Relevant bibliographies by topics / Folic acid deficiency

Academic literature on the topic 'Folic acid deficiency'

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Published: 4 June 2021
Last updated: 25 February 2023

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Journal articles on the topic "Folic acid deficiency"

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Ratajczak, Alicja Ewa, Aleksandra Szymczak-Tomczak, Anna Maria Rychter, Agnieszka Zawada, Agnieszka Dobrowolska, and Iwona Krela-Kaźmierczak. "Does Folic Acid Protect Patients with Inflammatory Bowel Disease from Complications?" Nutrients 13, no. 11 (November 12, 2021): 4036. http://dx.doi.org/10.3390/nu13114036.

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Folic acid, referred to as vitamin B9, is a water-soluble substance, which participates in the synthesis of nucleic acids, amino acids, and proteins. Similarly to B12 and B6, vitamin B9 is involved in the metabolism of homocysteine, which is associated with the MTHFR gene. The human body is not able to synthesize folic acid; thus, it must be supplemented with diet. The most common consequence of folic acid deficiency is anemia; however, some studies have also demonstrated the correlation between low bone mineral density, hyperhomocysteinemia, and folic acid deficiency. Patients with inflammatory bowel disease (IBD) frequently suffer from malabsorption and avoid certain products, such as fresh fruits and vegetables, which constitute the main sources of vitamin B9. Additionally, the use of sulfasalazine by patients may result in folic acid deficiency. Therefore, IBD patients present a higher risk of folic acid deficiency and require particular supervision with regard to anemia and osteoporosis prevention, which are common consequences of IBD.
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Khaitovich, M. V. "Folates: Modern Pregnant Health Support." HEALTH OF WOMAN, no. 4(150) (May 30, 2020): 37–42. http://dx.doi.org/10.15574/hw.2020.150.37.

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Folates (folic acid-based chemical compounds) got their name from the Latin “folio” - “leaf”, since they were first synthesized from spinach leaves, in which vitamin B9 is found in maximum quantities. As an important cofactor in carbon metabolism, folates are involved in the most important metabolic processes in the body, in particular, they play a key role in the synthesis of nucleotides and DNA replication. The article provides information on the physiological role of folates, their metabolism and its genetic aspects. The clinical significance of folate deficiency is examined, their sources and doses are described, and the interaction of folic acid and drugs is highlighted. Keywords: folate, metabolism, folic acid deficiency, pregnancy.
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Yasmin, Haleema, Shireen Bhutta, and Hasina -. "FOLIC ACID;." Professional Medical Journal 24, no. 12 (November 29, 2017): 1884–88. http://dx.doi.org/10.29309/tpmj/2017.24.12.602.

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Objectives: The objective of our study was to assess the effectiveness offolic acid in optimizing the red blood cells folate levels and to observe the frequency of folateresistance among Pakistani female patients. Setting: Outpatient Department of Obstetrics &Gynaecology, Jinnah Post graduate Medical Centre (JPMC), Karachi. Period: January–July2016. Methodology: Participants fulfilling the inclusion criteria were included after informedconsent. Detail history and physical examination was done in each participant. All studyparticipants received 5mg (400 μg) folic acid as a daily supplement for 24 weeks. Red bloodcell folate concentrations were measured at baseline and after 24 weeks of therapy. Pairedsample t-test was used to find out significant difference between folate levels. Results: A totalof 44 women (23 pregnant while 21 non pregnant) were included in the study. Mean age of theparticipants was 27.6 ± 5.9years and mean BMI was 23.9 ± 4.1kg/m2 respectively. The meanvalues of Red blood cells folate at baseline and at 24 weeks were 623.6 ± 406.6 and 861.9 ±432.4respectively. Paired sample t-test results showed that there was no significant difference.Thirty-two (70.4%) women showed an increase in RBC folate status while 13 (29.6%) womenhad steady or decreased levels of folate after taking folic acid for 24 weekswhich may be dueto RBS enzyme methylenetetrahydrofolate reductase (MTHFR) deficiency. Conclusion: Simplefolic acid supplementation is not very helpful in improving folate status in female Pakistanipatients. Resistant to improvement may be due to MTHFR deficiency in our study subjects.
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Diaz, Karina, Zhu Na, Sorab Gupta, Vikram Arya, Lourdes Martinez, Supreet Dhaliwal, Nora Ajdir, Bhavita Gaglani, Shradha Ahuja, and Ilmana Fulger. "Prevalence of Folic Acid Deficiency and Cost Effectiveness of Folic Acid Testing: A Single Center Experience." Blood 132, Supplement 1 (November 29, 2018): 4878. http://dx.doi.org/10.1182/blood-2018-99-111607.

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Abstract Study Objective According to the National Health and Nutrition Examination Survey (NHANES) data from 2003-2006 the prevalence of folic acid deficiency in the United States has decreased from 16% to 0.5% since the dietary folic acid fortification program started in the late 1990s. Routine testing for folic acid deficiency remains quite common in the workup of anemia, dementia, alcoholism and other high risk populations. The objective for this study were to determine the prevalence of folic acid deficiency in order to analyze whether routine testing for deficiency should be discouraged or targeted to specific patient populations. In addition to this, we want to assess the economic burden that folic acid level testing adds to the high cost of care of our health system. Methods Cross sectional chart review of all adults tested for folic acid level from March 2014 to March 2015 from the Hospital and Ambulatory Care Center of the Community Hospital was undertaken. Folic acid deficiency was defined as ≤4ng/dl. Folic acid level were further classified as low (≤10ng/dl ), intermediate (10-20ng/dl) and high (>20ng/dl). Age, race, body mass index, hemoglobin, mean corpuscular volume levels and billing details were recorded of all patients and information was also collected regarding known conditions correlated to the folic acid levels including Vitamin B12 deficiency( <300 ng/dl), dementia, alcoholism, pregnancy malabsorption, sickle cell disease, bariatric surgery, inflammatory bowel syndrome, and drug therapy with HAART (Highly Active Anti-Retroviral Therapy) , TMP-SMX(Trimethoprim/sulfamethoxazole), phenytoin, valproic acid and/or methotrexate (Table 1). Statistical testing using t-test, logistic / linear regressions with α level at 0.05 was used for analysis of data. Results A total of 957 charts of patients who were tested for folic acid between March 2014 to March 2015 at our Heath- Care System were reviewed. 413 (43%) patients were male and 544 (57%) were female. There were 394 (41 %) Hispanics, 325 (34%) African American, 202 (21%) Caucasian and 36 (4%) were from other ethnicity. The mean age was 59.7 years and a mean Hb was 11. 6 g/ dl. Mean folic acid level was 14.5 ng/dl. 16 patients from total of 957 (2 %) had folic acid deficiency with value ≤4ng/dl . Additional results from the study are described in Table 1, Table 2 and Table 3. Conclusion The prevalence of folic acid deficiency was 2%, About 33,000 dollars per year were used to identify such a low prevalent disease which can be treated at a low cost (2 cents/day) by oral supplementation. Low levels of folic acid were statistically associated with male sex, African American race, dementia and coexistence of vitamin B12 deficiency. Empiric supplementation of folic acid and possibly limiting testing for folic acid level to this group of patients may represent a more cost effective strategy. Disclosures No relevant conflicts of interest to declare.
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Cristina-Crenguța Albu, Dinu-Florin Albu, Emily-Alice Russu, and Ştefan-Dimitrie Albu. "Folic acid and its implications in genetic pathology." World Journal of Advanced Research and Reviews 16, no. 1 (October 30, 2022): 742–48. http://dx.doi.org/10.30574/wjarr.2022.16.1.1097.

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Vitamins are essential for the proper functioning of the body, and Folic Acid, also known as Vitamin B9, has many benefits for the body. Folic Acid contributes to the normal development of the fetus, preventing the risk of fetal birth defects, mainly represented by neural tube defects and orofacial clefts. At the same time, Folic Acid deficiency can cause serious health problems. That is why it is necessary to know the roles of Folic Acid in the body, the symptoms of Folic Acid deficiency, but also what foods are rich in Folic Acid and how to supplement the body's need for Folic Acid.
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Slagman, Anna, Linton Harriss, Sandra Campbell, Reinhold Muller, and 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, no. 18 (September 4, 2019): 3426–34. http://dx.doi.org/10.1017/s1368980019002258.

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AbstractObjective:To investigate the prevalence of folic acid deficiency in Queensland-wide data of routine laboratory measurements, especially in high-risk sub-populations.Design:Secondary health data analysis.Setting:Analysis of routine folic acid tests conducted by Pathology Queensland (AUSLAB).Participants:Female and male persons aged 0–117 years with routine folic acid testing between 1 January 2004 and 31 December 2015. If repeat tests on the same person were conducted, only the initial test was analysed (n 291 908).Results:Overall the prevalence of folic acid deficiency declined from 7·5 % before (2004–2008) to 1·1 % after mandatory folic acid fortification (2010–2015; P < 0·001) reflecting a relative reduction of 85 %. Levels of erythrocyte folate increased significantly from a median (interquartile range) of 820 (580–1180) nmol/l in 2008 before fortification to 1020 (780–1350) nmol/l in 2010 (P < 0·001) after fortification. The prevalence of folic acid deficiency in the Indigenous population (14 792 samples) declined by 93 % (17·4 v. 1·3 %; P < 0·001); and by 84 % in non-Indigenous residents (7·0 v. 1·1 %; P < 0·001). In a logistic regression model the observed decrease of folic acid deficiency between 2008 and 2010 was found independent of gender, age and ethnicity (ORcrude = 0·20; 95 % CI 0·18, 0·23; P < 0·001; ORadjusted = 0·21; 95 % CI 0·18, 0·23; P < 0·001).Conclusions:While voluntary folic acid fortification, introduced in 1995, failed especially in high-risk subgroups, the 2009 mandatory folic acid fortification programme coincided with a substantial decrease of folic acid deficiency in the entire population.
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Gordon, Neil. "Folic Acid Deficiency from Anticonvulsant Therapy." Developmental Medicine & Child Neurology 10, no. 4 (November 12, 2008): 497–504. http://dx.doi.org/10.1111/j.1469-8749.1968.tb02925.x.

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Marcus, David L., and Michael L. Freedman. "Folic Acid Deficiency in the Elderly." Journal of the American Geriatrics Society 33, no. 8 (August 1985): 552–58. http://dx.doi.org/10.1111/j.1532-5415.1985.tb04621.x.

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Speidel, B. D. "FOLIC ACID DEFICIENCY AND CONGENITAL MALFORMATION." Developmental Medicine & Child Neurology 15, no. 1 (November 12, 2008): 81–83. http://dx.doi.org/10.1111/j.1469-8749.1973.tb04872.x.

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Lewis, Dale P., Don C. Van Dyke, Laurie A. Willhite, Phyllis J. Stumbo, and Mary J. Berg. "Phenytoin-Folic Acid Interaction." Annals of Pharmacotherapy 29, no. 7-8 (July 1995): 726–35. http://dx.doi.org/10.1177/106002809502907-816.

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Objective: To review information regarding the dual and interdependent drug-nutrient interaction between phenytoin and folic acid and other literature involving phenytoin and folic acid. Data Sources: Information was retrieved from a MEDLINE search of English-language literature conducted from 1983 (time of the last review) to March 1995. Search terms included folic acid, phenytoin, and folic acid deficiency. Additional references were obtained from Current Contents and from the bibliographies of the retrieved references. Study Selection: All human studies examining the effects of phenytoin on serum folate concentrations and folic acid supplementation on serum phenytoin concentrations were selected. These included studies of patients with epilepsy and healthy volunteers as well as case reports. Case reports were included because of the extensive length of time needed to study this drug interaction. Data Extraction: Data extracted included gender, dosing, serum folate concentrations if available, pharmacokinetics, and adverse events. Data Synthesis: Serum folate decreases when phenytoin therapy is initiated alone with no folate supplementation. Folic acid supplementation in folate-deficient patients with epilepsy changes the pharmacokinetics of phenytoin, usually leading to lower serum phenytoin concentrations and possible seizure breakthrough. Folate is hypothesized to be a cofactor in phenytoin metabolism and may be responsible for the “pseudo-steady-state,” which is a concentration where phenytoin appears to be at steady-state, but in reality, is not. Phenytoin and folic acid therapy initiated concomitantly prevents decreased folate and phenytoin obtains steady-state concentrations sooner. Conclusions: Folic acid supplementation should be initiated each time phenytoin therapy commences because of the hypothesized cofactor mechanism, decreased adverse effects associated with folate deficiency, and better seizure control with no perturbation of phenytoin pharmacokinetics.
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Dissertations / Theses on the topic "Folic acid deficiency"

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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.

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Low-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.

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Methylenetetrahydrofolate reductase (MTHFR) reduces 5,10-methylene THF to 5-methyl THF, the carbon donor for the methylation of homocysteine to methionine. Patients with severe MTHFR deficiency (MRD) have neurologic abnormalities while a milder form (a thermolabile MTHFR variant) has been shown to be associated with coronary artery disease (CAD). Ten MRD patients, with reduced or non-detectable activity, were studied to characterize the nature of the mutation. Southern, Northern and Western analysis did not reveal any defects in the patients. These results suggest that the mutations may be minor insertions/deletions or single base substitutions that affect catalytic activity. Single strand conformation polymorphism (SSCP) analysis was used to detect base substitutions; 3 RFLPs were identified with this protocol. One was in the coding region (SphI) while the other two were in the 3$ sp prime$ untranslated region (MaeIII and MnlI). A difference in frequency of the SphI RFLP was found between control subjects and a small sample of CAD patients whose homocysteine levels were greater than the 99th percentile.
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Milan, 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.

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Mascisch, 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.

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MTHFD is a folate-dependent trifunctional protein comprised of three activities: N$ sp5$,N$ sp{10}$-methylenetetrahydrofolate dehydrogenase, N$ sp5$,N$ sp{10}$-methenyltetrahydrofolate cyclohydrolase and N$ sp{10}$-formyltetrahydrofolate synthetase. The enzymes catalyse the sequential interconversion of tetrahydrofolate derivatives required for purine, methionine and thymidylate synthesis. A Chinese hamster ovary cell line, reported to have reduced cyclohydrolase activity, was studied to characterize the nature of its mutation.
Enzymatic 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.
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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.

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Folate deficiency, a prevalent vitamin deficiency in America, can stem from environmental and/or genetic causes. The most common inborn error of folate metabolism is deficiency of methylenetetrahydrofolate reductase (MTHFR), which catalyzes the reduction of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate. Severe MTHFR deficiency results in hyperhomocysteinemia and homocystinuria; patients present with developmental delay, and various neurological and vascular disorders. This thesis describes three mutations identified in the MTHFR locus in patients with severe deficiency: 1025T→C (M→T), 1027T→G (W→G), and 1768G→A (E→K). Genotype-phenotype correlations are described, along with biochemical characterization of three mutations (983A→G (N→S), 1025T→C, 1027T→G). All three mutations exert their effect by decreasing Vmax without changing the enzyme's affinity for its substrate, 5-methyltetrahydrofolate. The 983A→G variant also conferred decreased affinity for FAD, a cofactor.
The 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.
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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.

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Reprints of the author's previously published articles included as an appendix. Bibliography: leaves 165-188. "This thesis describes a series of experiments that aimed to investigate the effects of folic acid deficiency and defects in folate metabolism on chromosome damage rates in human lymphocytes. The accumulation of chromosome damage over time is an important issue because it is thought to contribute to the mechanism of ageing and the aetiology of diseases of age such as cancer and Alzheimer's disease."
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Hilton, 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.

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Glutamate formiminotransferase deficiency (OMIM 229100) is an autosomal recessive disorder marked by clinical heterogeneity. The severe phenotype, first identified in patients of Japanese descent, includes high levels of formiminoglutamate (FIGLU) in the urine in response to histidine loading, megaloblastic anemia, and mental retardation. The mild phenotype is marked by high levels of FIGLU in the urine in the absence of histidine loading, mild developmental delay and no hematological abnormalities. The gene for human glutamate formiminotransferase-cyclodeaminase consists of 15 exons and is located at 21q22.3. The protein consists of a tetramer of dimers, with dimerization essential for both formiminotransferase and cyclodeaminase activity.
Genomic 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).
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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.

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Methylenetetrahydrofolate reductase (MTHFR), an important enzyme in folate metabolism, mediates the conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate which serves as the carbon donor for the conversion of homocysteine to methionine. It is also inhibited by S-adenosylmethionine which has shown to be actively demethylated to form S-adenosylhomocysteine, which is hydrolysed to homocysteine. MTHFR deficiency exhibits well-documented clinical and biochemical symptoms. The human MTHFR cDNA was isolated by Goyette et al (1994), and fifteen mutations have been identified at this locus.
An 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.
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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.

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We have studied the effect of S-adenosylmethionine (SAM) on tail flick latency in the rat. We also studied the effect of methionine the immediate precursor of SAM. Administration of methionine to the rat increases brain SAM, but little is known about its behavioral effects. Long-Evans rats were given SAM and methionine orally at different doses and tail-flick latency was measured at various times. Both methionine and SAM increased tail-flick latency, but methionine did so at a lower dose. A biochemical study showed that methionine was more effective than SAM in raising brain SAM probably because it is transported better into brain. The biochemical measurements were not consistent with the idea that the effects of SAM and methionine were mediated by an increase in brain 5-HT.
Folate 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.)
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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.

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Methylenetetrahydrofolate reductase catalyzes the reduction of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, a carbon donor for the remethylation of homocysteine to methionine. Patients with severe MTHFR deficiency have $<$20% residual enzyme activity, moderate hyperhomocysteinemia, vascular lesions and neurological dysfunction. Mildly-deficient individuals with a thermolabile enzyme are at increased risk for developing cardiovascular disease.
Two 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.
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Books on the topic "Folic acid deficiency"

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Frances, Picciano Mary, Stokstad E. L. Robert, Gregory Jesse F, and American Chemical Society. Food and Nutritional Biochemistry Subdivision., eds. Folic acid metabolism in health and disease. New York: Wiley-Liss, 1990.

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Bailey, Lynn B. Folate in health and disease. 2nd ed. Boca Raton: Taylor & Francis, 2010.

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1948-, Bailey Lynn B., ed. Folate in health and disease. New York: M. Dekker, 1995.

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Kurtzweil, Paula. How folate can help prevent birth defects. [Rockville, MD: Dept. of Health and Human Services, Public Health Service, Food and Drug Administration, 1996.

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Kurtzweil, Paula. How folate can help prevent birth defects. [Rockville, MD: Dept. of Health and Human Services, Public Health Service, Food and Drug Administration, 1997.

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Folic acid and the prevention of disease: Report of the Committee on Medical Aspects of Food and Nutrition Policy. London: Stationery Office, 2000.

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J, Massaro Edward, and Rogers John M, eds. Folate and human development. Totowa, N.J: Humana Press, 2002.

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World 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.

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Amouzou, 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.

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Folate in health and disease. 2nd ed. Boca Raton: Taylor & Francis, 2010.

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Book chapters on the topic "Folic acid deficiency"

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Desnick, Robert J., Orlando Guntinas-Lichius, George W. Padberg, Gustav Schonfeld, Xiaobo Lin, Maurizio Averna, Pin Yue, et al. "Folic Acid Deficiency." In 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.

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Theisler, Charles. "Folic Acid Deficiency." In Adjuvant Medical Care, 132. New York: CRC Press, 2022. http://dx.doi.org/10.1201/b22898-142.

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Rain, J. D., I. Blot, and G. Tchernia. "Folic Acid Deficiency in Developing Nations." In Folates and Cobalamins, 171–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74364-1_13.

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Link, H., P. Ostendorf, P. Wernet, K. Wilms, and D. Niethammer. "Folic Acid Deficiency After Bone Marrow Transplantation." In 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.

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Lakshmanan, Mageshwaran. "Pharmacotherapy of Vitamin B12 and Folic Acid Deficiency." In 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.

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Lemoine, A., G. Potier de Courcy, S. Hercberg, and C. Le Devehat. "Prevalence of Folic Acid Deficiency in the French Population." In Folates and Cobalamins, 129–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74364-1_9.

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Gillespie, Bronwen. "Nutritional Status and the Risk of Preterm Birth." In 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.

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AbstractA woman’s body mass index and nutritional status should be assessed in the antenatal period. The evidence indicates that maternal anemia is a risk factor for preterm birth. Ensuring adequate levels of iron and folic acid is essential for general pregnancy health and outcomes. To reduce the risk of pre-eclampsia, daily calcium supplementation for populations with low dietary calcium intake may be advised, although negative interactions between iron and calcium supplements may occur so these two nutrients should be administered several hours apart. In undernourished populations, balanced energy and protein supplementation should also be recommended for pregnant women (though not specifically linked to a reduction in preterm birth). For populations at risk of vitamin D deficiency, possible benefits for general pregnancy outcomes may be gained from vitamin D supplementation. Where dietary zinc is low, it has been suggested that zinc supplementation may reduce the risk of preterm birth. However, further research is required to clarify the benefits of supplementation. For example, vitamin D in combination with calcium may increase the risk of preterm birth. In the antenatal period, the most important focus should be on promoting a good quality diet in general, rather than a specific supplementation regime.
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Knowles, L., A. A. M. Morris, and 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." In JIMD Reports, 103–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/8904_2016_529.

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Knowles, L., A. A. M. Morris, and 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." In JIMD Reports, 117. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/8904_2016_574.

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"Anemia: Folic Acid Deficiency." In 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.

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Conference papers on the topic "Folic acid deficiency"

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Wyatt, Michael D., Katie Brady, Alexandra Litvinchuk, Virginia Noxon, Xiao-Hong Wang, and Robert W. Sobol. "Abstract 2549: Chromosomal instability and DNA repair status during folic acid deficiency in breast cancer cells." In 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.

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Akca, Emine Erdağ, Özlem Çağındı, and Ergun Köse. "The Importance of Cereal Based Foods to Prevention of Iron Deficiency." In 6th International Students Science Congress. Izmir International Guest Student Association, 2022. http://dx.doi.org/10.52460/issc.2022.025.

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Iron is vital for almost every organism, due to its role in a wide range of metabolic processes. For the human body, it contributes to crucial activities, especially haemoglobin synthesis and oxygen transport. Iron deficiency anaemia occurs when iron stores release inadequate amount of iron [1; 2; 3]. However, basic strategies can be used effectively in the prevention of iron deficiency and related anaemia. Although the applicability of these strategies mostly depends on the health infrastructure, the economy of the countries and people's access to resources, it is stated that food fortification is one of the most cost-effective methods [3; 4]. Cereals and pulses are often preferred in food fortification studies as they form the basis of daily nutrition. Around the world, 85 countries have already made it mandatory to fortify wheat flour (and corn/rice) with iron or folic acid [4; 5]. In this study, theoretical information and recent developments on the subject were evaluated in detail with a comprehensive literature review about the role of grain-based products in the prevention of iron deficiency and iron deficiency anaemia. Additionally, food fortification, complex food matrix, bioaccessibility/bioavailability, interaction with sensory and organoleptic properties and aimed to gain a current perspective for future studies on the selection of iron forms.
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