Academic literature on the topic 'Adenosine deaminase'
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Journal articles on the topic "Adenosine deaminase"
Roth, E. Jr, N. Ogasawara, and S. Schulman. "The deamination of adenosine and adenosine monophosphate in Plasmodium falciparum-infected human erythrocytes: in vitro use of 2'deoxycoformycin and AMP deaminase-deficient red cells." Blood 74, no. 3 (August 15, 1989): 1121–25. http://dx.doi.org/10.1182/blood.v74.3.1121.1121.
Full textRoth, E. Jr, N. Ogasawara, and S. Schulman. "The deamination of adenosine and adenosine monophosphate in Plasmodium falciparum-infected human erythrocytes: in vitro use of 2'deoxycoformycin and AMP deaminase-deficient red cells." Blood 74, no. 3 (August 15, 1989): 1121–25. http://dx.doi.org/10.1182/blood.v74.3.1121.bloodjournal7431121.
Full textKeegan, Liam P., André P. Gerber, Jim Brindle, Ronny Leemans, Angela Gallo, Walter Keller, and Mary A. O'Connell. "The Properties of a tRNA-Specific Adenosine Deaminase from Drosophila melanogaster Support an Evolutionary Link between Pre-mRNA Editing and tRNA Modification." Molecular and Cellular Biology 20, no. 3 (February 1, 2000): 825–33. http://dx.doi.org/10.1128/mcb.20.3.825-833.2000.
Full textZhu, Q., G. P. Matherne, R. R. Curnish, C. G. Tribble, and R. M. Berne. "Effect of adenosine deaminase on cardiac interstitial adenosine." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 4 (October 1, 1992): H1322—H1326. http://dx.doi.org/10.1152/ajpheart.1992.263.4.h1322.
Full textKroll, K., and E. O. Feigl. "Adenosine is unimportant in controlling coronary blood flow in unstressed dog hearts." American Journal of Physiology-Heart and Circulatory Physiology 249, no. 6 (December 1, 1985): H1176—H1187. http://dx.doi.org/10.1152/ajpheart.1985.249.6.h1176.
Full textHirschhorn, Rochelle. "Adenosine Deaminase Deficiency." Hospital Practice 22, no. 6 (June 15, 1987): 149–56. http://dx.doi.org/10.1080/21548331.1987.11703253.
Full textBagheri, S., A. A. Saboury, and T. Haertlé. "Adenosine deaminase inhibition." International Journal of Biological Macromolecules 141 (December 2019): 1246–57. http://dx.doi.org/10.1016/j.ijbiomac.2019.09.078.
Full textMartin, Margarita, Josep M. Aran, Dolors Colomer, Joan Huguet, Josep Joan Centelles, Joan Lluis Vives-Corrons, and Rafael Franco. "Surface adenosine deaminase." Human Immunology 42, no. 3 (March 1995): 265–73. http://dx.doi.org/10.1016/0198-8859(94)00097-a.
Full textSchrader, W. P., C. A. West, and N. L. Strominger. "Localization of adenosine deaminase and adenosine deaminase complexing protein in rabbit brain." Journal of Histochemistry & Cytochemistry 35, no. 4 (April 1987): 443–51. http://dx.doi.org/10.1177/35.4.3546489.
Full textHashikawa, T., M. Takedachi, M. Terakura, S. Yamada, L. F. Thompson, Y. Shimabukuro, and S. Murakami. "Activation of Adenosine Receptor on Gingival Fibroblasts." Journal of Dental Research 85, no. 8 (August 2006): 739–44. http://dx.doi.org/10.1177/154405910608500810.
Full textDissertations / Theses on the topic "Adenosine deaminase"
Abbott, C. M. "Adenosine deaminase in the wasted mouse." Thesis, University of Reading, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.374695.
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.
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.
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/.
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.
Dinjens, Winandus Nicolaas Maria. "Distribution of adenosine deaminase complexing protein in normal and neoplastic cells." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1988. http://arno.unimaas.nl/show.cgi?fid=5412.
Full textBjörkegren, Emma Katia Madeleine. "Development of gene therapy for the treatment of adenosine deaminase deficiency." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1444352/.
Full textOliveira, Camila Belmonte. "Atividade das enzimas ntpdase, 5´-nucleotidase e adenosina deaminase em plaquetas de ratos infectados por Trypanosoma evansi." Universidade Federal de Santa Maria, 2010. http://repositorio.ufsm.br/handle/1/10079.
Full textNucleotide- and nucleoside-degrading enzymes are present in the surface of platelets, blood cells involved in clotting disturbances of Trypanosoma evansi-infected animals. Thus, this study was aimed at evaluating the activity of the enzymes NTPDase, 5 - nucleotidase and adenosine deaminase in platelets of rats experimentally infected by T. evansi. Animals were divided into four groups, according to the degree of parasitemia. Samples were collected at days 3 (group A: at the beginning of parasitemia), 5 (group B: high parasitemia) and 15 (group C: chronic infection). Group D (control group) was composed of non-infected animals. Blood samples with citrate as the anticoagulant were collected and used for platelet separation and enzymatic assays. NTPDase, 5 - nucleotidase and adenosine deaminase (ADA) activities were decreased (p<0.05) in platelets from rats of groups A and B, when compared to the control group. In group C, only NTPDase and 5 -nucleoside activities were decreased (p<0.001), observed by ADP and AMP hydrolysis. The correlation between platelet count and nucleotide and nucleoside hydrolysis was positive and statistically significant (p<0.05) in groups A and B. Platelet aggregation of all infected groups was decreased in comparison to the control group (p<0.05). Based upon the results, it is concluded that the alterations observed in the activity of the enzymes NTPDase, 5 -nucleotidase and adenosine deaminase in platelets of T. evansi-infected animals might be related to thrombocytopenia.
Nucleotide- and nucleoside-degrading enzymes are present in the surface of platelets, blood cells involved in clotting disturbances of Trypanosoma evansi-infected animals. Thus, this study was aimed at evaluating the activity of the enzymes NTPDase, 5 - nucleotidase and adenosine deaminase in platelets of rats experimentally infected by T. evansi. Animals were divided into four groups, according to the degree of parasitemia. Samples were collected at days 3 (group A: at the beginning of parasitemia), 5 (group B: high parasitemia) and 15 (group C: chronic infection). Group D (control group) was composed of non-infected animals. Blood samples with citrate as the anticoagulant were collected and used for platelet separation and enzymatic assays. NTPDase, 5 - nucleotidase and adenosine deaminase (ADA) activities were decreased (p<0.05) in platelets from rats of groups A and B, when compared to the control group. In group C, only NTPDase and 5 -nucleoside activities were decreased (p<0.001), observed by ADP and AMP hydrolysis. The correlation between platelet count and nucleotide and nucleoside hydrolysis was positive and statistically significant (p<0.05) in groups A and B. Platelet aggregation of all infected groups was decreased in comparison to the control group (p<0.05). Based upon the results, it is concluded that the alterations observed in the activity of the enzymes NTPDase, 5 -nucleotidase and adenosine deaminase in platelets of T. evansi-infected animals might be related to thrombocytopenia.
Roura, Frigolé Helena. "Biomedical studies of human adenosine deaminase acting on transfer RNA and related therapeutic strategies." Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/650900.
Full textL’adenosina deaminasa específica per RNA de transferència (ADAT) és un enzim humà heterodimèric que catalitza la reacció de deaminació de l’adenosina (A) a inosina (I) a la primera posició de l’anticodó de RNAs de transferència (tRNAs) (també anomenada posició 34 o posició de balanceig); una de les poques modificacions post-transcripcionals essencials en tRNAs (1-5). La inosina 34 permet el reconeixement de tres nucleòtids diferents: citidina, uridina i adenosina, a la tercera posició del codó, augmentant per tant la capacitat de descodificació dels tRNAs a més d’un codó en l’RNA missatger (mRNA) (l’adenosina 34 en principi únicament pot aparellar-se amb uridina en la tercera posició) (6, 7). Això altera els nivells de tRNAs disponibles per cada codó i s’ha demostrat que alinea la correlació entre l’ús de codons i número de còpies gèniques de cada tRNA (8). També s’ha suggerit que millora la fidelitat i eficiència de la traducció (8, 9), especialment per mRNAs enriquits en codons traduïts per tRNA modificats (10, 11). Monitoritzar la deaminació produïda per ADAT és clau per la caracterització de l’enzim en termes d’activitat, substrats, regulació, així com també pel disseny de fàrmacs. No obstant, aquest anàlisi és sovint complex, laboriós i poc quantitatiu. Per això, hem desenvolupat un assaig de deaminació in vitro basat en el polimorfisme de longitud dels fragments de restricció (RFLP) amb el propòsit de monitoritzar l’activitat d’ADAT de manera eficient, cost-efectiva i semiquantitativa (12). Per superar una limitació del mètode essent la necessitat de transcripció reversa i amplificació del tRNA, hem dissenyat un mètode directe per quantificar la formació d’I34 in vitro utilitzant els primers anàlegs fluorescents d’àcids nucleics que són substrats de deaminacions enzimàtiques descrits fins al moment (13-15). ADAT ha estat conservat en l’evolució amb l’adquisició de multi-especificitat de substrat. Mentre que el seu homòleg bacterià TadA deamina exclusivament tRNAArg (2), l’enzim humà deamina vuit tRNAs diferents (3, 16). Tot i així, els mecanismes que van conduir a aquesta evolució romanen desconeguts. Mentre que el reconeixement de substrat en TadA es coneix bé, en ADAT eucariòtic ha estat poc estudiat. A través d’assajos enzimàtics in vitro amb diferents variants de tRNAArg i tRNAAla, hem elucidat els trets més importants per a una conversió eficient d’A34 a I34 i hem caracteritzat el reconeixement de substrat per part de l’enzim humà. També proposem un nou potencial mecanisme de control de l’activitat d’ADAT per part de fragments derivats de tRNAs humans, el qual ofereix noves perspectives en la regulació de la funció d’ADAT i que pot obrir la porta al desenvolupament de noves estratègies per modular-ne l’activitat. Una mutació sense sentit (V128M) en una de les dues subunitats en l’enzim ADAT humà s’ha associat a retard mental i estrabisme, encara que les bases moleculars de la patologia es desconeixen (17, 18). Hem caracteritzat ADAT humà en termes de cinètica enzimàtica i estructura, i n’hem investigat l’efecte de la mutació V128M. Hem descobert que la substitució de valina 128 per metionina redueix l’activitat deaminatòria d’ADAT i que altera severament l’estabilitat de l’estructura quaternària de l’enzim. En aquest aspecte, hem descobert molècules amb l’habilitat d’activar l’enzim, la qual cosa podria revertir potencialment la reducció en l’activitat enzimàtica causada per la mutació. References 1. Gerber AP, Keller W. An adenosine deaminase that generates inosine at the wobble position of tRNAs. Science. 1999;286(5442):1146-9. Epub 1999/11/05. 2. Wolf J, Gerber AP, Keller W. tadA, an essential tRNA-specific adenosine deaminase from Escherichia coli. The EMBO journal. 2002;21(14):3841-51. Epub 2002/07/12. 3. Torres AG, Pineyro D, Rodriguez-Escriba M, Camacho N, Reina O, Saint-Leger A, et al. Inosine modifications in human tRNAs are incorporated at the precursor tRNA level. Nucleic acids research. 2015;43(10):5145-57. Epub 2015/04/29. 4. Zhou W, Karcher D, Bock R. Identification of enzymes for adenosine-to-inosine editing and discovery of cytidine-to-uridine editing in nucleus-encoded transfer RNAs of Arabidopsis. Plant physiology. 2014;166(4):1985-97. Epub 2014/10/16. 5. Tsutsumi S, Sugiura R, Ma Y, Tokuoka H, Ohta K, Ohte R, et al. Wobble inosine tRNA modification is essential to cell cycle progression in G(1)/S and G(2)/M transitions in fission yeast. J Biol Chem. 2007;282(46):33459-65. Epub 2007/09/19. 6. Crick FH. Codon--anticodon pairing: the wobble hypothesis. Journal of molecular biology. 1966;19(2):548-55. Epub 1966/08/01. 7. Torres AG, Pineyro D, Filonava L, Stracker TH, Batlle E, Ribas de Pouplana L. A-to-I editing on tRNAs: biochemical, biological and evolutionary implications. FEBS Lett. 2014;588(23):4279-86. Epub 2014/09/30. 8. Novoa EM, Pavon-Eternod M, Pan T, Ribas de Pouplana L. A role for tRNA modifications in genome structure and codon usage. Cell. 2012;149(1):202-13. Epub 2012/04/03. 9. Schaub M, Keller W. RNA editing by adenosine deaminases generates RNA and protein diversity. Biochimie. 2002;84(8):791-803. Epub 2002/11/30. 10. Rafels-Ybern A, Attolini CS, Ribas de Pouplana L. Distribution of ADAT-Dependent Codons in the Human Transcriptome. International journal of molecular sciences. 2015;16(8):17303- 14. Epub 2015/08/01. 11. Rafels-Ybern A, Torres AG, Grau-Bove X, Ruiz-Trillo I, de Pouplana LR. Codon adaptation to tRNAs with Inosine modification at position 34 is widespread among Eukaryotes and present in two Bacterial phyla. RNA biology. 2017:0. Epub 2017/09/08. 12. Wulff TF, Arguello RJ, Molina Jordan M, Roura Frigole H, Hauquier G, Filonava L, et al. Detection of a Subset of Posttranscriptional Transfer RNA Modifications in Vivo with a Restriction Fragment Length Polymorphism-Based Method. Biochemistry. 2017;56(31):4029-38. Epub 2017/07/14. 13. Sinkeldam RW, McCoy LS, Shin D, Tor Y. Enzymatic interconversion of isomorphic fluorescent nucleosides: adenosine deaminase transforms an adenosine analogue into an inosine analogue. Angew Chem Int Ed Engl. 2013;52(52):14026-30. Epub 2013/11/30. 14. McCoy LS, Shin D, Tor Y. Isomorphic emissive GTP surrogate facilitates initiation and elongation of in vitro transcription reactions. Journal of the American Chemical Society. 2014;136(43):15176-84. Epub 2014/09/26. 15. Rovira AR, Fin A, Tor Y. Chemical Mutagenesis of an Emissive RNA Alphabet. J Am Chem Soc. 2015;137(46):14602-5. Epub 2015/11/03. 16. Juhling F, Morl M, Hartmann RK, Sprinzl M, Stadler PF, Putz J. tRNAdb 2009: compilation of tRNA sequences and tRNA genes. Nucleic acids research. 2009;37(Database issue):D159-62. Epub 2008/10/30. 17. Alazami AM, Hijazi H, Al-Dosari MS, Shaheen R, Hashem A, Aldahmesh MA, et al. Mutation in ADAT3, encoding adenosine deaminase acting on transfer RNA, causes intellectual disability and strabismus. Journal of medical genetics. 2013;50(7):425-30. Epub 2013/04/27. 18. El-Hattab AW, Saleh MA, Hashem A, Al-Owain M, Asmari AA, Rabei H, et al. ADAT3- related intellectual disability: Further delineation of the phenotype. American journal of medical genetics Part A. 2016;170A(5):1142-7. Epub 2016/02/05.
Samee, Abdus. "An analysis of the ADAT1 (adenosine deaminase, tRNA- specific 1) gene in cancer." Thesis, Keele University, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.530765.
Full textChielle, Eduardo Ottobelli. "EFEITO DA RUTINA SOBRE A ATIVIDADE DA ADENOSINA DEAMINASE EM RATOS DIABÉTICOS." Universidade Federal de Santa Maria, 2012. http://repositorio.ufsm.br/handle/1/5921.
Full textO Diabetes mellitus (DM) é uma disfunção metabólica de múltipla etiologia caracterizado por hiperglicemia crônica resultante da deficiência da produção e/ou ação da insulina. Esse estado de hiperglicemia pode provocar uma série de complicações cardiovasculares, renais, neurológicas e oculares. A Adenosina deaminase (ADA) é uma importante enzima responsável por regular os níveis de adenosina (ado), um importante nucleosídeo componente do sistema purinérgico. Alterações na atividade da ADA têm sido demonstradas em várias doenças, incluindo o DM. A rutina (RT) é um flavonoide polifenólico abundante nos alimentos que exibe múltiplas atividades farmacológicas como atividade antibacteriana, antitumoral, vasodilatadora e hepatoprotetora. O objetivo deste estudo foi verificar o efeito da RT sobre a atividade da ADA sérica e tecidual e parâmetros bioquímicos em modelos de diabetes induzidos por estreptozotocina (STZ). O diabetes foi induzido através de injeção única intraperitoneal (i.p.) de 55 mg/kg de STZ. A RT (100 mg / kg / dia) e a glibenclamida (10mg/kg/dia) foram administradas durante 30 dias, com exceção dos grupos controles (não diabéticos e diabéticos). Seis grupos de ratos foram utilizados no estudo e agrupados com base nos níveis de glicose em jejum após a indução de diabetes. Os resultados demonstraram um aumento na atividade da ADA no soro e no fígado de ratos diabéticos, assim como das transaminases (AST, ALT), -glutamiltransferase (-GT) e glicose. A RT na concentração de 100 mg/kg foi capaz de reduzir a atividade sérica e em tecido hepático da ADA quando comparado com o controle. O efeito protetor da RT também foi observado sobe a atividade das enzimas ALT e -GT. Reduções significativas foram observadas no colesterol total e LDL-colesterol, bem como, na concentração sérica de glicose no grupo diabético tratado com RT. Os resultados sugerem que a RT pode melhorar a hiperglicemia e dislipidemia, restabelecer danos à função hepática, bem como é capaz de prevenir o aumento da atividade da ADA no soro e no fígado de ratos diabéticos tratados com este flavonoide.
Books on the topic "Adenosine deaminase"
L, Tritsch George, New York Academy of Sciences., and Conference on Adenosine Deaminase in Disorders of Purine Metabolism and in Immune Deficiency (1984 : New York, N.Y.), eds. Adenosine deaminase in disorders of purine metabolism and in immune deficiency. New York, N.Y: New York Academy of Sciences, 1985.
Find full textAdenosine deaminases acting on RNA (ADARs) and A-to-I editing. Heidelberg: Springer, 2012.
Find full textChu, Peter Pui Tak. Retroviral-mediated human adenosine deaminase gene transfer into human hematopoietic progenitor and stem cells. Ottawa: National Library of Canada, 1995.
Find full textSamuel, Charles E., ed. Adenosine Deaminases Acting on RNA (ADARs) and A-to-I Editing. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-22801-8.
Full textGeha, Raif, and FRED Rosen. Case Studies in Immunology: Adenosine Deaminase Deficiency. W.W. Norton & Company, 2010. http://dx.doi.org/10.4324/9780203853566.
Full textGeha, Raif, and Fred Rosen. Case Studies in Immunology : Adenosine Deaminase Deficiency: A Clinical Companion. Norton & Company, Incorporated, W. W., 2010.
Find full textGeha, Raif, and Fred Rosen. Case Studies in Immunology : Adenosine Deaminase Deficiency: A Clinical Companion. Norton & Company, Incorporated, W. W., 2010.
Find full textGeha, Raif, and Fred Rosen. Case Studies in Immunology : Adenosine Deaminase Deficiency: A Clinical Companion. Norton & Company, Incorporated, W. W., 2010.
Find full textGeha, Raif, and Fred Rosen. Case Studies in Immunology : Adenosine Deaminase Deficiency: A Clinical Companion. Norton & Company, Incorporated, W. W., 2010.
Find full textGeha, Raif, and Fred Rosen. Case Studies in Immunology : Adenosine Deaminase Deficiency: A Clinical Companion. Taylor & Francis Group, 2010.
Find full textBook chapters on the topic "Adenosine deaminase"
Schomburg, Dietmar, and Margit Salzmann. "Adenosine deaminase." In Enzyme Handbook 4, 999–1003. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84437-9_199.
Full textAgarwal, Ram P. "Adenosine Deaminase." In Methods Used in Adenosine Research, 109–25. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4886-3_6.
Full textSchomburg, Dietmar, and Margit Salzmann. "Adenosine-phosphate deaminase." In Enzyme Handbook 4, 1059–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84437-9_212.
Full textScharnagl, Hubert, Winfried März, Markus Böhm, Thomas A. Luger, Federico Fracassi, Alessia Diana, Thomas Frieling, et al. "Adenosine Deaminase Deficiency." In Encyclopedia of Molecular Mechanisms of Disease, 36–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_52.
Full textBelmont, J. W., J. Henkel-Tigges, K. Wager-Smith, S. M. W. Chang, and C. Th Caskey. "Adenosine Deaminase Gene Transfer." In Human Genetics, 639–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71635-5_88.
Full textKelley, William N., Peter E. Daddona, and Martin B. van der Weyden. "Characterization of Human Adenosine Deaminase." In Ciba Foundation Symposium 48 - Purine and Pyrimidine Metabolism, 277–93. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720301.ch16.
Full textGeiger, Jonathan D., and James I. Nagy. "Adenosine Deaminase and [3H] Nitrobenzylthioinosine as Markers of Adenosine Metabolism and Transport in Central Purinergic Systems." In Adenosine and Adenosine Receptors, 225–88. Totowa, NJ: Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-4504-9_7.
Full textGeiger, J. D., R. A. Padua, and J. I. Nagy. "Adenosine Deaminase and Adenosine Transport Systems in the CNS." In Purines in Cellular Signaling, 20–25. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3400-5_3.
Full textOmbrello, Amanda, and Reeval Segel. "Deficiency of Adenosine Deaminase 2 (DADA2)." In Textbook of Autoinflammation, 417–31. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-98605-0_23.
Full textSimmonds, H. Anne, A. Sahota, C. F. Potter, D. Perrett, K. Hugh-Jones, and J. G. Watson. "Purine Metabolism in Adenosine Deaminase Deficiency." In Ciba Foundation Symposium 68 - Enzyme Defects and Immune Dysfunction, 255–79. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720516.ch16.
Full textConference papers on the topic "Adenosine deaminase"
Pereira, Flávio Ribeiro, Blanca Helena Rios Gomes Bica, Maria Pompeya Olmedo de Lopes de Figueiredo, Rodrigo Lousada, Virginia de Souza Guimarães Merat, Dimona Carvalho Vivas Amado, and Mariana Ferreira Vieira. "Deficiency of Adenosine Deaminase 2: a rare disease." In XXXIX Congresso Brasileiro de Reumatologia. Sociedade Brasileiro de Reumatologia, 2022. http://dx.doi.org/10.47660/cbr.2022.2212.
Full textSharoyan, S., L. Karapetyan, R. Harutyunyan, S. Mardanyan, and A. Antonyan. "SAT0051 Citrullination of adenosine deaminase isoforms in rheumatoid arthritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.1433.
Full textTofovic, Stevan P., Victor Bilan, Edwin K. Jackson, and OLGA Rafikova. "Role Of Plasma Adenosine Deaminase In Hemolysis-Induced Pulmonary Hypertension." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6335.
Full textPARENTE, JOSÉ SÁVIO MENEZES, AMANDA VIRGINIA BATISTA CAVALCANTE, and THAÍS GUERREIRO JORGE ROCHA. "POLYARTERITIS NODOSA OR DEFICIENCY OF ADENOSINE DEAMINASE 2?: CASE REPORT." In 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-207.
Full textCho, Yu Ji, Jong Deog Lee, Eun Young Yun, Young Sil Hwang, Jung Eun Ma, Yi Yeong Jeong, Ho Cheol Kim, and Hyeon Sik Kim. "Clinical Characteristics Of Tuberculous Pleurisy Patients With Low Adenosine Deaminase Levels." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1781.
Full textKiryukhina, Larisa, Marina Dyakova, and Diljara Esmedlyaeva. "Adenosine deaminase in the COPD pathogenesis in patients with pulmonary tuberculosis." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa2718.
Full textTrajcevska, Mirjana, and Aleksandar Sandevski. "Activity of lysozyme and adenosine deaminase in patients with pulmonary tuberculosis." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa4762.
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 textXie, Jing, Hua Wei, and Xiaoxing Xiang. "AB1111 RELATIONSHIP BETWEEN SERUM ADENOSINE DEAMINASE LEVELS AND DISEASE ACTIVITY IN AUTOIMMUNE HEPATITIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.3679.
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