Academic literature on the topic 'Adenosine'
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Journal articles on the topic "Adenosine"
Dibner-Dunlap, M. E., T. Kinugawa, and M. D. Thames. "Activation of cardiac sympathetic afferents: effects of exogenous adenosine and adenosine analogues." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 1 (July 1, 1993): H395—H400. http://dx.doi.org/10.1152/ajpheart.1993.265.1.h395.
Full textSundin, Emma M., John D. Ciubuc, Kevin E. Bennet, Katia Ochoa, and Felicia S. Manciu. "Comparative Computational and Experimental Detection of Adenosine Using Ultrasensitive Surface-Enhanced Raman Spectroscopy." Sensors 18, no. 8 (August 16, 2018): 2696. http://dx.doi.org/10.3390/s18082696.
Full textEisenach, James C., Regina Curry, and David D. Hood. "Dose Response of Intrathecal Adenosine in Experimental Pain and Allodynia." Anesthesiology 97, no. 4 (October 1, 2002): 938–42. http://dx.doi.org/10.1097/00000542-200210000-00028.
Full textChiari, Astrid I., and James C. Eisenach. "Intrathecal Adenosine." Anesthesiology 90, no. 5 (May 1, 1999): 1413–21. http://dx.doi.org/10.1097/00000542-199905000-00026.
Full textNair, Vasu, Steven Adah, and Seung Ha. "Strategically Functionalized Adenosines: Agonists for Adenosine Receptors." Nucleosides, Nucleotides and Nucleic Acids 14, no. 3 (May 1, 1995): 537–39. http://dx.doi.org/10.1080/15257779508012421.
Full textBantel, Carsten, Xinhui Li, and James C. Eisenach. "Intraspinal Adenosine Induces Spinal Cord Norepinephrine Release in Spinal Nerve-ligated Rats but not in Normal or Sham Controls." Anesthesiology 98, no. 6 (June 1, 2003): 1461–66. http://dx.doi.org/10.1097/00000542-200306000-00024.
Full textVidal, C. "Adenosine and adenosine receptors." Biochimie 74, no. 6 (June 1992): 591. http://dx.doi.org/10.1016/0300-9084(92)90165-b.
Full textSteinberg, Thomas H. "Adenosine and Adenosine Receptors." American Journal of Respiratory Cell and Molecular Biology 2, no. 2 (February 1990): 127–28. http://dx.doi.org/10.1165/ajrcmb/2.2.127.
Full textFredholm, Bertil. "Adenosine and adenosine receptors." Trends in Pharmacological Sciences 12 (January 1991): 76. http://dx.doi.org/10.1016/0165-6147(91)90503-k.
Full textShang, Liangcheng, Yaobiao Huang, Xin Xie, Sudan Ye, and Chun Chen. "Effect of Adenosine Receptor Antagonists on Adenosine-Pretreated PC12 Cells Exposed to Paraquat." Dose-Response 20, no. 2 (April 2022): 155932582210934. http://dx.doi.org/10.1177/15593258221093411.
Full textDissertations / Theses on the topic "Adenosine"
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.
Full textAbamectina 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.
Find full textSoledade, Cinira Santana. "O efeito do DMA (composto quinazolinico) sobre o processo inflamatorio." [s.n.], 2008. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310436.
Full textTese (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.
Full textBanca: 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.
Full textThe 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.
Full textWang, 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.
Full textCarlos, 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/.
Full textIn 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.
Full textMolaudzi, 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.
Full textMycobacterium 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.
Books on the topic "Adenosine"
Williams, Michael, ed. Adenosine and Adenosine Receptors. Totowa, NJ: Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-4504-9.
Full textWilliams, Michael, 1947 Jan. 3-, ed. Adenosine and adenosine receptors. Clifton, N.J: Humana Press, 1990.
Find full textMasino, Susan, and Detlev Boison, eds. Adenosine. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-3903-5.
Full textF, Cooper Dermot M., and Londos Constantine, eds. Adenosine receptors. New York: A.R. Liss, 1988.
Find full textBorea, Pier Andrea, Katia Varani, Stefania Gessi, Stefania Merighi, and Fabrizio Vincenzi, eds. The Adenosine Receptors. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-90808-3.
Full textPaton, David M., ed. Methods Used in Adenosine Research. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4886-3.
Full text1938-, Paton David M., ed. Methods used in adenosine research. New York: Plenum Press, 1985.
Find full textHiroshi, Kase, Richardson Peter J, and Jenner P. G, eds. Adenosine receptors and Parkinson's disease. San Diego, Calif: Academic, 2000.
Find full textHiroshi, Kase, Richardson Peter J, and Jenner Peter 1946-, eds. Adenosine receptors and Parkinson's disease. San Diego, CA: Academic Press, 2000.
Find full textW, Stone T., ed. Adenosine in the nervous system. London: Academic Press, 1991.
Find full textBook chapters on the topic "Adenosine"
Fredholm, Bertil B. "Adenosine and Metabolism—A Brief Historical Note." In Adenosine, 3–19. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_1.
Full textPorkka-Heiskanen, Tarja. "Sleep and Adenosine: Human Studies." In Adenosine, 201–12. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_10.
Full textMuheim, Christine, and Steven A. Brown. "Adenosine and Other Purinergic Products in Circadian Timing." In Adenosine, 213–32. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_11.
Full textHaskó, György, Balázs Koscsó, and Balázs Csóka. "Adenosine in the Immune System." In Adenosine, 233–51. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_12.
Full textDrew, Kelly L., and Tulasi R. Jinka. "The Bioenergetic Network of Adenosine in Hibernation, Sleep, and Thermoregulation." In Adenosine, 253–72. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_13.
Full textPedata, Felicita, Anna Maria Pugliese, Francesca Corti, and Alessia Melani. "Adenosine and Stroke." In Adenosine, 273–306. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_14.
Full textKochanek, Patrick M., Jonathan D. Verrier, Amy K. Wagner, and Edwin K. Jackson. "The Many Roles of Adenosine in Traumatic Brain Injury." In Adenosine, 307–22. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_15.
Full textNantwi, Kwaku D. "Therapeutic Perspectives of Adenosine Receptor Compounds in Functional Restitution After Spinal Cord Injury." In Adenosine, 323–42. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_16.
Full textSawynok, Jana. "Adenosine and Pain." In Adenosine, 343–60. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_17.
Full textPinna, Annalisa, Nicola Simola, Lucia Frau, and Micaela Morelli. "Symptomatic and Neuroprotective Effects of A2A Receptor Antagonists in Parkinson’s Disease." In Adenosine, 361–84. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_18.
Full textConference papers on the topic "Adenosine"
Lexmond, Anne J., Ilse Boudewijn, Paul Hagedoorn, Siebrig Schokker, Claire Cox, Judith Vonk, Nick ten Hacken, et al. "An improved bronchial provocation test with dry powder adenosine instead of nebulised adenosine monophosphate (AMP)." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa4756.
Full textFeng Zhang, Keisuke Tominaga, Jun-ichi Nishizawa, Ohki Kambara, Tetsuo Sasaki, Houng-Wei Wang, and Michitoshi Hayashi. "Terahertz spectroscopy of adenine and adenosine." In 2012 37th International Conference on Infrared, Millimeter, and Terahertz Waves (IRMMW-THz 2012). IEEE, 2012. http://dx.doi.org/10.1109/irmmw-thz.2012.6380157.
Full textSundaresan, Vishnu Baba, Stephen Andrew Sarles, and Donald J. Leo. "Chemoelectrical energy conversion of adenosine triphosphate." In The 14th International Symposium on: Smart Structures and Materials & Nondestructive Evaluation and Health Monitoring, edited by Yuji Matsuzaki, Mehdi Ahmadian, and Donald J. Leo. SPIE, 2007. http://dx.doi.org/10.1117/12.715715.
Full textLin, Juqiang, Yating Lin, Yiming Huang, Zhiwei Wu, Jianshu Xu, Ya Hu, and Shusen Xie. "Quantitative FRET measurement of the interaction of A1 adenosine receptors and A2A adenosine receptors in living cell." In Optics in Health Care and Biomedical Optics VIII, edited by Qingming Luo, Xingde Li, Yuguo Tang, and Ying Gu. SPIE, 2018. http://dx.doi.org/10.1117/12.2500692.
Full textDiRenzo, Daniel, Dana Piovesan, Joanne Tan, Dillon H. Miles, Manmohan R. Leleti, Timothy Park, Ferdie Soriano, et al. "Abstract A162: AB928, a dual antagonist of the A2aR and A2bR adenosine receptors, relieves adenosine-mediated immune suppression." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-a162.
Full textLondoño-R, Luz Marina, Jessica Cowell, Lin Wang, Qiping Zhao, Lei Huang, Chris Thanos, Michael J. LaBarre, Xiaoming Li, and Caglar Cekic. "Abstract 1755: PEGylated adenosine deaminase (ADA2) prevents adenosine-mediated increase in tumor growth and improves antitumor immune responses." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1755.
Full textSerra, Sara, Cinzia Bologna, Luz Londono, Lin Wang, Michael Shepard, Sanna Rosengren, Christopher Thanos, and Silvia Deaglio. "Abstract 5583: Pegylated adenosine deaminase 2 (PEG-ADA2) abrogates the cytoprotective effects of adenosine against chronic lymphocytic leukemia cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5583.
Full textHouthuys, Erica, Paola Basilico, Veronique Bodo, Margreet Brouwer, Michel Detheux, Gregory Driessens, Bruno Gomes, et al. "Abstract 3278: EOS100850 potently restores adenosine A2Areceptor-dependent suppression of T cell function in the adenosine rich tumor microenvironment." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3278.
Full textHouthuys, Erica, Paola Basilico, Veronique Bodo, Margreet Brouwer, Michel Detheux, Gregory Driessens, Bruno Gomes, et al. "Abstract 3278: EOS100850 potently restores adenosine A2Areceptor-dependent suppression of T cell function in the adenosine rich tumor microenvironment." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3278.
Full textVan Rompaey, Philippe, Kenneth A. Jacobson, Zhan-Guo Gao, Aishe Chen, Dov Barak, Soon-Ai Kim, Kyeong Lee, et al. "Amine-modified nucleosides as adenosine A3 neoceptor ligands." In XIIth Symposium on Chemistry of Nucleic Acid Components. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2002. http://dx.doi.org/10.1135/css200205267.
Full textReports on the topic "Adenosine"
Liou, Gregory I., Saif Ahmad, Mohammad Naime, Nadeem Fatteh, and Sohail Khan. Role of Adenosine Receptor A2A in Traumatic Optic Neuropathies. Fort Belvoir, VA: Defense Technical Information Center, December 2012. http://dx.doi.org/10.21236/ada581642.
Full textLiou, Gregory I., Saif Ahmad, and Ahmed Elsherbini. Role of Adenosine Receptor A2A in Traumatic Optic Neuropathies. Fort Belvoir, VA: Defense Technical Information Center, December 2013. http://dx.doi.org/10.21236/ada600384.
Full textSpychala, Jozef. Growth-Promoting and Angiogenic Functions of Adenosine in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2004. http://dx.doi.org/10.21236/ada432030.
Full textSpychala, Jozef. Growth-Promoting and Angiogenic Functions in Adenosine in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada420393.
Full textSchwarzshild, Michael A. Caffeine, Adenosine Receptors and Estrogen in Toxin Models of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, October 2006. http://dx.doi.org/10.21236/ada462198.
Full textSchwarzschild, Michael A. Caffeine, Adenosine Receptors and Estrogen in Toxin Models of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, October 2009. http://dx.doi.org/10.21236/ada625341.
Full textYe, Libin, Christopher Andrew Neale, Adnan Sljoka, Brent Lyda, Dmitry Pichugin, Nobuyuki Tsuchimura, Sacha T. Larda, et al. Mechanistic insights into allosteric regulation of the A2A adenosine G protein-coupled receptor by physiological cations. Office of Scientific and Technical Information (OSTI), April 2018. http://dx.doi.org/10.2172/1434450.
Full textDeutsch, Christopher. Discovery and Characterization of the Proteins Involved in the Synthesis of N⁶-Threonylcarbamoyl Adenosine, a Nucleoside Modification of tRNA. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.3075.
Full textXi, Yin, Zheng Gao, Jiyuan Ni, Yang Li, Wenyu Zhang, and Jie Hao. Comparative efficacy of “contact force” ablation, adenosine, cryoballoon and waiting time after PVI for freedom from arrhythmia recurrence undergoing PVI : A network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0076.
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