Gotowe bibliografie tematyczne / Adenosine

Gotowa bibliografia na temat „Adenosine”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 1 kwietnia 2023

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Artykuły w czasopismach na temat "Adenosine"

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Dibner-Dunlap, M. E., T. Kinugawa i M. D. Thames. "Activation of cardiac sympathetic afferents: effects of exogenous adenosine and adenosine analogues". American Journal of Physiology-Heart and Circulatory Physiology 265, nr 1 (1.07.1993): H395—H400. http://dx.doi.org/10.1152/ajpheart.1993.265.1.h395.

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Adenosine is released during myocardial ischemia and can cause angina-like chest pain when given by intracoronary administration. We tested the hypothesis that intracoronary adenosine activates cardiac sympathetic afferent fibers and results in reflex sympathoexcitation. In dogs with sinoaortic denervation and vagotomy, we administered 2 mg of adenosine into the left anterior descending artery over 2 min. Before dipyridamole infusion, intracoronary adenosine resulted in no change in blood pressure or renal sympathetic nerve activity. After dipyridamole infusion, which blocks adenosine uptake, intracoronary adenosine resulted in a peak increase in sympathetic activity of 34 +/- 7%. We also investigated the adenosine-receptor subtype responsible for this sympathoexcitatory response. We found that the adenosine1 agonist N6-cyclopentyladenosine elicited a dose-dependent sympathoexcitatory response similar to adenosine but that the adenosine2 agonist 5'-(N-cyclopropyl)carboxamidoadenosine failed to elicit a sympathoexcitatory response. We conclude that adenosine activates cardiac sympathetic afferent fibers and leads to a sympathoexcitatory response due to activation of adenosine1 receptors.
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Sundin, Emma M., John D. Ciubuc, Kevin E. Bennet, Katia Ochoa i Felicia S. Manciu. "Comparative Computational and Experimental Detection of Adenosine Using Ultrasensitive Surface-Enhanced Raman Spectroscopy". Sensors 18, nr 8 (16.08.2018): 2696. http://dx.doi.org/10.3390/s18082696.

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To better understand detection and monitoring of the important neurotransmitter adenosine at physiological levels, this study combines quantum chemical density functional modeling and ultrasensitive surface-enhanced Raman spectroscopic (SERS) measurements. Combined simulation results and experimental data for an analyte concentration of about 10−11 molar indicate the presence of all known molecular forms resulting from adenosine’s complex redox-reaction. Detailed analysis presented here, besides assessing potential Raman signatures of these adenosinic forms, also sheds light on the analytic redox process and voltammetric detection. Examples of adenosine Raman fingerprints for different molecular orientations with respect to the SERS substrate are the vibrational line around 920 ± 10 cm−1 for analyte physisorption through the carbinol moiety and around 1600 ± 20 cm−1 for its fully oxidized form. However, both hydroxyl/oxygen sites and NH2/nitrogen sites contribute to molecule’s interaction with the SERS environment. Our results also reveal that contributions of partially oxidized adenosine forms and of the standard form are more likely to be detected with the first recorded voltammetric oxidation peak. The fully oxidized adenosine form contributes mostly to the second peak. Thus, this comparative theoretical–experimental investigation of adenosine’s vibrational signatures provides significant insights for advancing its detection, and for future development of opto-voltammetric biosensors.
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Eisenach, James C., Regina Curry i David D. Hood. "Dose Response of Intrathecal Adenosine in Experimental Pain and Allodynia". Anesthesiology 97, nr 4 (1.10.2002): 938–42. http://dx.doi.org/10.1097/00000542-200210000-00028.

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Background Intrathecal adenosine reduces areas of mechanical hypersensitivity and provides analgesia in patients with neuropathic pain. Adenosine also causes side effects, yet its dose response for either efficacy or side effects has not been examined in double blind studies. We studied two doses of intrathecal adenosine in humans with experimental hypersensitivity and the ability of the adenosine receptor antagonist, aminophylline, to reverse adenosine's effects. Methods Following Internal Review Board approval and written informed consent, 35 volunteers were studied. Five volunteers were studied to confirm the stability of a new method of inducing hypersensitivity with capsaicin. The remaining 30 volunteers received, in a randomized, double-blind manner, saline, or adenosine, 0.5 or 2.0 mg, by intrathecal injection 40 min after areas of allodynia and hyperalgesia were established from capsaicin. Two hr later, volunteers were randomized to receive intravenous saline or aminophylline, 5 mg/kg. Results Topical capsaicin with intermittent heating resulted in stable areas of allodynia and hyperalgesia. Intrathecal adenosine, but not saline, reduced areas of allodynia and hyperalgesia from capsaicin, with no differences between doses. Side effects occurred in 1, 2, and 6 volunteers receiving saline, 0.5 mg and 2.0 mg adenosine, respectively. Aminophylline failed to reverse adenosine's effects. Conclusions There is no difference in efficacy to experimental hypersensitivity between the largest approved dose of intrathecal adenosine and a dose 25% this size, but side effects are more common with the larger dose. Failure of aminophylline to reverse adenosine's effects could reflect inadequate concentrations at receptors in the spinal cord after intravenous injection.
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Chiari, Astrid I., i James C. Eisenach. "Intrathecal Adenosine". Anesthesiology 90, nr 5 (1.05.1999): 1413–21. http://dx.doi.org/10.1097/00000542-199905000-00026.

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Background Spinal adenosine receptor agonists exert antinociception in animal models of acute and chronic pain, but adenosine itself has not been examined. The authors tested the antinociceptive and antihypersensitivity interactions of intrathecal adenosine and its interactions with intrathecal clonidine and neostigmine in rat models of acute thermal nociception and postoperative hypersensitivity. Methods Rats were prepared with lumbar intrathecal catheters. Responses to acute noxious stimulation were evaluated by latency to paw withdrawal from a radiant heat source focused on the hind paw. Postoperative hypersensitivity was measured after an incision in the rat hind paw by application of von Frey filaments to the heel adjacent to the wound. An isobolographic design was used to distinguish between additive and synergistic drug interactions. Results Spinal administration of clonidine and neostigmine, but not adenosine, produced dose-dependent antinociception to noxious thermal stimulation. Addition of adenosine enhanced the antinociceptive effect of clonidine but not neostigmine. In contrast, each of these three agents alone reversed postoperative hypersensitivity. Pretreatment with the alpha-adrenergic antagonist phentolamine completely reversed adenosine's antihypersensitivity action. Adenosine interacted synergistically with neostigmine and additively with clonidine in reducing postoperative hypersensitivity. Conclusions These data indicate that intrathecal adenosine by itself has no antinociceptive properties to acute noxious thermal stimulation in rats, but enhances clonidine's antinociception. In contrast, intrathecal adenosine is active against postoperative hypersensitivity by an adrenergic mechanism. Different interactions between adenosine, clonidine, and neostigmine in acute nociception and postoperative hypersensitivity models are consistent with altered central processing of sensory information after peripheral injury.
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Nair, Vasu, Steven Adah i Seung Ha. "Strategically Functionalized Adenosines: Agonists for Adenosine Receptors". Nucleosides, Nucleotides and Nucleic Acids 14, nr 3 (1.05.1995): 537–39. http://dx.doi.org/10.1080/15257779508012421.

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Bantel, Carsten, Xinhui Li i James C. Eisenach. "Intraspinal Adenosine Induces Spinal Cord Norepinephrine Release in Spinal Nerve-ligated Rats but not in Normal or Sham Controls". Anesthesiology 98, nr 6 (1.06.2003): 1461–66. http://dx.doi.org/10.1097/00000542-200306000-00024.

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Background Intrathecal adenosine is antinociceptive under conditions of central sensitization, but not in response to acute stimuli in normals. The reasons for this selective circumstance of action remain unclear, but some evidence links adenosine's antinociceptive effects to release of norepinephrine by terminals in the spinal cord. The purpose of this study was to test whether spinal adenosine induces norepinephrine release selectively in settings of hypersensitivity. Methods Rats randomly assigned to spinal nerve ligation, sham operation, or no operation were anesthetized. A microdialysis fiber was implanted in the spinal cord dorsal horn at the L5-L6 level and perfused with artificial cerebrospinal fluid. After washout and a baseline sample period, adenosine at various concentrations was infused through the fiber for 150 min, and samples were collected every 15 min. Results In ligated, but not in sham or normal animals, adenosine perfusion increased norepinephrine in spinal cord microdialysates in a concentration-dependent manner. The effects of adenosine plateaued after 75 min and remained stable until the end of the experiment. Intravenous injection of selective adenosine A1 and A2 receptor antagonists revealed that adenosine's effect on spinal norepinephrine release was A1 receptor mediated. Conclusions This is the first study to provide direct evidence that adenosine is able to release norepinephrine in spinal cord dorsal horns in living animals. However, this effect was only seen in animals after spinal nerve ligation. These data are consistent with behavioral studies demonstrating that adenosine's antinociceptive effects in rats after spinal nerve ligation is totally dependent on intact spinal noradrenergic terminals and can be blocked by spinal alpha 2-adrenergic receptor antagonists.
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Vidal, C. "Adenosine and adenosine receptors". Biochimie 74, nr 6 (czerwiec 1992): 591. http://dx.doi.org/10.1016/0300-9084(92)90165-b.

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Steinberg, Thomas H. "Adenosine and Adenosine Receptors". American Journal of Respiratory Cell and Molecular Biology 2, nr 2 (luty 1990): 127–28. http://dx.doi.org/10.1165/ajrcmb/2.2.127.

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Fredholm, Bertil. "Adenosine and adenosine receptors". Trends in Pharmacological Sciences 12 (styczeń 1991): 76. http://dx.doi.org/10.1016/0165-6147(91)90503-k.

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Shang, Liangcheng, Yaobiao Huang, Xin Xie, Sudan Ye i Chun Chen. "Effect of Adenosine Receptor Antagonists on Adenosine-Pretreated PC12 Cells Exposed to Paraquat". Dose-Response 20, nr 2 (kwiecień 2022): 155932582210934. http://dx.doi.org/10.1177/15593258221093411.

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Previous studies evaluated the adenosine receptor antagonists alone to determine their effects on oxidative stress, but little is known about adenosine’s protective efficacy when oxidative injury occurs in vivo. Adenosine is a crucial signaling molecule recognized by four distinct G-protein-coupled receptors (GPCRs) (i.e., A1R, A2AR, A2BR, and A3R) and protects cells against pathological conditions. The present study was performed to evaluate the role of antagonist modulation in the setting of paraquat toxicity with adenosine pretreatment. First, PC12 cells were exposed to paraquat (850 μM) and adenosine (30 μM) to develop an in vitro model for the antagonist effect assay. Second, we found that the A1R antagonist DPCPX enhanced the viability of paraquat-induced PC12 cells that underwent adenosine pretreatment. Moreover, the A2AR antagonist ZM241385 decreased the viability of paraquat-induced PC12 cells that underwent adenosine pretreatment. Our findings indicate that adenosine protection requires a dual blockade of A1R and activation of A2AR to work at its full potential, and the A2B and A3 adenosine receptor antagonists increased paraquat-induced oxidative damage. This represents a novel pharmacological strategy based on A1/A2A interactions and can assist in clarifying the role played by AR antagonists in the treatment of neurodegenerative diseases.
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Rozprawy doktorskie na temat "Adenosine"

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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.

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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
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
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Dulla, Chris. "Adenosine and adenosine triphosphate link Pco2 to cortical excitability via pH /". Connect to full text via ProQuest. IP filtered, 2005.

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Soledade, Cinira Santana. "O efeito do DMA (composto quinazolinico) sobre o processo inflamatorio". [s.n.], 2008. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310436.

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Orientadores: Lilian Tereza Lavras Costallat, Kleber Gomes Franchini
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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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
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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.

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Orientador: Fabio Erminio Mingatto
Banca: 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
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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.

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The 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.
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Chevallier, Olivier Paul. "Adenosine diphosphoribose synthetic analogues". Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501244.

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Wang, 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.

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Carlos, 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/.

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Na Anemia Falciforme em situações de baixa tensão de oxigênio, a hemoglobina mutante S (HbS) sofre polimerização promovendo a falcização das hemácias, que podem aderir ao endotélio vascular, causando a oclusão de vasos (VO) e isquemia tecidual (crises dolorosas) que caracterizam o quadro clínico da doença. Além disso, os pacientes falciformes apresentam outras manifestações clínicas como o priapismo, alterações ósseas, certas complicações pulmonares entre outros. Além das células eritróides, células endoteliais, leucócitos e plaquetas também desempenham um papel fundamental na fisiopatologia da anemia falciforme. A hidroxiuréia (HU), na anemia falciforme, aumenta a produção de hemoglobina fetal (HbF) em células eritróides, reduzindo a polimerização da HbS, diminuindo os sintomas clínicos dos pacientes. O aumento da HbF, no entanto, não implica necessariamente na melhora clínica, indicando desta forma a potencial ação da HU sobre outros processos. Estudos recentes vêm relacionando priapismo e asma com elevados níveis de adenosina. Devido a esta importância da adenosina relacionada a patologias comuns a AF, tivemos como objetivo identificar polimorfismos em genes de receptores de adenosina e na adenosina deaminase e verificar a possível associação entre as manifestações clínicas, além de investigar o papel da HU na modulação de marcadores envolvido na síntese e degradação da adenosina. Foram analisados diversos sítios polimórficos nos genes que codificam ADORA1, ADORA 2b, ADORA 3 e ADA, seguindo com a genotipagem em pacientes com AF, comparando afetados e não afetados. Em adição foi avaliada a expressão diferencial de mRNA de ADA pela HU em monócitos destes pacientes, comparando tratados e não tratados e também avaliamos por citometria de fluxo a modulação de marcadores de superfície CD39, CD73 e CD26, pela HU. As análises estatísticas foram realizadas utilizando os softwares GenePop 3.4 para análises de associação, cálculo do HWE, GraphPad Prism 5, Arlequin para identificação de desequilíbrio de ligação, haplótipos, heterozigozidade e SAS 9.13 para associação dos haplótipos as características. Os resultados mostraram que os pacientes sob tratamento com HU apresentaram um aumento da expressão de mRNA de ADA, aumento da expressão de CD26 em monócitos e diminuição de CD39 em linfócitos. Sem alterações significativas em relação a CD73. Encontramos também um aumento da freqüência do alelo T do SNP (rs1685103) presente no gene de ADORA 1 associado com pacientes afetados com síndrome torácica aguda. Apesar de não ter sido estatisticamente significante, concorda com dados da literatura. No gene ADORA 2B, verificamos associação do SNP 1007 C>T no desenvolvimento de STA indicando o alelo T como fator de risco e o alelo C para alterações ósseas. Para o SNP 968 G>T houve associação com alterações ósseas. Na análise haplotípica entre os SNPs 968 G>T e 1007 C>T encontramos associação dos haplótipos ht2 e ht3 com STA, como fator de risco, ht2 para hipertensão pulmonar. ht1 para priapismo, alterações ósseas e estenose/AVC. Os haplótipos formados pelos três SNPs 968 G>T, 1007 C>T e rs16851030, encontramos associação entre ht1, ht3 e ht4 entre os afetados com priapismo, caracterizando-o como haplótipo de risco e também ht1 e ht6 associados à estenose/AVC. Concluímos, que a hidroxiuréia participa na modulação da expressão da adenosina deaminase, de CD26 em monócitos e CD39 em linfócitos. Além disso, mostrou-se a importância de sítios polimórfico presente no gene ADORA 2B e ADORA1 envolvido na fisiopatologia das manifestações clínicas da doença falciforme. Associações dos SNPs em ADORA 1 e ADA, devem ser melhor estudados em um número maior de pacientes. A determinação destes polimorfismos associados com diferentes características clínicas pode levar a um melhor entendimento dos processos fisiopatológicos da anemia falciforme, levando à identificação de pacientes de risco, possibilitando um manejamento racional dos mesmos, em termos de cuidados específicos, ou mesmo à determinação de alvos para o desenvolvimento de terapias alternativas.
In 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.
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STEFANELLI, Angela. "Adenosine receptors in health and disease". Doctoral thesis, Università degli studi di Ferrara, 2014. http://hdl.handle.net/11392/2388942.

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Adenosine (Ado) is an endogenous nucleoside released from almost all cell types. It exerts neuroprotective and anti-inflammatory functions by acting through four receptor subtypes A1, A2A, A2B and A3 (ARs). These receptors differ in their affinity for Ado, in the type of G protein that they recruit and finally in the downstream signalling that are activated in target cells. The levels of Ado in the interstitial fluid are in the range of 20-200 nM, but many pathophysiological conditions such as asthma, neurodegenerative disorders, chronic inflammatory diseases and cancer are associated with changes in Ado levels. The primary aim of Ado is to reduce tissue injury and promote repair by different receptor-mediated mechanisms, including the increase of oxygen supply/demand ratio, anti-inflammatory effects and stimulation of angiogenesis. The investigation of ARs and their ligands is a rapidly growing field; there is extensive evidence for the involvement of ARs in the physiological regulation of several homeostatic processes and their implication in the ethiology of many diseases. The aim of this work was to analyse the expression of ARs and the signalling pathway, transcription factors and cytochines activated by them in different pathophysiological conditions linked to hypoxic and inflammatory conditions. At first, the role of ARs was studied in healthy and aneuploid pregnancies to understand reasons of spontaneous abortion (SA). It has been suggested that the causes of SA in aneuploidy are no different to those in euploidy, with the increased frequency in the former perhaps being ascribable to a genetically-determined imbalance in the mediators of placental perfusion and uterine contraction. So aneuploidy can be used as a model of this event. The ado transduction cascade appears to be disturbed in Trisomy 21 (TR21) through reduced expression of A2BAR and A1AR. These anomalies may be implicated in complications such as fetal growth restriction, malformation and/or SA, well known features of aneuploid pregnancies. Therefore A1AR and A2BAR could be potential biomarkers able to provide an early indication of SA risk and their stimulation may turn out to improve fetoplacental perfusion by increasing nitric oxide (NO) and vascular endothelial growth factor (VEGF). Next, the effects of ARs in glial cells under inflammatory conditions have been investigated. Glial cells, astrocytes and microglia, are important contributors to inflammatory immune responses and hypoxia-inducible factor 1 (HIF-1α) is the key transcription factor that is upregulated in response to hypoxia and inflammatory stimuli. Ado, through A1AR and A3AR activation, reduces lipopolysaccharide (LPS)-stimulated HIF-1α mRNA expression and protein accumulation by inhibiting LPS-triggered p42/p44 mitogen-activated protein kinase (p44/42 MAPK) and serine/threonine protein kinase (Akt) phosphorylation in normoxic and hypoxic conditions. This leads to an inhibition of genes involved in inflammation like Inducible Nitric Oxide Synthase (iNOS) and A2BARs, that are stimulated by LPS and further increased by LPS in concert with hypoxia, whilst does not affect angiogenesis and metabolic related genes, with the exception of glucose transporter 1 (GLUT1) and hexokinase 2 (HK2) that are stimulated by LPS in normoxia and reduced by A1AR and A3AR activation. These findings add a new molecular pathway activated by Ado in astrocytes to give a reduction of genes involved in inflammation and hypoxic injury that may cohexist in stroke, ischemia and other central nervous system (CNS) disorders.
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Molaudzi, 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.

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Thesis (MSc (Med)(Microbiology)) -- University of Limpopo, 2012.
Mycobacterium 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.
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Książki na temat "Adenosine"

1

Williams, Michael, red. Adenosine and Adenosine Receptors. Totowa, NJ: Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-4504-9.

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Williams, Michael, 1947 Jan. 3-, red. Adenosine and adenosine receptors. Clifton, N.J: Humana Press, 1990.

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Masino, Susan, i Detlev Boison, red. Adenosine. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-3903-5.

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F, Cooper Dermot M., i Londos Constantine, red. Adenosine receptors. New York: A.R. Liss, 1988.

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Borea, Pier Andrea, Katia Varani, Stefania Gessi, Stefania Merighi i Fabrizio Vincenzi, red. The Adenosine Receptors. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-90808-3.

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Paton, David M., red. Methods Used in Adenosine Research. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4886-3.

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1938-, Paton David M., red. Methods used in adenosine research. New York: Plenum Press, 1985.

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Hiroshi, Kase, Richardson Peter J i Jenner P. G, red. Adenosine receptors and Parkinson's disease. San Diego, Calif: Academic, 2000.

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Hiroshi, Kase, Richardson Peter J i Jenner Peter 1946-, red. Adenosine receptors and Parkinson's disease. San Diego, CA: Academic Press, 2000.

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W, Stone T., red. Adenosine in the nervous system. London: Academic Press, 1991.

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Części książek na temat "Adenosine"

1

Fredholm, Bertil B. "Adenosine and Metabolism—A Brief Historical Note". W Adenosine, 3–19. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_1.

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Porkka-Heiskanen, Tarja. "Sleep and Adenosine: Human Studies". W Adenosine, 201–12. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_10.

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Muheim, Christine, i Steven A. Brown. "Adenosine and Other Purinergic Products in Circadian Timing". W Adenosine, 213–32. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_11.

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Haskó, György, Balázs Koscsó i Balázs Csóka. "Adenosine in the Immune System". W Adenosine, 233–51. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_12.

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Drew, Kelly L., i Tulasi R. Jinka. "The Bioenergetic Network of Adenosine in Hibernation, Sleep, and Thermoregulation". W Adenosine, 253–72. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_13.

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Pedata, Felicita, Anna Maria Pugliese, Francesca Corti i Alessia Melani. "Adenosine and Stroke". W Adenosine, 273–306. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_14.

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Kochanek, Patrick M., Jonathan D. Verrier, Amy K. Wagner i Edwin K. Jackson. "The Many Roles of Adenosine in Traumatic Brain Injury". W Adenosine, 307–22. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_15.

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Nantwi, Kwaku D. "Therapeutic Perspectives of Adenosine Receptor Compounds in Functional Restitution After Spinal Cord Injury". W Adenosine, 323–42. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_16.

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Sawynok, Jana. "Adenosine and Pain". W Adenosine, 343–60. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_17.

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Pinna, Annalisa, Nicola Simola, Lucia Frau i Micaela Morelli. "Symptomatic and Neuroprotective Effects of A2A Receptor Antagonists in Parkinson’s Disease". W Adenosine, 361–84. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_18.

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Streszczenia konferencji na temat "Adenosine"

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Lexmond, Anne J., Ilse Boudewijn, Paul Hagedoorn, Siebrig Schokker, Claire Cox, Judith Vonk, Nick ten Hacken i in. "An improved bronchial provocation test with dry powder adenosine instead of nebulised adenosine monophosphate (AMP)". W ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa4756.

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Feng Zhang, Keisuke Tominaga, Jun-ichi Nishizawa, Ohki Kambara, Tetsuo Sasaki, Houng-Wei Wang i Michitoshi Hayashi. "Terahertz spectroscopy of adenine and adenosine". W 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.

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Sundaresan, Vishnu Baba, Stephen Andrew Sarles i Donald J. Leo. "Chemoelectrical energy conversion of adenosine triphosphate". W The 14th International Symposium on: Smart Structures and Materials & Nondestructive Evaluation and Health Monitoring, redaktorzy Yuji Matsuzaki, Mehdi Ahmadian i Donald J. Leo. SPIE, 2007. http://dx.doi.org/10.1117/12.715715.

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Lin, Juqiang, Yating Lin, Yiming Huang, Zhiwei Wu, Jianshu Xu, Ya Hu i Shusen Xie. "Quantitative FRET measurement of the interaction of A1 adenosine receptors and A2A adenosine receptors in living cell". W Optics in Health Care and Biomedical Optics VIII, redaktorzy Qingming Luo, Xingde Li, Yuguo Tang i Ying Gu. SPIE, 2018. http://dx.doi.org/10.1117/12.2500692.

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DiRenzo, Daniel, Dana Piovesan, Joanne Tan, Dillon H. Miles, Manmohan R. Leleti, Timothy Park, Ferdie Soriano i in. "Abstract A162: AB928, a dual antagonist of the A2aR and A2bR adenosine receptors, relieves adenosine-mediated immune suppression". W 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.

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Londoño-R, Luz Marina, Jessica Cowell, Lin Wang, Qiping Zhao, Lei Huang, Chris Thanos, Michael J. LaBarre, Xiaoming Li i Caglar Cekic. "Abstract 1755: PEGylated adenosine deaminase (ADA2) prevents adenosine-mediated increase in tumor growth and improves antitumor immune responses". W 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.

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Serra, Sara, Cinzia Bologna, Luz Londono, Lin Wang, Michael Shepard, Sanna Rosengren, Christopher Thanos i Silvia Deaglio. "Abstract 5583: Pegylated adenosine deaminase 2 (PEG-ADA2) abrogates the cytoprotective effects of adenosine against chronic lymphocytic leukemia cells". W 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.

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Houthuys, Erica, Paola Basilico, Veronique Bodo, Margreet Brouwer, Michel Detheux, Gregory Driessens, Bruno Gomes i in. "Abstract 3278: EOS100850 potently restores adenosine A2Areceptor-dependent suppression of T cell function in the adenosine rich tumor microenvironment". W 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.

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Houthuys, Erica, Paola Basilico, Veronique Bodo, Margreet Brouwer, Michel Detheux, Gregory Driessens, Bruno Gomes i in. "Abstract 3278: EOS100850 potently restores adenosine A2Areceptor-dependent suppression of T cell function in the adenosine rich tumor microenvironment". W 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.

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Van Rompaey, Philippe, Kenneth A. Jacobson, Zhan-Guo Gao, Aishe Chen, Dov Barak, Soon-Ai Kim, Kyeong Lee i in. "Amine-modified nucleosides as adenosine A3 neoceptor ligands". W 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.

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Raporty organizacyjne na temat "Adenosine"

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Liou, Gregory I., Saif Ahmad, Mohammad Naime, Nadeem Fatteh i Sohail Khan. Role of Adenosine Receptor A2A in Traumatic Optic Neuropathies. Fort Belvoir, VA: Defense Technical Information Center, grudzień 2012. http://dx.doi.org/10.21236/ada581642.

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Liou, Gregory I., Saif Ahmad i Ahmed Elsherbini. Role of Adenosine Receptor A2A in Traumatic Optic Neuropathies. Fort Belvoir, VA: Defense Technical Information Center, grudzień 2013. http://dx.doi.org/10.21236/ada600384.

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Spychala, Jozef. Growth-Promoting and Angiogenic Functions of Adenosine in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, grudzień 2004. http://dx.doi.org/10.21236/ada432030.

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Spychala, Jozef. Growth-Promoting and Angiogenic Functions in Adenosine in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2003. http://dx.doi.org/10.21236/ada420393.

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Schwarzshild, Michael A. Caffeine, Adenosine Receptors and Estrogen in Toxin Models of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, październik 2006. http://dx.doi.org/10.21236/ada462198.

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Schwarzschild, Michael A. Caffeine, Adenosine Receptors and Estrogen in Toxin Models of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, październik 2009. http://dx.doi.org/10.21236/ada625341.

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Ye, Libin, Christopher Andrew Neale, Adnan Sljoka, Brent Lyda, Dmitry Pichugin, Nobuyuki Tsuchimura, Sacha T. Larda i in. Mechanistic insights into allosteric regulation of the A2A adenosine G protein-coupled receptor by physiological cations. Office of Scientific and Technical Information (OSTI), kwiecień 2018. http://dx.doi.org/10.2172/1434450.

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Deutsch, Christopher. Discovery and Characterization of the Proteins Involved in the Synthesis of N⁶-Threonylcarbamoyl Adenosine, a Nucleoside Modification of tRNA. Portland State University Library, styczeń 2000. http://dx.doi.org/10.15760/etd.3075.

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Xi, Yin, Zheng Gao, Jiyuan Ni, Yang Li, Wenyu Zhang i 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, maj 2022. http://dx.doi.org/10.37766/inplasy2022.5.0076.

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