Gotowa bibliografia na temat „Folic acid deficiency”
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Artykuły w czasopismach na temat "Folic acid deficiency"
Ratajczak, Alicja Ewa, Aleksandra Szymczak-Tomczak, Anna Maria Rychter, Agnieszka Zawada, Agnieszka Dobrowolska i Iwona Krela-Kaźmierczak. "Does Folic Acid Protect Patients with Inflammatory Bowel Disease from Complications?" Nutrients 13, nr 11 (12.11.2021): 4036. http://dx.doi.org/10.3390/nu13114036.
Pełny tekst źródłaKhaitovich, M. V. "Folates: Modern Pregnant Health Support". HEALTH OF WOMAN, nr 4(150) (30.05.2020): 37–42. http://dx.doi.org/10.15574/hw.2020.150.37.
Pełny tekst źródłaYasmin, Haleema, Shireen Bhutta i Hasina -. "FOLIC ACID;". Professional Medical Journal 24, nr 12 (29.11.2017): 1884–88. http://dx.doi.org/10.29309/tpmj/2017.24.12.602.
Pełny tekst źródłaDiaz, Karina, Zhu Na, Sorab Gupta, Vikram Arya, Lourdes Martinez, Supreet Dhaliwal, Nora Ajdir, Bhavita Gaglani, Shradha Ahuja i Ilmana Fulger. "Prevalence of Folic Acid Deficiency and Cost Effectiveness of Folic Acid Testing: A Single Center Experience". Blood 132, Supplement 1 (29.11.2018): 4878. http://dx.doi.org/10.1182/blood-2018-99-111607.
Pełny tekst źródłaCristina-Crenguța Albu, Dinu-Florin Albu, Emily-Alice Russu i Ştefan-Dimitrie Albu. "Folic acid and its implications in genetic pathology". World Journal of Advanced Research and Reviews 16, nr 1 (30.10.2022): 742–48. http://dx.doi.org/10.30574/wjarr.2022.16.1.1097.
Pełny tekst źródłaSlagman, Anna, Linton Harriss, Sandra Campbell, Reinhold Muller i Robyn McDermott. "Folic acid deficiency declined substantially after introduction of the mandatory fortification programme in Queensland, Australia: a secondary health data analysis". Public Health Nutrition 22, nr 18 (4.09.2019): 3426–34. http://dx.doi.org/10.1017/s1368980019002258.
Pełny tekst źródłaGordon, Neil. "Folic Acid Deficiency from Anticonvulsant Therapy". Developmental Medicine & Child Neurology 10, nr 4 (12.11.2008): 497–504. http://dx.doi.org/10.1111/j.1469-8749.1968.tb02925.x.
Pełny tekst źródłaMarcus, David L., i Michael L. Freedman. "Folic Acid Deficiency in the Elderly". Journal of the American Geriatrics Society 33, nr 8 (sierpień 1985): 552–58. http://dx.doi.org/10.1111/j.1532-5415.1985.tb04621.x.
Pełny tekst źródłaSpeidel, B. D. "FOLIC ACID DEFICIENCY AND CONGENITAL MALFORMATION". Developmental Medicine & Child Neurology 15, nr 1 (12.11.2008): 81–83. http://dx.doi.org/10.1111/j.1469-8749.1973.tb04872.x.
Pełny tekst źródłaLewis, Dale P., Don C. Van Dyke, Laurie A. Willhite, Phyllis J. Stumbo i Mary J. Berg. "Phenytoin-Folic Acid Interaction". Annals of Pharmacotherapy 29, nr 7-8 (lipiec 1995): 726–35. http://dx.doi.org/10.1177/106002809502907-816.
Pełny tekst źródłaRozprawy doktorskie na temat "Folic acid deficiency"
Goyette, Philippe. "Molecular characterization of methylenetetrahydrofolate reductase deficiency". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0005/NQ44442.pdf.
Pełny tekst źródłaLow-Nang, Lawrence. "Investigation of mutations in methylenetetrahydrofolate reductase deficiency". Thesis, McGill University, 1991. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=60720.
Pełny tekst źródłaMilan, Julie E. "The Women's Folate Study: A Stage-Tailored, Web-Based Intervention for College Women". Fogler Library, University of Maine, 2004. http://www.library.umaine.edu/theses/pdf/MilanJE2004.pdf.
Pełny tekst źródłaMascisch, Allegra. "Characterization of a CHO cell line deficient in the folate-dependent trifunctional protein, MTHFD". Thesis, McGill University, 1990. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=60015.
Pełny tekst źródłaEnzymatic assays showed reduced activities of all three enzymes. Immunoblotting and immunoprecipitation of radiolabelled cell extracts indicated that the gene product was greatly reduced or absent in the mutant. Southern analysis showed no differences between normal and mutant cells, indicating that the defect was not due to a major gene rearrangement. RNA analysis, by Northern blotting and by RNA amplification using the polymerase chain reaction, showed that a mRNA for MTHFD of normal size was present in mutant cells. These results suggest that the mutation is post-transcriptional and that it disrupts the synthesis of MTHFD.
Sibani, Sahar. "Genetic and nutritional folate deficiency : implications for homocystinuria and intestinal neoplasia". Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=31539.
Pełny tekst źródłaThe more common and mild deficiency observed in the general healthy population is probably due in part to insufficient dietary intake of folate. Folate deficiency has been associated with increased risk for colon cancer. In a pilot study presented here, the impact of altered folate intake on tumor multiplicity in the Min mouse, a model for multiple intestinal neoplasia, was assessed. Folate deficient diets did not produce a consistent change in tumor numbers. However, a linear correlation between S-adenosylmethionine and S-adenosylhomocysteine content of preneoplastic tissue and tumor multiplicity was identified.
This thesis contributes to our understanding of the impact of genetic- and/or dietary-induced folate deficiency on cellular and organismal functions.
Crott, Jimmy. "The effects of folic acid deficiency and defects in folate metabolism on chromosome damage in vitro". Title page, table of contents and abstract only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phc9515.pdf.
Pełny tekst źródłaHilton, John Frederick. "The molecular basis of glutamate formiminotransferase deficiency /". Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=33776.
Pełny tekst źródłaGenomic DNA extracted from cell lines from three patients with suspected glutamate formiminotransferase deficiency was analyzed by PCR and sequencing of individual exons. Cell lines WG 1758 and WG 1759 are from two siblings of Germanic descent. Both siblings are heterozygous for the mutations c457 C → T and c940 G → C. The c457 C → T changes a conserved arginine to a cysteine in a loop involved in the binding of formiminotetrahydrofolate to the enzyme. The c940 G → C mutation converts an arginine to a proline in an alpha-helix essential for the dimerization of the formiminotransferase domain. Cell line WG 1795 is from a patient of Danish descent. The patient appears to be hemizygous for a c1033 insG mutation. Quantitative PCR suggests the presence of a deletion on the other chromosome, which minimally encompasses exon 9. All of the FTCD gene changes were absent in 100 control individuals (200 alleles).
Pai, 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.
Shalchi-Toosi, Marjan. "Implications of methionine and S-adenosylmethionine for the brain function". Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=26132.
Pełny tekst źródłaFolate deficiency can lower brain SAM levels and cause depression. Thus, methionine, which raises brain SAM, may overcome the effects of folate deficiency. Seven day food records were done by 26 psychiatric outpatients who were stable on lithium treatment. Eight patients had mean daily folate intakes below those recommended. Some of those with low folate intake had high methionine intake consistent with the idea that methionine could substitute metabolically for folate deficiency. Daily methionine intakes ranged from 13 to 304% of the recommended intake. As methionine had behavioral effects in the rat at doses much less than the daily dietary intake this raises the question of whether varying daily intakes of methionine in humans have behavioral implications. (Abstract shortened by UMI.)
Frosst, Phyllis D. "Investigation of methylenetetrahydrofolate reductase in vascular disease and neural tube effects". Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=23399.
Pełny tekst źródłaTwo MTHFR sequence changes were identified. The first was a C to T transition at bp 764 altering a proline to a leucine codon; this change was found in one severely-deficient patient. The second was a C to T transition at bp 677, substituting a valine for a highly-conserved alanine codon. The $ rm A to V$ substitution was identified on 35-40% of chromosomes. Expression of the $ rm A to V$ mutation in prokaryotic cells revealed increased thermolability over the wild-type enzyme. Genotyping for the $ rm A to V$ mutation in three vascular disease studies showed that it was associated with mild hyperhomocysteinemia, a risk factor for vascular disease.
The preventative effects of folate supplementation on the occurrence and recurrence of neural tube defects (NTDs) have been repeatedly demonstrated. The curly-tail (ct) mouse model for NTDs was used to investigate the involvement of MTHFR in these defects. Ct mice had significantly increased homocysteine levels although differences in MTHFR activity were not demonstrated. The mouse MTHFR gene was mapped to distal chromosome 4, close to the major gene for NTDs in ct. MTHFR is suggested as a candidate locus for the ct defect.
Książki na temat "Folic acid deficiency"
Frances, Picciano Mary, Stokstad E. L. Robert, Gregory Jesse F i American Chemical Society. Food and Nutritional Biochemistry Subdivision., red. Folic acid metabolism in health and disease. New York: Wiley-Liss, 1990.
Znajdź pełny tekst źródłaBailey, Lynn B. Folate in health and disease. Wyd. 2. Boca Raton: Taylor & Francis, 2010.
Znajdź pełny tekst źródła1948-, Bailey Lynn B., red. Folate in health and disease. New York: M. Dekker, 1995.
Znajdź pełny tekst źródłaKurtzweil, Paula. How folate can help prevent birth defects. [Rockville, MD: Dept. of Health and Human Services, Public Health Service, Food and Drug Administration, 1996.
Znajdź pełny tekst źródłaKurtzweil, Paula. How folate can help prevent birth defects. [Rockville, MD: Dept. of Health and Human Services, Public Health Service, Food and Drug Administration, 1997.
Znajdź pełny tekst źródłaFolic acid and the prevention of disease: Report of the Committee on Medical Aspects of Food and Nutrition Policy. London: Stationery Office, 2000.
Znajdź pełny tekst źródłaJ, Massaro Edward, i Rogers John M, red. Folate and human development. Totowa, N.J: Humana Press, 2002.
Znajdź pełny tekst źródłaWorld Health Organization. Regional Office for South-East Asia. Prevention of iron deficiency anaemia in adolescents: Role of weekly iron and folic acid supplementation. New Delhi, India: World Health Organization, Regional Office for South-East Asia, 2011.
Znajdź pełny tekst źródłaAmouzou, Kou'santa Sabiba. Evaluation des marqueurs nutritionnels et génétiques du statut en coenzymes B (cobalamines et folates) et de l'homocystéinemie plasmatique dans une population d'Afrique de l'Ouest (Benin-Togo). Lomé: [s.n., 2003.
Znajdź pełny tekst źródłaFolate in health and disease. Wyd. 2. Boca Raton: Taylor & Francis, 2010.
Znajdź pełny tekst źródłaCzęści książek na temat "Folic acid deficiency"
Desnick, Robert J., Orlando Guntinas-Lichius, George W. Padberg, Gustav Schonfeld, Xiaobo Lin, Maurizio Averna, Pin Yue i in. "Folic Acid Deficiency". W Encyclopedia of Molecular Mechanisms of Disease, 668. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8551.
Pełny tekst źródłaTheisler, Charles. "Folic Acid Deficiency". W Adjuvant Medical Care, 132. New York: CRC Press, 2022. http://dx.doi.org/10.1201/b22898-142.
Pełny tekst źródłaRain, J. D., I. Blot i G. Tchernia. "Folic Acid Deficiency in Developing Nations". W Folates and Cobalamins, 171–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74364-1_13.
Pełny tekst źródłaLink, H., P. Ostendorf, P. Wernet, K. Wilms i D. Niethammer. "Folic Acid Deficiency After Bone Marrow Transplantation". W 11th Annual meeting of the EBMT, 96. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-662-40457-7_75.
Pełny tekst źródłaLakshmanan, Mageshwaran. "Pharmacotherapy of Vitamin B12 and Folic Acid Deficiency". W Introduction to Basics of Pharmacology and Toxicology, 769–79. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-6009-9_50.
Pełny tekst źródłaLemoine, A., G. Potier de Courcy, S. Hercberg i C. Le Devehat. "Prevalence of Folic Acid Deficiency in the French Population". W Folates and Cobalamins, 129–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74364-1_9.
Pełny tekst źródłaGillespie, Bronwen. "Nutritional Status and the Risk of Preterm Birth". W Evidence Based Global Health Manual for Preterm Birth Risk Assessment, 41–51. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-04462-5_6.
Pełny tekst źródłaKnowles, L., A. A. M. Morris i J. H. Walter. "Treatment with Mefolinate (5-Methyltetrahydrofolate), but Not Folic Acid or Folinic Acid, Leads to Measurable 5-Methyltetrahydrofolate in Cerebrospinal Fluid in Methylenetetrahydrofolate Reductase Deficiency". W JIMD Reports, 103–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/8904_2016_529.
Pełny tekst źródłaKnowles, L., A. A. M. Morris i J. H. Walter. "Erratum to: Treatment with Mefolinate (5-Methyltetrahydrofolate), but Not Folic Acid or Folinic Acid, Leads to Measurable 5-Methyltetrahydrofolate in Cerebrospinal Fluid in Methylenetetrahydrofolate Reductase Deficiency". W JIMD Reports, 117. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/8904_2016_574.
Pełny tekst źródła"Anemia: Folic Acid Deficiency". W The APRN and PA’s Complete Guide to Prescribing Drug Therapy. New York, NY: Springer Publishing Company, 2019. http://dx.doi.org/10.1891/9780826179340.0016.
Pełny tekst źródłaStreszczenia konferencji na temat "Folic acid deficiency"
Wyatt, Michael D., Katie Brady, Alexandra Litvinchuk, Virginia Noxon, Xiao-Hong Wang i Robert W. Sobol. "Abstract 2549: Chromosomal instability and DNA repair status during folic acid deficiency in breast cancer cells". W Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2549.
Pełny tekst źródłaAkca, Emine Erdağ, Özlem Çağındı i Ergun Köse. "The Importance of Cereal Based Foods to Prevention of Iron Deficiency". W 6th International Students Science Congress. Izmir International Guest Student Association, 2022. http://dx.doi.org/10.52460/issc.2022.025.
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