Literatura académica sobre el tema "5-methylTHF"

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Artículos de revistas sobre el tema "5-methylTHF"

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Palmer, Ashley M., Elena Kamynina, Martha S. Field y Patrick J. Stover. "Folate rescues vitamin B12 depletion-induced inhibition of nuclear thymidylate biosynthesis and genome instability". Proceedings of the National Academy of Sciences 114, n.º 20 (1 de mayo de 2017): E4095—E4102. http://dx.doi.org/10.1073/pnas.1619582114.

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Clinical vitamin B12 deficiency can result in megaloblastic anemia, which results from the inhibition of DNA synthesis by trapping folate cofactors in the form of 5-methyltetrahydrofolate (5-methylTHF) and subsequent inhibition of de novo thymidylate (dTMP) biosynthesis. In the cytosol, vitamin B12 functions in the remethylation of homocysteine to methionine, which regenerates THF from 5-methylTHF. In the nucleus, THF is required for de novo dTMP biosynthesis, but it is not understood how 5-methylTHF accumulation in the cytosol impairs nuclear dTMP biosynthesis. The impact of vitamin B12 depletion on nuclear de novo dTMP biosynthesis was investigated in methionine synthase-null human fibroblast and nitrous oxide-treated HeLa cell models. The nucleus was the most sensitive cellular compartment to 5-methylTHF accumulation, with levels increasing greater than fourfold. Vitamin B12 depletion decreased de novo dTMP biosynthesis capacity by 5–35%, whereas de novo purine synthesis, which occurs in the cytosol, was not affected. Phosphorylated histone H2AX (γH2AX), a marker of DNA double-strand breaks, was increased in vitamin B12 depletion, and this effect was exacerbated by folate depletion. These studies also revealed that 5-formylTHF, a slow, tight-binding inhibitor of serine hydroxymethyltransferase (SHMT), was enriched in nuclei, accounting for 35% of folate cofactors, explaining previous observations that nuclear SHMT is not a robust source of one-carbons for de novo dTMP biosynthesis. These findings indicate that a nuclear 5-methylTHF trap occurs in vitamin B12 depletion, which suppresses de novo dTMP biosynthesis and causes DNA damage, accounting for the pathophysiology of megaloblastic anemia observed in vitamin B12 and folate deficiency.
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Pfeiffer, Christine M., Maya R. Sternberg, Zia Fazili, David A. Lacher, Mindy Zhang, Clifford L. Johnson, Heather C. Hamner et al. "Folate status and concentrations of serum folate forms in the US population: National Health and Nutrition Examination Survey 2011–2". British Journal of Nutrition 113, n.º 12 (28 de abril de 2015): 1965–77. http://dx.doi.org/10.1017/s0007114515001142.

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Serum and erythrocyte (RBC) total folate are indicators of folate status. No nationally representative population data exist for folate forms. We measured the serum folate forms (5-methyltetrahydrofolate (5-methylTHF), unmetabolised folic acid (UMFA), non-methyl folate (sum of tetrahydrofolate (THF), 5-formyltetrahydrofolate (5-formylTHF), 5,10-methenyltetrahydrofolate (5,10-methenylTHF)) and MeFox (5-methylTHF oxidation product)) by HPLC–MS/MS and RBC total folate by microbiologic assay in US population ≥ 1 year (n approximately 7500) participating in the National Health and Nutrition Examination Survey 2011–2. Data analysis for serum total folate was conducted including and excluding MeFox. Concentrations (geometric mean; detection rate) of 5-methylTHF (37·5 nmol/l; 100 %), UMFA (1·21 nmol/l; 99·9 %), MeFox (1·53 nmol/l; 98·8 %), and THF (1·01 nmol/l; 85·2 %) were mostly detectable. 5-FormylTHF (3·6 %) and 5,10-methenylTHF (4·4 %) were rarely detected. The biggest contributor to serum total folate was 5-methylTHF (86·7 %); UMFA (4·0 %), non-methyl folate (4·7 %) and MeFox (4·5 %) contributed smaller amounts. Age was positively related to MeFox, but showed a U-shaped pattern for other folates. We generally noted sex and race/ethnic biomarker differences and weak (Spearman's r< 0·4) but significant (P< 0·05) correlations with physiological and lifestyle variables. Fasting, kidney function, smoking and alcohol intake showed negative associations. BMI and body surface area showed positive associations with MeFox but negative associations with other folates. All biomarkers showed significantly higher concentrations with recent folic acid-containing dietary supplement use. These first-time population data for serum folate forms generally show similar associations with demographic, physiological and lifestyle variables as serum total folate. Patterns observed for MeFox may suggest altered folate metabolism dependent on biological characteristics.
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Taflin, Helena, Yvonne Wettergren, Elisabeth Odin, Göran Carlsson y Kristoffer Derwinger. "Folate Levels and Polymorphisms in the Genes MTHFR, MTR, and TS in Colorectal Cancer". Clinical Medicine Insights: Oncology 8 (enero de 2014): CMO.S12701. http://dx.doi.org/10.4137/cmo.s12701.

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Aim The aim of the study was to explore and describe the effect of polymorphisms in folate-associated genes regarding the levels of different folate forms and their distribution in tumors and mucosa in patients with colorectal cancer. Materials and Methods Tumor and mucosa tissues from 53 patients with colorectal cancer were analyzed. The concentrations of tetrahydrofolate (THF), 5-methylTHF, and 5,10-methyleneTHF were measured by liquid chromatography—mass spectrometry. Genotyping of polymorphisms in the folate-associated genes methylenetetrahydrofolate reductase ( MTHFR, C677T), methionine synthase ( MTR, A2756G), and thymidylate synthase ( TS, 5'-TSER 28 bp tandem repeat and 3'-TSUTR 6 bp deletion/insertion), were done by real-time polymerase chain reaction. Folate levels and distributions were determined in the total patient cohort and after subgrouping by genotypes. Results The total folate level, as well as the THF and 5,10-methyleneTHF levels, were significantly higher in the tumor compared with mucosa tissue ( P = 0.030, 0.031, and 0.015, respectively). The individual variation in folate levels in both tumor and mucosa were larger than the variation found when the patients were subgrouped by the gene polymorphisms. No significant differences in the mean concentration of any folate in the mucosa or tumor tissue were found in relation to the analyzed polymorphisms. The percentage level of 5,10-methyleneTHF in tumors was highest in patients with the MTHFR 677 CC genotype, and lowest in patients with the TT genotype ( P = 0.033). A significantly lower percentage level of the 5,10-methyleneTHF level was found in tumors of patients with the 5'-TSER 3R/3R genotype ( P = 0.0031). Conclusion A significant difference was found between the percentage level of 5,10-methyleneTHF in tumor tissues in relation to the MTHFR C677T and 5'-TSER 28 bp repeat polymorphisms. However, no differences were found in the actual tissue folate levels, or in their distribution, in relation to the polymorphisms in the MTHFR, MTR, or TS genes. These findings could be of importance for further research in the field by explaining some of the difficulties of obtaining reproducible and uniform results when using a few selected polymorphisms as predictive markers.
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Dattilo, Maurizio, Carolina Fontanarosa, Michele Spinelli, Vittorio Bini y Angela Amoresano. "Modulation of Human Hydrogen Sulfide Metabolism by Micronutrients, Preliminary Data". Nutrition and Metabolic Insights 15 (enero de 2022): 117863882110653. http://dx.doi.org/10.1177/11786388211065372.

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Background: Hydrogen sulfide (H2S) is a pivotal gasotransmitter networking with nitric oxide (NO) and carbon monoxide (CO) to regulate basic homeostatic functions. It is released by the alternative pathways of transulfuration by the enzymes Cystathionine Beta Synthase (CBS) and Cystathionine Gamma Lyase (CSE), and by Cysteine AminoTransferase (CAT)/ 3-Mercaptopyruvate Sulfur Transferase (3MPST). A non-enzymatic, intravascular release is also in place. We retrospectively investigated the possibility to modulate the endogenous H2S release and signaling in humans by a dietary manipulation with supplemented micronutrients (L-cystine, Taurine and pyridoxal 5-phopsphate/P5P). Methods: Patients referring for antiaging purposes underwent a 10-day supplementation. Blood was collected at baseline and after treatment and the metabolome was investigated by mass spectrometry to monitor the changes in the metabolites reporting on H2S metabolism and related pathways. Results: Data were available from 6 middle aged subjects (2 women). Micronutrients increased 3-mercaptopyruvate ( P = .03), reporting on the activity of CAT that provides the substrate for H2S release within mitochondria by 3MPST, decreased lanthionine ( P = .024), reporting the release of H2S from CBS, and had no significant effect of H2S release from CSE. This is compatible with a homeostatic balancing. We also recorded a strong increase of reporters of H2S-induced pathways including 5-MethylTHF ( P = .001) and SAME ( P = .022), reporting on methylation capacity, and of BH4 ( P = .021) and BH2 ( P = .028) reporting on nitric oxide metabolism. These activations may be explained by the concomitant induction of non-enzymatic release of H2S. Conclusions: Although the current evidences are weak and will need to be confirmed, the effect of micronutrients was compatible with an increase of the H2S endogenous release and signaling within the control of homeostatic mechanisms, further endorsing the role of feeding in health and disease. These effects might result in a H2S boosting effect in case of defective activity of pathologic origin, which should be checked in duly designed clinical trials.
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Mosnier, Hannah, Erin Kelly, Kamaya Lawrence, Sarah Cruickshank, Sarah Stacey, Adelina McCall, Sunny Dhatt, Erland Arning, Teodoro Bottiglieri y Nafisa Jadavji. "The Role of One-Carbon Metabolism After Ischemic Stroke in an Aged Mouse Model". Current Developments in Nutrition 4, Supplement_2 (29 de mayo de 2020): 1226. http://dx.doi.org/10.1093/cdn/nzaa057_042.

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Abstract Objectives Nutrition is a modifiable risk factor for stroke, which is one of the leading causes of death and disability world-wide. In humans deficiencies in one-carbon metabolism, including the methyltetrahydrofolate reductase (MTHFR) polymorphism, have been linked to increased risk of stroke. The Mthfr+/− mice mouse model mimics the phenotype of the MTHFR677C – &gt;T polymorphism. In our work using in vitro and in vivo models of ischemic stroke we have observed decreased recovery after stroke through reduced neuronal and astrocyte viability and increased apoptosis in MTHFR-deficient mice. In addition, we have previously shown dietary supplementation of one-carbon metabolites increases neuroplasticity and reduced oxidative stress after ischemic stroke. Using the MTHFR-deficient mouse model, the aim of this study was to investigate the impact of dietary supplementation with one-carbon metabolites on stroke outcome. Methods Male Mthfr+/− and wildtype littermate control mice were aged to 1.5-year-old and were placed on control diet (CD) 4-weeks prior to sensorimotor cortex damage using photothrombosis (PT), a model for ischemic stroke. Post-operatively, one group of Mthfr+/− and wildtype littermate mice were fed a supplemented diet (SD) containing 5-methylTHF, vitamin B12, and choline. Four weeks after PT damage and SD motor function was assessed and brain tissue was processed to assess lesion volume and investigate biochemical and molecular changes. Results Mthfr +/− mice fed a SD after PT did not have an impaired neuroscore compared to CD Mthfr+/− mice. When compared to CD, SD Mthfr+/− mice were able to stay on the accelerating rotarod longer and travelled further, they also used their impaired forepaw more. Total homocysteine levels in plasma and lesion volume were reduced in SD Mthfr+/+ and Mthfr+/− mice. In the brain, within the damage site, there were reduced levels of apoptotic cell death and an increased neuroprotective cellular response in SD treated Mthfr+/− mice. Conclusions This study reveals a critical role for one-carbon supplementation in supporting improvement of function after ischemic stroke. Our data suggests that in stroke affected patients, nutritional supplementation maybe an important component to post-operative care, in addition to pharmacological and rehabilitation therapies. Funding Sources NSERC.
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Sufrin, Janice R., Arthur J. Spiess, Debora L. Kramer, Paul R. Libby, John T. Miller, Ralph J. Bernacki, Younha Lee, Ronald T. Borchardt y Carl W. Porter. "Targeting 5'-deoxy-5'-(methylthio)adenosine phosphorylase by 5'-haloalkyl analogs of 5'-deoxy-5'-(methylthio)adenosine". Journal of Medicinal Chemistry 34, n.º 8 (agosto de 1991): 2600–2606. http://dx.doi.org/10.1021/jm00112a039.

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SUFRIN, J. R., A. J. SPIESS, D. L. KRAMER, P. R. LIBBY, J. T. MILLER, R. J. BERNACKI, Y. LEE, R. T. BORCHARDT y C. W. PORTER. "ChemInform Abstract: Targeting 5′-Epoxy-5′-(methylthio)adenosine Phosphorylase by 5′-Haloalkyl Analogues of 5′-Deoxy-5′-(methylthio)adenosine." ChemInform 23, n.º 2 (22 de agosto de 2010): no. http://dx.doi.org/10.1002/chin.199202319.

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Alam, L. V., R. V. Kharbash y G. I. Koldobskii. "2-Substituted 5-methylthio- and 5-methylsulfonyltetrazoles". Russian Journal of Electrochemistry 36, n.º 6 (junio de 2000): 916–18. http://dx.doi.org/10.1007/bf02757456.

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Yu-Xiu, Liu, Cui Ming-Bo, Zhao Qi-Qi, Wang Qing-Min, Liu Ying y Huang Run-Qiu. "Reduction of Pyrimidine Derivatives by LiAlH4". Journal of Chemical Research 2007, n.º 8 (agosto de 2007): 490–93. http://dx.doi.org/10.3184/030823407x240872.

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The reduction of ethyl 2-methylthio-(or 2-ethoxy)pyrimidine-5-carboxylate by LiAlH4 afforded ethyl 2-methylthio-(or 2-ethoxy)-1,6-dihydropyrimidine-5-carboxylate as the main product. Similarly, the reduction of 2-methylthio-(or 2-methoxy)pyrimidine-5-carboxamide by LiAlH4 gave 2-methylthio-(or 2-methoxy)-1,6-dihydropyrimidine-5-carbonitrile as main product.
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Singh, Okram Mukherjee, H. Junjappa y H. Ila. "A Facile Synthesis of 3-Cyclopropyl- and 5-Cyclopropyl-isoxazoles". Journal of Chemical Research 23, n.º 6 (junio de 1999): 398–99. http://dx.doi.org/10.1177/174751989902300627.

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Tesis sobre el tema "5-methylTHF"

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GOMES, DE LIMA LUIS CARLOS. "Reactions d'alcynes cyanes (monocyanoacethylene et dicyanoacethylene), vis-a-vis de complexes organometalliques du fer, du cobalt, du molybdene et du tungstene". Brest, 1986. http://www.theses.fr/1986BRES2009.

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Etude de la reactivite de complexes thiolates du fer et du tungstene (cp(co)::(n) m(sch::(3))) vis a vis du mono et du dicyanoacetylene. Aptitude des complexes de co(i) a intervenir dans la formation de molecules organiques. Nature des liaisons m-pb(m=mo ou w) dans les complexes cp(co)::(3)m-pbr::(3) et (cp(co)::(3)m)::(2) pbr::(2). Donnes de rmn de **(95)mo et **(207)pb
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FRISO, Simonetta. "GENE-NUTRIENT INTERACTIONS AND EPIGENETICS. BIOCHEMICAL BASES OF THE ROLE OF PLASMA AND RED BLOOD CELL FOLATE, THE MTHFR C677T POLYMORPHISM AND GENOMIC DNA METHYLATION". Doctoral thesis, 2002. http://hdl.handle.net/11562/364225.

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La metilazione del DNA, una caratteristica epigenetica essenziale del DNA che modula l'espressione genica e l'integrità del genoma, è catalizzata da metiltrasferasi che utilizzano la S-adenosilmetionina (SAM) quale donatore universale di gruppi metilici. L'enzima metilenetetraidrofolato reduttasi (MTHFR) catalizza la sintesi del 5-metiltetraidrofolato (5-methylTHF), il donatore di gruppi metilici per la sintesi di metionina dall'omocisteina e precursore della SAM. Nel presente studio si è voluto determinare l'effetto dello status dei folati sulla metilazione genomica del DNA con particolare enfasi sul ruolo di una possibile interazione genetico-nutrizionale con la mutazione comune a carico del gene MTHFR. Un nuovo metodo ad elevata sensibilità e specificità per l'analisi delle basi nucleotidiche, basato su tecnologia LC/ESI-MS, è stato da noi inventato e messo a punto per determinare la metilazione genomica del DNA da materiale nucleico isolato da cellule mononucleate da sangue periferico di 105 soggetti omozigoti per la mutazione comune del gene MTHFR (T/T) e 187 soggetti wild-type (C/C) per il medesimo polimorfismo genico. I risultati del presente lavoro hanno dimostrato che la metilazine genomica del DNA correla in modo diretto con lo status dei folati (P<0.01). I genotipi T/T hanno ridotti livelli di metilazione del DNA rispetto ai soggetti wild-type (C/C) (32.23 vs.62.24 ng 5-methylcytosine/mg DNA, P<0.0001). Tuttavia, solamente i soggetti con genotipo T/T con bassi livelli di folatemia rendevano conto dei ridotti livelli di metilazione genomica del DNA (P<0.0001). Dato particolarmente innovativo ed interessante è la scoperta che nei soggetti portatori del genotipo T/T la metilazione del DNA correlava con la porzione metilata dei folati eritrocitari (RBC folates) ed era inversamente proporzionale con la porzione formilata dei folati eritrocitari (P<0.03)che è noto essere presente solamente nei soggetti portatori del genotipo mutante MTHFR T/T. Questi risultati indiacano pertanto che il polimorfismo MTHFR C677T influenzano il principale meccanismo epigenetico del DNA attraverso una interazione genetico-nutrizionale con lo status dei folati.
DNA methylation, an essential epigenetic feature of DNA that modulates gene expression and genomic integrity, is catalyzed by methyltransferases that utilize the universal methyl donor S-adenosyl-L-methionine (SAM). Methylenetetrahydrofolate reductase (MTHFR) catalyzes the synthesis of 5-methyltetrahydrofolate (5-methylTHF), the methyl donor for synthesis of methionine from homocysteine and precursor of SAM. In the present study we sought to determine the effect of folate status on genomic DNA methylation with an emphasis on the interaction with the common C677T mutation in the MTHFR gene. A newly developed sensitive and selective LC/ESI-MS method for the analysis of nucleotide bases was used to assess genomic DNA methylation in peripheral blood mononuclear cell DNA from 105 subjects homozygous for this mutation (T/T) and 187 homozygous for the wild-type (C/C) genotype. The results show that genomic DNA methylation directly correlates with folate status (P<0.01). T/T genotypes had a diminished level of DNA methylation compared to those with the C/C wild-type (32.23 vs.62.24 ng 5-methylcytosine/mg DNA, P<0.0001). Only the T/T subjects with low levels of folate, however, accounted for the diminished DNA methylation (P<0.0001). In T/T subjects DNA methylation status correlated with the methylated proportion of red blood cell folate (RBC) and was inversely related to the formylated proportion of RBC folates (P<0.03) that is known to be solely represented in those individuals. These results indicate that the MTHFR C677T polymorphism influences DNA methylation status through an interaction with folate status.
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Capítulos de libros sobre el tema "5-methylTHF"

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Dombek, R. Duane, Robert J. Angelici, Ian S. Butler y Daniel Cozak. "Dicarbonyl(η5 -Cyclopentadienylxthio-Carbonyl)Iron(1 +) Hexafluorophosphate(1 -) and Dicarbonyl(η 5 -Cyclopentadienyl)-[(Methylthio)Thiocarbonyl]Iron". En Inorganic Syntheses, 100–103. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2007. http://dx.doi.org/10.1002/9780470132487.ch29.

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Actas de conferencias sobre el tema "5-methylTHF"

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Bosshard, Christian, Pan Feng, Man Shing Wong, Martin Bösch, Urs Meier y Peter Günter. "Thiophene Based Hydrazones: a New Class of Nonlinear Optical Molecular Crystals". En Organic Thin Films for Photonic Applications. Washington, D.C.: Optica Publishing Group, 1997. http://dx.doi.org/10.1364/otfa.1997.thd.2.

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Crystalline solids are often regarded as the best choice of material form for practical use as optical frequency converters because of the excellent long-term orientational stability and extremely high density of active components. Such materials can be combined with inexpensive diode lasers for optic parametric generation of a broad range of optical frequencies [1, 2]. We here report on our on-going efforts in the development of novel and highly efficient second-order nonlinear optical crystalline materials for frequency conversion, based on the hydrazone derivatives 5-(methylthio)-thiophenecarboxaldehyde-4-nitrophenylhydrazone (MTTNPH) and 5-nitro-2-thiophene-carboxaldehyde-4-methylphenylhydrazone (NTMPH).
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Żołnowska, Beata, Jarosław Sławiński y Anna Kawiak. "Synthesis of New N-Substituted N′-(2-methylthio-4-chloro-5-methylbenzenesulfonyl)guanidines with Anticancer Activity". En ECMC 2022. Basel Switzerland: MDPI, 2022. http://dx.doi.org/10.3390/ecmc2022-13255.

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Lyapustin, D. N., E. N. Ulomsky, E. K. Voinkov y V. L. Rusinov. "Preparation of new 5-methylthio-6-nitro-1,2,4-triazolo[1,5-a]pyrimidine-7-ones as structural analogues of antiviral drugs". En PROCEEDINGS OF THE 3RD INTERNATIONAL CONFERENCE ON AUTOMOTIVE INNOVATION GREEN ENERGY VEHICLE: AIGEV 2018. Author(s), 2019. http://dx.doi.org/10.1063/1.5087320.

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Smit, Biljana, Petar Stanic y Marija Zivkovic. "Synthesis, characterization and an extensive biological evaluation of 5-​[2-​(methylthio)​ethyl]​-​3-​(2-​propen-​1-​yl)​-​2-​thioxo-4-​imidazolidinone". En 4th International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2018. http://dx.doi.org/10.3390/ecmc-4-05625.

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Sohrabi, Beheshteh, Mehdi Kiasadegh y Javad Beheshtian. "Computational Studies of Optical Properties of (E)-2-(5-methacrylamido-2, 3-bis (methylthio) phenyl) Diazenesulfonate Dye for Solar Cell Using DFT and TD-DFT Methods". En The 16th International Electronic Conference on Synthetic Organic Chemistry. Basel, Switzerland: MDPI, 2012. http://dx.doi.org/10.3390/ecsoc-16-01158.

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