Rozprawy doktorskie na temat „Adenosine”
Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych
Sprawdź 50 najlepszych rozpraw doktorskich naukowych na temat „Adenosine”.
Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.
Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.
Przeglądaj rozprawy doktorskie z różnych dziedzin i twórz odpowiednie bibliografie.
Zanoli, Juliana Carla Castanha [UNESP]. "Efeitos da abamectina na bioenergética de mitocôndrias isoladas de fígado de rato: Juliana Carla Castanha Zanoli. -". Universidade Estadual Paulista (UNESP), 2011. http://hdl.handle.net/11449/94732.
Pełny tekst źródłaAbamectina é uma lactona macrocíclica pertencente à família das avermectinas, utilizada mundialmente como agente antiparasitário em animais de criação e estimação, além do emprego agrícola como princípio ativo dos inseticidas e nematicidas. Mitocôndrias são responsáveis pela conversão da energia liberada pelo transporte de elétrons e armazenamento como energia de ligação na molécula de ATP, um componente metabólico essencial. Interferências em sua síntese ou utilização caracterizam mecanismos pelos quais os xenobióticos podem expressar toxicidade aguda ou crônica. Neste trabalho, os efeitos da abamectina na bioenergética de mitocôndrias isoladas de fígado de rato foram avaliados. Nas concentrações utilizadas (5 a 25 µM), abamectina causou inibição da cadeia respiratória, sem afetar a atividade das enzimas NADH desidrogenase, succinato desidrogenase e o potencial de membrana, comportando-se de maneira semelhante à oligomicina e ao atractilosídeo. A principal atuação da abamectina foi reduzir o potencial mitocondrial de fosforilação oxidativa, diminuindo os níveis de ATP provavelmente como resultado de sua ação direta sobre a FoF1-ATPase, uma vez que inibiu a atividade desta enzima, e/ou sobre o translocador de ADP/ATP. A inibição mais acentuada da atividade fosfohidrolase em mitocôndrias intactas desacopladas do que em mitocôndrias rompidas juntamente com a inibição da despolarização do potencial de membrana induzida pelo ADP sugerem que a abamectina atuou inibindo mais especificamente o translocador de ADP/ATP do que a FoF1-ATPase
Abamectin is a macrocyclic lactone belonging to the avermectin family, used worldwide as antiparasitic agent in farm animals and pets, and agricultural employment as the active ingredient of insecticides and nematicides. Mitochondria are responsible for converting the energy released by electron transport and storage as the binding energy molecule ATP, an essential metabolic component. Interference in its synthesis or utilization characterize mechanisms by which xenobiotics can express acute or chronic toxicity. In this study, the effects of abamectin in the bioenergetics of mitochondria isolated from rat liver were evaluated. At the concentrations used (5-25 mM), abamectin caused inhibition of the respiratory chain without affecting the activity of enzymes NADH dehydrogenase, succinate dehydrogenase and the membrane potential, behaving similarly to oligomycin and Atractyloside. The main activity of abamectin was to reduce the potential of mitochondrial oxidative phosphorylation, decreasing ATP levels probably as a result of its direct action on the Fo-F1 ATPase, since it inhibited the activity of this enzyme, and/or the ADP/ATP translocator. The more pronounced inhibition of the fosfohydrolase activity in intact uncoupled mitochondria than in disrupted mitochondria, in addition to the inhibition of the ADP-stimulated depolarization of mitochondrial membrane potential suggest that abamectin acted more specifically by inhibiting the ADP/ATP translocator than the FoF1-ATPase
Dulla, Chris. "Adenosine and adenosine triphosphate link Pco2 to cortical excitability via pH /". Connect to full text via ProQuest. IP filtered, 2005.
Znajdź pełny tekst źródłaSoledade, Cinira Santana. "O efeito do DMA (composto quinazolinico) sobre o processo inflamatorio". [s.n.], 2008. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310436.
Pełny tekst źródłaTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
Made available in DSpace on 2018-08-13T01:28:13Z (GMT). No. of bitstreams: 1 Soledade_CiniraSantana_D.pdf: 1680992 bytes, checksum: 98f3f468653137a8796c59f9d6297f89 (MD5) Previous issue date: 2008
Resumo: A inflamação é apontada como o principal processo mediador das diversas doenças do tecido conjuntivo e um componente importante da fisiopatologia das doenças infecciosas. Mais recentemente também tem lhe sido atribuído papel de destaque na obesidade, diabetes e doenças cardiovasculares, em especial a aterosclerose. Dentre os vários mediadores envolvidos no processo inflamatório, a adenosina tem sido apontada como um potente mediador endógeno. A adenosina é um autacóide, cuja ação se dá pela interação com quatro receptores de superfície celular (A1, A2A, A2B e A3), sendo a sua concentração modulada pelo equilíbrio entre os processos de síntese (5- nucleotidases), fosforilação (adenosina quinase), e deaminação (adenosina deaminase). A adenosina sabidamente age em múltiplos aspectos do processo inflamatório, como: apoptose, migração de leucócitos, liberação de mediadores (citocinas, quimiocinas) e mecanismos vasoregulatórios. No nível celular os efeitos da adenosina incluem várias vias de sinalização, modulando a ativação de importantes fatores de transcrição como o NF-?B. Neste contexto, a imunomodulação exercida pela adenosina tem seu potencial terapêutico reconhecido e avaliado na literatura, através do estudo de compostos que agem sobre seus receptores específicos ou através do aumento de sua concentração. O objetivo geral deste trabalho foi avaliar as propriedades antiinflamatórias e mecanismos de ação de um novo composto, inibidor de adenosina quinase (6,7-dimetóxi-4-N-(3'-N,N-dimetilfenil)aminoquinazolina, DMA), cuja ação resulta no aumento da concentração tecidual de adenosina. Para isso, foram utilizados modelos de inflamação aguda em animais de experimentação e ensaios in vitro em cultura de células. No modelo de peritonite aguda induzida por thioglicolato em camundongos, o tratamento com DMA reduziu o acúmulo de neutrófilos, (?55%, p < 0,05) e esse efeito foi bloqueado por um antagonista de receptor de adenosina, a 8-sulpho-phenil- theophilina. Ainda neste modelo, houve diminuição de Interleucina-6 no exudato dos animais tratados com DMA (?35%; p < 0,005). O DMA também foi efetivo na redução da inflamação nos modelos de artrite aguda em ratos, reduzindo o volume articular (?30% na segunda hora e ?35% na quarta hora; p < 0,05), número de leucócitos no líquido sinovial (?50% ; 28,6 x 106 ± 5,2 células/ml vs. 13,8 x 106 ± 1,7 células/ml; p < 0,05) e escala de dor (2,62 ± 0,18 vs. 1,53 ± 0,136; p < 0,05). No modelo de edema de pata induzidos por carragenina demonstrou-se uma redução do edema
Abstract: : Inflammation has a main role in several connective tissue diseases and is an important element of infectious disease physiopathology. Recently it has been linked to obesity, diabetes and cardiovascular diseases. Adenosine, among the various inflammatory process mediators, is a potent autocoid and its bioavailability is limited by catabolism to inosine by adenosine deaminase or by salvage following cellular uptake via adenosine kinase (ADK). Once in extracellular space adenosine interacts with specific cell-surface receptors (A1, A2, A2B, A3) and acts on multiples aspects of the inflammatory process: apoptosis, leukocyte migration, release of proinflammatory cytokines and vascular regulation. At cellular level adenosine acts in a wide-range of pathways, modulating important transcription factors like NF-?B. Based on these premises, adenosine immune regulatory properties and potential in therapeutics have been acknowledged and investigated through the study of specific receptors agonists and compounds able to increase its concentration. The main objective of this study was to evaluate the antiinflammatory properties and mechanisms of DMA, a novel adenosine kinase inhibitor, which increases adenosine tissue concentration. In order to accomplished that, animal models of acute inflammation and cell culture assay were used. DMA was orally effective to reduce neutrophils migration (~55%; p < 0,05) and IL-6 concentration (~35%; p < 0,005) in the aseptic thioglycollate peritonitis model. DMA significantly inhibited arthritis in an acute arthritis carrageenan model, decreasing articular volume (~30% second hour and ~35% fourth hour, p < 0,05), leukocytes on synovial liquid (~50% ; 28,6 x 106 ± 5,2 cells/ml vs. 13,8 x 106 ± 1,7 cells/ml; p < 0,05) and pain score (2,62 ± 0,18 vs. 1,53 ± 0,136; p <0 ,05). DMA was also effective in reducing edema in the carrageenan-induced paw edema model (~30% second hour and 36% fourth hour; p < 0,05) and pain in the second phase of the "Liking test" induced by formalin (~40% in liking time; p < 0,01). In vitro, macrophage expression of TLR4, an important cell receptor in recognizing and processing antigens, was decreased after DMA treatment. The results suggest that DMA also impacts the inflammatory cascade by modulating inflammatory related nuclear transcription. It was demonstrated that DMA was also able to inhibit macrophages and neutrophils, LPS induced NF-?B activation and promote PPAR activation in THP-1 cells. Antiinflammatories are drugs in high demand, but their use is still limited by side-effects. The DMA is a novel, potent non-nucleoside ADK inhibitor, orally effective to improve inflammation in some well characterized animal models and in vitro assays. New studies, based on this data, will be design to further explore the therapeutic use of DMA in inflammatory diseases
Doutorado
Ciencias Basicas
Doutor em Clínica Médica
Zanoli, Juliana Carla Castanha. "Efeitos da abamectina na bioenergética de mitocôndrias isoladas de fígado de rato / Juliana Carla Castanha Zanoli. -". Araçatuba : [s.n.], 2011. http://hdl.handle.net/11449/94732.
Pełny tekst źródłaBanca: Flavia Thomaz Verechia Pereira
Banca: Tiago Rodrigues
Resumo: Abamectina é uma lactona macrocíclica pertencente à família das avermectinas, utilizada mundialmente como agente antiparasitário em animais de criação e estimação, além do emprego agrícola como princípio ativo dos inseticidas e nematicidas. Mitocôndrias são responsáveis pela conversão da energia liberada pelo transporte de elétrons e armazenamento como energia de ligação na molécula de ATP, um componente metabólico essencial. Interferências em sua síntese ou utilização caracterizam mecanismos pelos quais os xenobióticos podem expressar toxicidade aguda ou crônica. Neste trabalho, os efeitos da abamectina na bioenergética de mitocôndrias isoladas de fígado de rato foram avaliados. Nas concentrações utilizadas (5 a 25 µM), abamectina causou inibição da cadeia respiratória, sem afetar a atividade das enzimas NADH desidrogenase, succinato desidrogenase e o potencial de membrana, comportando-se de maneira semelhante à oligomicina e ao atractilosídeo. A principal atuação da abamectina foi reduzir o potencial mitocondrial de fosforilação oxidativa, diminuindo os níveis de ATP provavelmente como resultado de sua ação direta sobre a FoF1-ATPase, uma vez que inibiu a atividade desta enzima, e/ou sobre o translocador de ADP/ATP. A inibição mais acentuada da atividade fosfohidrolase em mitocôndrias intactas desacopladas do que em mitocôndrias rompidas juntamente com a inibição da despolarização do potencial de membrana induzida pelo ADP sugerem que a abamectina atuou inibindo mais especificamente o translocador de ADP/ATP do que a FoF1-ATPase
Abstract: Abamectin is a macrocyclic lactone belonging to the avermectin family, used worldwide as antiparasitic agent in farm animals and pets, and agricultural employment as the active ingredient of insecticides and nematicides. Mitochondria are responsible for converting the energy released by electron transport and storage as the binding energy molecule ATP, an essential metabolic component. Interference in its synthesis or utilization characterize mechanisms by which xenobiotics can express acute or chronic toxicity. In this study, the effects of abamectin in the bioenergetics of mitochondria isolated from rat liver were evaluated. At the concentrations used (5-25 mM), abamectin caused inhibition of the respiratory chain without affecting the activity of enzymes NADH dehydrogenase, succinate dehydrogenase and the membrane potential, behaving similarly to oligomycin and Atractyloside. The main activity of abamectin was to reduce the potential of mitochondrial oxidative phosphorylation, decreasing ATP levels probably as a result of its direct action on the Fo-F1 ATPase, since it inhibited the activity of this enzyme, and/or the ADP/ATP translocator. The more pronounced inhibition of the fosfohydrolase activity in intact uncoupled mitochondria than in disrupted mitochondria, in addition to the inhibition of the ADP-stimulated depolarization of mitochondrial membrane potential suggest that abamectin acted more specifically by inhibiting the ADP/ATP translocator than the FoF1-ATPase
Mestre
Silva, Aleksandro Schafer da. "Atividade da adenosina desaminase, concentração de nucleotideos e nucleosideo de adenina em ratos Infectados com Trypanosoma evansi". Universidade Federal de Santa Maria, 2011. http://repositorio.ufsm.br/handle/1/4058.
Pełny tekst źródłaThe purinergic system is known to be an important signaling pathway in different tissues. Among the components of this system have adenosine, a modulator of central nervous, circulatory and immune systems. The concentration of adenosine in the host is controlled by the enzyme adenosine deaminase (ADA), present in tissues, cells and fluids. As a result, the objectives of this study were (1) to determine the ADA activity in Trypanosoma evansi, (2) evaluate the activity of ADA in serum, erythrocytes, lymphocytes and brain of infected rats, and (3) determine the concentration of nucleotides and nucleosides in serum and cerebral cortex of rats infected with T. evansi. In the first study two mice were infected with T. evansi. When these animals showed high parasitemia (±108 parasites/uL) was performed with blood collection and separation of trypomastigotes by DEAE-cellulose column for performing the assays. Spectrometry was performed by the biochemical detection of ADA in the form trypomastigotes of T. evansi. In a second study, we used 39 rats divided into three groups: group A and B (infected) and group C (C1 and C2 control group) Samples of blood and brain samples were collected on day 4 PI (A and C1) and 20 PI (B and C2). From the blood (with anticoagulant) were separated lymphocytes and erythrocytes for measurement of ADA activity, since the serum was obtained from blood samples stored in tubes without anticoagulant. The brain was separated into cerebellum, cerebral cortex, hippocampus and striatum to evaluate the ADA activity in each structure. Decrease of ADA activity in serum and erythrocytes in rats infected with T. evansi when compared not-infected (P<0.05). ADA activity in lymphocytes was decreased at day 4 PI and increased in day 20 PI. There was no difference in ADA activity in the cerebellum. In the cerebral cortex caused a reduction of ADA activity on days 4 and 20 PI. Decrease of ADA activity in hippocampus and striatum in the day 4 and day 20 PI, respectively. In a third study, 24 rats were used, 12 used as a negative control and 12 infected with T. evansi. On day 4 (n = 6 per group) and 20 PI (n = 6 per group) were performed to obtain blood samples of serum and cerebral cortex for analysis. The samples were prepared for quantification of ATP, ADP, AMP and adenosine. This study found increased concentrations of ATP, AMP and adenosine in the brain and serum of rats infected with T. evansi in both periods, except that the levels of adenosine decreased on day 4 PI. The ADP concentration did not change in this study. Therefore, the infection by T. evansi purinergic system components can be changed, may be involved in immune response, in anemia and neurological signs.
O sistema purinérgico é conhecido por ser uma via de sinalização importante em diversos tecidos. Entre os componentes desse sistema destacamos a adenosina, um modulador do sistema nervoso central, circulatório e imunológico. A concentração de adenosina no hospedeiro é controlada pela enzima adenosina deaminase (ADA), presentes em tecidos, células e fluidos. Em virtude disso, os objetivos deste estudo foram (1) determinar a atividade da ADA no Trypanosoma evansi; (2) avaliar a atividade da ADA no soro, eritrócitos, linfócitos e encéfalo e (3) determinar a concentração de nucleotídeos e nucleosideos no soro e córtex cerebral de ratos infectados com T. evansi. Para um primeiro estudo foram infectados dois camundongos com T. evansi. Quando estes animais apresentavam elevada parasitemia (±108 parasito/μL) foi realizada a coleta de sangue e separação dos flagelados por coluna de DEAE-celulose, a fim realização dos ensaios enzimáticos no parasito. Atividade da ADA nas formas trypomastigotas de T. evansi foi determinada por espectofotometria. Em um segundo estudo foi utilizado 39 ratos, divididos em três grupos: grupo A e B (infectado) e grupo C (C1 e C2/controle). Amostras de sangue e encéfalo foram colhidas nos dias 4 pós-infecção (PI) (grupos A e C1) e 20 PI (grupos B e C2). A partir do sangue total colhido com anticoagulante foram separados os linfócitos e eritrócitos para mensuração da atividade da ADA, já o soro foi obtido de amostras de sangue armazenadas em tubos sem anticoagulante. O encéfalo foi separado em cerebelo, córtex cerebral, hipocampo e estriado para avaliar a atividade da ADA em cada estrutura. Então, observou-se redução da atividade de ADA no soro e eritrócitos em ratos infectados com T. evansi em comparação com não-infectados (P <0,05). A atividade de ADA em linfócitos estava diminuída no dia 4 PI e aumentou no dia 20 PI. Não houve diferença da ADA no cerebelo. No córtex cerebral, no hipocampo e estriado ocorreu redução da atividade da ADA nos dia 4 e 20 PI, respectivamente. Em todas as estruturas do encéfalo foi detectada a presença do parasito por PCR. Em um terceiro estudo foram utilizados 24 ratos, sendo 12 controles negativos e outros 12 infectados com T. evansi. Nos dias 4 (n=6 por grupo) e 20 (n=6 por grupo) foram realizadas as coletas de sangue para obtenção do soro e amostras do córtex cerebral para mensuração dos níveis de ATP, ADP, AMP e adenosina. Neste estudo, foi constatado aumento das concentrações de ATP, AMP e adenosina no encéfalo e soro de ratos infectados com T. evansi nos dois períodos avaliados, com exceção dos níveis de adenosina que reduziram no dia 4 PI. Não houve alteração na concentração de ADP. Portanto, na infecção por T. evansi os componentes do sistema purinérgico pode ser alterados, podendo estar envolvido na resposta imunológica, na anemia e nos sinais neurológicos.
Chevallier, Olivier Paul. "Adenosine diphosphoribose synthetic analogues". Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501244.
Pełny tekst źródłaWang, Jianjie. "Modulation of coronary and skeletal muscle exchange by adenosine : role of adenosine receptors /". Free to MU Campus, others may purchase, 2005. http://wwwlib.umi.com/cr/mo/fullcit?p3204635.
Pełny tekst źródłaCarlos, Carolina Dias. "Polimorfismos nos Receptores de Adenosina, suas Associações com Características Fisiopatológicas e Avaliação de Componentes na Biossíntese da Adenosina em Pacientes com Doença Falciforme". Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/17/17135/tde-12062013-074600/.
Pełny tekst źródłaIn sickle cell disease in low oxygen tension, mutant hemoglobin S (HbS) undergoes polymerization promoting sickling of red blood cells that can adhere to vascular endothelium, causing vessel occlusion (VO) and tissue ischemia (painful crises) that characterize the clinical disease. In addition, sickle cell patients have other clinical manifestations such as priapism, bone disorders, certain pulmonary complications among others. In addition to the erythroid cells, endothelial cells, white cells and platelets also play a key role in the pathophysiology of sickle cell anemia. Hydroxyurea (HU) in sickle cell anemia, increases the production of fetal hemoglobin (HbF) in erythroid cells, reducing the HbS polymerization, reducing the clinical symptoms of patients. The increase in HbF, however, does not necessarily imply clinical improvement, thus indicating the potential effects of HU on other processes. Recent studies relating asthma and priapism with high levels of adenosine. Due to this importance of adenosine-related pathologies common to AF, we aimed to identify gene polymorphisms in adenosine receptors and adenosine deaminase and verify the possible association between clinical manifestations, and to investigate the role of HU in the modulation of markers involved synthesis and degradation of adenosine. We analyzed several polymorphic sites in genes that encode ADORA1, ADORA 2b, 3 and ADORA ADA, according to the genotype in patients with AF, comparing affected and unaffected. In addition we assessed the differential expression of ADA mRNA by HU in monocytes of these patients, comparing treated and untreated, and also evaluated by flow cytometry modulation of surface markers CD39, CD73 and CD26 by HU. Statistical analysis was performed using the software GenePop 3.4 for association analysis, calculation of HWE, GraphPad Prism 5, Arlequin for identification of linkage disequilibrium, haplotypes, heterozygosity and SAS 9.13 for association of haplotypes features. The results showed that patients treated with HU showed an increase in mRNA expression of ADA, increased expression of CD26 on monocytes and decreased CD39 on lymphocytes. No significant changes in relation to CD73. We also found an increased frequency of allele T (SNP rs1685103) present in a gene associated with ADORA affected patients with acute chest syndrome. Although not statistically significant, agrees with literature data. ADORA 2B gene, we found association of the SNP 1007 C> T in the development of STA indicating the T allele as a risk factor for the C allele and bone changes. For the SNP 968 G> T was associated with bone disorders. In haplotype analysis between SNPs 968 G> T and 1007 C> T found association of haplotypes ht2 and HT3 with STA as a risk factor for pulmonary hypertension ht2. ht1 for priapism, stenosis and bone disorders / stroke. The three haplotypes formed by SNPs 968 G> T, 1007 C> T and rs16851030, we found association between ht1, HT3 and HT4 among those affected with priapism, characterizing it as a risk haplotype and also ht1 ht6 associated with renal and / AVC. We conclude that hydroxyurea participates in modulating the expression of adenosine deaminase of CD26 on monocytes and CD39 on lymphocytes. Moreover, he showed the importance of polymorphic sites in this gene and ADORA 2B ADORA1 involved in the pathophysiology of clinical manifestations of sickle cell disease. Associations of SNPs in ADORA 1 and ADA should be better studied in a larger number of patients. The determination of these polymorphisms associated with different clinical characteristics can lead to a better understanding of the pathophysiological processes of sickle cell anemia, leading to the identification of patients at risk, enabling a rational handling of the same in terms of specific care, or even the determination of targets for the development of alternative therapies.
STEFANELLI, Angela. "Adenosine receptors in health and disease". Doctoral thesis, Università degli studi di Ferrara, 2014. http://hdl.handle.net/11392/2388942.
Pełny tekst źródłaMolaudzi, Mulalo. "The usefulness of the adenosine deaminase assay for diagnosing tuberculosis pleuritis in immunocompromised patients at Dr George Mukhari tertiary laboratory, Pretoria". Thesis, University of Limpopo (Medunsa Campus), 2012. http://hdl.handle.net/10386/671.
Pełny tekst źródłaMycobacterium tuberculosis is the most common cause of death world-wide and its incidence has been steadily increasing, which is more evident when comparing the global tuberculosis (T8) incidence of 9.24 million in 2006 to 9.27 million cases in 2007. African countries are the second most affected by the epidemic and South Africa is among the 22 highest burden countries most affected by T8 with a very high number of cases relative to the total population. The early diagnosis of tuberculosis and screening of contacts is the cornerstone for controlling spread of active T8 infection. T8 diagnosis becomes even more challenging in patients with immunosuppression (for example in human immunodeficiency virus (HIV) infected), in the case of latent infection and extra pulmonary T8 such as pleural T8. The definitive diagnosis of pleural T8 depends on the demonstration of M. tuberculosis in sputum, pleural fluid and pleural biopsy. Although acid fast bacilli (AF8) microscopy is a rapid, inexpensive and relatively simple method, it has low sensitivity. The culture method is more sensitive than AF8 microscopy, detecting 25-37% of all pleural tuberculosis cases however it takes 4 to 8 weeks for a visible growth on a solid medium. Therefore it is important to find a rapid and reliable test for the diagnosis of pleural T8 particularly in developing countries such as South Africa where there is a high T8 incidence and HIV infection rate.
Crummy, F. "Adenosine, mast cells and asthma". Thesis, Queen's University Belfast, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403238.
Pełny tekst źródłaSvenningsson, Per. "Striatal adenosine A₂A receptors /". Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19981015sven.
Pełny tekst źródłaConn, Michael Morgan. "Molecular recognition of adenosine derivatives". Thesis, Massachusetts Institute of Technology, 1994. http://hdl.handle.net/1721.1/17346.
Pełny tekst źródłaNiebauer, Ronald Thomas. "Engineering yeast cells for optimal expression of the human adenosine (A2a) receptor". Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file 4.52 Mb., 175 p, 2005. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:3181857.
Pełny tekst źródłaNewton, Adam J. H. "Modelling adenosine dynamics in neural tissues". Thesis, University of Warwick, 2015. http://wrap.warwick.ac.uk/81484/.
Pełny tekst źródłaJackson, Andrew M. "Aâ†2â†B adenosine receptor signalling". Thesis, University of Nottingham, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251985.
Pełny tekst źródłaAbbott, C. M. "Adenosine deaminase in the wasted mouse". Thesis, University of Reading, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.374695.
Pełny tekst źródłaCohen, Fiona Rachel. "The allosteric regulation of adenosine receptors". Thesis, University College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309286.
Pełny tekst źródłaJames, Stephen. "Adenosine at the striatal chlorinergic synapse". Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314824.
Pełny tekst źródłaBaines, Abigail. "Adenosine receptor trafficking : implications for epilepsy". Thesis, University of Warwick, 2011. http://wrap.warwick.ac.uk/51350/.
Pełny tekst źródłaLivingston, Mark. "The role of adenosine in asthma". Thesis, Queen's University Belfast, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.649365.
Pełny tekst źródłaWillems, Laura E., i n/a. "Adenosine and Ischaemia in Young To Aged Hearts". Griffith University. School of Medical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20061011.163451.
Pełny tekst źródłaWillems, Laura E. "Adenosine and Ischaemia in Young To Aged Hearts". Thesis, Griffith University, 2006. http://hdl.handle.net/10072/365196.
Pełny tekst źródłaThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Full Text
Freitas, Helder Teixeira de. "Papel da sinalização da adenosina na geração de células T regulatórias a partir de células T naive de cordão umbilical e na imunomodulação por células-tronco estromais mesenquimais de medula óssea". Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/17/17153/tde-19072018-135504/.
Pełny tekst źródłaRegulatory T cells (Tregs) are essential for the maintenance of peripheral tolerance, prevention of autoimmune and limiting diseases in chronic inflammatory diseases. In addition, these cells play a key role in the control of transplant rejection. Different protocols have shown that it is possible to obtain Tregs from naive CD4+ T cells in vitro. To this end, there is consensus that TGF-? and interleukin-2 (IL-2) are capable of directing the naive CD4 + T cells to become regulatory following an antigenic stimulus (anti-CD3/CD28).. Our group recently noted that during the immunomodulation of T lymphocytes by mesenchymal stromal cells (MSCs), they were able to produce adenosine which in turn participates in the immunoregulation process. Other studies indicate that MSCs suppress the proliferation of T lymphocytes by generation of Tregs and that MSCs induce generation of Tregs by downregulation of the TCR pathway and the AKT-mTOR pathway. Evidence indicates that adenosine may act by downregulating the mTOR pathway. Therefore, it is believed that adenosine may participate in the generation of Tregs by modulating the mTOR pathway. In addition, recent studies indicate that activation of adenosine receptors, more specifically A2a, with agonist agents, leads to increased production of Treg cells, whereas the use of antagonistic agents of these receptors leads to a decrease in Treg differentiation.. However, these studies show the generation of Tregs from naive T cells of mice. In view of the great importance of Tregs in the immunological context, the efficient production of Tregs in vitro is of fundamental importance for the development of new therapeutic protocols for the treatment of autoimmune diseases and in the fight against transplant rejection. Thus, the central objective of this study was to evaluate the participation of adenosine receptor agonists and antagonists in induction of regulatory T cells generated in vitro (iTreg) by the activation of naive CD4+ T cells isolated from human umbilical cord blood (SCU). For this, mononuclear cells were isolated from SCU and naive T cells were immunomagnetic isolated. These cells were activated with beads bound to anti-CD2/CD3/CD28 antibodies and cultured for five days in the presence of IL-2 and different concentrations of agonist drugs and antagonists of adenosine receptors. Next, the major regulatory T-cell markers were assessed by flow cytometry and the culture medium was collected at the end of the generation for quantification of cytokines. In addition, total RNA was extracted from all culture conditions for the analysis of the expression of genes involved in the generation and development of Tregs by quantitative PCR. The potential for suppression of effector T cells was also evaluated.
Rodenko, Boris. "A new entry to adenosine analogues via purine nitration combinatorial synthesis of antiprotozoal agents and adenosine receptor ligands /". [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2004. http://dare.uva.nl/document/71739.
Pełny tekst źródłaYonally, Sarah K. "The mitochondrial F{207}F{206} ATP synthase : multienzyme associations and membrane locations /". view abstract or download file of text, 2006. http://proquest.umi.com/pqdweb?did=1188872031&sid=1&Fmt=2&clientId=11238&RQT=309&VName=PQD.
Pełny tekst źródłaTypescript. Includes vita and abstract. Includes bibliographical references (leaves 63-68). Also available for download via the World Wide Web; free to University of Oregon users.
Brown, Ruth Elizabeth. "Investigations of adenosine as a vascular modulator". Thesis, Queen Mary, University of London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397335.
Pełny tekst źródłaKhan, Zeenatul. "Adenosine diphosphoribosyl transferase in granulocyte-monocyte differentiation". Thesis, Brunel University, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.255772.
Pełny tekst źródłaAtterbury, Alison. "Development of adenosine signalling in the cerebellum". Thesis, University of Warwick, 2010. http://wrap.warwick.ac.uk/35147/.
Pełny tekst źródłaLarner, Carrie Jayne Byrom. "Selective targeting of the adenosine A2A receptor". Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608592.
Pełny tekst źródłaVarley, David Robert. "The synthesis of novel analogues of adenosine". Thesis, University of Exeter, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307291.
Pełny tekst źródłaHussey, Martin John. "Adenosine Aâ‚‚A receptors and peripheral nociception". Thesis, University of Surrey, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441903.
Pełny tekst źródłaGurden, Mark Francis. "Studies on the classification of adenosine receptors". Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386645.
Pełny tekst źródłaHern, Jonathan A. "Studies on the human adenosine A₁ receptor". Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1445552/.
Pełny tekst źródłaMoscoso, Castro Maria 1988. "Study of the involvement of adenosine A2A receptors in the pathophysiology of schizophrenia". Doctoral thesis, Universitat Pompeu Fabra, 2016. http://hdl.handle.net/10803/565401.
Pełny tekst źródłaEl sistema adenosinèrgic és un neuromodulador que actua sobre quatre subtipus de receptors amb diferents distribucions en el sistema nerviós central. Aquest sistema contribueix a l’homeòstasi i a la vegada regula diverses funcions fisiològiques com per exemple la son, la funció motora, la plasticitat sinàptica o la cognició. L’adenosina pot exercir un control “upstream” sobre diferents sistemes de neurotransmissió, incloent la dopamina i el glutamat, neurotransmissors implicats en la fisiopatologia de les malalties neuropsiquiàtriques, especialment en la psicosis. L’esquizofrènia es considera una malaltia psicòtica que cursa de forma crònica i debilitant provocada per la interacció de diferents factors genètics, ambientals i del desenvolupament. La malaltia es manifesta en tres dominis de símptomes, incloent símptomes positius, negatius i cognitius, i actualment té importants limitacions terapèutiques. Estudis preclínics i clínics suggereixen que la disfunció en el sistema d’adenosina pot contribuir a la patofisiologia de l’esquizofrènia. Per tant, l’objectiu principal d’aquesta tesi és l’estudi dels efectes induïts per la supressió completa dels receptors A2A d’adenosina en la fisiopatologia de la malaltia, parant especial atenció al domini de símptomes cognitius. L’ús de mètodes bioquímics i comportamentals ens ha permès avaluar la validesa dels KO pel receptor A2A d’adenosina com a possible model animal per a l’estudi de l’esquizofrènia.
Junqueira, Ana FlÃvia Torquato de AraÃjo. "Estudo do efeito do inibidor da enzima adenosina desaminase, EHNA, sobre a enterite induzida pela toxina a do Clostridium difficile em alÃa ileal isolada de camundongos". Universidade Federal do CearÃ, 2008. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=1305.
Pełny tekst źródłaO Clostridium difficile tem como principal fator de virulÃncia a toxina A (TxA), a qual provoca inflamaÃÃo e destruiÃÃo tecidual aguda em intestinos de animais experimentais e de pacientes com a doenÃa induzida por esta bactÃria. Em locais de injÃria tecidual, adenosina à produzida em altas concentraÃÃes, onde exerce uma sÃrie de efeitos antiinflamatÃrios, limitados por sua rÃpida degradaÃÃo pela enzima adenosina desaminase. O objetivo deste trabalho foi investigar o efeito da inibiÃÃo da enzima adenosina desaminase pelo EHNA (eritro-9-(2-hidrÃxi-3-nonil)-adenina) sobre a enterite induzida pela TxA do C. difficile em alÃa ileal de camundongos. Para isto, injetamos EHNA (90 μmol/kg) ou PBS i.p. 30 minutos antes da administraÃÃo de TxA (10 a 100 μg) ou PBS na alÃa ileal isolada. Os animais foram sacrificados 3 horas depois da induÃÃo da enterite e as alÃas foram retiradas para estudo. As razÃes peso/comprimento da alÃa e volume de secreÃÃo/comprimento da alÃa foram calculadas e amostras de tecido foram coletadas para histopatologia, dosagem de atividade de mieloperoxidase (MPO), dosagem de TNF-α, IL-1β e IL-10 por ELISA, imunohistoquÃmica para TNF-α, IL-1β, NOS induzÃvel e PTX3, e PCR para TNF-α, IL-1β e PTX3. A injeÃÃo de TxA (10 a 100 μg) nas alÃas ileais aumentou significativamente (p<0,05) as razÃes peso/comprimento da alÃa e volume de secreÃÃo/comprimento da alÃa com resultados consistentes a partir de 50 μg. A TxA promoveu significativa (p<0,05) destruiÃÃo tecidual, edema, infiltraÃÃo de cÃlulas inflamatÃrias, aumento das citocinas TNF-α e IL-1β, e elevaÃÃo de iNOS e PTX3. Todos esses parÃmetros foram significativamente revertidos com o uso do EHNA (p<0,05). Em adiÃÃo, a TxA nÃo alterou os nÃveis de IL-10 em relaÃÃo ao controle, mas o prÃ-tratamento com EHNA promoveu uma elevaÃÃo nos nÃveis desta citocina. Assim, concluÃmos que na enterite induzida pela TxA em camundongos o EHNA demonstrou um potente efeito antiinflamatÃrio, reduzindo consideravelmente a lesÃo tecidual, a migraÃÃo neutrofÃlica, a expressÃo e os nÃveis de citocinas prÃinflamatÃrias (TNF-α, IL-1β) e produzindo um aumento nos nÃveis de IL-10. AlÃm disso, a administraÃÃo de TxA induziu um aumento na expressÃo da proteÃna PTX3 e no nÃmero de cÃlulas imunomarcadas para iNOS no tecido ileal, ambos revertidos pelo EHNA
The main factor of virulence in Clostridium difficile is toxin A (TxA), which can induce inflammation and acute tissue injury in the bowels of animals and humans affected by this organism. The high concentration of adenosine generated upon injury produces a number of antiinflammatory effects limited by rapid degradation by adenosine deaminase. The objective of this study was to determine the effect of EHNA (erythro-9-(2-hydroxy-3-nonyl)-adenine) inhibition of adenosine deaminase upon TxA-induced ileal loop enteritis in mice. EHNA (90 μmol/kg) or PBS was injected i.p. 30 minutes prior to TxA (10-100 μg) or PBS instillation into the ligated ileal loop. The animals were euthanized 3 hours after enteritis induction and the ileal loops were retrieved for analysis. The weight/length ratio and the secretion volume/length ratio were calculated and tissue samples were submitted to histopathological study, myeloperoxidase assay (MPO), measurement of TNF-α, IL-1β and IL-10 levels with ELISA, immunohistochemical tests for TNF-α, IL-1β, inducible NOS and PTX3, and PCR assay for TNF-α, IL-1β and PTX3. The instillation of TxA (10-100 μg) into the ileal loop significantly increased (p<0.05) the weight/length ratio and the secretion volume/length ratio with consistent results above 50 μg. TxA induced a significant amount (p<0.05) of histological damage, edema and inflammatory cell infiltration and increased the production of TNF-α, IL-1β, iNOS and PTX3. All changes were significantly reverted by treatment with EHNA (p<0.05). Moreover, IL-10 levels remained unchanged in animals treated with TxA, but increased in animals receiving EHNA. In conclusion, in mice with TxA-induced enteritis EHNA produced considerable antiinflammatory effects, reducing tissue injury, neutrophil migration, the expression and levels of proinflammatory cytokines (TNF-α and IL-1β) and producing an increase in IL-10 levels. In addition, TxA instillation increased PTX3 expression and the number of cells immunolabeled for iNOS in the ileal tissue, both of which were reverted by EHNA
TARGA, Martina. "ADENOSINE RECEPTORS IN RESPIRATORY DISORDERS AS CHRONIC OBSTRUCTIVE PULMONARY DISEASE AND MALIGNANT PLEURAL MESOTHELIOMA". Doctoral thesis, Università degli studi di Ferrara, 2012. http://hdl.handle.net/11392/2388779.
Pełny tekst źródłaThevenin, Damien. "Roles of transmembrane domains in the folding and assembly of the adenosine A2A receptor". Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 170 p, 2007. http://proquest.umi.com/pqdweb?did=1260822171&sid=2&Fmt=2&clientId=8331&RQT=309&VName=PQD.
Pełny tekst źródłaCoy, David Laughlin. "The activation and chemomechanical stoichiometry of cargo-loaded kinesin /". Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/10530.
Pełny tekst źródłaLau, Siu-ling. "Characterization of adenosine transport in rat cardiomyocytes, H9c2 /". View the Table of Contents & Abstract, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31494894.
Pełny tekst źródłaWright, Denis Matthew John, i mikewood@deakin edu au. "Potential antiarrhythmic and cardioprotective agents based on adenosine". Deakin University. School of Biological and Chemical Sciences, 1998. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20050915.160941.
Pełny tekst źródłaBeauglehole, Anthony Robert, i anthony@adenrx com. "N3-substituted xanthines as irreversible adenosine receptor antagonists". Deakin University. School of Biological and Chemical Sciences, 2000. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20080612.084330.
Pełny tekst źródłaTandon, Anurag. "Adenosine and acetylcholine synthesis in a sympathetic ganglion". Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=28539.
Pełny tekst źródłaActivity-dependent modulation of synaptic transmission is known to occur in sympathetic ganglia. One such form of adaptive behavior is the increase in ACh content ('rebound ACh') after high frequency preganglionic stimulation. The possibility that adenosine might play a role in the rebound phenomenon was examined in the second study. The accumulation of rebound ACh was sensitive to nucleoside transport inhibitors; dipyridamole reduced rebound ACh if it wzs present only after the stimulation, but not if it was present only during stimulation. After its synthesis, rebound ACh was released by preganglionic stimulation, but not if vesamicol was present, as if the extra transmitter had to be mobilized from a reserve pool. Because the dipyridamole-sensitive step occurred after the conditioning period, it seemed possible that a retrograde messenger triggered the post-stimulation change in ACh synthesis.
Thus, the final series of experiments tested whether a postsynaptic signal could alter presynaptic ACh synthesis. Antidromic stimulation increased ganglionic ACh synthesis, and, consequently, ACh content. Subsequent evoked ACh release was potentiated, as if the additional transmitter was releasable. The antidromic stimulation-induced increase in AZh content was blocked by dipyridamole suggesting that adenosine might be involved.
Overall, the results presented in this thesis are consistent with the notion that adenosine acts as a retrograde messenger after high frequency orthodromic stimulation to induce an increase in presynaptic ACh synthesis.
Lau, Siu-ling, i 劉少玲. "Characterization of adenosine transport in rat cardiomyocytes, H9c2". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B45010237.
Pełny tekst źródłaDonaghy, Kevin M. "Actions of adenosine and anoxia in rat brain". Thesis, Queen's University Belfast, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333806.
Pełny tekst źródłaHarper, Laura. "A[2A subscript] adenosine receptors, dopamine and reward". Thesis, University of Nottingham, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408638.
Pełny tekst źródłaDale, Clare Louise. "Fluorescent Aâ‚-adenosine agonists : a structure activity relationship". Thesis, University of Nottingham, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.440124.
Pełny tekst źródłaDexter, Emily Jane. "The role of adenosine in mast cell degranulation". Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314292.
Pełny tekst źródłaWatt, A. H. "Cardiac and respiratory effects of adenosine in man". Thesis, University of Aberdeen, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.379168.
Pełny tekst źródłaMann, J. S. "Adenosine : A putative mediator of bronchoconstriction in asthma". Thesis, University of Southampton, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.379583.
Pełny tekst źródła