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Libros sobre el tema "Riboflavin"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 29 de julio de 2024

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1

Schneeman, Barbara O., Ann L. Yaktine y Alice Vorosmarti, eds. Scanning for New Evidence on Riboflavin to Support a Dietary Reference Intake Review. Washington, D.C.: National Academies Press, 2021. http://dx.doi.org/10.17226/26188.

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2

Madigan, Sharon M. Riboflavin status, intake and inter-relationship with other nutrients in a healthy elderly population in NorthernIreland. [S.l: The Author], 1993.

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3

1909-, Bourne Geoffrey H., ed. Nutritional disorders and requirements. Basel: Karger, 1987.

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4

Institute of Medicine (U.S.). Standing Committee on the Scientific Evaluation of Dietary Reference Intakes., Institute of Medicine (U.S.). Panel on Folate, Other B Vitamins, and Choline. y Institute of Medicine (U.S.). Subcommittee on Upper Reference Levels of Nutrients., eds. DRI, dietary reference intakes for thiamin, riboflavin, niacin, vitamin B₆, folate, vitamin B₁₂, pantothenic acid, biotin, and choline. Washington, D.C: National Academy Press, 1998.

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5

Hannover, Tierärztliche Hochschule, ed. Untersuchungen zu [beta]-Carotin-, Vitamin E-, Thiamin-, Riboflavin- und Vitamin B₆-Gehalten verschiedener fett- beziehungsweise kohlenhydratreicher Einzelfuttermittel für Ziervögel. Hannover: [s.n.], 1999.

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6

Rivlin, Richard. Riboflavin. Springer, 2011.

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7

Riboflavin. Springer, 2011.

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8

Rivlin, Richard. Riboflavin. Springer London, Limited, 2012.

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9

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng y Anne Bardsley. Vitamin B2 (riboflavin) in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0008.

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Riboflavin is a cofactor for enzymes involved in energy generation, biosynthesis, detoxification, and electron-scavenging pathways, as well as in the metabolism of other B vitamins. Deficiency is rare in developed countries; it is encountered almost invariably in combination with deficit of other B vitamins in areas of poor overall nutrition. Deficiency is endemic in populations whose staple diet consists of rice and wheat, with low or no consumption of meat and dairy products. Infants of riboflavin-deficient mothers tend to be deficient themselves at birth and remain deficient through breastfeeding and weaning. To ensure adequate riboflavin supply in both mother and infant, an increase in dairy products and/or meat consumption, particularly during lactation, may be necessary in some women.
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10

A. R. (Alexander R. ) Robblee y University of Alberta Dept of Animal. Use of Crystalline Riboflavin in Poultry Rations. Creative Media Partners, LLC, 2021.

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11

Schwechheimer, Susanne Katharina. Riboflavin Production with Ashbya Gossypii (Band 6). Cuvillier Verlag, 2018.

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12

Ottinger, Joan Marie. Influence of riboflavin doses on the urinary excretion of riboflavin and 4-pyridoxic acid in young men. 1985.

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13

El-Samaraie, Susanne. Wechselwirkungen von Cyclodextrinen und Cyclodextrinethern mit Riboflavin und Riboflavin-5-phosphat sowie mit deren Molekülfragmenten Lumichrom und Ribose. 1995.

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14

Yeh, Shih-ya. Riboflavin status of Orientals in a U.S. town. 1985.

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15

Murphy, Elaine, Yann Nadjar y Christine Vianey-Saban. Fatty Acid Oxidation, Electron Transfer and Riboflavin Metabolism Defects. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0008.

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The fatty acid oxidation disorders are a group of autosomally recessively inherited disorders of energy metabolism that may present with life-threatening hypoketotic hypoglycemia, encephalopathy and hepatic dysfunction, muscle symptoms, and/or cardiomyopathy. Milder phenotypes may present in adulthood, causing exercise intolerance, episodic rhabdomyolysis, and neuropathy. Specific investigations include acylcarnitine profiling, urine organic acid analysis, fibroblast or leucocyte studies of fatty acid oxidation flux/enzyme activity, and genetic testing. Management varies depending on the condition but includes avoidance of precipitants such as fasting, fever, and intense exercise, a high-carbohydrate, low-fat diet, and supplementation with carnitine or riboflavin. Inborn errors of riboflavin transport mainly present with Brown-Vialetto-Van Laere syndrome. Some patients respond dramatically to riboflavin supplementation; therefore it has to be tried in all suspected patients.
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16

Hertz, Joel John. Stability and Solubility Study of Riboflavin and Some Derivatives. Creative Media Partners, LLC, 2021.

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17

Brean, Suzanne E. Dietary riboflavin and the production of clubbed down in chick embryos. 1989.

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18

Stasch, Ann Rita 1927. Studies on the Respiration of Ashbya Gossypii: A Riboflavin Producing Organism. Creative Media Partners, LLC, 2021.

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19

Kozobolis, Vassilios. Corneal Collagen Cross-Linking Using Riboflavin and Ultraviolet-A Irradiation in Keratitis Treatment. INTECH Open Access Publisher, 2012.

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20

National Academies of Sciences, Engineering, and Medicine. Scanning for New Evidence on Riboflavin to Support a Dietary Reference Intake Review. National Academies Press, 2021.

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21

Board, Food and Nutrition, National Academies of Sciences, Engineering, and Medicine, Health and Medicine Division, Alice Vorosmarti y Committee on Scanning for New Evidence on Riboflavin to Support a Dietary Reference Intake Review. Scanning for New Evidence on Riboflavin to Support a Dietary Reference Intake Review. National Academies Press, 2021.

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22

Board, Food and Nutrition, National Academies of Sciences, Engineering, and Medicine, Health and Medicine Division, Alice Vorosmarti y Committee on Scanning for New Evidence on Riboflavin to Support a Dietary Reference Intake Review. Scanning for New Evidence on Riboflavin to Support a Dietary Reference Intake Review. National Academies Press, 2021.

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23

Zamboni, Nicola. Metabolic engineering of respiration for improved riboflavin production and elucidation of NADPH metabolism in Bacillus subtilis. 2003.

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24

Board, Food and Nutrition, Institute of Medicine, Subcommittee on Upper Reference Levels of Nutrients y Standing Committee on the Scientific Evaluation of Dietary Reference Intakes and its Panel on Folate, Other B Vitamins, and Choline. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline. National Academies Press, 2000.

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25

Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline. Washington, D.C.: National Academies Press, 1998. http://dx.doi.org/10.17226/6015.

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26

Board, Food and Nutrition, Institute of Medicine, Subcommittee on Upper Reference Levels of Nutrients y Committee on the Scientific Evaluation of Dietary Reference Intakes and its Panel on Folate Other B. Vitamins and Choline Standing. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline. National Academies Press, 2000.

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27

Board, Food and Nutrition, Institute of Medicine, Subcommittee on Upper Reference Levels of Nutrients y Standing Committee on the Scientific Evaluation of Dietary Reference Intakes and its Panel on Folate, Other B Vitamins, and Choline. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline. National Academies Press, 2000.

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28

Board, Food and Nutrition, Institute of Medicine y Other B Vitamins, and Choline and Subcommittee on Upper Reference Levels of Nutrients A Report of the Standing Committee on the Scientific Evaluation of Dietary Reference Intakes and its Panel on Folate. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline (Dietary Reference Series). National Academies Press, 2000.

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29

Medicine, Institute of. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline (Dietary Reference Series). National Academy Press, 2000.

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30

Lachmann, Robin H. y Nigel Manning. Trimethylaminuria. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0064.

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Trimethylaminuria (TMAU) or “Fish Odor Syndrome” is a disorder caused by increased concentrations of the volatile amine trimethylamine (TMA) in body fluids resulting in an unpleasant odor. The excess TMA may occur either due to deficient hepatic oxidation (primary) or increased bacterial generation (secondary). Testing urine for TMA concentration is the first line of investigation, preferably following a dietary load of a TMA precursor such as choline. Measurement of TMA and TMA-oxide are used as a guide to determine a primary or secondary cause, which can be confirmed by DNA analysis. FMO3 deficiency may have further clinical consequences due to the wide range of substrates oxidized by the enzyme including many drugs. Treatment of both primary and secondary TMAU relies on restriction of dietary precursors of TMA, antibiotic-based reduction of gut flora, and odor chelators. Riboflavin may also benefit some patients.
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31

B. Thesing*, S. Göppel, P. Weindl, C. Lambertz, K. Damme y G. Bellof. Efficiency of an organic farming compatible yeast product to ensure the Riboflavin-supply of organically raised B.U.T. 6 turkey poults – Effects on animal performance and health. Verlag Eugen Ulmer, 2021. http://dx.doi.org/10.1399/eps.2021.338.

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32

Silva, Aminda De, J. A. Saunders y M. A. Stroud. Vitamin deficiencies. Editado por Patrick Davey y David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0333.

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Vitamins are organic compounds required by the body in small amounts to perform specific cellular functions. Nine vitamins (thiamine (vitamin B1), riboflavin (vitamin B2), pyridoxine (vitamin B6), cyanocobalamin (vitamin B12), niacin (nicotinic acid; vitamin B3), pantothenic acid (vitamin B5), biotin (vitamin B7; vitamin H), folic acid (folate; vitamin B9), and ascorbic acid (vitamin C)) are water soluble, while four (vitamins A, D, E, and K) are fat soluble. The importance of vitamins was first appreciated through recognition of their clinical deficiency state. However, this approach has led to the concept that the primary purpose of a vitamin is to prevent the associated clinical deficiency state and, consequently, unless patients exhibit signs of a specific clinical deficiency state, they are thought to be replete in the corresponding vitamin. This is a misunderstanding. In reality, most vitamins have many different functions which are incompletely understood, and impaired biochemical function and even functional problems affecting metabolic, immunological, or cognitive status can occur with marginal vitamin depletion long before overt clinical deficiency becomes evident. A high index of suspicion is thus essential in all patients who have malnutrition or malabsorption, to ensure that levels that might compromise health, resistance to disease, and recovery from injury or illness are not left untreated.
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