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Książki na temat „Pyruvate”

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Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 14 marca 2023

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1

B, Keech D., i Wallace J. C, red. Pyruvate carboxylase. Boca Raton, Fla: CRC Press, 1985.

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2

Yazdanpanah, Mehrdad. Pyruvate improves myocardial functional recovery after ischemia and reperfusion. Ottawa: National Library of Canada, 1998.

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3

Dykshoorn, Philip. Identification of an upstream activating sequence of the yeast pyruvate kinase gene (PYK). Ottawa: National Library of Canada, 1990.

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4

Lesicki, Andrzej. Fosfofruktokinaza i kinaza pirogronianowa w tkankach skorupiaków i owadów. Wyd. 3. Poznań: Wydawn. Nauk. Uniwersytetu im. Adama Mickiewicza, 1993.

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5

Staples, Elizabeth M. The effects of R(+)-lipoic acid supplementation on regulation of human skeletal muscle pyruvate dehydrogenase. St. Catharines, Ont: Brock University, Faculty of Applied Health Science, 2006.

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6

MacPherson, Laura Lynn. Adaptations of skeletal muscle pyruvate dehydrogenase kinase in response to food-restriction in mitochondrial subpopulations. St. Catharines, Ont: Brock University, Faculty of Applied Health Sciences, 2007.

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7

International Meeting on the Function of Thiamin Diphosphate Enzymes (1990 Blaubeuren, Germany). Biochemistry and physiology of thiamin diphosphate enzymes: Proceedings of the International Meeting on the Function of Thiamin Diphosphate Enzymes, held in Blaubeuren, October 1990. Weinheim: VCH, 1991.

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8

Parker, James N., i Philip M. Parker. Pyruvate carboxylase 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

Pyruvate: The natural dietary supplement that increases exercise endurance, promotes fat loss, and regulates blood sugar metabolism. New Canaan, Conn: Keats Pub., 1997.

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10

Bornemann, Stephen. Studies on pyruvate decarboxylase-catalysed acyloin formation and the effects of surfactants on lipase-catalysedhydrolysis of esters. [s.l.]: typescript, 1992.

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11

Bigrigg, Jonathan Kent. Carbohydrate refeeding rapidly reverses the adaptive upregulation of human skeletal muscle pyruvate dehydrogenase kinase following a high fat diet. St. Catharines, Ont: Brock University, Dept. of Physical Education and Kinesiology, 2004.

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12

Shahi, B. Chopra. Studies on the uptake and utilization of pyruvate and glucose by isolated segmental ganglia of the leech Haemopis Sanguisuga. Salford: University of Salford, 1987.

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13

Keogh, Adrian Colin. Anti-mitochondrial antigen on human biliary epithelial cells [: A study of membrane expression of dihydrolipoamide acetyltransferase sub unit of pyruvate dehydrogenase on human biliary epithelial cells]. Birmingham: University of Birmingham, 2001.

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14

Bjorkman, Camilla. Methodological and biochemical aspects of acetylcholinesterase and acetate in blood from cattle , and acetyl-CoA synthesizing enzymes in spinal cord from ruminants and monogastric animals. Uppsala: Sveriges Lantbruksuniversitet, 1989.

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15

Burke, Edmund R. Pyruvate. McGraw-Hill, 1998.

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16

Keech. Pyruvate Carboxylase. Redaktorzy D. B. Keech i J. C. Wallace. CRC Press, 2018. http://dx.doi.org/10.1201/9781351076142.

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17

Pyruvate Carboxylase. Taylor & Francis Group, 2017.

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18

Keech. Pyruvate Carboxylase. Taylor & Francis Group, 2018.

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19

Keech. Pyruvate Carboxylase. Taylor & Francis Group, 2018.

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20

Keech. Pyruvate Carboxylase. Taylor & Francis Group, 2018.

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21

Keech. Pyruvate Carboxylase. Taylor & Francis Group, 2018.

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22

The Power of Pyruvate. Keats Publishing, 1999.

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23

Janssen, Mirian C. H., i Shamima Rahman. Pyruvate Dehydrogenase Complex Deficiency. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0006.

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Pyruvate dehydrogenase complex (PDHc) deficiency usually first manifests at a young age and is rarely diagnosed in adulthood. The clinical picture varies from neonatal death with overwhelming lactic acidosis to a relatively benign course early in life. The three main presentations are congenital lactic acidosis, Leigh syndrome, and episodic ataxia. Treatment consists of a ketogenic diet and cofactor supplementation with thiamine. Successful therapy is rare.

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24

Grace, Rachael. Fast Facts: Pyruvate Kinase Deficiency. Health Press Limited, 2018.

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25

Glader, B., W. Barcellini i R. Grace. Fast Facts: Pyruvate Kinase Deficiency. Karger AG, S., 2018.

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26

Molly Theresa L.V Smith. Studies in the purification of phosphoenol-pyruvate. 1985.

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27

Seyda, Agnieszka. Pyruvate dehydrogenase complex-correlation between structure and function. 2001.

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28

The Pyruvate Phenomenon: The Facts, the Benefits, the Unanswered Questions. Woodland Publishing, 1999.

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29

Roy, Shukla. Regulation of hepatic pyruvate carboxylase in 2,3,7,8-Tetrachlorodibenzo-p-dioxin treated C57BL/6J mice and their pair-fed controls. 1998.

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30

Gish, Gerald Daniel. A mechanistic investigation of the thiamin diphosphate-dependent enzyme pyruvate decarboxylase. 1986.

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31

Sparrow, Barney R. Characterization of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced modification of hepatic pyruvate carboxylase gene expression in C57BL/6J male mice. 1997.

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32

Sparrow, Barney R. Characterization of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced modification of hepatic pyruvate carboxylase gene expression in C57BL/6J male mice. 1997.

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33

Prokop, David. Pyruvate: The Super Strength, Stamina and Weight-Loss Supplement (Woodland Health Series). Woodland Publishing, 1997.

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34

Glader, B., W. Barcellini i R. Grace. Fast Facts : déficit en Pyruvate Kinase: Sensibilisation à Cette Maladie Génétique Rare. Karger AG, S., 2019.

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35

Carbone, Mary Anna. Human pyruvate carboxylase deficiency: Correlation of genotypes with the clinical and biochemical phenotypes. 2002.

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36

Chun, Kathy M. Characterization of mutations in the E1[alpha] subunit of the pyruvate dehydrogenase complex. 1995.

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37

Schellenberger, Alfred. Thiamin Pyrophosphate Biochemistry, Vol. II: The Pyruvate Dehydrogenase Complex and Prospects for the Future. Crc Pr I Llc, 1988.

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38

Bevacqua, Robert Francis. Mineral nutrition, pyruvate kinase activity, and protein concentration in 'd'Anjou' pear fruit affected by cork spot. 1989.

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39

Veech, Richard L., i M. Todd King. Alzheimer’s Disease. Redaktor Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0026.

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Deficits in cerebral glucose utilization in Alzheimer’s disease (AD) arise decades before cognitive impairment and accumulation of amyloid plaques and neurofibrillary tangles in brain. Addressing this metabolic deficit has greater potential in treating AD than targeting later disease processes – an approach that has failed consistently in the clinic. Cerebral glucose utilization requires numerous enzymes, many of which have been shown to decline in AD. Perhaps the most important is pyruvate dehydrogenase (PDH), which links glycolysis with the Krebs cycle and aerobic metabolism, and whose activity is greatly suppressed in AD. The unique metabolism of ketone bodies allows them to bypass the block at pyruvate dehydrogenase and restore brain metabolism. Recent studies in mouse genetic models of AD and in a human Alzheimer’s patient showed the potential of ketones in maintaining brain energetics and function. Oral ketone bodies might be a promising avenue for treatment of Alzheimer’s disease.

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40

Grace, Rachael. Fast Facts : Pyruvate Kinase Deficiency for Patients and Supporters: A Rare Genetic Disease That Affects Red Blood Cells. Karger AG, S., 2019.

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41

Christofk, Heather Renee. The M2 splice isoform of pyruvate kinase is a phosphotyrosine binding protein critical for tumor cell metabolism and proliferation. 2007.

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42

S, Patel Mulchand, Roche Thomas E i Harris Robert A. 1939-, red. Alpha-keto acid dehydrogenase complexes. Boston: Birkhäuser Verlag, 1996.

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43

Sherwood, Dennis, i Paul Dalby. The bioenergetics of living cells. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198782957.003.0024.

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Living systems create order, and appear to break the Second Law. This chapter explains, and resolves, this apparent paradox, drawing on the concept of coupled reactions (as introduced in Chapters 13 and 16), as mediated by ‘energy currencies’ such as ATP and NADH. The chapter then examines the key energy-capturing systems in biological systems – glycolysis and the citric acid cycle, and also photosynthesis. Topics covered include how energy is captured in the conversion of glucose to pyruvate, the mitochondrial membrane, respiration, electron transport, ATP synthase, chloroplasts and thylakoids, photosystems I and II, and the light-independent reactions of photosynthesis.

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44

Grace, Rachael. Fast Facts : le déficit en Pyruvate Kinase Pour les Patients et les Accompagnants: Une Maladie Génétique Rare Qui Affecte les Globules Rouges. Karger AG, S., 2019.

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45

Hsieh, David T., i Elizabeth A. Thiele. Ketogenic Diet for Other Epilepsies. Redaktor Eric H. Kossoff. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0007.

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The ketogenic diet is the treatment of choice for epilepsy in certain disorders of brain metabolism, in particular glucose transporter protein 1 deficiency and pyruvate dehydrogenase deficiency. The International Ketogenic Diet Study Group has listed several other conditions for which the ketogenic diet has been reported as being particularly beneficial and could be offered earlier. Whether efficacy in these conditions is due in part to the broad-spectrum efficacy of the ketogenic diet or to specific mechanisms specific to these conditions is still under investigation. This chapter discusses the use of dietary therapies for the treatment of epilepsy in certain genetic disorders, including Rett syndrome and tuberous sclerosis complex, as listed by the International Ketogenic Diet Study Group, and additionally discusses the use of epilepsy dietary therapies in patients with Angelman syndrome and Sturge-Weber syndrome.

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46

Provan, Drew, Trevor Baglin, Inderjeet Dokal i Johannes de Vos. Red cell disorders. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0002.

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The peripheral blood film in anaemias - Anaemia in renal disease - Anaemia in endocrine disease - Anaemia in joint disease - Anaemia in gastrointestinal disease - Anaemia in liver disease - Iron (Fe) deficiency anaemia - Vitamin B12 deficiency - Folate deficiency - Other causes of megaloblastic anaemia - Anaemia in other deficiency states - Haemolytic syndromes - Genetic control of haemoglobin production - Sickling disorders - HbS—sickle-modifying therapies - Sickle cell trait (HbAS) - Other sickling disorders - Other haemoglobinopathies - Unstable haemoglobins - Thalassaemias - α thalassaemia - β thalassaemia - Other thalassaemias - Hereditary persistence of fetal haemoglobin - Hb patterns in haemoglobin disorders - Non-immune haemolysis - Hereditary spherocytosis - Hereditary elliptocytosis - Glucose-6-phosphate dehydrogenase (G6PD) deficiency - Pyruvate kinase deficiency - Other red cell enzymopathies - Drug-induced haemolytic anaemia - Methaemoglobinaemia - Microangiopathic haemolytic anaemia - Acanthocytosis - Autoimmune haemolytic anaemia - Cold haemagglutinin disease - Leucoerythroblastic anaemia - Aplastic anaemia - Paroxysmal nocturnal haemoglobinuria - Pure red cell aplasia - Iron (Fe) overload - Transfusion haemosiderosis

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47

Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, Banu Kaya i Angela Theodoulou. Red cell disorders. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0002_update_001.

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The peripheral blood film in anaemias - Anaemia in renal disease - Anaemia in endocrine disease - Anaemia in joint disease - Anaemia in gastrointestinal disease - Anaemia in liver disease - Iron (Fe) deficiency anaemia - Vitamin B12 deficiency - Folate deficiency - Other causes of megaloblastic anaemia - Anaemia in other deficiency states - Haemolytic syndromes - Genetic control of haemoglobin production - Sickling disorders - HbS—sickle-modifying therapies - Sickle cell trait (HbAS) - Other sickling disorders - Other haemoglobinopathies - Unstable haemoglobins - Thalassaemias - α‎ thalassaemia - β‎ thalassaemia - Other thalassaemias - Hereditary persistence of fetal haemoglobin - Hb patterns in haemoglobin disorders - Non-immune haemolysis - Hereditary spherocytosis - Hereditary elliptocytosis - Glucose-6-phosphate dehydrogenase (G6PD) deficiency - Pyruvate kinase deficiency - Other red cell enzymopathies - Drug-induced haemolytic anaemia - Methaemoglobinaemia - Microangiopathic haemolytic anaemia - Acanthocytosis - Autoimmune haemolytic anaemia - Cold haemagglutinin disease - Leucoerythroblastic anaemia - Aplastic anaemia - Paroxysmal nocturnal haemoglobinuria - Pure red cell aplasia - Iron (Fe) overload - Transfusion haemosiderosis

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48

Buchaklian, Adam H., i David P. Dimmock. Citrin Deficiency. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0018.

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Citrin deficiency is an inborn error of metabolism that appears to affect both the urea cycle and energy generation. Worldwide, citrin deficiency is likely one of the commonest inborn errors of metabolism, 60,000–80,000 individuals are estimated to have citrin deficiency in China alone. Children typically present with an abnormal newborn screen or neonatal intrahepatic cholestasis with citrin deficiency (NICCD). Adults typically present clinically with neuropsychiatric symptoms, hepatic dysfunction and hyperammonemia. As plasma amino acids typically show an elevated citrulline at the time of crisis, this presentation is known as citrullinemia type II (CTLN2). Without therapy, cases may progress to liver failure. Individuals may also suffer recurrent pancreatitis. In contrast to other urea cycle defects, the treatment for citrin deficiency requires a high protein, low carbohydrate diet. Acute hyperammonemia responds to arginine therapy. Sodium pyruvate has been reported to provide benefit. In addition many cases will require restriction of galactose. Liver transplant fully corrects the CTLN2 phenotype.

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