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Libri sul tema "Amino acids Metabolism Disorders"

Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 28 gennaio 2023

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1

Kollegger, Harald. Excitatory amino acids and brain damage. Wien: Facultas-Universitätsverlag, 1993.

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2

Pisters, Peter W. T., 1960- e Brennan Murray F, a cura di. Protein and amino acid metabolism in cancer cachexia. New York: Chapman & Hall, 1996.

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3

1918-, Bickel Horst, e Wachtel U, a cura di. Inherited diseases of amino acid metabolism: Recent progress in the understanding, recognition, and management : international symposium in Heidelberg 1984. Stuttgart ; New York: Thieme, 1985.

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4

M, Ostrovskiĭ I͡U. Aminokisloty v patogeneze, diagnostike i lechenii alkogolizma. Minsk: Navuka i tėkhnika, 1995.

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5

Jones, Patricia M. Quick guide to organic acid interpretation. Washington D.C: AACC Press, 2011.

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6

Toshihiko, Andō, a cura di. Aminosan to seikatsu shūkanbyō: Saishin aminoguramu de saguru "inochi" no kagaku = Amino acids. Tōkyō: Joshi Eiyō Daigaku Shuppanbu, 2010.

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7

Parker, James N., e Philip M. Parker. Maple syrup urine disease: A bibliography and dictionary for physicians, patients, and genome researchers [to Internet references]. San Diego, CA: ICON Health Publications, 2007.

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8

Parker, James N., e Philip M. Parker. Beta-ketothiolase deficiency: A bibliography and dictionary for physicians, patients, and genome researchers [to Internet references]. San Diego, CA: ICON Health Publications, 2007.

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9

Parker, James N., e Philip M. Parker. 3-hydroxy-3-methylglutaryl-coenzyme A lyase deficiency: A bibliography and dictionary for physicians, patients, and genome researchers [to internet references]. San Diego, CA: ICON Health Publications, 2007.

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10

Bender, David A. Amino acid metabolism. 3a ed. Chichester, West Sussex: John Wiley & Sons, 2012.

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11

Amino acid metabolism. 2a ed. Chichester: Wiley, 1985.

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12

A, Cynober Luc, a cura di. Amino acid metabolism and therapy in health and nutritional disease. Boca Raton: CRC Press, 1995.

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13

M, Wallsgrove R., e Rothamsted Experimental Station, a cura di. Amino acids and their derivatives in higher plants. Cambridge [England]: Cambridge University Press, 1995.

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14

D'Mello, J. P. F., a cura di. The handbook of microbial metabolism of amino acids. Wallingford: CABI, 2017. http://dx.doi.org/10.1079/9781780647234.0000.

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15

Masella, Roberta. Glutathione and sulfur amino acids in human health and disease. Hoboken: Wiley, 2009.

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16

Workshop on the Biosynthesis of Branched Chain Amino Acids (1988 Beer-sheva, Israel). Biosynthesis of branched chain amino acids. Weinheim: VCH, 1990.

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17

Rhodes, Jeremy David. The metabolism of sucrose and amino acids by aphids. Norwich: University of East Anglia, 1992.

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18

1940-, Barak Z., Chipman D. M e Schloss J. V, a cura di. Biosynthesis of branched chain amino acids: Proceedings of the Workshop on the Biosynthesis of Branched Chain Amino Acids, Beer-sheva, Israel, November 1988. [S.l.]: Balaban Publishers, 1990.

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19

Seymour, Kaufman, G.D. Searle & Co., University of California, Los Angeles. e UCLA Symposium "Amino Acids in Health and Disease: New Perspectives" (1986 : Keystone, Colo.), a cura di. Amino acids in health and disease: New perspectives : proceedings of a Searle-UCLA symposium held at Keystone, Colorado, May 30-June 4, 1986. New York: Liss, 1987.

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20

Purich, Daniel L. Advances in Enzymology and Related Areas of Molecular Biology, 72: Amino Acid Metabolism. 7a ed. Hoboken: John Wiley & Sons, 1998.

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21

Clinical psycho-oncology: An international perspective. Chichester, West Sussex: John Wiley & Sons, 2012.

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22

Prunty, Helen, Jamie L. Fraser, Charles P. Venditti e Robin H. Lachmann. Branched Chain Amino Acids. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0016.

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Abstract (sommario):
This chapter describes the four most common disorders affecting the degradation of branched chain amino acids: maple syrup urine disease, methylmalonic acidemia, propionic acidemia and isovaleric acidemia. These conditions most commonly present with encephalopathy in the newborn period, although cases with later onset have also been described. Although adult patients are less prone to acute metabolic decompensations, they do develop a number of long-term complications, both neurological and visceral. Management shares features with other disorders of protein metabolism and centers on a low-protein diet and the use of disease-specific amino acid supplements.
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23

Rovenský, Jozef, Tibor Urbánek, Boldišová Oľga e James A. Gallagher. Alkaptonuria and Ochronosis. Springer, 2015.

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24

Rovenský, Jozef, Tibor Urbánek, Boldišová Oľga e James A. Gallagher. Alkaptonuria and Ochronosis. Springer, 2016.

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25

Oľga, Boldisová, Jozef Rovenský, Tibor Urbánek e James A. Gallagher. Alkaptonuria and Ochronosis. Springer, 2015.

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26

Pisters, Peter W. T., e Murray F. Brennan. Protein and Amino Acid Metabolism in Cancer Cachexia. Springer London, Limited, 2013.

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27

Hartman, Adam L. Amino Acids in the Treatment of Neurological Disorders. A cura di Dominic P. D’Agostino. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0035.

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Abstract (sommario):
Studies of metabolism- and diet-based therapies in epilepsy and neuroprotection have focused primarily on the quality and quantity of fat supplementation or carbohydrate restriction. However, protein is another key dietary component that has not been as thoroughly studied. A number of amino acids have been shown to stop, terminate, or prevent seizures. In addition, some have been shown to exert neuroprotective effects in other neurological disorders. Amino acids (and their metabolites) may exert their effects by acting at membrane or cytoplasmic receptors, serving as substrates for membrane transporters and as modulators of signaling pathway activity. This chapter highlights examples of each of these mechanisms of action in select nervous system disorders.
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28

Carmel, Ralph, e Donald W. Jacobsen. Homocysteine in Health and Disease. University of Cambridge ESOL Examinations, 2011.

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29

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

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Abstract (sommario):
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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30

Lachmann, Robin, e Elaine Murphy. Aminoacidopathies, urea cycle disorders, and organic acidurias. A cura di Patrick Davey e David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0180.

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Abstract (sommario):
Aminoacidopathies are caused by deficiencies in enzymes involved in amino acid metabolism and are often characterized by the accumulation of a toxic amino acid. The two diseases most likely to be encountered in adult medicine are phenylketonuria, which is caused by a deficiency of phenylalanine hydroxylase, and maple syrup urine disease (MSUD), which is due to a branched-chain amino acid decarboxylase deficiency. High levels of phenylalanine progressively damage the developing brain, leading to severe learning difficulties. The high levels of leucine which accumulate in MSUD produce an acute encephalopathy which, if not treated, can rapidly become fatal.
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31

Rabier, Daniel. Amino Acids. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0083.

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Abstract (sommario):
Amino acids present in the different biological fluids belong to two groups: the protein group, with the 21 classical amino acids constituting the backbone of the protein, and the nonprotein group, appearing in different metabolic pathways as intermediate metabolites. It is important to know and to be able to recognize the latter, as they are the markers of many inherited metabolic diseases. Three kinds of pathways must be considered: the catabolic pathways, the synthesis pathways, and the transport pathways. A disorder on a catabolic pathway induces an increase of all metabolites upstream and so an increase of the starting amino acid in all fluids. Any disorder on the synthetic pathway of a particular amino acid will induce a decrease of this amino acid in all fluids. When a transporter is located on a plasma membrane, its deficiency will result in normal or low concentration in plasma concomitant to a high excretion in urine.
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32

Bender, David A. Amino Acid Metabolism. Wiley & Sons, Incorporated, John, 2012.

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33

Bender, David A. Amino Acid Metabolism. Wiley & Sons, Incorporated, John, 2012.

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34

Bender, David A. Amino Acid Metabolism. Wiley & Sons, Incorporated, John, 2012.

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35

Bender, David A. Amino Acid Metabolism. Wiley & Sons, Limited, John, 2012.

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36

Heales, Simon, Simon Pope, Viruna Neergheen e Manju Kurian. Abnormalities of CSF Neurotransmitters/Folates. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0082.

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Abstract (sommario):
The term Neurotansmitter disorder, in the area of metabolic disease, focuses particularly on inborn errors affecting monoamine (dopamine & serotonin), pyridoxal phosphate (B6) and folate metabolism. Whilst there has been considerable focus on these disorders with regards to the paediatric population, it is clear that an increasing number of adult patients are being identified. Adult neurologists need to be aware of the clinical presentation of such patients and the appropriate tests that need to be requested to ensure a correct diagnosis is achieved. CSF profiling, by a specialist laboratory, is often required. This has the ability to very often identify the nature of a primary defect with regards to implementation of appropriate treatment. For some of these disorders, treatment can be effective. This may be in the form of monoamine/vitamin replacement. However there are exceptions, e.g. aromatic amino acid decarboxylase and dopamine transporter deficiencies. There also needs also to be an awareness of the growing list of secondary factors that can cause impaired dopamine and serotonin metabolism.
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37

Ahmed, Ahmed I., Sarah Aldhaheri e Allison Bannick. Inherited Metabolic Diseases (IMDs) and Pregnancy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190667351.003.0030.

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Abstract (sommario):
Inherited metabolic diseases (IMDs) are rare genetic disorders: clinically heterogeneous, and they can present at any age. With the expanded newborn screening panels, many of the IMDs have been successfully screened. Early diagnosis and treatment of these conditions have led to improved neurological outcomes and overall survival of these individuals, and now many of them are reaching childbearing age. Despite treatment, the potential presence of preexisting organ involvement may not only impact their fertility potentials but also may impose a higher risk of adverse maternal and fetal outcomes. Pregnancy leads to an extra strain on maternal metabolism; this may result in the manifestation of symptoms of a previously unknown disease or a progression of a known disease. This chapter will address the possible complications of some inherited disorders of metabolism that are associated with maternal or fetal neurological manifestations such as disorders of energy metabolism (eg, mitochondrial disorders, adult onset urea cycle disorders, ornithine transcarbamylase (OTC) deficiency, amino acidopathies, phenylketonuria (PKU), and impaired fatty acid oxidation disorders). We will provide special emphasis on the available potential treatments and plan of care during pregnancy and postpartum periods.
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38

Amino Acids in Higher Plants. CABI, 2015.

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39

Khillare, Jayant. Amino Acids in Higher Plants. Scitus Academics LLC, 2015.

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40

Grassi, Luigi, e Michelle Riba. Clinical Psycho-Oncology: An International Perspective. Wiley & Sons, Incorporated, John, 2012.

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41

Grassi, Luigi, e Michelle Riba. Clinical Psycho-Oncology: An International Perspective. Wiley & Sons, Incorporated, John, 2012.

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42

Grassi, Luigi, e Michelle Riba. Clinical Psycho-Oncology: An International Perspective. Wiley & Sons, Incorporated, John, 2012.

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43

Nishikawa, Toru, Tohru Yoshimura e Hiroshi Homma. D-Amino Acids: Physiology, Metabolism, and Application. Springer, 2018.

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44

Handbook of Microbial Metabolism of Amino Acids. CABI, 2017.

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45

Nishikawa, Toru, Tohru Yoshimura e Hiroshi Homma. D-Amino Acids: Physiology, Metabolism, and Application. Springer London, Limited, 2016.

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46

Nishikawa, Toru, Tohru Yoshimura e Hiroshi Homma. D-Amino Acids: Physiology, Metabolism, and Application. Springer, 2016.

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47

Metabolism of Aromatic Amino Acids and Amines. Elsevier, 1987. http://dx.doi.org/10.1016/s0076-6879(00)x0055-9.

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48

Kaufman, Seymour, Nathan P. Colowick e Nathan P. Kaplan. Metabolism of Aromatic Amino Acids and Amines. Elsevier Science & Technology Books, 1987.

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49

Pardee, Joel D., e Suresh Tate. Metabolism of Protein: Fates of Amino Acids. Morgan & Claypool Life Science Publishers, 2011.

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50

Iversen, Leslie L. Amino Acid Neurotransmitters. Springer, 2013.

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