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Books on the topic 'Amino acid- based systems'

Author: Grafiati
Published: 6 September 2023

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1

M, Lesk Arthur, and CODATA. Task Group on Coordination of Protein Sequence Data Banks., eds. Computational molecular biology: Sources and methods for sequence analysis. Oxford: Oxford University Press, 1988.

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2

L, Wang Jason T., Shapiro Bruce A, and Shasha Dennis Elliott, eds. Pattern discovery in biomolecular data: Tools, techniques, and applications. New York: Oxford University, 1999.

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3

B, Calne Donald, ed. Therapeutic manipulation of excitatory amino acid systems. New York: Advanstar Communications, 1994.

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4

H, Schlesinger David, ed. Macromolecular sequencing and synthesis: Selected methods and applications. New York: A.R. Liss, 1988.

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5

Entrez user's guide: Release 24.0. Bethesda, Md: National Library of Medicine, 1996.

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6

Harren, Jhoti, and Leach Andrew R, eds. Structure-based drug discovery. Dordrecht: Springer, 2007.

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7

1947-, Sillince Maria, ed. Molecular databases for protein sequences and structure studies: An introduction. Berlin: Springer-Verlag, 1991.

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8

Abelson, John N., Melvin I. Simon, and Russell F. Doolittle. Molecular Evolution: Computer Analysis of Protein and Nucleic Acid Sequences. Elsevier Science & Technology Books, 1990.

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9

(Editor), John N. Abelson, Melvin I. Simon (Editor), and Russell F. Doolittle (Editor), eds. Molecular Evolution: Computer Analysis of Protein and Nucleic Acid Sequences, Volume 183: Volume 183: Molecular Evolution (Methods in Enzymology). Academic Press, 1990.

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10

(Editor), John N. Abelson, Melvin I. Simon (Editor), and Russell F. Doolittle (Editor), eds. Molecular Evolution: Computer Analysis of Protein and Nucleic Acid Sequences, Volume 183: Volume 183: Molecular Evolution (Methods in Enzymology). Academic Press, 1990.

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11

Teichberg, Vivian I., and Lechoslaw Turski. Excitatory Amino Acids and Second Messenger Systems. Springer London, Limited, 2013.

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12

Teichberg, Vivian I., and Lechoslaw Turski. Excitatory Amino Acids and Second Messenger Systems. Springer, 2014.

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13

Excitatory amino acids and second messenger systems. Berlin: Springer-Verlag, 1992.

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14

1934-, Colwell Rita R., Swartz David G, MacDonell Michael Terrell, CODATA, and CODATA Workshop on Nucleic Acid and Protein Sequencing Data (1st : 1987 : National Bureau of Standards), eds. Biomolecular data: A resource in transition. Oxford: Oxford University Press, 1989.

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15

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

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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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16

(Editor), Rita R. Colwell, David G. Swartz (Editor), and Michael T. MacDonell (Editor), eds. Biomolecular Data: A Resource in Transition (Oxford science publications). Oxford University Press, USA, 1989.

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17

Skarja, Gary Alan. The development and characterization of degradable, segmented polyurethanes containing amino acid-based chain extenders. 2001.

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18

Columb, Malachy O. Local anaesthetic agents. Edited by Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0017.

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Local anaesthetic agents cause a pharmacologically induced reversible neuropathy characterized by axonal conduction blockade. They act by blocking the sodium ionophore and exhibit membrane stabilizing activity by inhibiting initiation and propagation of action potentials. They are weak bases consisting of three components: a lipophilic aromatic ring, a link, and a hydrophilic amine. The chemical link classifies them as esters or amides. Local anaesthetics diffuse through the axolemma as unionized free-base and block the ionophore in the quaternary ammonium ionized form. The speed of onset of block is therefore dependent on the pKa of the agent and the ambient tissue pH. Esters undergo hydrolysis by plasma esterases and amides are metabolized by hepatic microsomal mixed-function oxidases. Local anaesthetics are bound in the blood to α‎1-acid glycoproteins. Pharmacological potency is dependent on the lipid solubility of the drug as is the potential for systemic toxicity. The blood concentrations required to cause cardiovascular system (CVS) collapse and early central nervous system (CNS) toxicity are used to quantify the CVS:CNS toxicity ratio. Local anaesthetics also have the potential to induce direct neuronal damage. Intravenous lipid emulsion is used for the treatment of systemic toxicity but the scientific evidence is inconsistent. With regard to the pipecoloxylidine local anaesthetics, early evidence indicated that the S- was less toxic than the R-enantiomer. However, clinical research using minimum local analgesic concentration designs suggests that reduced systemic toxicity and motor block sparing is mainly explained by potency rather than enantiomerism.
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19

Acid, acid everywhere: Exploring chemical, ecological, and transportation systems : a problem-based learning unit designed for 4th-6th grade learners. 2nd ed. Dubuque, Iowa: Kendall/Hunt Pub. Co., 2007.

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20

Nozière, Pierre. INRA feeding system for ruminants. Edited by Daniel Sauvant and Luc Delaby. Wageningen Academic Publishers, 2018. http://dx.doi.org/10.3920/978-90-8686-872-8.

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The INRA Feeding System for Ruminants has been renewed to better address emerging challenges for animal nutrition: prevision of productive responses, product quality, animal health and emissions to the environment, in a larger extent of breeding contexts. The new system is mainly built from meta-analyses of large data bases, and modelling. The dietary supply model accounts for digestive interactions and flows of individual nutrients, so that feed values depend on the final ration. Animal requirements account for variability in metabolic efficiency. Various productive and non-productive animal responses to diets are quantified. This book presents the whole system for dairy and meat, large and small ruminant production, including specificities for tropical and Mediterranean areas. The first two sections present biological concepts and equations (with their field of application and statistical accuracy) used to predict intake (including at grazing) and nutrient supply (Section 1), animal’s requirements and multiple responses to diets (Section 2). They apply to net energy, metabolisable protein and amino acids, water, minerals and vitamins. Section 3 presents the use of concepts and equations in rationing with two purposes: (1) diet calculation for a given performance objective; and (2) prediction of the multiple responses of animal to diet changes. Section 4 displays the tables of feed values, and their prevision. All the equations and concepts are embedded in the fifth version of INRAtion® software for practical use.
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21

R, Leach· Andrew, and Harren Jhoti. Structure-based Drug Discovery. Springer, 2010.

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22

(Editor), John N. Abelson, Melvin I. Simon (Editor), and Russell F. Doolittle (Editor), eds. Computer Methods for Macromolecular Sequence Analysis (Methods in Enzymology). Academic Press, 1996.

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23

Abelson, John N., Melvin I. Simon, and Russell F. Doolittle. Computer Methods for Macromolecular Sequence Analysis. Elsevier Science & Technology Books, 1996.

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24

(Editor), Harren Jhoti, and Andrew R. Leach (Editor), eds. Structure-based Drug Discovery. Springer, 2007.

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25

Hanning, Rhona Mary. The effectiveness and metabolic consequences of the case of amino acid versus glucose based dialysis solutions in infants and children receiving continuous ambulatory peritoneal dialysis (CAPD). 1986.

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26

Data in Modern Biology (Codata Bulletin,). Elsevier Science Pub Co, 1985.

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27

S. Göppel*, P. Weindl, C. Lambertz, B. Thesing, S. Born, E. Schmidt, and G. Bellof. Effects of reduced energy and amino acid contents in complete feed mixtures on fattening and slaughter performance of slow or fast growing turkey genotypes in different organic housing systems. Verlag Eugen Ulmer, 2022. http://dx.doi.org/10.1399/eps.2022.362.

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28

Sillince, Maria, and John Sillince. Molecular Databases for Protein Sequences and Structure Studies: An Introduction. Springer, 1992.

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29

Molecular Databases for Protein Sequences and Structure Studies: An Introduction. Springer, 2011.

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30

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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31

Hodgkiss, Andrew. Introduction to biological and molecular psychiatry. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0002.

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An introduction to biological and molecular psychiatry is offered, intended for oncology and palliative medicine clinicians. A recent historical perspective is used, beginning with a summary of monoaminergic and cholinergic neurotransmission as understood in the 1980s. One endocrine theory of depression, based on HPA axis dysfunction, is described. Recognition of the limits of these models has led to a deeper molecular psychiatry ‘beyond the synapse’ and to an appreciation of the importance of amino acid neurotransmission. Selective expression of proteins, and their covalent and allosteric modification, is now seen as central to neuroplasticity. The NMDA receptor and excitotoxicity are introduced. The chapter closes with an overview of the amygdala and of hippocampal neurogenesis.
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32

Servais, Aude, and Bertrand Knebelmann. Cystinuria. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0024.

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Cystinuria (OMIM #220100) is an autosomal recessive disorder of a dibasic amino acid transport in the apical membrane of epithelial cells of the renal proximal tubule and small intestine. It leads to increased urinary cystine excretion and recurrent urolithiasis. The cystine transporter is an heterodimeric transporter which is composed of a heavy subunit, rBAT, linked to a light subunit, b0,+AT. Two genes, SLC3A1 (solute carrier family 3 member 1) and SLC7A9, coding for rBAT and b0,+AT, account for the genetic basis of cystinuria. Cystinuria may lead to obstruction, infections, and ultimately to renal insufficiency. The diagnosis of cystinuria mainly relies on stone analysis, urinary cystine measurement, or urinary cystine crystal identification. Medical treatment is based upon a stepwise strategy using hydration and alkalinization as basic measures, with the addition of thiol derivatives in refractory cases. Urological interventions are often indicated for the management of cystine stones >5 mm in diameter.
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33

Septic Shock: Methods and Protocols (Methods in Molecular Medicine). Humana Press, 2000.

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34

Litell, John M., and Nathan I. Shapiro. Pathophysiology of septic shock. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0297.

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The pathophysiology of sepsis is the result of a dysregulated host response to infection. Interactions between conserved pathogenic signals and host recognition systems initiate a systemic reaction to local infection. Pro- and anti-inflammatory intermediates and associated coagulatory abnormalities lead to altered macrovascular, microvascular, and mitochondrial function. Uncorrected, these processes yield similar patterns of failure in multiple organ systems. Mortality increases with successive organ failures. Although commonly thought to be a manifestation of impaired renal circulation, septic acute kidney injury may be due primarily to non-haemodynamic factors. Pulmonary parenchymal dysfunction in sepsis also contributes to failures in other organ systems. Sepsis involves complex alterations in myocardial function, vascular tone, and capillary integrity, which are mediated by elevated concentrations of inflammatory cytokines, inducible nitric oxide, and reactive oxygen species, among others. Gut hypomotility and translocation of enteric flora likely contribute to a persistent inflammatory response. This perpetuates the pathophysiological pattern of sepsis, and can lead to the delayed onset of these features in patients with other types of critical illness. The neurological manifestations of sepsis include acquired delirium, which is also probably due to circulatory and inflammatory abnormalities, as well as alterations in cerebral amino acid metabolism. Critical illness-related corticosteroid insufficiency and derangements in glucose metabolism are among the endocrine abnormalities commonly seen in septic patients. Restoration of homeostasis requires early haemodynamic resuscitation and aggressive infectious source control.
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