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Books on the topic 'Pyridosin'

Author: Grafiati

Published: 4 June 2021

Last updated: 4 February 2022

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1

Torshin, Ivan Y. Magnesium and pyridoxine: Fundamental studies and clinical practice. Hauppauge, NY: Nova Science Publishers, 2009.

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2

1941-, Leklem James E., and Reynolds Robert D. 1943-, eds. Clinical and physiological applications of vitamin B-6: Proceedings of the Third International Conference on Vitamin B-6, held in Goslar-Hahnenklee, Germany, August 24-28, 1987. New York: Liss, 1988.

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3

1943-, Reynolds Robert D., and Leklem James E. 1941-, eds. Vitamin B-6: Its role in health and disease : proceedings of a Conference on Vitamin B-6 Nutrition and Metabolism, held at the Banff Conference Centre, Banff, Alberta, Canada, October 8-10, 1984. New York: Liss, 1985.

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4

Gaby, Alan. B6, the natural healer. New Canaan, Conn: Keats Pub., 1987.

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5

1945-, Korpela Timo, Christen Philipp 1937-, and International Union of Biochemistry, eds. Biochemistry of vitamin B6: Proceedings of the 7th International Congress on Chemical and Biological Aspects of Vitamin B6 Catalysis, held in Turku, Finland, June 22-26, 1987. Basel: Birkhäuser, 1987.

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6

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Vitamin B6 (pyridoxine) in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0010.

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Vitamin B6 is required for the activity of a large number of enzymes with varied essential functions. Along with other B vitamins, it is involved in the metabolism of homocysteine to cysteine; if this reaction is disrupted, blood homocysteine levels rise, along with increased risks for cardiovascular disease, neuropsychiatric problems, and other adverse effects. Elevated homocysteine in pregnancy it is associated with anaemia, pre-eclampsia, preterm birth, and low birthweight. Vitamin B6 deficiency can also affect fetal brain development, as well as weight gain and linear growth in infancy. Although vitamin B6 is widely available in foods, mild to moderate deficiency is still common, even in developed countries. A #amp;#x2018;Mediterranean-style#amp;#x2019; diet is recommended to supply sufficient amounts of vitamin B6. In individuals with an adequate and balanced diet and healthy lifestyle, supplementation is generally unnecessary.

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7

1928-, Dakshinamurti Krishnamurti, New York Academy of Sciences., and International Multidisciplinary Conference on Vitamin B6 (1989 : Philadelphia, Pa.), eds. Vitamin B6. New York, N.Y: New York Academy of Sciences, 1990.

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8

Yoon, Soon Ah Kang. RELATIONSHIP OF PYRIDOXINE SUPPLEMENTATION TO THE NUTRITIONAL STATUS OF MOTHERS AND THEIR BREASTFED INFANTS. 1991.

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9

Sindihebura-Ruhumba, Pascaline. Effect of controlled vitamin B-6 intake and pyridoxine supplementation on B-6 status of smokers. 1999.

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10

Chemistry and Metabolism of 4' - Deoxypyridoxine. Taylor & Francis Group, 2017.

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11

David, Dolphin, Poulson Rozanne, and Avramović Olga, eds. Vitamin B6 pyridoxal phosphate: Chemical, biochemical, and medical aspects. New York: Wiley, 1986.

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12

Clinical and physiological applications of vitamin B-6: Proceedings of the Third International Conference on Vitamin B-6, held in Goslar-Hahnenklee, Germany, ... (Current topics in nutrition and diseases). Liss, 1988.

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13

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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14

Vitamin B-6: Its role in health and disease : Proceedings of a Conference on Vitamin B-6 Nutrition and Metabolism, held at the Banff Conference Centre, ... (Current topics in nutrition and disease). Liss, 1985.

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15

Bills, Nathan D. In vivo and in vitro determination of the bioavailability of vitamin B-6 from plant foods containing pyridoxine glucoside. 1990.

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16

Leung, Doris G. Neuropathies Associated with Infection or Toxic Exposure. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0113.

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Among the many causes of peripheral neuropathy are those mediated by environmental exposure to infectious and toxic agents. The most common neuropathy associated with HIV is HIV-associated distal sensory polyneuropathy (HIV-DSP). The clinical presentation of HIV-DSP is one of a distal, symmetric, often painful, small-fiber sensory axonal polyneuropathy. Other infectious causes of neuropathy include hepatitis C, leprosy, Lyme disease, rabies, and diphtheria, and antibiotic drugs such as isoniazid can also cause neuropathy. Heavy metals and a variety of other toxins including chemotherapeutic agents such as platinum, vincristine, and thalidomide disrupt peripheral nerve function. High doses of pyridoxine can cause damage to the dorsal root ganglia and foodbourne toxins such as saxitoxins found in shellfish.

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17

1938-, Marino G., Sannia G, Bossa Francesco, and International Meeting on Vitamin B₆ and Carbonyl Catalysis (1994 : Capri, Italy), eds. Biochemistry of vitamin B₆ and PQQ. Basel: Birkhäuser Verlag, 1994.

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18

Pearl, Phillip L., and William P. Welch. Pediatric Neurotransmitter Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0059.

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The pediatric neurotransmitter disorders represent an enlarging group of neurological syndromes characterized by inherited abnormalities of neurotransmitter synthesis, metabolism, and transport. Disorders involving monoamine synthesis include guanosine triphosphate cyclohydrolase deficiency (Segawa disease or classical Dopa-responsive dystonia as the heterozygous form), aromatic amino acid decarboxylase deficiency, tyrosine hydrolase deficiency, sepiapterin reductase deficiency, and disorders of tetrahydrobiopterin synthesis. These disorders can be classified according to whether they feature elevated serum levels of phenylalanine. Disorders of γ-amino butyric acid (GABA) metabolism include succinic semialdehyde dehydrogenase deficiency and GABA-transaminase deficiency. Glycine encephalopathy is typically manifested by refractory neonatal seizures due to a defect in the glycine degradative pathway. Pyridoxine-responsive seizures have now been associated with deficiency of α-aminoadipic semialdehyde dehydrogenase as well as a variants requiring therapy with pyridoxal-5-phosphate and folinic acid.

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19

Christen, P., and Korpela. Biochemistry of Vitamin B6: Porceedings of the 7th International Congress (Advances in Life Sciences). Birkhauser, 1987.

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20

Gaitanis, John, Phillip L. Pearl, and Howard Goodkin. The EEG in Degenerative Disorders of the Central Nervous System. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0013.

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Nervous system alterations can occur at any stage of prenatal or postnatal development. Any of these derangements, whether environmental or genetic, will affect electrical transmission, causing electroencephalogram (EEG) alteration and possibly epilepsy. Genetic insults may be multisystemic (for example, neurocutaneous syndromes) or affect only the brain. Gene mutations account for inborn errors of metabolism, channelopathies, brain malformations, and impaired synaptogenesis. Inborn errors of metabolism cause seizures and EEG abnormalities through a variety of mechanisms, including disrupted energy metabolism (mitochondrial disorders, glucose transporter defect), neuronal toxicity (amino and organic acidopathies), impaired neuronal function (lysosomal and peroxisomal disorders), alteration of neurotransmitter systems (nonketotic hyperglycinemia), and vitamin and co-factor dependency (pyridoxine-dependent seizures). Environmental causes of perinatal brain injury often result in motor or intellectual impairment (cerebral palsy). Multiple proposed etiologies exist for autism, many focusing on synaptic development. This chapter reviews the EEG findings associated with this myriad of pathologies occurring in childhood.

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21

Groothoff, Jaap W. Primary Hyperoxaluria. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0065.

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Primary hyperoxalurias (PH) are rare autosomal recessive metabolic disorders characterized by an increased endogenous oxalate production which leads to the development of urolithiasis, nephrocalcinosis, and ultimately to renal failure.PH patients with severe renal failure develop life-threatening systemic oxalosis, which affects many organs such as bone, skin, retina, myocardium, vessel walls, and the central nervous system. So far, combined or sequential liver-kidney transplantation is the only therapeutic option for patients with advanced disease. Contrary to the former impression of a relatively mild course of disease in patients diagnosed as adults, recent data have shown that patients diagnosed in adulthood mostly present with established ESRD and systemic oxalosis. The fact that some of these patients respond to pyridoxine therapy underlines the importance of early diagnosis and measures to prevent renal failure and systemic oxalosis. All children with stone disease or nephrocalcinosis and all adults with recurrent stone disease should therefore be screened for PH.

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22

Silva, Aminda De, J. A. Saunders, and M. A. Stroud. Vitamin deficiencies. Edited by Patrick Davey and 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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