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Books on the topic 'Formic acid synthesis'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

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1

Fu, Ming-Chen. Studies on Green Synthetic Reactions Based on Formic Acid from Biomass. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-7623-2.

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2

Crichton, Michael. Three Complete Novels: The Andromeda Strain / The Terminal Man / The Great Train Robbery. New York: Wings Books, 1993.

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3

Crichton, Michael. Tian wai si jun. Hong Kong: Bo Yi, 1995.

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4

Crichton, Michael. The Andromeda Strain. New York, USA: Ballantine Books, 1999.

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5

Crichton, Michael. The Andromeda Strain. 4th ed. New York: Dell, 1987.

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6

Crichton, Michael. The Andromeda strain. Hampton, N.H: Eagle Large Print, 1994.

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7

Crichton, Michael. The Andromeda Strain. New York, USA: Ballantine Books, 1993.

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8

Crichton, Michael. The Andromeda strain. New York: Dell Pub. Co., 1987.

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9

Crichton, Michael. The Andromeda strain. London: Century, 1993.

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10

Crichton, Michael. La amenaza de Andromeda. México: Origen/Planeta, 1985.

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11

Crichton, Michael. The Andromeda strain. London: Arrow Bks., 1993.

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12

Crichton, Michael. The Andromeda strain. London: Pan, 1988.

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13

Crichton, Michael. Nejade Andromeda. [Tehran?]: [s.n.], 2000.

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14

Crichton, Michael. Tian wai si jun. Hong Kong: Bo Yi, 1995.

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15

Crichton, Michael. The Andromeda Strain. New York, USA: Avon Books, 2003.

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16

Crichton, Michael. The Andromeda Strain. New York: Ballantine Books, 1994.

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17

Crichton, Michael. The Andromeda Strain / The Terminal Man. New York: Harper, 2009.

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18

Crichton, Michael. Rising Sun / The Andromeda Strain / Binary. London: Cresset, 1994.

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19

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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20

Mochel, Fanny. Spastic Paraplegia Type 5. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0041.

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Spastic paraplegia type 5 (SPG5) is an autosomal recessive hereditary spastic paraplegia due to mutations in CYP7B1, which encodes oxysterol 7α‎-hydroxylase. Oxysterol 7α‎-hydroxylase is involved in the synthesis of bile acids from cholesterol. CYP7B1 mutations are responsible for rare forms of liver failure in infancy as well as lower motor neuron degeneration in adults with no obvious genotype-phenotype correlation. SPG5 is mostly characterized by spastic paraplegia with prominent posterior column sensory impairment that can lead to sensory ataxia and bladder dysfunction. SPG5 can easily be diagnosed thanks to the significant elevation of two plasma oxysterols: 27- and 25-hydroxycholesterol. Accordingly, plasma oxysterols are biomarkers that should be included in the screening of any spastic paraplegia of unknown etiology. Furthermore, the dramatic therapeutic response of a child with liver failure due to CYP7B1 mutations using chenodeoxycholic acid opens promising therapeutic perspectives for SPG5 patients, possibly as in cerebrotendinous xanthomatosis.

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21

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Vitamin B9 (folate) in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0012.

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Folate is a coenzyme in multiple biochemical pathways involving one-carbon metabolism, including amino acid metabolism, DNA and RNA synthesis, homocysteine metabolism, and methylation of DNA. The most overt consequence of folate deficiency is megaloblastic anaemia caused by the inhibition of DNA synthesis in red blood cell production. Folate deficiency may also influence the ability to maintain DNA methylation patterns in replicating cells, resulting in lasting phenotypic changes. Embryogenesis and fetal growth require higher levels of folate, which must be supplied maternally during pregnancy. A link between low maternal folate levels and the occurrence of neural tube defects has long been recognized. Other effects in pregnancy include increased risks of pre-eclampsia and placental vascular disorders. The general recommendation is for supplementation prior to conception and throughout pregnancy with 400 #amp;#x03BC;g of folic acid in tablet form, in addition to dietary sources, which can reduce the risk of neural tube defects.

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22

de Koning, Tom J. Serine Deficiency. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0023.

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Serine deficiency is a rare cause of intractable seizures and severe psychomotor retardation in infants and young children. However, in recent years it has become clear that serine deficiency in adolescents and adults can give rise to milder forms of seizure disorders and mild mental retardation or to a phenotype with severe progressive polyneuropathy. Serine deficiency can be diagnosed on the basis of low values of serine in plasma and CSF using routine amino acid analysis. However, with the introduction of next generation sequencing in clinical diagnostics the majority of patients are diagnosed through molecular testing of the three genes of the synthesis pathway. L-serine therapy is highly effective in the treatment of seizures and improvement of wellbeing and daily activities. Early diagnosis and timely treatment are important to prevent irreversible damage to the central or peripheral nervous system.

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23

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Vitamin B3 (niacin) in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0009.

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Niacin (as nicotinamide) is a component of coenzyme systems that function in the reductive biosynthesis of fatty acids and steroids, including cholesterol, and are involved in cell signalling. Niacin deficiency is rare, as the daily requirement can usually be met by food sources, and also via synthesis from tryptophan, which is present in dietary proteins. The prevalence of niacin deficiency is higher in populations consuming mainly corn or sorghum as a dietary staple. Corn contains niacin, but only in a bound form that is nutritionally unavailable. The additional needs for niacin during pregnancy are mirrored by the increased energy intake needs, and dietary supplementation is only necessary in cases of overall poor nutritional intake.

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24

Lee, Gregory. Epitope/Peptide-Based Monoclonal Antibodies for Immunotherapy of Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0007.

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Two monoclonal antibodies, RP215 and GHR106, were selected, respectively, for the research and development of anti-cancer drugs targeting ovarian cancer and other types of human cancer. RP215 was shown to react with a carbohydrate-associated epitope located mainly in the variable regions of immunoglobulin heavy chains expressed on the surface of almost all cancer cells in humans. GHR106 was generated against a synthetic peptide corresponding to N1-29 amino acid residues in the extracellular domains of human GnRH receptor, which is surface-expressed by most cancer cells as well as the anterior pituitary. This monoclonal antibody was shown to serve as a bioequivalent analog to GnRH-derived decapeptides currently used clinically. The molecular mechanisms of action of these two antibody-based anti-cancer drug candidates were well elucidated following numerous biochemical, immunological, and molecular biological studies, mainly by using ovarian cancer as the model. Further preclinical studies with humanized forms of these two antibodies are essential.

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25

Sarphare, Geeta, Ryan Lee, and Elaine Tierney. Smith-Lemli-Opitz Syndrome and Role of Cholesterol in Autism. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199744312.003.0012.

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Cholesterol is manufactured throughout the body, but predominantly in the liver, and is essential for many metabolic processes. Cholesterol plays a critical role in forming membranes and myelin sheaths and is a precursor molecule for the synthesis of steroid hormones, neuroactive steroids, oxysterols, and vitamin D. It is also essential in the production of bile acids, which in turn helps the body absorb cholesterol and fat-soluble vitamins. Cholesterol is essential in embryonic and fetal development and is also critical in regulating lipid raft processes such as signaling and trafficking (Korade & Kenworthy, 2008). Cholesterol biosynthesis begins with the formation of squalene and ends with the reduction of 7-dehydrocholesterol (7DHC) into cholesterol by the enzyme 7DHC reductase, and then its spontaneous isomer, 8-dehydrocholesterol (8DHC). Smith-Lemli-Opitz syndrome (SLOS, Mendelian Inheritance in Man #270400) is an autosomal recessive disorder due to an inborn error of cholesterol biosynthesis (Elias et al., 1993; Irons, Elias, Salen, Tint, & Batta, 1993; Tint et al., 1994). Smith-Lemli-Opitz syndrome has an estimated incidence among individuals of European ancestry in Canada and the United States of 1 in 15,000 to 1 in 60,000 births (Bzdúch, Behulova, & Skodova, 2000; Lowry & Yong, 1980; Opitz, 1999; Ryan, Bartlett, Clayton, Eaton, Mills, Donnai, & Burn, 1998) and a carrier frequency of 1 in 30 to 1 in 50 (Nowaczyk & Waye, 2001).

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26

Crichton, Michael. The Andromeda Strain. 9th ed. New York: Vintage Books, 2017.

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27

The Andromeda Strain. Tandem Library, 1999.

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28

Crichton, Michael. The Andromeda Strain. 2008.

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29

Crichton, Michael. The Andromeda Strain. Ballantine Books, 1997.

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30

The Andromeda Strain. Ballantine Books, 1993.

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31

The Andromeda Strain. Turtleback, 1993.

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32

Crichton, Michael. Anenaza de Andromeda, La. Ediciones B, 1996.

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33

Crichton, Michael. The Andromeda strain. Firecrest, 1989.

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34

Crichton, Michael. The Andromeda Strain. Ulverscroft Large Print, 1997.

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35

Crichton, Michael. The Andromeda Strain. RH Audio Price-less, 2004.

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36

Crichton, Michael. La Amenaza de Andromeda. B Ediciones S.A., 2002.

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37

Crichton, Michael. La Variete Andromede. Pocket, 2001.

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38

The Andromeda Strain. Brilliance Audio, 2015.

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39

Crichton, Michael. The Andromeda Strain/The Terminal Man. Avon A, 2007.

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40

Crichton, Michael. O Enigma de Andromeda (Em Portugues do Brasil). ALEPH, 2018.

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41

Crichton, Michael. Andromeda - SF-Roman. n/a, 1994.

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42

Crichton, Michael. The Andromeda Strain. Avon, 2003.

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43

Andromeda. Milano: Garzanti, 2005.

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44

Crichton, Michael. The Andromeda Strain. Harper, 2008.

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