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1
Granger, Herbert. "Cinematic Philosophy in Le Feu follet." Film and Philosophy 8 (2004): 74–90. http://dx.doi.org/10.5840/filmphil200488.
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Sharpe, Mani. "Gender and the politics of decolonization in early 1960s French cinema." Journal of European Studies 49, no. 2 (2019): 163–83. http://dx.doi.org/10.1177/0047244119837478.
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In a recent monograph, Todd Shepard has implored us to examine the ways in ‘which the Algerian War modified the form and the content of debates surrounding contemporary sexuality in France’, from the nationalist revolution spearheaded by the FLN in Algeria, to the sexual paradigm shift of May ’68 (2017: 21). An important injunction, undoubtedly. But also an injunction that, as I will show, could also be inverted to examine how, in the world of cinema, the radicalization of identity politics catalysed by decolonization found itself similarly distorted by a tendency among male directors to imagine the war through the lens of their own androcentric preoccupations, fantasies and anxieties: anxieties that, in the case of Jacques Rivette’s Paris nous appartient (1961), Louis Malle’s Le Feu Follet (1963), and Jacques Dupont’s Les Distractions (1960), ricochet erratically between masochistic and misogynistic tales of impotence and carnal retribution; anxieties that subtly twist the dynamics of the decolonial debate into strange shapes, places and meanings.
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Gallissot, René. "Au-delà du multiculturel : nationaux, étrangers et citoyens. Urbanisation généralisée et transnationalisation." I. Nationalité et citoyenneté à l’épreuve du pluriculturalisme, no. 21 (November 17, 2015): 27–33. http://dx.doi.org/10.7202/1034074ar.
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Le multiculturel n’est peut-être qu’un feu follet courant sur une transformation de base : l’urbanisation généralisée et la généralisation des cultures urbaines. Retardée en France, l’urbanisation ne s’accomplit que dans les trois dernières décennies. C’est donc pour la première fois que les générations jeunes sont, dans leur masse, socialisées et acculturées par la ville. Pour les jeunes issus de l’immigration, la ville est en outre le lieu de francisation, et c’est donc en ville que se produit une surexcitation des conflits dits ethniques, suivant la ligne de partage entre les nationaux français, les nationaux européens auxquels l’on reconnaît l’équivalence nationale et les immigrés. L’immigré est celui qui n’est pas français d’origine. Cette discrimination lui dénie et une nationalité propre et la pleine citoyenneté française, pour l’ethniciser comme musulman, noir, asiatique, etc. La différence dite d’origine et de culture masque la différenciation raciale qui sépare l’Europe du Tiers Monde. Sous couvert multiculturel, la culture des jeunes répercute les cultures urbaines; celles-ci sont le signe d’un cosmopolitisme nouveau; elles révèlent qu’opère en profondeur un procès de transnationalisation qui met en cause la centralité nationale et dissocie la citoyenneté de la nationalité.
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Emanuele, Canzaniello. "«Voir un corps». Pierre Drieu La Rochelle e l'anatomia dell'impotenza." Aura, no. 1 (March 15, 2022): 1–11. https://doi.org/10.5281/zenodo.11779994.
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It is from the body that Drieu allows the evocation of decadence to germinate, or conversely, the most vital explosions of privilege, of arrogance, of the mortifying beauty of the world enclosed in a body. A certain taste for physiology inherited from Nietzsche leads Drieu to consider how in the santé corporelle one has the measure of civilisations, and hence an enormous symbolic charge granted to the corporeal presence of beings and life. A refined interpreter of the drifts and changes of virility in the convulsive phase of the compromises with fascism, Drieu consigns to the body and on the body every trace of the struggles and gestations taking place.
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Stoner, A., and W. T. Wilson. "TOXICITY EFFECTS AND CHALKBROOD INCIDENCE IN HONEY BEE1 COLONIES FED CONTROLLED DOSES OF FUNGICIDES2,3." Journal of Entomological Science 20, no. 2 (1985): 172–78. http://dx.doi.org/10.18474/0749-8004-20.2.172.
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Folpet and a combination with folpet, benomyl, citral, sodium propionate, and sorbic acid were fed or exposed to honey bee, Apis mellifera L., field colonies to: 1) determine their long-term toxic effects on the bees; and 2) to determine if chalkbrood (CB) disease, Ascosphaera apis (Maassen ex Claussen) Olive et Spiltor, is inhibited or controlled by the compounds. When folpet was fed to honey bee colonies in sucrose syrup, the group fed the highest rate (1000 ppm) never differed significantly (P > 0.05) from the control colonies. There was an equal number of adult bees, an equal amount of sealed brood, and mortality was identical. Analysis indicated significantly (P < 0.05) fewer CB mummies in treatment groups fed 10 or 1000 ppm folpet, but this apparent benefit may have been due to seasonal changes of reduced CB infection that occur in late summer. Folpet or a combination of folpet, benomyl, citral, sodium propionate, and sorbic acid (1000 ppm each, total 5000 ppm) incorporated into lipid/sucrose extender patties produced no significant (P > 0.05) effect of any kind on colonies to which they were applied, including CB infection. However, when the combination of five fungicides (5000 ppm) was impregnated into beeswax foundation and exposed to honey bee colonies, only a small amount of comb was drawn on the test foundation, indicating a repellent effect. Otherwise, the test foundation had no significant (P > 0.05) effect on the honey bees or the CB infection.
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Han, Young-Hee, Miyong Yon, Heon-Seok Han, Kwang-Yup Kim, Tsunenobu Tamura, and Taisun H. Hyun. "Folate contents in human milk and casein-based and soya-based formulas, and folate status in Korean infants." British Journal of Nutrition 101, no. 12 (2008): 1769–74. http://dx.doi.org/10.1017/s0007114508158974.
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We assessed folate nutritional status from birth to 12 months in fifty-one infants who were fed human milk (HM;n20), casein-based formula (CBF;n12) or soya-based formula (SBF;n19). Folate contents in ninety-five HM samples obtained from twenty mothers for the first 6-month period and twelve CBF and nineteen SBF samples were measured by bioassay after trienzyme extraction. Folate intake was estimated by weighing infants before and after feeding in the HM group and by collecting formula intake records in the formula-fed groups. After solid foods were introduced, all foods consumed were included to estimate folate intake. Serum folate and total homocysteine (tHcy) concentrations were determined at 5 and 12 months of age, and infant growth was monitored for the first 12 months. Mean HM folate contents ranged from 201 to 365 nmol/l with an overall mean of 291 nmol/l, and the contents peaked at 2 months postpartum. HM folate contents were higher than those reported in North America. Folate contents in CBF and SBF were markedly higher than those in HM and those claimed on the product labels. The overall folate intakes in formula-fed infants were significantly higher than those in HM-fed infants, and this was associated with significantly higher folate and lower tHcy in formula-fed infants than HM-fed infants at 5 months. At 12 months, serum folate was significantly higher in the SBF group than the other groups, whereas serum tHcy and overall growth were similar among all groups.
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Salmenperä, Leena, Jaakko Perheentupa, and Martti A. Siimes. "Folate Nutrition is Optimal in Exclusively Breast‐Fed Infants but Inadequate in Some of Their Mothers and in Formula‐Fed Infants." Journal of Pediatric Gastroenterology and Nutrition 5, no. 2 (1986): 283–89. http://dx.doi.org/10.1002/j.1536-4801.1986.tb09064.x.
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Summary:Plasma concentrations of folate were studied in a group of exclusively breast‐fed infants and their mothers (their numbers gradually decreased from 200 at birth to 7 at 12 months) and in infants completely weaned to a cow's milk formula (containing 35 μg of folate/L) and solid foods. The exclusively breast‐fed infants were in no danger of folate deficiency; their plasma levels were elevated after the age of 2 months and, on average, were 2.0‐3.3‐fold higher than maternal levels throughout the study. None of these infants ?? whereas up to 5% of the mothers had values ≤ 3 μg/L, despite supplementation during lactation with 0.1 mg folate/day. In the formula‐fed infants, 69‐94% of the plasma folate concentrations lay below the lowest concentration for the breast‐fed infants. Although no infant had signs of anemia or macrocytosis in red cell indices, the infants weaned earliest had the lowest hemoglobin concentrations (p = 0.09) and the highest mean corpuscular volume (MCV) values (p = 0.06) at 9 months of age. Thus, an infant fed a formula containing the recommended amount of ??
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Wang, Xinyan, Wen Li, Zhenshu Li, et al. "Maternal Folic Acid Supplementation During Pregnancy Promotes Neurogenesis and Synaptogenesis in Neonatal Rat Offspring." Cerebral Cortex 29, no. 8 (2018): 3390–97. http://dx.doi.org/10.1093/cercor/bhy207.
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Abstract Maternal folic acid supplementation during pregnancy is associated with improved cognitive performances in offspring. However, the effect of supplementation on offspring’s neurogenesis and synaptogenesis is unknown, and whether supplementation should be continued throughout pregnancy is controversial. In present study, 3 groups of female rats were fed a folate-normal diet, folate-deficient diet, or folate-supplemented diet from 1 week before mating until the end of pregnancy. A fourth group fed folate-normal diet from 1 week before mating until mating, then fed folate-supplemented diet for 10 consecutive days, then fed folate-normal diet until the end of pregnancy. Offspring were sacrificed on postnatal day 0 for measurement of neurogenesis and synaptogenesis by immunofluorescence and western blot. Additionally neural stem cells (NSCs) were cultured from offspring’s hippocampus for immunocytochemical measurement of their rates of proliferation and neuronal differentiation. The results demonstrated that maternal folic acid supplementation stimulated hippocampal neurogenesis by increasing proliferation and neuronal differentiation of NSCs, and also enhanced synaptogenesis in cerebral cortex of neonatal offspring. Hippocampal neurogenesis was stimulated more when supplementation was continued throughout pregnancy instead of being limited to the periconceptional period. In conclusion, maternal folic acid supplementation, especially if continued throughout pregnancy, improves neurogenesis and synaptogenesis in neonatal offspring.
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Balaghi, M., D. W. Horne, and C. Wagner. "Hepatic one-carbon metabolism in early folate deficiency in rats." Biochemical Journal 291, no. 1 (1993): 145–49. http://dx.doi.org/10.1042/bj2910145.
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Glycine N-methyltransferase (GNMT) is inhibited by 5-methyltetrahydrofolate polyglutamate in vitro. It is believed to play a regulatory role in the synthesis de novo of methyl groups. We have used the amino-acid-defined diet of Walzem and Clifford [(1988) J. Nutr. 118, 1089-1096] to determine whether folate deficiency in vivo would affect GNMT activity, as predicted by the studies in vitro. Weanling male rats were fed on the folate-deficient diet or a folate-supplemented diet pair-fed to the deficient group. A third group was fed on the folate-supplemented diet ad libitum. Development of folate deficiency rapidly resulted in decreased levels of S-adenosylmethionine (SAM) and elevation of S-adenosylhomocysteine (SAH). The ratios of SAM to SAH were 1.8, 2.7 and 1.5 in the deficient group for weeks 2, 3 and 4 of the experiment, and the values were 9.7, 7.1 and 8.9 for the pair-fed control group and 10.3, 8.8 and 8.0 for the control group ad libitum fed. The activity of GNMT was significantly higher in the deficient group than in either of the two control groups at each time period. This was not due to increased amounts of GNMT protein, but reflected an increase in specific enzyme activity. Levels of folate in both the cytosol and mitochondria were severely lowered after only 2 weeks on the diet. The distribution of folate coenzymes was also affected by the deficiency, which resulted in a marked increase in the percentage of tetrahydrofolate polyglutamates in both cytosol and mitochondria and a very large decrease in cytosolic 5-methyltetrahydrofolate. The increased GNMT activity is therefore consistent with decreased folate levels and decreased inhibition of enzyme activity.
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Sneh, A., and E. Jerby. "Coaxially fed folded foil electromagnet wiggler." Nuclear Instruments and Methods in Physics Research Section A: Accelerators, Spectrometers, Detectors and Associated Equipment 285, no. 1-2 (1989): 294–98. http://dx.doi.org/10.1016/0168-9002(89)90468-3.
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Koury, Mark J., Donald W. Horne, Zoe A. Brown, et al. "Apoptosis of Late-Stage Erythroblasts in Megaloblastic Anemia: Association With DNA Damage and Macrocyte Production." Blood 89, no. 12 (1997): 4617–23. http://dx.doi.org/10.1182/blood.v89.12.4617.
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Abstract An in vitro model of folate-deficient erythropoiesis has been developed using proerythroblasts isolated from the spleens of Friend virus-infected mice fed an amino acid-based, folate-free diet. Control proerythroblasts were obtained from Friend virus-infected mice fed the same diet plus 2 mg folic acid/kg diet. Our previous studies showed that, after 20 to 32 hours of culture in folate-deficient medium with 4 U/mL of erythropoietin, the folate-deficient proerythroblasts underwent apoptosis, whereas control erythroblasts survived and differentiated into reticulocytes over a period of 48 hours. The addition of folic acid or thymidine to the folate-deficient medium prevented the apoptosis of the folate-deficient erythroblasts, thereby implicating decreased thymidylate synthesis as the main cause of apoptosis in the folate-deficient erythroblasts. In the study reported here, we examined intracellular folate levels, uracil misincorporation into DNA, p53 and p21 proteins, and reticulocyte formation in erythroblasts cultured in folate-deficient or control medium. In all experiments, the folate-deficient erythroblasts cultured in folate-deficient medium gave results that varied significantly from folate-deficient erythroblasts cultured in control medium or control erythroblasts cultured in either folate-deficient or control media. Folate-deficient erythroblasts cultured in folate-deficient medium had marked decreases in all coenzyme forms of folate that persisted throughout culture, increased uracil misincorporation into DNA, persistent accumulations of p53 and p21, and decreased reticulocyte production but increased size of individual reticulocytes. A model of folate-deficient erythropoiesis based on apoptosis of late stage erythroblasts is presented. This model provides explanations for the clinical findings in megaloblastic anemia.
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Bills, ND, MJ Koury, AJ Clifford, and EN Dessypris. "Ineffective hematopoiesis in folate-deficient mice." Blood 79, no. 9 (1992): 2273–80. http://dx.doi.org/10.1182/blood.v79.9.2273.2273.
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Abstract A folate-free amino acid-based diet provided an opportunity to characterize the effects of folate depletion on growth, tissue folate levels, and hematopoiesis of mice under well-standardized conditions. Weanling mice were fed a folate-free, amino acid-based diet supplemented with either 0 or 2 mg folic acid/kg diet for 35 to 48 days. Folate concentrations were decreased in liver, kidney, serum, and erythrocytes in mice fed the folate-free diet. The folate-deficient mice had anemia, reticulocytopenia, thrombocytopenia, and leukopenia, all of which reverted to normal after folic acid was reintroduced to the diet. Hematopoietic organs of folate-deficient mice had alterations that were similar to those seen in folate-deficient humans except that in mice, the hyperplasia of hematopoietic tissue occurred in the spleen rather than in the marrow. Ferrokinetic studies showed a normal 59Fe- transferrin half-life, but the percentage of 59Fe-incorporation into red blood cells at 48 hours was markedly subnormal. The number of committed hematopoietic progenitors at the stages of erythroid colony- forming units (CFUs), megakaryocyte CFUs, and granulocyte-macrophage CFUs were all increased in folate-deficient mice. However, the progeny of these progenitors was markedly decreased in folate-deficient mice. Thus, the folate-deficient mice had “ineffective hematopoiesis” leading to pancytopenia, and they therefore provide a murine model of megaloblastic anemia.
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Bills, ND, MJ Koury, AJ Clifford, and EN Dessypris. "Ineffective hematopoiesis in folate-deficient mice." Blood 79, no. 9 (1992): 2273–80. http://dx.doi.org/10.1182/blood.v79.9.2273.bloodjournal7992273.
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A folate-free amino acid-based diet provided an opportunity to characterize the effects of folate depletion on growth, tissue folate levels, and hematopoiesis of mice under well-standardized conditions. Weanling mice were fed a folate-free, amino acid-based diet supplemented with either 0 or 2 mg folic acid/kg diet for 35 to 48 days. Folate concentrations were decreased in liver, kidney, serum, and erythrocytes in mice fed the folate-free diet. The folate-deficient mice had anemia, reticulocytopenia, thrombocytopenia, and leukopenia, all of which reverted to normal after folic acid was reintroduced to the diet. Hematopoietic organs of folate-deficient mice had alterations that were similar to those seen in folate-deficient humans except that in mice, the hyperplasia of hematopoietic tissue occurred in the spleen rather than in the marrow. Ferrokinetic studies showed a normal 59Fe- transferrin half-life, but the percentage of 59Fe-incorporation into red blood cells at 48 hours was markedly subnormal. The number of committed hematopoietic progenitors at the stages of erythroid colony- forming units (CFUs), megakaryocyte CFUs, and granulocyte-macrophage CFUs were all increased in folate-deficient mice. However, the progeny of these progenitors was markedly decreased in folate-deficient mice. Thus, the folate-deficient mice had “ineffective hematopoiesis” leading to pancytopenia, and they therefore provide a murine model of megaloblastic anemia.
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Bills, N. D., A. D. Jones, and A. J. Clifford. "Biological Activity of Racemic Folate Mixtures Fed to Folate-Depleted Rats." Journal of Nutrition 121, no. 10 (1991): 1643–48. http://dx.doi.org/10.1093/jn/121.10.1643.
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Ayala-López, Wilfredo, Wei Xia, Walter A. Henne, and Philip S. Low. "Targeting the Activated Macrophage with Folate-Conjugated Compounds in Experimental Atherosclerosis (92.11)." Journal of Immunology 182, no. 1_Supplement (2009): 92.11. http://dx.doi.org/10.4049/jimmunol.182.supp.92.11.
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Abstract Macrophages are central to the development of atherosclerosis. Folate-receptor positive (FR+) macrophages have been reported to orchestrate inflammatory processes in multiple inflammatory diseases, but the role of FR+ macrophages in atherosclerosis is unknown. Here, we report the use of folate to target radioactive and fluorescent imaging agents to macrophages present within aortas of atherosclerotic ApoE-/- mice. Folate-targeted 99m-Tc and folate-DyLight680 were synthesized and injected into ApoE-/- mice that were fed either normal or Western chow for 25 weeks. Mice and their excised aortas were then imaged to assess accumulation of both folate conjugates. Flow cytometric analysis of single cell suspensions of collagenase-digested aortas was also performed. Folate-targeted compounds, but not nontargeted compounds, were found to accumulate in atherosclerotic lesions of ApoE-/- mice, with greater uptake in mice fed Western chow than normal chow. The targeted cells were also confirmed to be FR+ macrophages. These data demonstrate that FR+ macrophages are present in atherosclerotic lesions and that they can be targeted with folate-conjugated compounds. Folate targeting could conceivably be developed for the staging of atherogenesis and treating of the associated disease.
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Choi, S.-W., Y.-I. Kim, J. N. Weitzel, and J. B. Mason. "Folate depletion impairs DNA excision repair in the colon of the rat." Gut 43, no. 1 (1998): 93–99. http://dx.doi.org/10.1136/gut.43.1.93.
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Background/Aims—Diminished folate status appears to promote colonic carcinogenesis by, as of yet, undefined mechanisms. Impaired DNA repair plays a significant role in the evolution of many colon cancers. Since folate is essential for thede novo synthesis of nucleotides and since folate depletion has previously been associated with excessive DNA strand breaks, it was hypothesised that folate depletion may impair DNA repair. Studies were therefore performed to examine whether folate depletion affects the two major categories of DNA repair.Methods—Study 1: eight weanling male Sprague-Dawley rats were fed on diets containing either 0 or 8 mg folate/kg diet with 1% succinylsulphathiazole for four weeks. After viable colonocytes had been harvested, DNA excision repair was evaluated by a single cell gel electrophoresis assay. Study 2: eighteen animals were fed on similar diets for five weeks. Also in study 2, 18 additional rats were fed on the same defined diet without succinylsulphathiazole for 15 weeks. Weekly injections with the procarcinogen, 1,2-dimethylhydrazine (20 mg base/kg), were administered to the latter group of animals. Five microsatellite loci from different chromosomes were investigated for instability in hepatic and colonic DNA.Results—In study 1, a significantly retarded rate of DNA excision repair was observed in the folate deficient colonocytes compared with controls (p<0.05). In study 2, there was no evidence of instability at the five microsatellite loci associated with either short or long term folate depletion.Conclusions—Folate deficiency impairs DNA excision repair in rat colonic mucosa; a similar degree of deficiency, even when administered in conjunction with a colonic carcinogen, did not produce evidence of a widespread defect in mismatch repair.
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Chan, Chun-Wai, and Bi-Fong Lin. "Folate Deficiency Enhanced Inflammation and Exacerbated Renal Fibrosis in High-Fat High-Fructose Diet-Fed Mice." Nutrients 15, no. 16 (2023): 3616. http://dx.doi.org/10.3390/nu15163616.
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The prevalence of obesity and chronic kidney disease (CKD) is increasing simultaneously and rapidly worldwide. Our previous study showed that folate deficiency increased lipid accumulation and leptin production of adipocytes. Whether folate plays a role in CKD, particularly obesity-related nephropathy remains unclear. To investigate the effects of folate deficiency on CKD in diet-induced obese mice, four groups of male C57BL/6 mice were fed either a normal-fat diet (NF) with folate (NF+f); NF without folate (NF−f); high-fat high-fructose diet (HFF) with folate (HFF+f); or HFF without folate (HFF−f) for 12 months during the study. The results showed that HFF increased not only body weight, fasting blood glucose, total cholesterol (TC), low-density lipoprotein (LDL)-cholesterol, and blood pressure, but also cytokines levels, such as interleukin (IL)-2, interferon (IFN)-γ, IL-17A/F, IL-6, monocyte chemoattractant protein (MCP)-1, and transforming growth factor (TGF)-β1. The indicators of kidney failure including urinary protein, neutrophil gelatinase-associated lipocalin (NGAL), renal type I and IV collagen deposits and leptin content, and serum creatinine were also increased by HFF. Folate-deficient diets further elevated serum TC, LDL-cholesterol, IL-6, tumor necrosis factor (TNF)-α, MCP-1, TGF-β1, and leptin, but decreased IL-10 level, and thus exacerbated renal fibrosis. To investigate the possible mechanisms of folate deficiency on renal injury, phosphorylation of pro-fibrosis signaling molecules, including signal transducer and activator of transcription (STAT)3 and small mothers against decapentaplegic (Smad)2/3, were assayed. Both HFF and folate deficiency significantly increased the phosphorylation of STAT3 and Smad2/3, suggesting synergistic effects of HFF−f on chronic renal inflammation and fibrosis. In conclusion, the results demonstrated that folate deficiency might aggravate inflammatory status and enhance renal fibrosis.
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Norsidah, Ku-Zaifah, Ahmad Yusof Asmadi, Ayob Azizi, Othman Faizah, and Yusof Kamisah. "Palm Tocotrienol-Rich Fraction Improves Vascular Proatherosclerotic Changes in Hyperhomocysteinemic Rats." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/976967.
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This study investigated the effects of palm tocotrienol-rich fraction (TRF) on aortic proatherosclerotic changes in rats fed with a high methionine diet. Forty-two male Wistar rats were divided into six groups. The first group was the control (fed with a basal diet). Another five groups were fed with 1% methionine diet for 10 weeks. From week 6 onward, folate (8 mg/kg diet) or palm TRF (30, 60, and 150 mg/kg diets) was added into the diet of the last four rat groups, respectively. The high methionine diet raised the plasma total homocysteine and aortic lipid peroxidation, which were reduced by the palm TRF and folate supplementations. Plasma nitric oxide was reduced in the high methionine group compared to the control (3.72±0.57versus6.65±0.53 μmol/L,P<0.05), which reduction was reversed by the palm TRF (60 and 150 mg/kg) and folate supplementations. The increased aortic vascular cell adhesion molecule-1 expression in the methionine group (2.58±0.29) was significantly reduced by the folate (1.38±0.18) and palm TRF at 150 mg/kg (1.19±0.23). Palm TRF was comparable to folate in reducing high methionine diet-induced plasma hyperhomocysteinemia, aortic oxidative stress, and inflammatory changes in rats.
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Sharma, Jaspreet, Blake R. Rushing, Madeline S. Hall, et al. "Sex-Specific Metabolic Effects of Dietary Folate Withdrawal in Wild-Type and Aldh1l1 Knockout Mice." Metabolites 12, no. 5 (2022): 454. http://dx.doi.org/10.3390/metabo12050454.
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ALDH1L1 (10-formyltetrahydrofolate dehydrogenase), an enzyme of folate metabolism, is highly expressed in the liver. It regulates the overall flux of folate-bound one-carbon groups by converting 10-formyltetrahydrofolate to tetrahydrofolate and CO2 in a NADP+-dependent reaction. Our previous study revealed that Aldh1l1 knockout (KO) mice have an altered liver metabotype with metabolic symptoms of folate deficiency when fed a standard chow diet containing 2 ppm folic acid. Here we performed untargeted metabolomic analysis of liver and plasma of KO and wild-type (WT) male and female mice fed for 16 weeks either standard or folate-deficient diet. OPLS-DA, a supervised multivariate technique that was applied to 6595 and 10,678 features for the liver and plasma datasets, respectively, indicated that genotype and diet, alone or in combination, gave distinct metabolic profiles in both types of biospecimens. A more detailed analysis of affected metabolic pathways based on most confidently identified metabolites in the liver and plasma (OL1 and OL2a ontology level) indicated that the dietary folate restriction itself does not fully recapitulate the metabolic effect of the KO. Of note, dietary folate withdrawal enhanced the metabolic perturbations linked to the ALDH1L1 loss only for a subset of metabolites. Importantly, both the ALDH1L1 loss and dietary folate deficiency produced sex-specific metabolic effects.
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Maxwell, M. H., C. C. Whitehead, and J. Armstrong. "Haematological and tissue abnormalities in chicks caused by acute and subclinical folate deficiency." British Journal of Nutrition 59, no. 1 (1988): 73–80. http://dx.doi.org/10.1079/bjn19880011.
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1. Haematological, histological and ultrastructural findings in young chicks fed on a purified diet severely deficient in folate are reported.2. Growth of the birds was greatly depressed and they had a macrocytic anaemia. Other haematological changes included abnormal nuclear formations in erythrocytes, numerous mitoses and hypersegmented granulocytes.3. Megaloblasts were observed in bone marrow and their fine structure is described for the first time in an avian species.4. Morphological changes occurred also in the liver. The parenchyma had damaged sinusoidal endothelium, inflammatory cells and no glycogen. Mitochondria were damaged and many were associated with unusual crystalline structures.5. Chickens fed on a semi-purified diet of low folate content showed no growth depression or clinical signs of deficiency but had abnormal haematological values and morphological changes that resembled those seen in birds fed on the purified diet.6. These abnormalities responded to dietary supplements of pteroylmonoglutamic acid in a dose-related manner and may be useful in diagnosing subclinical folate deficiency.
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Cho, Clara E. "Role of methyl group vitamins in hypothalamic development of food intake regulation in Wistar rats." Applied Physiology, Nutrition, and Metabolism 39, no. 7 (2014): 844. http://dx.doi.org/10.1139/apnm-2014-0094.
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High multivitamin diets (HV; 10-fold AIN-93G) fed during pregnancy to Wistar rats produce offspring with increased food intake, obesity, and characteristics of metabolic syndrome. The hypothesis that methyl group vitamins in HV gestational and pup diets modify expression of the obesogenic phenotypes in the offspring through their effects on hypothalamic feeding pathways was tested by 4 studies. In studies 1 and 2, dams were fed the AIN-93G diet with recommended vitamin (RV), HV, high methyl vitamins (10-fold folate, vitamin B12 and vitamin B6) (HMethyl), or HV with normal folate (HVNF) and male offspring were weaned to a high-fat diet for 8 weeks. In studies 3 and 4, dams were fed RV, HV, or high 10-fold folate (HFol), and male offspring were weaned to RV, HV, or HFol diets for 29 weeks. The results were as follows: (i) HV and HMethyl diets increased obesogenic phenotypes and altered hypothalamic regulation of food intake and metabolism concurrent with epigenetic effects on gene expression. (ii) Removing folate additions to the HV diet showed that folate contributes to the obesogenic phenotype in the offspring and epigenetic alterations in the hypothalamus that favour increased food intake. (iii) Matching pup diet vitamin content with that of the HV and HFol diet-fed dams prevented their increased food intake, body weight, and insulin resistance when weaned to the RV diet. (iv) Both HFol gestational and pup diets altered hypothalamic feeding pathways through DNA methylation, showing that epigenetic effects of these vitamins occur not only in utero but also postnatally. In conclusion, methyl group vitamins in HV gestational and pup diets modify expression of the obesogenic phenotypes and hypothalamic food intake regulatory systems in the Wistar rat offspring.
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Engeham, Sarah F., Andrea Haase, and Simon C. Langley-Evans. "Supplementation of a maternal low-protein diet in rat pregnancy with folic acid ameliorates programming effects upon feeding behaviour in the absence of disturbances to the methionine–homocysteine cycle." British Journal of Nutrition 103, no. 7 (2009): 996–1007. http://dx.doi.org/10.1017/s0007114509992662.
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Maternal protein restriction in rat pregnancy is associated with altered feeding behaviour in later life. When allowed to self-select their diet, rats subject to prenatal undernutrition show an increased preference for fatty foods. The main aim of the present study was to evaluate the contribution of folic acid in the maternal diet to programming of appetite, since disturbances of the folate and methionine–homocysteine cycles have been suggested to impact upon epigenetic regulation of gene expression and hence programme long-term physiology and metabolism. Pregnant rats were fed diets containing either 9 or 18 % casein by weight, with folate provided at either 1 or 5 mg/kg diet. Adult male animals exposed to low protein (LP) in fetal life exhibited increased preference for high-fat food. Providing the higher level of folate in the maternal diet prevented this effect of LP, but offspring of rats fed 18 % casein diet with additional folate behaved in a similar manner to LP-exposed animals. Among day 20 gestation fetuses, it was apparent that both protein restriction and maternal folate supplementation could have adverse effects upon placental growth. Examination of methionine–homocysteine and folate cycle intermediates, tissue glutathione concentrations and expression of mRNA for methionine synthase, DNA methyltransferase 1 and methyltetrahydrofolate reductase revealed no gross disturbances of folate and one-carbon metabolism in either maternal or fetal tissue. The present findings indicated that any role for DNA methylation in programming of physiology is not related to major perturbations of folate metabolism, and is likely to be gene-specific rather than genome-wide.
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Hill, Sarah A., Nicholas J. Cave, and Sandra Forsyth. "Effect of age, sex and body weight on the serum concentrations of cobalamin and folate in cats consuming a consistent diet." Journal of Feline Medicine and Surgery 20, no. 2 (2017): 135–41. http://dx.doi.org/10.1177/1098612x17699680.
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Objectives Multiple feline diseases involving the gastrointestinal tract, pancreas, liver and biliary tract are known to cause abnormal serum cobalamin and folate concentrations. Measuring the serum concentration of these vitamins can therefore be a helpful diagnostic tool. However, factors other than disease, in particular age, have also been suggested to have an effect on the serum concentration of cobalamin and folate. In previous studies, the dietary intake was not standardised, or even known, despite diet being the prinicpal source of both vitamins. Therefore, we evaluated the effect of age, sex and body weight on the serum concentration of folate and cobalamin in cats fed the same diet. Methods The serum cobalamin and folate concentrations were measured in 65 apparently healthy cats in a nutrition colony that had been fed an identical diet. A linear model was used to test the relationship between the serum concentration of cobalamin and folate with the variables age, sex and body weight. Results There was a large variation in the serum concentration of both folate and cobalamin, despite identical intake. Serum cobalamin was inversely associated with age ( P = 0.002), and males had higher concentrations than females ( P = 0.039). Serum folate was positively associated with age ( P = 0.01). Conclusions and relevance Independent of diet, serum cobalamin concentration decreases with age. Changes in gastrointestinal function, microflora or metabolism may be responsible. Older cats may be more susceptible to cobalamin deficiency secondary to inappetence or gastrointestinal disease.
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Huot, Pedro S. P., David W. Dodington, Rebecca C. Mollard, et al. "High Folic Acid Intake during Pregnancy Lowers Body Weight and Reduces Femoral Area and Strength in Female Rat Offspring." Journal of Osteoporosis 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/154109.
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Rats fed gestational diets high in multivitamin or folate produce offspring of altered phenotypes. We hypothesized that female rat offspring born to dams fed a gestational diet high in folic acid (HFol) have compromised bone health and that feeding the offspring the same HFol diet attenuates these effects. Pregnant rats were fed diets with either recommended folic acid (RFol) or 10-fold higher folic acid (HFol) amounts. Female offspring were weaned to either the RFol or HFol diet for 17 weeks. HFol maternal diet resulted in lower offspring body weights (6%,P=0.03) and, after adjusting for body weight and femoral length, smaller femoral area (2%,P=0.03), compared to control diet. After adjustments, HFol pup diet resulted in lower mineral content (7%,P=0.01) and density (4%,P=0.002) of lumbar vertebra 4 without differences in strength. An interaction between folate content of the dam and pup diets revealed that a mismatch resulted in lower femoral peak load strength (P=0.01) and stiffness (P=0.002). However, the match in folate content failed to prevent lower weight gain. In conclusion, HFol diets fed to rat dams and their offspring affect area and strength of femurs and mineral quantity but not strength of lumbar vertebrae in the offspring.
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Suliburska, Joanna, Katarzyna Skrypnik, and Agata Chmurzyńska. "Folic Acid Affects Iron Status in Female Rats with Deficiency of These Micronutrients." Biological Trace Element Research 195, no. 2 (2019): 551–58. http://dx.doi.org/10.1007/s12011-019-01888-z.
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Abstract Although simultaneous supplementation with iron and folic acid is justified, the potential interactions between these micronutrients are unknown. The aim of this study was to determine the effects of oral iron and folic acid, administered together or separately, on iron concentration in tissues in rats with a deficiency of both these micronutrients. In the first stage of the experiment (28 days), 150 8-week-old female Wistar rats were randomly assigned to a control group (C; n = 30) fed the standard diet and to a study group (n = 120) fed a diet deficit in iron and folate. The study group was then randomly divided to four groups: D group fed a deficit diet, FE group fed a deficit diet with iron gluconate, the FOL group fed a deficit diet with folate acid, and the FEFOL group fed a deficit diet with iron gluconate and folate acid. After 2, 10, and 21 days of supplementation, ten animals from each group were killed. Morphological parameters were measured in whole blood. Iron concentration was assayed in serum, liver, spleen, pancreas, heart, and kidneys. Folic acid supplementation more significantly decreased iron concentrations in the pancreas and spleen than in the D group after 10 and 21 days of supplementation. Moreover, the combination of iron with folic acid markedly decreased iron levels in the liver and spleen, in comparison with iron alone, after 10 and 21 days of the experiment. In conclusion, folic acid affects iron status in female rats deficient in these micronutrients in moderate and long-term supplementation.
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Maloney, Christopher A., Susan M. Hay, and William D. Rees. "Folate deficiency during pregnancy impacts on methyl metabolism without affecting global DNA methylation in the rat fetus." British Journal of Nutrition 97, no. 6 (2007): 1090–98. http://dx.doi.org/10.1017/s0007114507670834.
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The methionine cycle and methyl group metabolism are implicated in the long-term programming of metabolism. Diets deficient in folic acid, methionine and choline have been fed to pregnant rats to examine the effects on amino acid metabolism, choline reserves and DNA methylation in dam and fetuses. Animals were fed folate-deficient, folate-deficient with low methionine, folate-deficient with low choline and folate-deficient, low-methionine, low-choline diets starting 2 weeks before mating. The dams and their fetuses were subsequently killed on day 21 of gestation for analysis. Diets low in methionine reduced fetal and maternal weight. Folate deficiency increased the concentrations of homocysteine, glycine, serine and threonine in the maternal plasma, and this was exacerbated by the low-methionine diets. The changes in the amino acid profile in the fetal serum were similar but less pronounced. This result suggests that fetal metabolism was less perturbed. Folate deficiency increased free choline in the maternal liver at the expense of phosphocholine stores. It has been suggested that a deficiency in methyl donors in the diet during pregnancy may impact on key methylation reactions, including the methylation of DNA. Despite widespread changes in the metabolism of choline and amino acids, there was no change in the global methylation of cytosine in DNA from either maternal or fetal livers. This suggests a more indirect mechanism in which gene–nutrient interactions modify the process of differential methylation during development
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Kulkarni, Medha V., C. P. Parameswaran Nair, and Gomathy Viswanathan. "Varying Folate Pattern in Different Strains of Mice Fed Coconut Oil and Sesame Seed Oil Diet." Pteridines 7, no. 4 (1996): 143–47. http://dx.doi.org/10.1515/pteridines.1996.7.4.143.
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Summary The effect of coconut oil feeding with and without cholesterol on folate metabolism in the two strains of mice, C57BL/6 and AKR have been studied. Liver total folate levels are higher in AKR mice. Coconut oil feeding markedly decreased the ratio of nonmethyl/methyl folates in C57BL/6 strain but not in AKR. Cholesterol supplementation to the coconut oil diet increased the percentage of monoglutamyl folates at the expense of polyglutamyl folates in both strains. Only C57BL/6 strain showed growth retardation on coconut oil feeding. The differences in hepatic folate metabolism between the two strains could possibly have an important role in determining their differences in susceptibility to diet induced atherosclerosis.
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Nyska, Abraham, Trevor Waner, Zvi Paster, Peretz Bracha, Elliot B. Gordon, and Baruch Klein. "Induction of Gastrointestinal Tumors in Mice Fed the Fungicide Folpet: Possible Mechanisms." Japanese Journal of Cancer Research 81, no. 6-7 (1990): 545–49. http://dx.doi.org/10.1111/j.1349-7006.1990.tb02604.x.
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Balkanski, Stefan V., Joana I. Simeonova, Stanislav R. Gueorguiev, Elina S. Petkova-Gueorguieva, Ivan G. Gitev, and Ilko N. Getov. "Pilot Study of Pharmacists’ Attitudes towards and Expectations for Remuneration of Valueadded Pharmacy Services (VAPS) in Bulgaria." Folia Medica 62, no. 2 (2020): 324–30. http://dx.doi.org/10.3897/folmed.62.e39371.
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Introduction: Value-added pharmacy services (VAPS) are additional services to the traditional pharmacy activities, which do not in&shy;clude dispensing of medicinal products and professional consultation. These services have cost reduction effect on the healthcare system and add value to the work of the pharmacist as a healthcare professional. Aim: To assess the pharmacists&rsquo; attitudes and expectations towards the remuneration of value-added pharmacy services (VAPS) in Bulgaria. Materials and methods: A cross-sectional study including pharmacists working in community pharmacies was carried out between August 2018 and October 2018. A web-based 15-item questionnaire was developed. The questionnaire was distributed to all members of the Bulgarian Pharmaceutical Union (n=5165). Two hundred thirty-three questionnaires were filled in and returned (response rate of 4.5%). Data were processed by SPSS v. 24.0. Results: Over 51% of the community pharmacies in Bulgaria offer VAPS, mainly measuring blood pressure (67.4%) and blood glucose (12.9%). Over two-thirds of the pharmacists considered charging a remuneration fee for blood pressure measurement irrelevant. About 30.5% of those who held the opposite opinion proposed that the fee charged should not be higher than EUR 2.56. Over 44% of the re&shy;spondents proposed that the fee for blood glucose measurement should not be higher than the same amount. Most pharmacists (98.3%) supported the idea of charging a remuneration fee for injections and influenza vaccination in a pharmacy. Conclusion: The study shows that pharmacists in Bulgaria are ready to offer VAPS, but additional remuneration for the services should be provided.
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Mwachaka, Philip Maseghe, Peter Gichangi, Adel Abdelmalek, Paul Odula, and Julius Ogeng’o. "Effect of Maternal Folate Use on Offsprings' Cerebellar Morphometric Parameters: An Experimental Study in A Rat Model." International Journal of Anatomy and Research 11, no. 3 (2023): 8685–91. http://dx.doi.org/10.16965/ijar.2023.161.
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Background: Folate is an important nutrient in fetal and early postnatal brain development, and its supplementation during pregnancy has been widely recommended. Folate supplementation has been linked to improved cerebellar function, specifically motor and neuropsychological abilities. It is still unclear exactly how folate affects the cerebellum's structural growth. This study aimed to describe the effects of maternal folate use on cerebellum postnatal development. Methods: Twelve adults (6–8 week old) female rats (Rattus norwegicus) were randomly divided into four groups and fed one of four premixed diets: a standard diet (folate 2 mg/kg), a folate-supplemented diet (folate 8 mg/kg), or a folate supra-supplemented diet (folate 40 mg/kg). The rats were introduced to their respective diets 14 days before mating, and remained on the same diet throughout gestation and lactation. On postnatal days 1, 7, 21, and 35, five pups from each group were sacrificed and their brains harvested for analysis. The data gathered included the brain's weight, brain length and width, cerebellar length and width, and vermis length and width. Results: The folate-deficient offspring's brains weighed significantly less at birth than the other groups' brains (p<0.05). As they aged, the folate-deficient group gained weight more slowly than the others. The folate-deficient group had significantly smaller cerebellar length, cerebellar width, vermis length, and vermis width than the other study groups. The folate-supplemented group had larger cerebellar dimensions than the folate supra-supplemented group, but these differences were not statistically significant. Conclusion: Folate deficiency during pregnancy and breastfeeding is linked to a smaller cerebellum in the offspring. These results could affect the health of the children. Furthermore, there is no additional benefit to folate supra-supplementation over recommended folate supplementation in cerebellum development. KEYWORDS: Folate deficiency, folate supplementation, cerebellum.
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Bajwa, Asif Azeem, Sohail Ali, Sikandar Ali Khan, Hassan Raza, Fayyaz Hussain, and Tashfeen Bin Nazir. "Folate Deficiency: Is it Related to the Development of Depression." Pakistan Armed Forces Medical Journal 73, no. 4 (2023): 989–92. http://dx.doi.org/10.51253/pafmj.v73i4.9187.
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Objectives: To determine the frequency of serum folate deficiency among patients with depression and to compare mean serum folate levels with the severity level of depression.
 Study Design: Cross-sectional study.
 Place and Duration of Study: Armed Forces Institute of Mental Health, Rawalpindi Pakistan, from Sep 2021 to Feb 2022.
 Methodology: We consecutively recruited 155 study subjects. Basic demographic data were recorded. The severity of depression was assessed using the Hamilton Depression Rating Scale–Urdu version (HAM-D U). Blood samples were collected to determine serum folate before commencing any treatment for depression; serum Folate levels were assessed at the Armed Forces Institute of Pathology.
 Results: The mean HAM-D score was 17.14±4.29, with minimum and maximum scores of 8 and 22. 97(62.6%) cases had mild– moderate depression, and 58(37.4%) patients had severe depression. The mean serum folate levels were 3.10±1.40 ng/ml. There were 57(36.8%) cases that had normal folate levels, 45(29%) cases that had borderline folate levels, and 53(34.2%) cases that had folate deficiency. The frequency of borderline folate deficiency was statistically higher in cases with severe depression, (p-value<0.001).
 Conclusion: Results of this study highlight that the frequency of borderline–folate deficiency was statistically higher in cases with moderate and severe depression.
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PESTI, GENE M., GEORGE N. ROWLAND, and KYEONG-SEON RYU. "Folate Deficiency in Chicks Fed Diets Containing Practical Ingredients." Poultry Science 70, no. 3 (1991): 600–604. http://dx.doi.org/10.3382/ps.0700600.
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Yang, Jin, Qiang Cheng, Mustafa K. Taher Al-Nuaimi, Ahmed Kishk, and Abd-Elhady Mahmoud. "Broadband Folded Reflectarray Fed by a Dielectric Resonator Antenna." IEEE Antennas and Wireless Propagation Letters 19, no. 1 (2020): 178–82. http://dx.doi.org/10.1109/lawp.2019.2957288.
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Zhang, G. M., J. S. Hong, B. Z. Wang, Q. Y. Qin, J. B. Mo, and D. M. Wan. "A Novel Multi-Folded UBW Antenna Fed by CPW." Journal of Electromagnetic Waves and Applications 21, no. 14 (2007): 2109–19. http://dx.doi.org/10.1163/156939307783152911.
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Ooi, B. L. "A double-folded, capacitive-fed, cavity-backed microstrip antenna." Microwave and Optical Technology Letters 30, no. 4 (2001): 240–41. http://dx.doi.org/10.1002/mop.1278.
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Yang, Steven S. L., and K. M. Luk. "Wideband folded-patch antennas fed by L-shaped probe." Microwave and Optical Technology Letters 45, no. 4 (2005): 352–55. http://dx.doi.org/10.1002/mop.20821.
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Lui, W. J. "Ultra-wideband folded loop antenna fed by coplanar waveguide." Microwave and Optical Technology Letters 50, no. 12 (2008): 3075–77. http://dx.doi.org/10.1002/mop.23890.
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Kim, Kyong-Chol, Hyeran Jang, Julia Sauer, et al. "Folate supplementation differently affects uracil content in DNA in the mouse colon and liver." British Journal of Nutrition 105, no. 5 (2011): 688–93. http://dx.doi.org/10.1017/s0007114510004332.
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High folate intake may increase the risk of cancer, especially in the elderly. The present study examined the effects of ageing and dietary folate on uracil misincorporation into DNA, which has a mutagenic effect, in the mouse colon and liver. Old (18 months; n 42) and young (4 months; n 42) male C57BL/6 mice were pair-fed with four different amino acid-defined diets for 20 weeks: folate deplete (0 mg/kg diet); folate replete (2 mg/kg diet); folate supplemented (8 mg/kg diet); folate deplete (0 mg/kg diet) with thymidine supplementation (1·8 g/kg diet). Thymidylate synthesis from uracil requires folate, but synthesis from thymidine is folate independent. Liver folate concentrations were determined by the Lactobacillus casei assay. Uracil misincorporation into DNA was measured by a GC/MS method. Liver folate concentrations demonstrated a stepwise increase across the spectrum of dietary folate levels in both old (P = 0·003) and young (P < 0·001) mice. Uracil content in colonic DNA was paradoxically increased in parallel with increasing dietary folate among the young mice (P trend = 0·033), but differences were not observed in the old mice. The mean values of uracil in liver DNA, in contrast, decreased with increasing dietary folate among the old mice, but it did not reach a statistically significant level (P < 0·1). Compared with the folate-deplete group, thymidine supplementation reduced uracil misincorporation into the liver DNA of aged mice (P = 0·026). The present study suggests that the effects of folate and thymidine supplementation on uracil misincorporation into DNA differ depending on age and tissue. Further studies are needed to clarify the significance of increased uracil misincorporation into colonic DNA of folate-supplemented young mice.
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McNeil, Christopher J., Susan M. Hay, Garry J. Rucklidge, et al. "Disruption of lipid metabolism in the liver of the pregnant rat fed folate-deficient and methyl donor-deficient diets." British Journal of Nutrition 99, no. 2 (2008): 262–71. http://dx.doi.org/10.1017/s0007114507798999.
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The importance of folic acid and the methionine cycle in fetal development is well recognised even though the mechanism has not been established. Since the cycle is active in the maternal liver, poor folate status may modify hepatic metabolism. Pregnant rats were fed diets deficient in folic acid (–F) or in three key methyl donors, folic acid, choline and methionine (–FLMLC) and the maternal liver was analysed on day 21 of gestation. Two-dimensional gel electrophoresis of soluble proteins identified differentially abundant proteins, which could be allocated into nine functional groups. Five involved in metabolic processes, namely, folate/methionine cycle, tyrosine metabolism, protein metabolism, energy metabolism and lipid metabolism, and three in cellular processes, namely, endoplasmic reticulum function, bile production and antioxidant defence. The mRNA for sterol regulatory element-binding protein-1c and acetyl-CoA carboxylase-1 (fatty acid synthesis) were decreased by both –F and –FLMLC diets. The mRNA for PPARα and PPARγ and carnitine palmitoyl transferase (fatty acid oxidation) were increased in the animals fed the –FLMLC diets. Changes in the abundance of proteins associated with intracellular lipid transport suggest that folate deficiency interferes with lipid export. Reduced fatty acid synthesis appeared to prevent steatosis in animals fed the –F diet. Even with increased oxidation, TAG concentrations were approximately three-fold higher in animals fed the –FLMLC diet and were associated with an increase in the relative abundance of proteins associated with oxidative stress. Fetal development may be indirectly affected by these changes in hepatic lipid metabolism.
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Alférez, María JM, Emilio Rivas, Javier Díaz-Castro, et al. "Folic acid supplemented goat milk has beneficial effects on hepatic physiology, haematological status and antioxidant defence during chronic Fe repletion." Journal of Dairy Research 82, no. 1 (2014): 86–94. http://dx.doi.org/10.1017/s0022029914000624.
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The aim of the current study was to asses the effect of goat or cow milk-based diets, either normal or Fe-overloaded and folic acid supplement on some aspects of hepatic physiology, enzymatic antioxidant defence and lipid peroxidation in liver, brain and erythrocyte of control and anaemic rats after chronic Fe repletion. 160 male Wistar rats were placed on 40 d in two groups, a control group receiving normal-Fe diet and the Fe-deficient group receiving low Fe diet. Lately, the rats were fed with goat and cow milk-based diets during 30 d, with normal-Fe content or Fe-overload and either with normal folic or folic acid supplemented. Fe-overload increased plasma alanine transaminase and aspartate transaminase levels when cow milk was supplied. Dietary folate supplementation reduced plasma transaminases levels in animals fed goat milk with chronic Fe overload. A remarkable increase in the superoxide dismutase activity was observed in the animals fed cow milk. Dietary folate supplement lead to a decrease on the activity of this enzyme in all the tissues studied with both milk-based diets. A concomitant increment in catalase was also observed. The increase in lipid peroxidation products levels in rats fed cow milk with Fe-overload, suggest an imbalance in the functioning of the enzymatic antioxidant defence. In conclusion, dietary folate-supplemented goat milk reduces both plasma transaminases levels, suggesting a hepatoprotective effect and has beneficial effects in situation of Fe-overload, improving the antioxidant enzymes activities and reducing lipid peroxidation.
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Esfandiari, Farah, Jesus A. Villanueva, Donna H. Wong, Samuel W. French, and Charles H. Halsted. "Chronic ethanol feeding and folate deficiency activate hepatic endoplasmic reticulum stress pathway in micropigs." American Journal of Physiology-Gastrointestinal and Liver Physiology 289, no. 1 (2005): G54—G63. http://dx.doi.org/10.1152/ajpgi.00542.2004.
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Previously, we showed that feeding micropigs ethanol with a folate-deficient diet promoted the development of hepatic injury while increasing hepatic levels of homocysteine and S-adenosylhomocysteine (SAH) and reducing the level of S-adenosylmethionine (SAM) and the SAM-to-SAH ratio. Our present goals were to evaluate mechanisms for hepatic injury using liver specimens from the same micropigs. The effects of ethanol feeding or folate-deficient diets, singly or in combination, on cytochrome P-450 2E1 (CYP2E1) and signal pathways for apoptosis and steatosis were analyzed using microarray, real-time PCR, and immunoblotting techniques. Apoptosis was increased maximally by the combination of ethanol feeding and folate deficiency and was correlated positively to liver homocysteine and SAH. Liver CYP2E1 and the endoplasmic reticulum stress signals glucose-regulated protein 78 (GRP78), caspase 12, and sterol regulatory element binding protein-1c (SREBP-1c) were each activated in pigs fed folate-deficient or ethanol diets singly or in combination. Liver mRNA levels of CYP2E1, GRP78, and SREBP-1c, and protein levels of CYP2E1, GRP78, nuclear SREBP, and activated caspase 12 each correlated positively to liver levels of SAH and/or homocysteine and negatively to the SAM-to-SAH ratio. The transcripts of the lipogenic enzymes fatty acid synthase, acetyl-CoA carboxylase, and stearoyl-CoA desaturase were elevated in the ethanol-fed groups, and each was positively correlated to liver homocysteine levels. The induction of abnormal hepatic methionine metabolism through the combination of ethanol feeding with folate deficiency is associated with the activation of CYP2E1 and enhances endoplasmic reticulum stress signals that promote steatosis and apoptosis.
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Choi, Sang-Woon, Simonetta Friso, Mary K. Keyes, and Joel B. Mason. "Folate supplementation increases genomic DNA methylation in the liver of elder rats." British Journal of Nutrition 93, no. 1 (2005): 31–35. http://dx.doi.org/10.1079/bjn20041283.
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The availability of folate is implicated as a determinant of DNA methylation, a functionally important feature of DNA. Nevertheless, when this phenomenon has been examined in the rodent model, the effect has not always been observed. Several reasons have been postulated for the inconsistency between studies: the rodent is less dependent on folate as a methyl source than man; juvenile animals, which most studies use, are more resistant to folate depletion than old animals; methods to measure genomic DNA methylation might not be sensitive enough to detect differences. We therefore examined the relationship between folate and genomic DNA methylation in an elder rat model with a newly developed method that can measure genomic DNA methylation sensitively and precisely. Thirty-nine 1-year-old rats were divided into three groups and fed a diet containing 0, 4·5 or 18 μmol folate/kg (folate-deplete, -replete and -supplemented groups, respectively). Rats were killed at 8 and 20 weeks. At both time points, mean liver folate concentrations increased incrementally between the folate-deplete, -replete and -supplemented rats (Pfor trend <0·001) and by 20 weeks hepatic DNA methylation also increased incrementally between the folate-deplete, -replete and -supplemented rats (Pfor trend=0·025). At both time points folate-supplemented rats had significantly increased levels of DNA methylation compared with folate-deplete\ rats (P<0·05). There was a strong correlation between hepatic folate concentration and genomic DNA methylation in the liver (r0·48,P=0·004). In the liver of this animal model, dietary folate over a wide range of intakes modulates genomic DNA methylation.
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Cui, Can, and Wen Bo Sun. "Application of Folded Plate Structure with Flat Truss in Long-Span Steel Roof Structure." Advanced Materials Research 243-249 (May 2011): 625–29. http://dx.doi.org/10.4028/www.scientific.net/amr.243-249.625.
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Folded plate structure with flat truss is applied in the roof steel structure of the natatorium in Huai’an sports center. In this paper, mechanical analysis on loading case and dynamic characteristics of the roof steel structure is accomplished. Overall stability analysis is also completed by FEM software STRAND7. Analysis results indicate the scheme is in accordance with safety and aesthetic is appropriately designed, which could figure out that bearing capacity and seismic performance of the folded plate structure are satisfactory.
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O'Leary, K., and P. J. A. Sheehy. "Influence of folic acid-fortified foods on folate status in a folate depletion–repletion rat model." British Journal of Nutrition 85, no. 4 (2001): 441–46. http://dx.doi.org/10.1079/bjn2000288.
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An increasing number of foods fortified with varying levels of folic acid are appearing in the market place, targeted either at the general population or at specific consumer groups. Although it is assumed that the folate in these products should be highly bioavailable, there is a need to carry out studies to ascertain that this is, in fact, the case. The present study investigated the ability of selected folic acid-fortified foods (targeted at different types of consumer) to increase the folate status of folate-deficient rats. Forty-two weanling male rats (Wistar strain) were fed a folate-deficient diet containing 1 % succinyl sulfathiazole (w/w) for 28 d. Following depletion, seven rats were randomly assigned to each of five repletion diets containing folic acid, Complan®, Slim Fast®, Opti-Fuel2®or Cola Coa®calculated to provide 200 μg folate/kg of each diet. Calculations were based on folate information from the product labels. After a further 28 d, plasma, liver and kidney folate concentrations were determined by microbiological assay. Plasma homocysteine was measured by HPLC as a functional indicator of folate status. The folate content of the foods was measured by tri-enzyme extraction followed by microbiological assay. Our analyses suggest that there may be considerable inaccuracies on the part of the manufacturers in relation to the folate declarations on the product labels. Despite this, the four foods evaluated were highly effective in elevating plasma, liver and kidney folate and lowering plasma homocysteine concentrations in rats. These results lend support to the policy of food fortification with folic acid as a means of raising the folate status of the population, and in particular to the fortification of specific foods which may target areas of the population where increased folate status is most needed.
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Thoma, Green, and Ferguson. "Citrus Pectin and Oligofructose Improve Folate Status and Lower Serum Total Homocysteine in Rats." International Journal for Vitamin and Nutrition Research 73, no. 6 (2003): 403–9. http://dx.doi.org/10.1024/0300-9831.73.6.403.
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Low folate status leads to increased total homocysteine (tHcy) concentration, and this has been associated with an increased risk of several diseases. Many colonic bacteria are capable of synthesizing folate, and certain dietary fibers may enhance this effect. We assessed the ability of non-fermentable (cellulose) and fermentable (citrus pectin and oligofructose) fibers to improve folate status and lower tHcy in rats. Weanling Sprague-Dawley rats were fed a folate-deficient diet with 5% cellulose for four weeks. Rats were then randomly assigned to one of five folate-adequate (400 mug/kg diet) test diets for 24 days. Diets were as follows: Basal; Basal + Sulfa Drug (succinylsulfathiazole); Cellulose; Citrus Pectin; and Oligofructose. High-fiber diets were formulated by diluting the basal diet such that the final diets contained 10% of the added fiber. Twenty-one days later, 3H-r-aminobenzoic acid was injected into the cecum, and rats were terminated three days later. Rats receiving the Citrus Pectin diet had significantly higher plasma (p = 0.011), erythrocyte (p = 0.035), and colonic tissue folate concentrations (p = 0.013) and lower tHcy (p = 0.003) than rats given the Cellulose diet. Rats receiving the Oligofructose had significantly higher plasma folate (p < 0.001) and lower tHcy (p = 0.032) concentrations than rats receiving the Cellulose diet. 3H-folate was detected in the livers of all rats except those receiving Sulfa Drug. Our study indicates that Citrus Pectin and Oligofructose, but not Cellulose, can significantly increase indices of folate status in rats and lower tHcy. It also confirms the ability of the large bowel to absorb folate.
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Lentz, Steven R., Rochelle A. Erger, Sanjana Dayal та ін. "Folate dependence of hyperhomocysteinemia and vascular dysfunction in cystathionine β-synthase-deficient mice". American Journal of Physiology-Heart and Circulatory Physiology 279, № 3 (2000): H970—H975. http://dx.doi.org/10.1152/ajpheart.2000.279.3.h970.
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Hyperhomocysteinemia is a risk factor for stroke, myocardial infarction, and venous thrombosis. Moderate hyperhomocysteinemia is associated with impaired endothelial function, but the mechanisms responsible for endothelial dysfunction in hyperhomocysteinemia are poorly understood. We have used genetic and dietary approaches to produce hyperhomocysteinemia in mice. Heterozygous cystathionine β-synthase-deficient mice (CBS +/−), which have a selective defect in homocysteine transsulfuration, and wild-type (CBS +/+) littermates were fed either a control diet or a diet that is relatively deficient in folic acid for 6 wk. Plasma total homocysteine was 5.3 ± 0.7 μM in CBS +/+ mice and 6.4 ± 0.6 μM in CBS +/− mice ( P = 0.3) given the control diet. Plasma total homocysteine was 11.6 ± 4.5 μM in CBS +/+ mice and 25.1 ± 3.2 μM in CBS +/− mice ( P = 0.004) given a low-folate diet. In mice fed the control diet, relaxation of aortic rings in response to the endothelium-dependent vasodilator acetylcholine did not differ significantly between CBS +/+ mice and CBS +/− mice. In contrast, in mice fed a low-folate diet, maximal relaxation to acetylcholine was markedly impaired in CBS +/− mice (58 ± 9%) compared with CBS +/+ mice (84 ± 4%) ( P = 0.01). No differences in relaxation to the endothelium-independent vasodilator sodium nitroprusside were observed among the four groups of mice. These data indicate that CBS-deficient mice are predisposed to hyperhomocysteinemia during dietary folate deficiency, and moderate hyperhomocysteinemia is associated with marked impairment of endothelial function in mice.
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Biswas, Arundhati, Sundar Rajan Senthilkumar, and Hamid M. Said. "Effect of chronic alcohol exposure on folate uptake by liver mitochondria." American Journal of Physiology-Cell Physiology 302, no. 1 (2012): C203—C209. http://dx.doi.org/10.1152/ajpcell.00283.2011.
Full textAbstract:
Mammalian cells obtain folate, a water-soluble vitamin, from their surroundings via transport across cell membrane. Intracellular folate is compartmentalized between the cytoplasm and the mitochondria. Transport of folate from the cytoplasm into the mitochondria is via a specific carrier-mediated process involving the mitochondrial folate transporter (MFT). Chronic alcohol use negatively impacts folate homeostasis, but its effect on mitochondrial folate uptake is not clear. We addressed this issue using mitochondrial preparations isolated from the liver of rats chronically fed an alcohol liquid diet and from human liver HepG2 cells chronically exposed to alcohol. The results showed that chronic alcohol feeding of rats leads to a significant inhibition in mitochondrial carrier-mediated folate uptake. This inhibition was associated with a significant reduction in the level of expression of the MFT protein, mRNA, and heterogenous nuclear RNA (hnRNA). Similarly, chronic alcohol exposure (96 h) of HepG2 cells led to significant inhibition in mitochondrial carrier-mediated folate uptake, which was associated with a marked reduction in the level of expression of the human MFT (hMFT). To determine whether the latter effect is, in part, being exerted at the transcriptional level, we cloned the 5′-regulatory region of the human SLC25A32 gene (which encodes the hMFT) and showed that chronic alcohol exposure of HepG2 cells leads to a significant inhibition in its promoter activity. These studies show for the first time that chronic alcohol feeding/exposure leads to a significant inhibition in mitochondrial carrier-mediated folate uptake and that the inhibition is, in part, being exerted at the level of transcription of the SLC25A32 gene.
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Nieman, Kristin M., Cara S. Hartz, Sandra S. Szegedi, Timothy A. Garrow, Janet D. Sparks, and Kevin L. Schalinske. "Folate status modulates the induction of hepatic glycine N-methyltransferase and homocysteine metabolism in diabetic rats." American Journal of Physiology-Endocrinology and Metabolism 291, no. 6 (2006): E1235—E1242. http://dx.doi.org/10.1152/ajpendo.00237.2006.
Full textAbstract:
A diabetic state induces the activity and abundance of glycine N-methyltransferase (GNMT), a key protein in the regulation of folate, methyl group, and homocysteine metabolism. Because the folate-dependent one-carbon pool is a source of methyl groups and 5-methyltetrahydrofolate allosterically inhibits GNMT, the aim of this study was to determine whether folate status has an impact on the interaction between diabetes and methyl group metabolism. Rats were fed a diet containing deficient (0 ppm), adequate (2 ppm), or supplemental (8 ppm) folate for 30 days, after which diabetes was initiated in one-half of the rats by streptozotocin treatment. The activities of GNMT, phosphatidylethanolamine N-methyltransferase (PEMT), and betaine-homocysteine S-methyltransferase (BHMT) were increased about twofold in diabetic rat liver; folate deficiency resulted in the greatest elevation in GNMT activity. The abundance of GNMT protein and mRNA, as well as BHMT mRNA, was also elevated in diabetic rats. The marked hyperhomocysteinemia in folate-deficient rats was attenuated by streptozotocin, likely due in part to increased BHMT expression. These results indicate that a diabetic state profoundly modulates methyl group, choline, and homocysteine metabolism, and folate status may play a role in the extent of these alterations. Moreover, the upregulation of BHMT and PEMT may indicate an increased choline requirement in the diabetic rat.
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Chen, S. Y., and P. Hsu. "CPW-fed folded-slot antenna for 5.8 GHz RFID tags." Electronics Letters 40, no. 24 (2004): 1516. http://dx.doi.org/10.1049/el:20046780.
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Shamsinejad, Souren, Franco De Flaviis, and Pedram Mousavi. "Microstrip-Fed 3-D Folded Slot Antenna on Cubic Structure." IEEE Antennas and Wireless Propagation Letters 15 (2016): 1081–84. http://dx.doi.org/10.1109/lawp.2015.2493146.
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