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Artykuły w czasopismach na temat "MTHFR"
Thompson, Henry R., Gayle M. Jones i Michael R. Narkewicz. "Ontogeny of hepatic enzymes involved in serine- and folate-dependent one-carbon metabolism in rabbits". American Journal of Physiology-Gastrointestinal and Liver Physiology 280, nr 5 (1.05.2001): G873—G878. http://dx.doi.org/10.1152/ajpgi.2001.280.5.g873.
Pełny tekst źródłaElsadig Babiker, Nihad. "Detection of Mthfr (C667t) and Mthfd (G1958a) Polymorphisms Among Sudanese Women with The Recurrent Miscarriages". Archives of Gynaecology and Women Health 1, nr 1 (6.02.2023): 01–04. http://dx.doi.org/10.58489/2836-497x/006.
Pełny tekst źródłaCole, Leslie, Alina Cernasev, Katie Webb, Santosh Kumar i A. Shaun Rowe. "A Study of the MTHFR Gene Prevalence in a Rural Tennessee Opioid Use Disorder Treatment Center Population". International Journal of Environmental Research and Public Health 19, nr 6 (10.03.2022): 3255. http://dx.doi.org/10.3390/ijerph19063255.
Pełny tekst źródłaKaragur, Ege, Mustafa Alay, Aydin Demiray, Nedim Karagenc, Onur Tokgün, Taner Durak i Hakan Akca. "The impact of hereditary thrombophilias in recurrent pregnancy loss". Genetika 54, nr 3 (2022): 1399–410. http://dx.doi.org/10.2298/gensr2203399k.
Pełny tekst źródłaMarosi, Krisztina, Annamária Ágota, Veronika Végh, József Gábor Joó, Zoltán Langmár, Ildikó †Kriszbacher i Zsolt B. Nagy. "The role of homocysteine and methylenetetrahydrofolate reductase, methionine synthase, methionine synthase reductase polymorphisms in the development of cardiovascular diseases and hypertension". Orvosi Hetilap 153, nr 12 (marzec 2012): 445–53. http://dx.doi.org/10.1556/oh.2012.29326.
Pełny tekst źródłaLiu, Zhiping, Hong Jiang, Justin H. Townsend i Jianhua Wang. "Effects of Ocufolin on retinal microvasculature in patients with mild non-proliferative diabetic retinopathy carrying polymorphisms of the MTHFR gene". BMJ Open Diabetes Research & Care 9, nr 1 (wrzesień 2021): e002327. http://dx.doi.org/10.1136/bmjdrc-2021-002327.
Pełny tekst źródłaLu, Mong-Liang, Wei-Chi Ku, Nailis Syifa, Shu-Chin Hu, Chia-Te Chou, Yi-Hsio Wu, Po-Hsiu Kuo, Chun-Hsin Chen, Wei J. Chen i Tzu-Hua Wu. "Developing a Sensitive Platform to Measure 5-Methyltetrahydrofolate in Subjects with MTHFR and PON1 Gene Polymorphisms". Nutrients 14, nr 16 (13.08.2022): 3320. http://dx.doi.org/10.3390/nu14163320.
Pełny tekst źródłaTsaousidou, Maria M. K. T., Fotis F. I. G. Girtovitis, Afroditi A. K. Boutou, Elefteria E. P. Pithara i Pantelis M. E. P. Makris. "Appliance of the DNA-Micro Array Technique for the Identification of Patients with Thrombophilic Diathesis. I-Comparison to the Classic PCR Analysis." Blood 104, nr 11 (16.11.2004): 4049. http://dx.doi.org/10.1182/blood.v104.11.4049.4049.
Pełny tekst źródłaSimonian, Rebecca, Emanuela Pannia, Rola Hammoud, Xiucheng Cui, Ruslan Kubant, Brandi Wasek, Terry Bottiglieri, James Dowling, Ramil Noche i G. Harvey Anderson. "Methylenetetrahydrofolate Reductase Deficiency Reduces Brain Microglia in Zebrafish During Embryonic Development and Is Not Corrected by Folic Acid". Current Developments in Nutrition 5, Supplement_2 (czerwiec 2021): 925. http://dx.doi.org/10.1093/cdn/nzab049_038.
Pełny tekst źródłaDevlin, Angela M., Erland Arning, Teodoro Bottiglieri, Frank M. Faraci, Rima Rozen i Steven R. Lentz. "Effect of Mthfr genotype on diet-induced hyperhomocysteinemia and vascular function in mice". Blood 103, nr 7 (1.04.2004): 2624–29. http://dx.doi.org/10.1182/blood-2003-09-3078.
Pełny tekst źródłaRozprawy doktorskie na temat "MTHFR"
Roy, Marc André 1981. "Investigation of MTHFR in birth defects : pharmacogenetic studies with valproic acid and MTHFR promoter analyses". Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=101801.
Pełny tekst źródłaSILVA, A. B. "Associação do carcinoma epidermóide oral com os polimorfismos MTHFR C677T, MTHFR A1298C e CBS 844ins68 na população do Espírito Santo". Universidade Federal do Espírito Santo, 2013. http://repositorio.ufes.br/handle/10/4473.
Pełny tekst źródłaAssociação do carcinoma epidermóide oral com os polimorfismos MTHFR C677T, MTHFR A1298C e CBS 844ins68 na população do Espírito Santo
Матлай, Ольга Іванівна, Ольга Ивановна Матлай i Olha Ivanivna Matlai. "Зв'язок алельного поліморфізму гена метилентетрагідрофолатредуктази (MTHFR) з розвитком ішемічних інсультів". Thesis, Вид-во СумДУ, 2015. http://essuir.sumdu.edu.ua/handle/123456789/42758.
Pełny tekst źródłaДиссертация посвящена выявлению влияния генетических факторов (однонуклеотидных полиморфизмов С677Т и А1298С гена метилентетрагидро-фолатредуктазы (MTHFR)) на развитие ишемического атеротромботического инсульта (ИАТИ). Установлено частоты аллелей и генотипов полиморфных вариантов С677Т и А1298С гена MTHFR у представителей украинской популяции и впервые исследованы их ассоциации с ишемическим атеротромботическим инсультом. Установлено, что существует связь между ишемическим атеротромботическим инсультом, с одной стороны, и С677Т и А1298С полиморфными вариантами гена MTHFR, с другой. Риск ИАТИ у гомозигот по минорному аллелю (Т/Т и С/С) по изученным полиморфизмам выше, чем у носителей других генотипов (Р = 0,044; Р = 0,039). У лиц с генотипом С/С по А1298С полиморфизму ИАТИ возникает в 2,3 раза чаще, чем у носителей основного аллеля (Р = 0,027; OR = 2,309). Выявлено, что влияние генетического фактора на развитие цереброваскулярной патологии имеет половые особенности. Лица мужского пола с генотипом С/Т по С677Т полиморфизму гена MTHFR в 2,3 раза более стойки к ИАТИ, чем больные с генотипом С/С (Р = 0,010; OR = 0,433). У мужчин-гомозигот по минорному аллелю (С/С) по А1298С полиморфизму риск развития ИАТИ в 3,5 раза выше, чем у носителей генотипа А/А (Р = 0,016; OR = 3,474). Изучена связь исследованных полиморфизмов с некоторыми факторами риска ИАТИ: индексом массы тела (ИМТ), артериальной гипертензией, курением. Выявлено, что гомозиготы по минорному аллелю (полиморфизм А1298С) с ИМТ ≥ 25 кг/м² в 3,2 раза более подвержены ИАТИ, чем гомозиготы по основному аллелю (Р = 0,013, OR = 3,195). У лиц с нормальным артериальным давлением - носителей Т/Т-генотипа, у пациентов с гипертензией с генотипом С/С по С677Т полиморфному варианту гена MTHFR, а также у гетерозигот А/С с гипертензией (А1298С полиморфизм) ишемический атеротромботический инсульт возникает чаще (P = 0,039; P = 0,010 и P = 0,025 соответственно). Риск развития ИАТИ больше в группе лиц с генотипом Т/Т по полиморфизму С677Т, которые не курят (Р = 0,029). Установлено влияние С677Т и А1298С полиморфных вариантов гена MTHFR на характеристики ИАТИ. У гомозигот по основному аллелю С/С (полиморфизм С677Т) с нормальной массой тела чаще поражению подвергаются вертебральные и базилярная артерии (Р = 0,026). У лиц с генотипом С/С по полиморфному варианту С677Т с нормальным артериальным давлением развивается легкая степень тяжести болезни (Р = 0,021). Гомозиготы С/С по А1298С полиморфизму мужского пола более склонны к повторным инсультам (Р = 0,041).
Dissertation is devoted to revealing the influence of genetic factors (SNPs C677T and A1298C gene methylenetetrahydrofolatereductase (MTHFR)) on the development of atherothrombotic ischemic stroke. The frequency of allele and genotype polymorphisms C677T and A1298C MTHFR gene from representatives of the Ukrainian population, and for the first time their association with atherothrombotic ischemic stroke was investigated. It was established that there is a relationship between atherothrombotic ischemic stroke and C677T and A1298C polymorphic variants of the gene MTHFR. Risk of atherothrombotic ischemic stroke homozygotes for the minor allele (T/T and C/C) of the studied polymorphisms is higher than that of the carriers of other genotypes (P = 0,044; P = 0,039). In patients with genotype C/C of A1298C polymorphism atherothrombotic ischemic stroke occurs 2,3 more frequently than that in the main allele carriers (P = 0,027; OR = 2,309). It was found that the influence of genetic factors on the development of cerebrovascular disease has sexual features. Males with genotype C/T polymorphism of C677T MTHFR gene is 2,3 times more resistant to atherothrombotic ischemic stroke than in patients with genotype C/C (P = 0,010; OR = 0,433). Men-minor allele homozygotes (C/C) at the risk of A1298C polymorphism atherothrombotic ischemic stroke is 3,5 times higher than that of genotype A/A (P = 0,016; OR = 3,474). The relationship between studied polymorphisms with some risk factors ATIS: body mass index (BMI), hypertension, smoking. It was revealed that homozygotes for the minor allele (polymorphism A1298C) with a BMI ≥ 25 kg/m² are 3,2 times more prone to atherothrombotic ischemic stroke I than homozygotes for the main allele (P = 0,013; OR = 3,195). In individuals with normal blood pressure - the carriers of T/T genotype in hypertensive patients with genotype C/C for C677T polymorphic variant of the gene MTHFR, as well as in the heterozygote A/C with hypertension (A1298C polymorphism) ischemic atherothrombotic stroke occurs more frequently (P = 0,039; P = 0,010 and P = 0,025 respectively). The risk of atherothrombotic ischemic stroke is greater in the group with genotype T/T polymorphism C677T who do not smoke (Р = 0,029). The effect of the C677T and A1298C polymorphisms of MTHFR gene on the characteristics of atherothrombotic ischemic stroke is established. At the main allele homozygotes for the C/C (C677T polymorphism) with normal body weight often defeat exposed vertebral and basilar artery (P = 0,026). In patients with genotype C/C for C677T polymorphic variant with normal blood pressure developes mild disease (P = 0,021). Homozygotes C/C A1298C polymorphism of males are more prone to recurrent stroke (P = 0,041).
McAuley, Emma. "Riboflavin, MTHFR genotype and blood pressure : implications for personalised nutrition". Thesis, Ulster University, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.706468.
Pełny tekst źródłaNeaga, Oana-Raisa. "Male germ cell development in the methylenetetrahydrofolate reductase (MTHFR) mouse model". Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=81366.
Pełny tekst źródłaMassa, Nayara Moreira. "Avaliação do efeito da Citrullus Lanatus (melancia) e análise Da influência de polimorfismos genéticos em adultos Dislipidêmicos". Universidade Federal da Paraíba, 2013. http://tede.biblioteca.ufpb.br:8080/handle/tede/4296.
Pełny tekst źródłaCoordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES
Dyslipidemia and genetic polymorphisms are associated with increased risk for developing cardiovascular diseases and watermelon appears to possess the potential to improve hyperlipidemia due to the presence of nutrients such as arginine and citrulline. We investigated the hypolipidemic effect of the extract of watermelon and influence of genotype of methylenetetrahydrofolate reductase (MTHFR C677T) and apolipoprotein E in response to supplementation. We developed an experimental, clinical phase II, randomized, double blind placebo controlled. Initially biochemical tests were performed to evaluate the lipid profile with 92 employees of a public institution, randomly. Of these, forty-three subjects diagnosed with dyslipidemia were randomly divided into two groups, the experimental (n = 22) and control (n = 21). The subjects were supplemented daily (6 g) for 42 days with extract of watermelon or a mixture of carbohydrates (sucrose / glucose / fructose). We evaluated anthropometric parameters (weight, body mass index, waist circumference and waist-hip ratio), biochemical (lipid profile), systemic arterial pressure and cardiac autonomic activity. The use of the extract of watermelon reduced plasma total cholesterol (p <0.05) and low density lipoprotein (p <0.01) without modifying values triglyceride, high density lipoprotein and very low density lipoprotein in human adults with dyslipidemia, pre hypertensive, overweight and glucose levels close to the upper limit. T allele carriers (C677T) in the experimental group apresentarm reduction of low density lipoprotein (p <0.01), longer allele C did not reduce the levels of this variable. The subjects in the experimental group and control had stimulated the sympathetic system, without modifications after supplementation in both groups. Beneficial effect of the extract on blood pressure levels, significantly reducing systolic blood pressure (p <0.01) and diastolic (p <0.01) in the experimental group, no significant changes in the control group. There were no changes in anthropometric parameters in both groups after supplementation with the extract of watermelon. In summary, the present study first demonstrated the beneficial effect of the consumption of watermelon extract in reducing plasma levels of lipids and systolic and diastolic blood pressure in humans, where MTHFR C677T polymorphism did not influence the levels of plasma lipids, but makes individuals more responsive to treatment with watermelon. The consumption of functional food may be an alternative therapy in the adjuvant treatment of patients with dyslipidemia, causing health promotion and minimizing the development of risk factors for cardiovascular disease.
A dislipidemia e polimorfismos genéticos estão relacionados com risco aumentado para desenvolver doenças cardiovasculares e a melancia parece possuir potencial para melhorar hiperlipidemia devido à presença de nutrientes como arginina e citrulina. Investigou-se o efeito hipolipemiante do extrato de melancia e a influência do genótipo da metilenotetrahidrofolato redutase (MTHFR C677T) e da apolipoproteína E na resposta a suplementação. Foi desenvolvido um estudo experimental, clínico de fase II, randomizado, duplo cego com placebo controlado. Inicialmente foram realizados exames bioquímicos para avaliação do perfil lipídico com 92 funcionários de uma instituição pública, de forma aleatória. Destes, quarenta e três sujeitos diagnósticados com dislipidemia foram randomicamente divididos em dois grupos, o experimental (n=22) e controle (n=21). Os sujeitos foram suplementados diariamente (6 g) durante 42 dias com extrato de melancia ou uma mistura de hidratos de carbono (sacarose/glicose/frutose). Foram avaliados parâmetros antropométricos (peso, índice de massa corporal, circunferência da cintura e relação cintura quadril), bioquímicos (perfil lipídico), pressão arterial sistêmica e atividade autonômica cardíaca. O consumo do extrato de melancia reduziu concentrações plasmáticas de colesterol total (p<0,05) e lipoproteína de baixa densidade (p<0,01), sem modificar valores de triglicerídeo, lipoproteína de alta densidade e lipoproteína de muito baixa densidade em humanos adultos com dislipidemia, pré hipertensos, com sobrepeso e glicemia próximo ao limite superior. Portadores do alelo T (MTHFR C677T) do grupo experimental apresentarm redução da lipoproteína de baixa densidade (p<0,01), já portadores do alelo C não reduziram os níveis desta variável. Os sujeitos do grupo experimental e controle apresentaram o sistema simpático estimulado, sem modificações após suplementação em ambos os grupos. Efeito benéfico do extrato sobre níveis de pressão arterial, reduzindo significativamente valores de pressão arterial sistólica (p<0,01) e diastólica (p<0,01) no grupo experimental, sem alterações significativas no grupo controle. Não foram encontradas modificações dos parâmetros antropométricos em ambos os grupos após a suplementação com o extrato de melancia. Em resumo, o presente estudo demonstrou pela primeira vez efeito benéfico do consumo do extrato de melancia na redução dos níveis plasmáticos de lipídios e pressão arterial sistólica e diastólica em seres humanos, onde polimorfismo MTHFR C677T não influenciou os níveis de lipídios plasmáticos, mas torna os indivíduos mais responsivos ao tratamento com a melancia. O consumo deste alimento funcional pode representar uma alternativa terapêutica no tratamento coadjuvante de pacientes com dislipidemia, acarretando promoção da saúde e minimização do desenvolvimento de fatores de risco para as doenças cardiovasculares.
Hessing, Sabine. "Die Rolle der MTHFR-C677T-Mutation bei der akuten Abstossung von Nierentransplantaten". [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=967954932.
Pełny tekst źródłaChan, Manuel. "Characterization of the 5' region of the human methylenetetrahydrofolate reductase, MTHFR, gene". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0026/MQ50734.pdf.
Pełny tekst źródłaTran, Pamela. "Regulation of mouse methylenetetrahydrofolate reductase (Mthfr) and its role in early development". Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=38426.
Pełny tekst źródłaPai, Aditya P. "Isolation and partial characterization of the mouse gene for methylenetetrahydrofolate reductase (MTHFR)". Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=22868.
Pełny tekst źródłaAn animal model would prove to be useful for designing therapeutic approaches for understanding the pathogenesis of this genetic disease at the molecular level. The mouse MTHFR gene and cDNA have been isolated and partially characterized. Four genomic clones were isolated by library screening. One of these clones (clone 3) contained the 5$ sp prime$ end of the gene and was completely characterized. The clone was shown to have no rearrangements and is to be used to design targeting vectors for 'knockout mice' and mice carrying a common mutation which has been postulated to be a genetic risk factor for cardiovascular disease. The other three clones contain the remaining 3$ sp prime$ portion of the gene. The coding portion has approximately 90% homology with the human cDNA and also shows a similar gene structure.
A 2.2 Kb mouse MTHFR cDNA was isolated by library screening and was found to contain a 320 base pair extension at the 5$ sp prime$ end which has not been found in the human cDNA. The cDNA contains exons -1 -3, but also contains two possibly unspliced introns. A portion of this cDNA can however still be used to rescreen libraries to isolate a full length cDNA. The above research is the first genetic data on the mouse MTHFR gene and provides the basis for future research involving mouse models of MTHFR deficiency.
Książki na temat "MTHFR"
Magne, Ueland Per, i Rozen Rima, red. MTHFR polymorphisms and disease. Georgetown, Tex: Landes Bioscience/ Eurekah.com, 2005.
Znajdź pełny tekst źródłaUeland, Per Magne, i Rima Rozen. MTHFR polymorphisms and disease. Georgetown, Tex: Landes Bioscience, 2005.
Znajdź pełny tekst źródłaLibrary of Tibetan Works & Archives., red. Mthar gtam mthoṅ ba ʼdzum śor. Dharamsala, H.P: Bod kyi dpe mdzod khaṅ, 2001.
Znajdź pełny tekst źródłaRig-ʼdzin Kun-grol-grags-paʼ [i.e. paʼi] rnam mthar [i.e. thar]. Swayambhunath, Kathmandu, Nepal: Tritan Narbutse Bon Education Centre Ichangu Narayan, 1990.
Znajdź pełny tekst źródłaDge-ʼdun-bsam-gtan, red. Tshaṅs thig: Sprul sku ched sbyor ʼdzin grwaʼi mthar phyin dran rten. [Zi-liṅ]: Mtsho-sṅon naṅ bstan slob gliṅ, 2004.
Znajdź pełny tekst źródłaSa mthar skor baʼi mthoṅ snaṅ: Rṅa-rgod Yon-tan gyi sñan rtsom phyogs bsgrigs. [India: ʼBras Sgo-maṅ dpe mdzod glog klad sde tshan, 1999.
Znajdź pełny tekst źródłaCenter, Buddhist Digital Resource. Snga ʼgyur mtho slob chen moʼi bslab pa mthar son gyi mdzad sgo thengs drug paʼi dran deb. Bylakuppe, karnataka: Ngagyur rigzod editorial committee, 2010.
Znajdź pełny tekst źródłaRi chos ṅes don rgya mtsho źes bya ba mthar thug thun moṅ ma yin paʼi man ṅag. Pe-cin: Mi rigs dpe skrun khaṅ, 1998.
Znajdź pełny tekst źródłaCenter, Buddhist Digital Resource. Mkhas grub chen po rnam grol bzan po'i rnam thar dad pa'i spu lon gyo byed no mthar can. Dalhousie, h.p: Damchoe sangpo, 1985.
Znajdź pełny tekst źródłaṄag-dbaṅ-kun-dgaʼ-ʼjam-dbyaṅs-blo-gros, red. Ri chos ṅes don rgya mtsho źes bya ba mthar thug thun moṅ ma yin paʼi man ṅag bźugs. [Pe-cin]: Mi rigs dpe skrun khaṅ, 2007.
Znajdź pełny tekst źródłaCzęści książek na temat "MTHFR"
Oette, Mark, Marvin J. Stone, Hendrik P. N. Scholl, Peter Charbel Issa, Monika Fleckenstein, Steffen Schmitz-Valckenberg, Frank G. Holz i in. "MTHFR Deficiency". W Encyclopedia of Molecular Mechanisms of Disease, 1356. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6947.
Pełny tekst źródłaBoisdron-Celle, M., V. Guérin-Meyer i O. Capitain. "5-fluorouracile : MSI, pharmacocinétique, DPD, TYMS et MTHFR". W Médecine personnalisée en cancérologie digestive, 75–92. Paris: Springer Paris, 2013. http://dx.doi.org/10.1007/978-2-8178-0527-6_6.
Pełny tekst źródłaRozen, Rima. "Molecular Biology of Methylenetetrahydrofolate Reductase (MTHFR): Interrelationships with Folic Acid, Homocysteine and Vascular Disease". W Homocysteine and Vascular Disease, 271–89. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-017-1789-2_16.
Pełny tekst źródłaWoitalla, D., W. Kuhn i T. Müller. "MTHFR C677T polymorphism, folic acid and hyperhomocysteinemia in levodopa treated patients with Parkinson’s disease". W Focus on Extrapyramidal Dysfunction, 15–20. Vienna: Springer Vienna, 2004. http://dx.doi.org/10.1007/978-3-7091-0579-5_2.
Pełny tekst źródłaIolascon, A., B. Coppola, E. Miraglia Del Giudice, R. Carbone, D. Del Gaizo, M. T. Carbone, G. Aceto, M. F. Faienza, G. Del Gado i R. Del Gado. "MTHFR 677C-T and Neural Tube Defects: An Evaluation in a Population from Southern Italy". W Spina Bifida, 509–12. Tokyo: Springer Japan, 1999. http://dx.doi.org/10.1007/978-4-431-68373-5_116.
Pełny tekst źródłaCui, Lian-Hua, Meng Liu, Hong-Zong Si, Min-Ho Shin, Hee Nam Kim i Jin-Su Choi. "Correlation of Aberrant Methylation of APC Gene to MTHFR C677T Genetic Polymorphisms in Hepatic Carcinoma". W Lecture Notes in Electrical Engineering, 2961–68. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7618-0_376.
Pełny tekst źródłaRoschitz, B., W. Muntean, C. Mannhalter i M. Koestenberger. "Deep Venous Thrombosis of the Lower Extremity in a 16-Year-Old Girl with Homozygous MTHFR- and Heterozygous Factor V Leiden-Mutation". W 33rd Hemophilia Symposium, 176–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18260-0_25.
Pełny tekst źródłaSchröder, W., C. Spitzer, M. Koesling, Ch Kessler i F. H. Herrmann. "Molekulare Marker bei Schlaganfallpatienten: Die G 20210 A-Prothrombin-Variante, die Faktor-V-Leiden-Mutation und der C 677 T-MTHFR-Polymorphismus". W 29. Hämophilie-Symposion, 312–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-59633-9_55.
Pełny tekst źródłaSchröder, W., A. Siegemund, J. Berrouschot, H. Voigt, B. Vorberg, H. Scheel i F. H. Herrmann. "Molekulargenetische Marker bei Patienten mit venösen und arteriellen Thrombosen: Der G20210A-Prothrombin-Polymorphismus, die C677T MTHFR-Mutation und die Faktor-V-Leiden (G1691A) Mutation". W 28. Hämophilie-Symposion Hamburg 1997, 67–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59915-6_10.
Pełny tekst źródłaHerrmann, F. H., W. Schröder, R. Altman, R. Jimenez Bonilla, J. L. Perez-Requejo i J. R. Singh. "Zur Prävalenz des G20210A-Prothrombin-Polymorphismus, der C677T-Mutation des MTHFR-Gens und der Faktor-V-Leiden-Mutation in Nordostdeutschland, Argentinien, Venezuela, Costa Rica und Indien". W 28. Hämophilie-Symposion Hamburg 1997, 55–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59915-6_8.
Pełny tekst źródłaStreszczenia konferencji na temat "MTHFR"
Machado, Vitor Pereira, Edis Bellini Júnior, Lucas Gazarini, Clarisse Lobo i Claudia Bonini-Domingos. "Association of genetic markers with ischemic stroke in pediatric patients with sickle cell anemia". W XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.293.
Pełny tekst źródłaGomes, Sérgio de Oliveira, Thaísa Guedes de Freitas Almeida, Cláudia Sampaio de Andrade Lima i Ricardo Yara. "ESTUDO SOBRE A FORMAÇÃO DA ENZIMA MTHFR HUMANA POR HOMOLOGIA". W Encontro Anual da Biofísica 2017. São Paulo: Editora Blucher, 2017. http://dx.doi.org/10.5151/biofisica2017-015.
Pełny tekst źródłaAstaf'eva, E. A., T. A. Tolochko i A. A. Timofeeva. "THE EFFECT OF POLYMORPHISM OF THE MTHFR C677T GENE ON THE MORPHOFUNCTIONAL STATE OF LYMPHOCYTES DURING DRUG INTOXICATION". W I International Congress “The Latest Achievements of Medicine, Healthcare, and Health-Saving Technologies”. Kemerovo State University, 2023. http://dx.doi.org/10.21603/-i-ic-8.
Pełny tekst źródłaGiannelou, Maira, Andrianos Nezos, Kyriaki Maselou, Nikolaos Drakoulis, Dimitrios Ioakeimidis, Michael Koutsilieris, Haralampos M. Moutsopoulos i Clio P. Mavragani. "07.11 Contribution of mthfr gene variants in lupus related subclinical atherosclerosis". W 37th European Workshop for Rheumatology Research 2–4 March 2017 Athens, Greece. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2016-211054.11.
Pełny tekst źródłade Lucas-Ramos, Pilar, Jose Miguel Rodriguez Gonzalez-Moro, Zoraida Verde Rello, Jose Luis Izquierdo Alonso, Jose Mª Bellón Cano i Catalina Santiago Dorrego. "Metylene Tetrahydrofolate Reductase (MTHFR) C677T Gene Polymorphisms In Patients With COPD". W American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2623.
Pełny tekst źródłaMagadan, Eduarda Druck, Eduarda Kotlinsky Weber, Esthela Rodegheri Trevisan, Luiza Fernandes Xavier i Virgínia Tafas Da Nóbrega. "TROMBOFILIA EM CRIANÇA PORTADORA DE SÍNDROME DE DOWN: UM RELATO DE CASO". W II Congresso Brasileiro de Hematologia Clínico-laboratorial On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/hematoclil/127.
Pełny tekst źródłaMuthmainah, Muthmainah, Nova Kurniasari, Mohammad Fanani, Septiawan Debree i Herdaetha Adriestri. "C677T Methylenetetrahydrofolate Reductase (MTHFR) Gene Polymorphism and Treatment Response in Schizophrenia Patients". W Health Science International Conference (HSIC 2017). Paris, France: Atlantis Press, 2017. http://dx.doi.org/10.2991/hsic-17.2017.33.
Pełny tekst źródłaLampalo, Marina, Irena Jukic, Jasna Bingulac-Popovic, Ana Hecimovic, Nikola Ferara i Sanja Popovic-Grle. "Effect of MTHFR C677T polymorphism on allergic airway disease in asthma patients". W ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa4460.
Pełny tekst źródłaFragkioudaki, Sofia, Adrianos Nezos, Aggeliki A. Saetta, Nikolaos Drakoulis, Vasilis L. Souliotis, Petros P. Sfikakis, Athanasios G. Tzioufas i in. "07.08 Contribution of mthfr gene polymorphisms in primary sjögren’s syndrome related lymphomagenesis". W 37th European Workshop for Rheumatology Research 2–4 March 2017 Athens, Greece. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2016-211054.8.
Pełny tekst źródłaFalchi, Alessandra, Michela Barsotelli, Laurianne Giovannoni, Laurent Varesi i Giuseppe Vona. "Prevalence of MTHFR gene polymorphisms among Mediteanean populations: a possible genetic selection from malaria?" W 2006 First International Symposium on Environment Identities and Mediterranean Area. IEEE, 2006. http://dx.doi.org/10.1109/iseima.2006.344998.
Pełny tekst źródłaRaporty organizacyjne na temat "MTHFR"
Iyshwarya, B. K., Ilibagiza Regine i Ramakrishnan Veerabathiran. Association of MTHFR Gene Polymorphism in Diabetic Nephropathy. Peeref, lipiec 2022. http://dx.doi.org/10.54985/peeref.2207p7008018.
Pełny tekst źródłaOwens, Greg D., Nafisa M. Jadavji i Patrice D. Smith. Neurogenesis Unchanged by MTHFR Deficiency in Three-Week-Old Mice. Journal of Young Investigators, grudzień 2016. http://dx.doi.org/10.22186/jyi.31.6.39-43.
Pełny tekst źródłaZhao, Lili, Tao Li, Meijuan Dang, Ye Li, Hong Fan, Qian Hao, Dingli Song i in. Association of methylenetetrahydrofolate reductase (MTHFR) C677T gene polymorphism with ischemic stroke risk in different populations: an updated meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, listopad 2022. http://dx.doi.org/10.37766/inplasy2022.11.0037.
Pełny tekst źródłaLiu, Xudong. MTHFR Functional Polymorphism C677T and Genomic Instability in the Etiology of Idiopathic Autism in Simplex Families. Revision. Fort Belvoir, VA: Defense Technical Information Center, październik 2013. http://dx.doi.org/10.21236/ada600503.
Pełny tekst źródłaEl Bairi, Khalid, i Falak Azzam. Polymorphisms of Folate-Metabolizing Enzymes (MTHFR, MTR and MTRR) and Colorectal Cancer Risk: An Updated Systematic Review and Meta-analysis of Case-control Studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, czerwiec 2020. http://dx.doi.org/10.37766/inplasy2020.6.0037.
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