Relevant bibliographies by topics / Uracila

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  2. Dissertations / Theses
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  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Uracila'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "Uracila"

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Fernandes, Roberta Siqueira, and Anderson José de Oliveira. "Extensão de Galois GF(2^6) Aplicada na Modelagem do Código Genético." INTERMATHS 2, no. 1 (2021): 35–52. http://dx.doi.org/10.22481/intermaths.v2i1.8412.

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Para a comunidade científica, um dos maiores desafios é analisar a existência de uma estrutura matemática relacionada com o DNA. Muitas pesquisas vêm sendo realizadas envolvendo o código genético, entre outros fenômenos biológicos, utilizandoa Matemática para contribuir na análise e descrição desses conceitos teóricos. Os códons são formados por uma trinca de bases nitrogenadas, com 64 combinações possíveis. As bases nitrogenadas são a adenina, citosina, guanina e timina/uracila, que são representa das pelas letras A,C,GeT/U, respectivamente, e representamo alfabeto do DNA e por meio da bijeção desse alfabeto com anel Z_4 = {0,1,2,3} é possível obter 24 permutações, que podem ser divididas em 3 rotulamentos (A, B e C). O objetivo deste trabalho é apresentar a utilização de elementos de álgebra na modelagem do código genético. Serão apresentadas uma representação polinomial, vetorial e por potência para a estrutura do código genético, onde para cada códon foi associado um elemento da extensão GF(2^6), uma vez que vemos que existe uma associação um-a-um dos códons do código genético com um elemento da extensão de Galois. Foi obtida a caracterização algébrica para os rotulamentosA, B e C do código genético, por meio dessas representações mencionadas anteriormente, as quais poderão ser utilizadas em futuros estudos envolvendo a análise do código genético.
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Bojarska, Elżbieta, Jarosław Kamiński, Ryszard Stolarski, and Zygmunt Kazimierczuk. "Novel Electrochemically Derived Dimers of Methylated Uracils." Zeitschrift für Naturforschung B 52, no. 6 (1997): 742–48. http://dx.doi.org/10.1515/znb-1997-0612.

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Abstract Electrolysis of acetic acid/sodium acetate solutions of N-methylated uracils results in the formation of 5-substituted methyl and acethoxy derivatives. Electrolysis of trifluoroacetic acid/potassium trifluoroacetate solutions of N-1-and N-3-methylated uracils provided, be­ sides 5-trifluoromethyl derivatives, novel N-C uracil dimers. In the case of 1,3-dimethyluracil in trifluoroacetic acid. N-l demethylathion was also observed.
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Maruyama, Tokumi, Shigetada Kozai, Tetsuo Yamasaki, et al. "Synthesis and Antiviral Activity of 1,3-Disubstituted Uracils against HIV-1 and HCMV." Antiviral Chemistry and Chemotherapy 14, no. 5 (2003): 271–79. http://dx.doi.org/10.1177/095632020301400506.

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The development of new non-nucleoside reverse transcriptase inhibitors (NNRTIs) is an efficient strategy for finding new therapeutic agents against human immunodeficiency virus (HIV). A large number of 6-substituted uracil derivatives have been prepared in order to explore new NNRTIs. However, there are few approaches to anti-HIV agents from 1,3-disubstituted uracil derivatives. Therefore, we tried to prepare several 1,3-disubstituted uracils, which were easily obtainable from uracil by preparation under alkali and Mitsunobu conditions, and examined their antiviral activity against HIV-1 and human cytomegalovirus (HCMV). We found that 1-benzyl-3-(3,5-dimethylbenzyl)uracil and 1-cyanomethyl-3-(3,5-dimethylbenzyl)-4-thiouracil showed powerful inhibition against HCMV and HIV-1, respectively.
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Girelli Zubani, Giulia, Marija Zivojnovic, Annie De Smet, et al. "Pms2 and uracil-DNA glycosylases act jointly in the mismatch repair pathway to generate Ig gene mutations at A-T base pairs." Journal of Experimental Medicine 214, no. 4 (2017): 1169–80. http://dx.doi.org/10.1084/jem.20161576.

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During somatic hypermutation (SHM) of immunoglobulin genes, uracils introduced by activation-induced cytidine deaminase are processed by uracil-DNA glycosylase (UNG) and mismatch repair (MMR) pathways to generate mutations at G-C and A-T base pairs, respectively. Paradoxically, the MMR-nicking complex Pms2/Mlh1 is apparently dispensable for A-T mutagenesis. Thus, how detection of U:G mismatches is translated into the single-strand nick required for error-prone synthesis is an open question. One model proposed that UNG could cooperate with MMR by excising a second uracil in the vicinity of the U:G mismatch, but it failed to explain the low impact of UNG inactivation on A-T mutagenesis. In this study, we show that uracils generated in the G1 phase in B cells can generate equal proportions of A-T and G-C mutations, which suggests that UNG and MMR can operate within the same time frame during SHM. Furthermore, we show that Ung−/−Pms2−/− mice display a 50% reduction in mutations at A-T base pairs and that most remaining mutations at A-T bases depend on two additional uracil glycosylases, thymine-DNA glycosylase and SMUG1. These results demonstrate that Pms2/Mlh1 and multiple uracil glycosylases act jointly, each one with a distinct strand bias, to enlarge the immunoglobulin gene mutation spectrum from G-C to A-T bases.
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Isono, Yohei, Norikazu Sakakibara, Paula Ordonez, et al. "Synthesis of 1-benzyl-3-(3,5-dimethylbenzyl)Uracil Derivatives with Potential Anti-HIV Activity." Antiviral Chemistry and Chemotherapy 22, no. 2 (2011): 57–65. http://dx.doi.org/10.3851/imp1844.

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Background: Nine novel uracil analogues were synthesized and evaluated as inhibitors of HIV-1. Methods: Key structural modifications included replacement of the 6-chloro group of 1-benzyl-6-chloro-3-(3,5-dimethylbenzyl)uracil by other functional groups or N1-alkylation of 3-(3,5-dimethylbenzyl)-5-fluorouracil. Results: These compounds showed only micromolar potency against HIV-1 in MT-4, though two of them; 6-azido-1-benzyl-3-(3,5-dimethylbenzyl) uracil and 6-amino-1-benzyl-3-(3,5-dimethylbenzyl) uracil were highly potent (half maximal effective concentration =0.067 and 0.069 μM) and selective (selectivity index =685 and 661), respectively. Structure–activity relationships among the newly synthesized uracil analogues suggest the importance of the H-bond formed between 6-amino group of 6-amino-1-benzyl-3-(3,5-dimethylbenzyl) uracil and amide group of HIV-1 reverse transcriptase. Conclusions: We discovered two 6-substituted 1-benzyl-3-(3,5-dimethylbenzyl) uracils, (6-azido-1-benzyl-3-(3,5-dimethylbenzyl) uracil and 6-amino-1-benzyl-3-(3,5-dimethylbenzyl) uracil) as novel anti-HIV agents. These compounds should be further pursued for their toxicity and pharmacokinetics in vivo as well as antiviral activity against non-nucleoside reverse transcriptase inhibitor-resistant strains.
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Heidari, Ali, Arash Ghorbani-Choghamarani, Maryam Hajjami, and Robert H. E. Hudson. "Fluorescent Biaryl Uracils with C5-Dihydro- and Quinazolinone Heterocyclic Appendages in PNA." Molecules 25, no. 8 (2020): 1995. http://dx.doi.org/10.3390/molecules25081995.

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There has been much effort to exploit fluorescence techniques in the detection of nucleic acids. Canonical nucleic acids are essentially nonfluorescent; however, the modification of the nucleobase has proved to be a fruitful way to engender fluorescence. Much of the chemistry used to prepare modified nucleobases relies on expensive transition metal catalysts. In this work, we describe the synthesis of biaryl quinazolinone-uracil nucleobase analogs prepared by the condensation of anthranilamide derivatives and 5-formyluracil using inexpensive copper salts. A selection of modified nucleobases were prepared, and the effect of methoxy- or nitro- group substitution on the photophysical properties was examined. Both the dihydroquinazolinone and quinazolinone modified uracils have much larger molar absorptivity (~4–8×) than natural uracil and produce modest blue fluorescence. The quinazolinone-modified uracils display higher quantum yields than the corresponding dihydroquinazolinones and also show temperature and viscosity dependent emission consistent with molecular rotor behavior. Peptide nucleic acid (PNA) monomers possessing quinazolinone modified uracils were prepared and incorporated into oligomers. In the sequence context examined, the nitro-substituted, methoxy-substituted and unmodified quinazolinone inserts resulted in a stabilization (∆Tm = +4.0/insert; +2.0/insert; +1.0/insert, respectively) relative to control PNA sequence upon hybridization to complementary DNA. All three derivatives responded to hybridization by the “turn-on” of fluorescence intensity by ca. 3-to-4 fold and may find use as probes for complementary DNA sequences.
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Colasurdo, Diego D., Matías N. Pila, Dacio A. Iglesias, Sergio L. Laurella, and Danila L. Ruiz. "Tautomerism of uracil and related compounds: A mass spectrometry study." European Journal of Mass Spectrometry 24, no. 2 (2017): 214–24. http://dx.doi.org/10.1177/1469066717712461.

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It has been demonstrated that uracil has a preponderant tautomeric form, but it is also known that different tautomers co-exist in this equilibrium. In this work, mass spectrometry is used as a helpful tool to analyse the equilibria, using derivative compounds to forbid the presence of some tautomers and ion trap mass spectrometry to follow relevant fragmentation pathways. Theoretical calculations were performed to confirm tautomers abundance by energy minimization in gas phase. Analysis of mass spectra of uracil, three methyl-substituted uracils, 2-thiouracil and three benzouracils suggest that uracil exists mainly as three tautomers in gas phase: one major structure that corresponds to the classical structure of uracil (pyrimidine-2,4(1H,3H)-dione) bearing two carbonyls and two NH moieties, and two minor enolic forms (4-hydroxypyrimidin-2(1H)-one and 2-hydroxypyrimidin-4(1H)-one). Such tautomeric distribution is supported by theoretical calculations, which show that they are the three most stable tautomers.
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Focher, F., A. Verri, S. Spadari, R. Manservigi, J. Gambino, and G. E. Wright. "Herpes simplex virus type 1 uracil-DNA glycosylase: isolation and selective inhibition by novel uracil derivatives." Biochemical Journal 292, no. 3 (1993): 883–89. http://dx.doi.org/10.1042/bj2920883.

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We have purified Herpes simplex type 1 (HSV1) uracil-DNA glycosylase from the nuclei of HSV1-infected HeLa cells harvested 8 h post-infection, at which time the induction of the enzyme is a maximum. The enzyme has been shown to be distinct from the host enzyme, isolated from HeLa cells, by its lack of sensitivity to a monoclonal antibody to human uracil-DNA glycosylase. Furthermore, several uracil analogues were synthesized and screened for their capacity to discriminate between the viral and human uracil-DNA glycosylases. Both enzymes were inhibited by 6-(p-alkylanilino)uracils, but the viral enzyme was significantly more sensitive than the HeLa enzyme to most analogues. Substituents providing the best inhibitors of HSV1 uracil-DNA glycosylase were found to be in the order: p-n-butyl < p-n-pentl = p-n-hexyl < p-n-heptyl < p-n-octyl. The most potent HSV1 enzyme inhibitor, 6-(p-n-octylanilino)uracil (OctAU), with an IC50 of 8 microM, was highly selective for the viral enzyme. Short-term [3H]thymidine incorporation into the DNA of HeLa cells in culture was partially inhibited by OctAU, whereas it was unchanged when 6-(p-n-hexylanilino)uracil was present at concentrations that completely inhibited HSV1 uracil-DNA glycosylase activity. These compounds represent the first class of inhibitors that inhibit HSV1 uracil-DNA glycosylase at concentrations in the micromolar range. The results suggest their possible use to evaluate the functional role of HSV1 uracil-DNA glycosylase in viral infections and re-activation in nerve cells.
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Di Noia, Javier M., Gareth T. Williams, Denice T. Y. Chan, Jean-Marie Buerstedde, Geoff S. Baldwin, and Michael S. Neuberger. "Dependence of antibody gene diversification on uracil excision." Journal of Experimental Medicine 204, no. 13 (2007): 3209–19. http://dx.doi.org/10.1084/jem.20071768.

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Activation-induced deaminase (AID) catalyses deamination of deoxycytidine to deoxyuridine within immunoglobulin loci, triggering pathways of antibody diversification that are largely dependent on uracil-DNA glycosylase (uracil-N-glycolase [UNG]). Surprisingly efficient class switch recombination is restored to ung−/− B cells through retroviral delivery of active-site mutants of UNG, stimulating discussion about the need for UNG's uracil-excision activity. In this study, however, we find that even with the overexpression achieved through retroviral delivery, switching is only mediated by UNG mutants that retain detectable excision activity, with this switching being especially dependent on MSH2. In contrast to their potentiation of switching, low-activity UNGs are relatively ineffective in restoring transversion mutations at C:G pairs during hypermutation, or in restoring gene conversion in stably transfected DT40 cells. The results indicate that UNG does, indeed, act through uracil excision, but suggest that, in the presence of MSH2, efficient switch recombination requires base excision at only a small proportion of the AID-generated uracils in the S region. Interestingly, enforced expression of thymine-DNA glycosylase (which can excise U from U:G mispairs) does not (unlike enforced UNG or SMUG1 expression) potentiate efficient switching, which is consistent with a need either for specific recruitment of the uracil-excision enzyme or for it to be active on single-stranded DNA.
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Kavli, Bodil, Tobias S. Iveland, Edith Buchinger, et al. "RPA2 winged-helix domain facilitates UNG-mediated removal of uracil from ssDNA; implications for repair of mutagenic uracil at the replication fork." Nucleic Acids Research 49, no. 7 (2021): 3948–66. http://dx.doi.org/10.1093/nar/gkab195.

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Abstract Uracil occurs at replication forks via misincorporation of deoxyuridine monophosphate (dUMP) or via deamination of existing cytosines, which occurs 2–3 orders of magnitude faster in ssDNA than in dsDNA and is 100% miscoding. Tethering of UNG2 to proliferating cell nuclear antigen (PCNA) allows rapid post-replicative removal of misincorporated uracil, but potential ‘pre-replicative’ removal of deaminated cytosines in ssDNA has been questioned since this could mediate mutagenic translesion synthesis and induction of double-strand breaks. Here, we demonstrate that uracil-DNA glycosylase (UNG), but not SMUG1 efficiently excises uracil from replication protein A (RPA)-coated ssDNA and that this depends on functional interaction between the flexible winged-helix (WH) domain of RPA2 and the N-terminal RPA-binding helix in UNG. This functional interaction is promoted by mono-ubiquitination and diminished by cell-cycle regulated phosphorylations on UNG. Six other human proteins bind the RPA2-WH domain, all of which are involved in DNA repair and replication fork remodelling. Based on this and the recent discovery of the AP site crosslinking protein HMCES, we propose an integrated model in which templated repair of uracil and potentially other mutagenic base lesions in ssDNA at the replication fork, is orchestrated by RPA. The UNG:RPA2-WH interaction may also play a role in adaptive immunity by promoting efficient excision of AID-induced uracils in transcribed immunoglobulin loci.
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Dissertations / Theses on the topic "Uracila"

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Galarza, Andrés Fernando Andrade. "Avaliação genotípica e fenotípica da enzima diidropirimidina desidrogenase (DPD) e risco de toxicidade com o uso de fluoropirimidinas." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2016. http://hdl.handle.net/10183/143351.

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Base teórica: As fluoropirimidinas possuem significativa variabilidade na resposta terapêutica e na ocorrência de toxicidade, o que tem sido relacionado à deficiência na depuração metabólica mediada pela enzima diidropirimidina desidrogenase (DPD). Mutações nos genes codificadores da enzima, bem como fatores ambientais podem levar à baixa ou nula expressão enzimática, provocando efeitos adversos graves devido ao acúmulo destes fármacos. Até o presente, nenhum teste reconhecidamente valido para a identificação de indivíduos em risco de toxicidade severa está estabelecido na prática oncológica. A genotipagem para o gene DPYD apresenta poder preditivo limitado, pois é capaz de rastrear somente as mutações já conhecidas, que apresentam baixa frequência populacional. Por esta razão, ensaios funcionais baseados na avaliação da redução fisiológica do uracil (U) para diidrouracil (UH2), igualmente medidada pela DPD, têm sido propostos na identificação de pacientes predispostos à toxicidade. Nesta abordagem são estimadas as razões plasmáticas [UH2]/[U] em níveis basais ou após uma dose oral do U. Recentemente, foi sugerida a realização do teste funcional em saliva como amostra alternativa ao plasma, com maior estabilidade dos analitos. Entretanto, a associação entre as razões metabólicas nesta matriz e a toxicidade não foi validada em amostras clínicas. Objetivos: Avaliar a efetividade dos métodos de determinação da razão metabólica [UH2]/[U] em plasma e saliva e a genotipagem para o gene DPYD como preditores de toxicidade por fluoropirimidinas em pacientes com neoplasias gastrointestinais. Adicionalmente, o trabalho propôs o desenvolvimento de um método bioanalítico para a determinação de U e UH2 por cromatografia líquida de alta eficiência. Métodos: Foram obtidas amostras pareadas de plasma e saliva de 60 pacientes diagnosticados com neoplasia gastrointestinal e com indicação de tratamento com fluoropirimidinas. As concentrações de U e UH2 foram determinadas nas duas matrizes através de LC-MS/MS. Os efeitos adversos do primeiro ciclo de quimioterapia foram classificados de acordo com o NCI-CTCAE versão 4. A genotipagem da DYDP foi realizada por PCR tempo real e incluiu os alelos *2A; *13, Y186C; I560S, *7 Y186C. Resultados: 35% dos pacientes apresentaram toxicidade severa (graus 3/4), sendo a neutropenia a mais frequente (n=11). A genotipagem da DYDP não foi capaz de identificar pacientes em risco de toxicidade, uma vez que não foram encontrados portadores de alelos variáveis. As razões [UH2]/[U] variaram amplamente entre os pacientes, de 0,09 a 26,73 no plasma e de 0,08 a 24 na saliva. As razões [UH2]/[U] no plasma e na saliva demonstraram correlação elevada (rs=-0,575; P<0,01), porém, a saliva demonstrou maior correlação com o grau de toxicidade quando comparada ao plasma (rs=-0,515; P<0,01 vs rs=-0,282 P<0,05). Pacientes com grau de toxicidade 3/4 (n=21) apresentaram menor razão metabólica em comparação a pacientes com grau 1/2 (n=26) ou com ausência de toxicidade (n=13) (média 0.59 vs 2.22 e 2.83 no plasma e 1.62 vs 6.88 e 6.75 na saliva, P<0.01). A partir de curva ROC foi determinado o valor de corte de 1,16 para a razão em saliva com 86% de sensibilidade e 77% de especificidade para a identificação de pacientes com toxicidade severa. Nas amostras de plasma o valor de corte foi 4.0 com 71% de sensibilidade e 76% de especificidade. Adicionalmente, foi desenvolvido e validado um método bioanalítico para a dosagem de U e UH2 com exatidão (98.4–105.3%) e precisão precisão intra-ensaio (5.1–12.1%) e inter-ensaios (5.3–10.1%) satisfatórios. Conclusão: Neste grupo de pacientes a genotipagem dos alelos *2A; Y186C; I560S, Y186C e *7 da DPYD não mostrou-se útil na identificação de indivíduos com deficiência severa da DPD. Entretanto, as razões metabólicas [UH2]/[U] demonstraram ser um promissor teste para avaliar a funcionalidade da enzima e identificar a maioria dos casos de pacientes com sujeitos a toxicidade grave à fluoropirimidinas, com sensibilidade superior da saliva.<br>Background: Variation on therapeutic response to fluoropirimidines and toxicity have been related to impaired dihydropyrimidine dehydrogenase (DPD) mediated metabolism. Mutations in genes encoding the enzyme as well as environmental factors can lead to reduced or absent enzyme expression, causing serious adverse effects due to the accumulation of these drugs. To date, there is no clinically recognized valid assay, for the identification of individuals at risk of severe toxicity in oncological practice. DPYD genotyping has a limited prediction power, since it is able to identify only the already known mutations, which have low frequency in population. Therefore, functional DPD assays based on the assessment of uracil (U) to dihydrouracil (UH2) metabolism, which is also dependent on DPD, have been proposed to identify patients prone to toxicity. Thus, endogenous metabolic ratios of [UH2]/[U] or after an oral dose of U are determined in plasma. Recently, the use of saliva has been suggested as alternative matrix to plasma, with higher stability of analytes. However, the association between salivary metabolic ratios and toxicity has not been validated in clinical samples. Objective: To evaluate the use of plasma and saliva uracil (U) to dihydrouracil (UH2) metabolic ratios and DPYD genotyping, as a means to identify patients with dihydropyrimidine dehydrogenase (DPD) deficiency and fluoropyrimidine toxicity. Additionally, the work proposed the development of a bioanalytical method for the determination of U and UH2 by high-performance liquid chromatography. Methods: Paired plasma and saliva samples were obtained from 60 patients with gastrointestinal cancer before fluoropyrimidine treatment. U and UH2 concentrations were measured by LC-MS/MS. DPYD was genotyped for alleles *2A; Y186C; I560S, Y186C and *7. Results: 35% of the patients had severe toxicity. There was no variant allele carrier for DPYD. The [UH2]/[U] metabolic ratios were 0.09-26.73 in plasma and 0.08-24.0 in saliva, with higher correlation with toxicity grade in saliva compared to plasma (rs=-0.515 vs rs=-0.282). Median metabolic ratios were lower in patients with severe toxicity as compared to those with absence of toxicity (0.59 vs 2.83 plasma; 1.62 vs 6.75 saliva, P<0.01). A cut-off of 1.16 for salivary ratio was set with 86% sensitivity and 77% specificity for the identification of patients with severe toxicity. Similarly, a plasma cut-off of 4.0 revealed a 71% sensitivity and 76% specificity. Additionally, a bioanalytical method for the quantification of U and UH2, with adequate accuracy (98.4–105.3%) and precision (intra-assay CV 5.1–12.1% and inter-assay CV 5.3–10.1%) was develop and validated. Conclusions: DPYD genotyping for alleles *2A; Y186C; I560S, Y186C and *7 was not helpful in the identification of patients with severe DPD deficiency in this series of patients. The [UH2]/[U] metabolic ratios, however, proved to be a promising functional test to identify the majority of cases of severe DPD activity, with saliva performing better than plasma.
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Hoff, Paulo Marcelo Gehm. "Estudo de fase II avaliando eficácia e toxicidade de UFT (uracil e tegafur) e leucovorin, administrados duas vezes ao dia, no tratamento de pacientes com câncer metastático de cólon e reto." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/5/5154/tde-31052007-162509/.

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Infusões prolongadas de 5-fluorouracil são mais seguras e potencialmente mais efetivas no tratamento do câncer de cólon metastático do que infusões rápidas da mesma medicação. No entanto, infusões prolongadas requerem a disponibilidade de um acesso venoso central, bem como de bombas de infusão dispendiosas. O desenvolvimento de fluoropirimidinas orais permitiu que pacientes fossem expostos ao 5-fluorouracil por longo tempo, com maior conveniência. UFT e leucovorin administrados três vezes ao dia demonstraram previamente uma eficácia equivalente, com menor toxicidade, quando comparados a um regime convencional de infusão rápida de 5- fluorouracil e leucovorin. Este estudo com 98 pacientes foi desenhado e conduzido com objetivo de demonstrar equivalência no tempo de progressão com o uso de UFT e leucovorin administrados duas vezes ao dia, com o uso da mesma combinação administrada três vezes ao dia. Objetivos secundários incluíram análise de toxicidade, resposta objetiva e sobrevida global. O tempo mediano de progressão foi de 3,8 meses, comparado com 3,5 meses observados com o uso da medicação três vezes ao dia e a taxa de resposta foi de 11%, com uma sobrevida mediana de 12,8 meses, sendo comparável aos resultados de 12% e 12,4 meses obtidas com o uso da combinação três vezes ao dia. A incidência de diarréia com graus 3 e 4 foi de 30% no regime de administração duas vezes ao dia, e 21% no de três vezes ao dia. Esses resultados sugerem que o uso de UFT e leucovorin duas vezes ao dia tem eficácia e toxicidade similares àquelas obtidas com o uso da mesma medicação três vezes ao dia.<br>Prolonged infusions have been shown to be safer and potentially more effective than bolus regimens of 5- fluorouracil as treatment for advanced colorectal cancer. However, infusional 5- fluorouracil requires central venous access and costly infusion pumps. Development of oral fluoropyrimidines has allowed longer exposures to 5-fluorouracil with increased convenience. UFT and leucovorin given thrice daily showed improved safety and no significant difference in survival or response rate compared with bolus 5- fluorouracil and leucovorin. This study with 98 patients was conducted to evaluate whether UFT and leucovorin given twice daily provided comparable time to progression (TTP) to the same combination administered three times a day. Secondary objectives included evaluation of toxicity, overall tumor response rate, and survival. Median time to progression was 3.8 months, compared with 3.5 months observed with the thrice-daily regimen. The twice-daily regimen had a response rate of 11% and median survival of 12.8 months, comparable to the 12% and 12.4 months seen with the thrice-daily regimen. The incidence of grade 3-4 drug-related diarrhea was 30% on the twice-daily and 21% on the thrice-daily schedule. Results suggest that the twice-daily schedule has similar safety and efficacy to the thrice-daily schedule.
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Guillet, Marie. "Les sites abasiques, leur origine et les systèmes de répération chez Saccharomyces cerevisiae." Paris 11, 2003. http://www.theses.fr/2003PA112149.

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Les cellules sont constamment soumises à des stress endogène et exogène qui provoquent la formation de lésions de l'ADN. Il a été estimé que les lésions les plus abondantes dans l'ADN sont les sites abasiques (sites AP) provenant du clivage du lien glycosidique entre la base et le désoxyribose. Ce clivage peut être spontané ou médié par une ADN glycosylase au cours la réparation par excision de bases (BER) endommagées ou anormales de l'ADN. Le clivage des sites AP en 5' ou en 3' provoquent la formation de cassures simple brin avec une extrémité 5' ou 3' bloquée, respectivement. Au début de ma thèse, seul le BER était connu comme intervenant dans la réparation des sites AP via les deux AP endonucléases Apn1 et Apn2 chez Saccharomyces cerevisiae. Cependant, alors que les sites AP sont mutagènes et potentiellement létaux, le double mutant apn1 apn2 est viable, ce qui suggère la présence d'autres voies de réparation des sites AP. J'ai pu montré que le système de réparation par excision de nucléotides (NER) intervient dans la réparation des sites AP. L'hétérodimère Rad1-Rad10 (flap-endonucléase) possède également un rôle dans la réparation des sites AP, en effet, le triple mutant apn1 apn2 rad1 est létal et forme une microcolonie composée d'environ 300 cellules 4 jours après dissection. Ce phénotype nous a permis de montrer que l'hétérodimère Mus81-Mms4 permet une réparation partielle des cassures simple brin avec une extrémité 3' bloquée responsables de la létalité du triple mutant apn1 apn2 rad1. La suppression de la létalité du triple mutant apn1 apn2 rad1 est possible par la délétion d'UNG1 codant pour l'uracile glycosylase ou par la surexpression de DUT1 codant pour la désoxyuridine triphosphate pyrophosphatase. Ces derniers résultats montrent qu'une source majoritaire spontanée de sites AP est la réparation de l'uracile dans l'ADN provenant de l'incorporation de dUTP du stock de dNTP par les ADN polymérases au cours de la réplication ou de la réparation<br>Cellular DNA is continuously damaged by exogenous and endogenous reactive species. One of the most frequent lesion in DNA is abasic sites (AP sites) that come from the cleavage of the glycosidic bond between the base and the deoxyribose. This cleavage could be spontaneous or due to the action of a DNA glycosylase during the base excision repair (BER) of damaged or abnormal bases. The cleavage of AP sites on the 5' or the 3' side leads to the formation of single strand breaks with a 5' or a 3' blocked end, respectively. At the beginning of my thesis, only the BER pathway was known to repair AP sites via the action of the two AP endonucleases Apn1 and Apn2 in Saccharomyces cerevisiae. However, while AP sites are known to be mutagenic and potentially lethal, the double mutant apn1 apn2 is viable that suggests the presence of other pathway(s) for AP site repair. I showed that the nucleotide excision repair (NER) pathway occurs a role in the repair of AP sites. The Rad1-Rad10 heterodimer is also implicated in the repair of AP sites since the apn1 apn2 rad1 triple mutant is lethal. This triple mutant forms a micro-colony of an average of 300 cells 4 days after dissection. This phenotype helps us to show that the Mus81-Mms4 can partially repair single strand break with 3' blocked end that are damages that cause the death of the apn1 apn2 rad1 triple mutant. The lethality of the apn1 apn2 rad1 triple mutant is suppressed by the deletion of UNG1 coding for the uracil DNA glycosylase or the overexpression of DUT1 coding for the deoxyuridine triphosphate pyrophosphatase. These results show that a critical spontaneous source of AP sites is the repair of uracil in DNA that come from the incorporation of dUTP from the dNTP pool by DNA polymerases during replication or repair
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Studebaker, Adam W. "Targeting uracil exclusion mechanisms for development of anti-viral and anti-cancer therapies." Connect to this title online, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1056034774.

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Thesis (Ph. D.)--Ohio State University, 2003.<br>Title from first page of PDF file. Document formatted into pages; contains xiii, 210 p.; also includes graphics (some col.). Includes bibliographical references (p. 174-210). Available online via OhioLINK's ETD Center
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Kandasamy, Dineshkumar. "Study on yeast enzymes Urc1p and Urc4p in a novel uracil catabolism pathway (URC)." Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-185013.

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Purine and pyrimidine bases are the central precursors of DNA and RNA and theirintracellular concentration is balanced by three pathways- de novo, salvage and catabolicpathways. Uracil catabolism pathway has been found in several bacteria and in some fungi(including yeast). Seven genes, URC1-7 have been found to be involved in this novelpathway. There are two “unknown genes” in the yeast Lachancea (Saccharomyces) kluyveri,namelyURC1 and URC4, which play a central role in this pathway and their exact functionremains a mystery.In this project, two S. kluyveri genes, URC1&amp;URC4, were over-expressed in the bacterialsystem and successfully purified. Our preliminary functional assay showed that uridinemonophosphate (UMP) is a likely substrate for Urc1p at pH7, 25ºC. It was shown clearly thatboth uracil and uridine were not the substrate for Urc1p. We tried to phosphorylatechemically synthesized ribosylurea using Drosophila melanogaster deoxyribonucleosidekinase and compared the activity between phosphorylated and non- phosphorylated RU atdifferent conditions. Phosphorylated ribosylurea seemed to be a likely substrate for Urc4p atpH7, 37ºC. Keywords: Uridine monophosphate (UMP), ribosylurea (RU), uracil catabolism.
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Kemmerich, Kristin. "Studies of genomic uracil and its excision." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610133.

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Brom, Jacques. "Squelettes pyrimidohétérocycliques dérivés d'amino- et d'hydrazino- uraciles." Mulhouse, 1991. http://www.theses.fr/1991MULH0205.

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Les 6-amino-, 6-hydrazino- et 6-(azavinyl) pyrimidinediones riches en électrons réagissent par leur carbone 5 avec différents électrophiles (l’O-tosylisonitrosomalodinitrile (OTMD), le tétracyanoéthylène (TCNE), l'acétylènedicarboxylate de diméthyle (DMAD), et le diméthylacétal du diméthylformamide (DMFDMA) pour conduire après cyclisation à toute une série d'hétérocycles polycycliques. La 6-amino-1,3-diméthylpyrimidine-2,4(1H, 3H)-dione fournit ainsi, avec l'OTMD, une lumazine précurseur de pyrimido [5,4-g] ptéridines, et avec le TCNE, une pyrido [2,3-d] pyrimidine. Une isomérisation du squelette carboné est mise en évidence dans le cas de la réaction entre la 6-hydrazino-1,3-diméthylpyrimidine-2,4(1H, 3H) dione et le TCNE. Des réactions analogues sur carbone sont également observées dans les séries naphtaléniques et anthracéniques
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HANNIER, REGIS. "Les cardiomyopathies au 5 fluoro-uracile (5 fu)." Lille 2, 1990. http://www.theses.fr/1990LIL2M281.

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Dingler, Felix. "Investigations into origin and fate of uracil in the mouse genome." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708713.

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Dworkin, Jason P. "Alternatives to uracil in the pre-RNA world /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1997. http://wwwlib.umi.com/cr/ucsd/fullcit?p9804027.

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Books on the topic "Uracila"

1

Pavittiran̲. Uracal ōcaikaḷ. Tēciya Kalai Ilakkiyap Pēravai, 2002.

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McKinnell, Denise. Phototransformation of 5-[inferior t]-butyl uracil derivatives. University of Birmingham, 1997.

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Bouzid, Bachir. Electrochemical behaviour and flow injection determination of uracil derivatives. University of Birmingham, 1987.

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Rondón, Francisco Gómez. Cantares a mi tierra Uracoa. Fragor, 2002.

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Mutikainen, Ilpo. X-ray structural studies on metal complexes of uracil and orotic acid: A survey of coordination induced changes in the uracil fragment. Suomalainen Tiedeakatemia, 1988.

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National Institute for Clinical Excellence. Guidance on the use of capecitabine and tegafur with uracil for metastatic colorectal cancer. National Institute for Clinical Excellence, 2003.

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Paramacivam, Mu. Ti. Ka. Ci. en̲n̲umoru tir̲an̲āyvut ten̲r̲al: 1950-90kaḷil Tamil̲ilakkiya varalāṛṛōṭu tōḷ uraci naṭanta oru man̲itarin̲ carittiram. Narmatā Patippakam, 1999.

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Slupphaug, Geir, and Hans Einar Krokan. Genomic Uracil. WORLD SCIENTIFIC, 2018. http://dx.doi.org/10.1142/10803.

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Urachima: El valiente/ Urachima: The Valiant/ Spanish Edition. Public Square Books, 2007.

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Krokan, Hans Einar, and Geir Slupphaug. Genomic Uracil: Evolution, Biology, Immunology and Disease. World Scientific Publishing Co Pte Ltd, 2018.

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Book chapters on the topic "Uracila"

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Miyakawa, Shin. "Uracil (Ura)." In Encyclopedia of Astrobiology. Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27833-4_1631-3.

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Miyakawa, Shin. "Uracil (Ura)." In Encyclopedia of Astrobiology. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-11274-4_1631.

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Schomburg, Dietmar, and Dörte Stephan. "Uracil phosphoribosyltransferase." In Enzyme Handbook 12. Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61117-9_215.

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Miyakawa, Shin. "Uracil (Ura)." In Encyclopedia of Astrobiology. Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-44185-5_1631.

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Schomburg, Dietmar, and Dörte Stephan. "Uracil dehydrogenase." In Enzyme Handbook 10. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-57756-7_148.

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Henriques, Vanessa, Maria Rosaria Raspollini, and Antonio Lopez-Beltran. "Urachal Carcinoma." In Encyclopedia of Pathology. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-41894-6_4965.

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Fahmy, Mohamed. "Urachal Anomalies." In Umbilicus and Umbilical Cord. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-62383-2_35.

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Al-Salem, Ahmed H. "Urachal Remnants." In An Illustrated Guide to Pediatric Urology. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-44182-5_16.

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Henriques, Vanessa, Maria Rosaria Raspollini, and Antonio Lopez-Beltran. "Urachal Carcinoma." In Encyclopedia of Pathology. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-28845-1_4965-1.

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Schomburg, Dietmar, and Ida Schomburg. "uracil-DNA glycosylase 3.2.2.27." In Class 2–3.2 Transferases, Hydrolases. Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-36240-8_123.

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Conference papers on the topic "Uracila"

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Stewart, Jessica, Shanqiao Wei, Madhurima Datta, Umesh Varshney, and Ashok Bhagwat. "Abstract 3802: A novel uracil-DNA glycosylase, UdgX, as a new biochemical tool to directly detect uracils in DNA." 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.am2017-3802.

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Kowalski, Konrad, Joanna Skiba, Ingo Ott, Jolanta Solecka, and Bruno Therrien. "Ferrocenylated uracils: synthesis and biology." In XVIth Symposium on Chemistry of Nucleic Acid Components. Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2014. http://dx.doi.org/10.1135/css201414310.

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Shih, Yu-Chiao, Ying-Shun Liao, Chun-Chi Lin, et al. "Synthesis of 6-substituted uracil and uridine derivatives." In XVIth Symposium on Chemistry of Nucleic Acid Components. Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2014. http://dx.doi.org/10.1135/css201414129.

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Fritz, Hans-Joachim. "Mechanistic and evolutionary aspects of DNA-uracil glycosylases." In XIIth Symposium on Chemistry of Nucleic Acid Components. Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2002. http://dx.doi.org/10.1135/css200205230.

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Lin, Xiumei, Tanja Deckert-Gaudig, Regina Treffer, Volker Deckert, P. M. Champion, and L. D. Ziegler. "Tip-Enhanced Raman Scattering (TERS) Of Uracil Strands." In XXII INTERNATIONAL CONFERENCE ON RAMAN SPECTROSCOPY. AIP, 2010. http://dx.doi.org/10.1063/1.3482412.

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Elkin, P. M., M. A. Erman, and O. V. Pulin. "Anharmonic analysis of vibrational spectra of substituted uracil." In SPIE Proceedings, edited by Vladimir L. Derbov, Leonid A. Melnikov, and Lev M. Babkov. SPIE, 2006. http://dx.doi.org/10.1117/12.696923.

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Grof, P., S. Gaspar, and A. Berces. "Uracil thin layers in dosimetry of UV-radiation." In Europto Biomedical Optics '93, edited by Kazuhiko Atsumi, Cornelius Borst, Frank W. Cross, et al. SPIE, 1994. http://dx.doi.org/10.1117/12.169152.

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Bulgar, Alina, Lachelle D. Weeks, Yanling Miao, et al. "Abstract A104: Removal of uracil by uracil DNA glycosylase limits pemetrexed cytotoxicity: Overriding the limit with methoxyamine (TRC102) to inhibit base excision repair." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-a104.

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Villar, Vincent, Carlos Casanova, Mari Luz Moreno Sancho, et al. "Antioxidant activity of 5-FU and new fluorinated uracil derivates." In MOL2NET 2017, International Conference on Multidisciplinary Sciences, 3rd edition. MDPI, 2017. http://dx.doi.org/10.3390/mol2net-03-04968.

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Fujita, Marta Akemi, Carla Marisa Brito Carvalho, Timothy John Brocksom та Kleber Thiago de Oliveira. "Synthesis and photophysical evaluations of β-fused Uracil- Porphyrin derivatives". У 15th Brazilian Meeting on Organic Synthesis. Editora Edgard Blücher, 2013. http://dx.doi.org/10.5151/chempro-15bmos-bmos2013_2013912183035.

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Reports on the topic "Uracila"

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Niedenzu, K., and L. Komorowski. New Boron-Nitrogen Analogues of Uracil Derivatives. Defense Technical Information Center, 1989. http://dx.doi.org/10.21236/ada210164.

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González-Pacanowska, Dolores. La dUTPasa, una NTP-pirofosfatasa todo-α que controla el nivel de uracilo en el ADN. Sociedad Española de Bioquímica y Biología Molecular (SEBBM), 2014. http://dx.doi.org/10.18567/sebbmdiv_anc.2014.09.1.

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Su, Ning, Jerald S. Bradshaw, Xian X. Zhang, Paul B. Savage, and Krzystof E. Krakowiak. Syntheses of Diaza-18-Crown-6 Ligands Containing Two Units Each of 4-Hydroxyazobenzene, Benzimidazole, Uracil, Anthraquinone, or Ferrocene Groups. Defense Technical Information Center, 1999. http://dx.doi.org/10.21236/ada361715.

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Management of urachal anomalies. BJUI Knowledge, 2019. http://dx.doi.org/10.18591/bjuik.0216.

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