National Technical Information Service, 1997. http://handle.dtic.mil/100.2/ADA333358.

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Bühler-Paschen, Silke. "Electron transport in polymer composites /." [S.l.] : [s.n.], 1995. http://library.epfl.ch/theses/?nr=1365.

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Emberly, Eldon. "Electron transport in molecular wires." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ51858.pdf.

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Hirst, Judy. "Electron transport in redox enzymes." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364043.

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Nandha, Beena. "Regulation of photosynthetic electron transport." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.502263.

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Investigations in this thesis aimed to understand the mechanisms that regulate the photosynthetic electron transport chain in C3 plants and therefore also the significance of cyclic electron flow (CEF). Physiological analysis of Arabidopsis thaliana photosynthetic pgr5 mutant, which had previously been reported to be a CEF mutant, were undertaken. The reduced state of P700 in the light meant that standard assays for P700 and CEF, using P700 absorbance could not be applied. Design and development of flash spectrophotometric techniques were necessary. This primarily involved P700 oxidation kinetics at 820 nm combined with the electrochromic shift at 520 nm to measure electrical field generation.

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Ng, Tao-Cheung Timothy. "Electron transport in narrow channels." Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385955.

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Wilowska, A. C. "Modelling electron transport in photosynthesis." Thesis, Imperial College London, 1985. http://hdl.handle.net/10044/1/37899.

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Nilwala, Gamaralalage Premasiri Kasun Viraj Madusanka. "Electron Transport in Chalcogenide Nanostructures." Case Western Reserve University School of Graduate Studies / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=case1572259784431038.

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Bell, Louise Carol. "Electron transport reactions of denitrification." Thesis, University of Oxford, 1990. https://ora.ox.ac.uk/objects/uuid:9625557a-fe52-4c94-bc1f-a544275df344.

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A study is reported which demonstrates that electron transport to the reductase reactions of denitrification in the bacterium Thiosphaera pantotropha can occur aerobically. Use of dark-type electrodes has demonstrated that the N₂O reductase enzyme of this organism is active under aerobic conditions, and that O₂ and N₂O reduction can occur simultaneously. The reduction of NO₃^- to N₂ gas, even under aerobic conditions, is shown to proceed via NO as an intermediate. It is concluded that the reaction of NO with O₂ must be sufficiently slow that it does not effectively compete with the reduction of NO to N₂O. The ability of T. pantotropha to catalyse aerobic NO₃^- reduction, the first step of the aerobic denitrification process, is shown to correlate with the expression of a NO₃^- reductase enzyme that is located in the periplasm. This periplasmic enzyme is expressed, and is active, under both aerobic and anaerobic conditions. A membrane bound NO₃^- reductase is also expressed, but only under anaerobic conditions, by this organism. This latter reductase resembles the NO₃^- reductase of Paracoccus denitrificans in respect of both its catalytic properties and the inhibition of activity in intact cells under aerobic conditions. Mutants of T. pantotropha that lack the membrane bound NO₃^- reductase, and not only retain but overproduce the periplasmic enzyme, have been obtained via Tn5 mutagenesis. The periplasmic NO₃^- reductase identified in T. pantotropha bears catalytic and structural similarities to an enzyme previously characterised in some strains of Rhodobacter capsulatus. The ability of strains of R. capsulatus to reduce NO to N₂O is reported together with evidence that there is a discrete NO reductase in this organism. The electron transport pathway to NO reductase has been elucidated. The first identification of a denitrifying strain of R. capsulatus is reported.

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Carroll, Bryan Thomas. "Characterization of Stomatin Suppressors ssu-1 AND ssu-2." Connect to text online, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1121454937.

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Negri, Carlotta. "Controlling electron transport : quantum pumping and single-electron tunneling oscillations." Thesis, Bordeaux 1, 2012. http://www.theses.fr/2012BOR14670/document.

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Exploiter des effets dépendants du temps pour induire et contrôler des courants à travers des conducteurs mésoscopiques et nanoscopiques est un enjeu majeur dans le domaine du transport quantique. Dans cette thèse, nous considérons deux systèmes de taille nanométrique pour lesquels un courant est induit grâce au couplage entre champs extérieurs dépendants du temps et le transport d'électrons. Nous étudions d'abord un problème de pompage quantique au sein d'un système à trois sites en configuration d'anneau, en considérant la possibilité d'induire un courant continu par modulation temporelle des paramètres de contrôle. Nous nous intéressons en particulier à la transition entre régime adiabatique et antiadiabatique en présence d'un mécanisme de dissipation modélisé par un couplage entre le système et un bain extérieur.Nous montrons que le modèle dissipatif admet une solution analytique complète valable pour la composante DC du courant à fréquence arbitraire. Ceci nous permet de bien comprendre comment le courant induit dépend de la fréquence de pompage. Nous nous concentrons ensuite sur un autre système de contrôle du courant exploitant le phénomène des oscillations tunnel à un électron (SETOs). Contrairement au cas précédent, ici la circulation d'un courant continu à travers un circuit comportant une jonction tunnel produit, pour le régime approprié, un courant quasi-périodique d'électrons. On étudie le spectre de bruit à température nulle d'une jonction tunnel dans différents environnements résistifs dans le but de déterminer les limites du régime des SETOs et de quantifier leur degré de périodicité. Nous généralisons par la suite les résultats à température finie et discutons des effets des fluctuations quantiques
Exploiting time-dependent effects to induce and control currents through mesoscopic and nano\-scopic conductors is a major challenge in the field of quantum transport. In this dissertation we consider two nanoscale systems in which a current can be induced through intriguing mechanisms of coupling between excitations by external fields and electron transport.We first study a quantum pumping problem, analyzing the possibility to induce a DC response to an AC parametric driving through a three-site system in a ring configuration. We are interested in particular in the crossover between adiabatic and antiadiabatic driving regimes and in the presence of dissipation, which is accounted for by coupling with an external bath. We show that for a clever choice of this coupling the dissipative model admits a full analytical solution for the steady state current valid at arbitrary frequency, which allows us to fully understand the pumping-frequency dependence of the induced current. We then focus on a different current-controlling scheme exploiting the phenomenon of single-electron tunneling oscillations (SETOs). In this case, opposite to what happens for pumping, an AC effect, an almost periodic current of single electrons, arises through a tunnel junction circuit as a consequence of a DC bias. We study the zero-temperature noise spectrum of a tunnel junction in different resistive environments with the aim to determine the boundaries of the SETOs regime and quantify their quality in terms of periodicity. We then discuss the finite-temperature generalization and the possibility to account for the effects of quantum fluctuations

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42

Nicolaides, Christos. "Anomalous transport in complex networks." Thesis, Massachusetts Institute of Technology, 2011. http://hdl.handle.net/1721.1/66871.

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Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Civil and Environmental Engineering, 2011.
Cataloged from PDF version of thesis.
Includes bibliographical references (p. 43-45).
The emergence of scaling in transport through interconnected systems is a consequence of the topological structure of the network and the physical mechanisms underlying the transport dynamics. We study transport by advection and diffusion in scale-free and Erdős-Rényi networks. Using stochastic particle simulations, we find anomalous (nonlinear) scaling of the mean square displacement with time. We show the connection with existing descriptions of anomalous transport in disordered systems, and explain the mean transport behavior from the coupled nature of particle jump lengths and transition times. Moreover, we study epidemic spreading through the air transportation network with a particle-tracking model that accounts for the spatial distribution of airports, detailed air traffic and realistic (correlated) waitingtime distributions of individual agents. We use empirical data from US air travel to constrain the model parameters and validate the model's predictions of traffic patterns. We formulate a theory that identifies the most influential spreaders from the point of view of early-time spreading behavior. We find that network topology, geography, aggregate traffic and individual mobility patterns are all essential for accurate predictions of spreading.
by Christos Nicolaides.
S.M.

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Dasgupta, Subho. "Tuneable electron transport in metallic nanostructures." Eggenstein-Leopoldshafen Forschungszentrum Karlsruhe GmbH, 2009. http://d-nb.info/999765485/34.

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Diaconescu, Dorina. "Ballistic electron transport in mesoscopic samples." [S.l. : s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=962295191.

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Smedja, Bäcklund Anna. "Electron transport in microbial chlorate respiration." Licentiate thesis, Karlstad University, Faculty of Technology and Science, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:kau:diva-3777.

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Several bacterial species are capable to use perchlorate and/or chlorate as an alternative electron acceptor in absence of oxygen. Microbial respiration of oxochlorates is important for biotreatment of effluent from industries where oxochlorates are produced or handled. One of these species, the Gram-negative Ideonella dechloratans, is able to reduce chlorate but not perchlorate. Two soluble enzymes, chlorate reductase and chlorite dismutase, participate in the conversion of chlorate into chloride and molecular oxygen. The present study deals with the electron transport from the membrane-bound components to the periplasmic chlorate reductase. Soluble c cytochromes were investigated for their ability to serve as electron donors to chlorate reductase. The results show that a 6 kDa c cytochrome serves as electron donor for chlorate reductase. This cytochrome also serves as electron donor for a terminal oxidase in the reduction of oxygen that is produced in the course of chlorate respiration. A gene encoding a soluble c cytochrome was found in close proximity to the gene cluster for chlorate reduction. This gene was cloned and expressed heterologously, and the resulting protein was investigated as a candidate electron donor for chlorate reductase. Electron transfer from this protein could not be demonstrated, suggesting that the gene product does not serve as immediate electron donor for chlorate reductase.

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Rolfe, Stephen Alexander. "Electron transport in cyanobacterial photosystem II." Thesis, University of Cambridge, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.258430.

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47

Burrows, P. E. "Electron Transport in Langmuir-Blodgett films." Thesis, Queen Mary, University of London, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531005.

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Hoffmann, James A. "Electron transport in interacting quantum wires." Virtual Press, 2003. http://liblink.bsu.edu/uhtbin/catkey/1259758.

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Nanoscale wires and molecules have remarkable electrical properties that make them well suited for new electronic devices. The projected device densities result in very small separation distances and therefore the possibility of device-device interactions. However, we do not know what impacts wire-wire interactions might have on the properties of closely spaced devices. If two quantum wires interact, what types of effects will there be on transport properties such as conductance? How would the coupling strength, length of wire, position of contact, or the energy of the electrons affect conductance? Understanding the effects of the interactions will assist the construction of efficient nanoscale devices.This thesis examined the effects of interaction on the low-field conductance using a simple classical model and two quantum models of coupled quantum wires fabricated electrostatically in the two-dimensional electron gas at the interface of the heterostructure A1GaAs/GaAs. We considered the effect of position and length of an interaction between two parallel quantum wires formed by hard wall boundaries and connected to electron reservoirs. Our second model consisted of two artificial molecular wires, i.e., parallel chains of quantum dots. We used a one-electron Schrodinger equation in the envelope approximation, a tight-binding Hamiltonian, and a recursive Green's function method to study the electron transport properties. Multi-parameter computations using a fortran-95 computer model provided data for an analysis of the relationships among conductance, the interaction strength, interaction location, and electron energy.In contrast to the monotonic changes predicted by the classical model, the lowfield conductance of interacting hard wall quantum wires varies in an oscillatory manner with the perturbing interaction strength and position. For electron energies below the first conductance plateau, Breit-Wigner resonances appear as a consequence of coupling. These conductance properties are explained with reference to quasi-bound states created by reflections at the end boundaries of the wires and the separating wall.At low electron energies, the conductance signature of a symmetric artificial molecule composed of serial quantum dots is a band of resonances. Coupled artificial molecular wires display a split-off molecular band with an energy separation that grows with the coupling strength and a bandwidth that narrows. The position of the Fermi energy relative to the molecular band states plays a dominant role in determining the lowfield conductance of interacting artificial molecules. The conductance variation with coupling ranges from oscillatory to monotonic, depending on the Fermi energy. Varying the atom-atom coupling position in the molecular wires causes a relatively small shift in the resonance band energies.
Department of Physics and Astronomy

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Bailey, Steven W. D. "Single electron transport in carbon nanotubes." Thesis, Lancaster University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289056.

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Mavroidis, Constantinos. "Electron transport in GaN epitaxial layers." Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407135.

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Dissertations / Theses on the topic 'Electron transport Complex I'

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