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Libros sobre el tema "Carbohydrate receptors"

Autor: Grafiati
Publicado: 8 de febrero de 2025

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1

Gregory, Bock, Harnett Sara y Symposium on Carbohydrate Recognition in Cellular Function (1988 : Ciba Foundation), eds. Carbohydrate recognition in cellular function. Chichester [England]: Wiley, 1989.

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2

Bellissimo, Nicola. Fat and carbohydrate induced suppression of food intake via CCK(A) receptors in rats. Ottawa: National Library of Canada, 2003.

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3

C, Wong Simon Y. y Arsequell Gemma, eds. Immunobiology of carbohydrates. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2003.

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4

Quesenberry, Michael Stephen. Molecular analysis of calcium-dependent carbohydrate-recognition domains. 1991.

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5

Hartman, Adam L. Amino Acids in the Treatment of Neurological Disorders. Editado por 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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6

Droz, Anne Sophie. Synthesis of chiral macrocyclic receptors for Carbohydrates. 2000.

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7

Immunobiology of carbohydrates. Georgetown, TX: Eurekah.com/Landes Bioscience ; Kluwer Academic/Plenum, 2004.

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8

(Editor), Thomas Schrader y Andrew D. Hamilton (Editor), eds. Functional Synthetic Receptors. Wiley-VCH, 2005.

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9

Schrader, Thomas y Andrew D. Hamilton. Functional Synthetic Receptors. Wiley-VCH Verlag GmbH, 2005.

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10

Schrader, Thomas y Andrew D. Hamilton. Functional Synthetic Receptors. Wiley & Sons, Incorporated, John, 2006.

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11

(Editor), Simon Wong y Gemma Arsequell (Editor), eds. Immunobiology of Carbohydrates (Molecular Biology Intelligence Unit). Springer, 2003.

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12

Zorca, Suzana. The role of N-linked carbohydrates in von Willebrand factor receptor function. 2008.

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13

Nikravan, Sara y Frederick Mihm. Pathophysiology and management of functional endocrine tumours in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0264.

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Thyroid hormones act on most tissues via nuclear T3 receptors. Thyroid hormones stimulate oxygen consumption and heat production, influence cell growth and maturation (central nervous system, bone), and modulate metabolism (carbohydrates, lipids, proteins, drugs). Treatment for presumed thyroid disease frequently has to be initiated before the results of diagnostic tests are available. Treatment of hyperthyroidism should result in the reduction of serum thyroid hormone levels and their action on peripheral tissues with concurrent treatment of the precipitating event. In severe hypothyroidism the choice of thyroid hormone (thyroxine or tri-iodothyronine), optimal dosing, and the route of administration remain controversial
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14

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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15

Biochemical Roles Of Eukaryotic Cell Surface Macromolecules 2011 Iscsm Proceedings. Springer, 2012.

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16

Macdougall, Iain C. Erythropoiesis-stimulating agents in chronic kidney disease. Editado por David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0124.

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The advent of recombinant human erythropoietin (epoetin) in the late 1980s transformed the management of renal anaemia, liberating many dialysis patients from lifelong regular blood transfusions, in turn causing severe iron overload and human leucocyte antigen sensitization. Epoetin can be administered either intravenously or subcutaneously, but the half-life of the drug is fairly short at around 6–8 hours, necessitating frequent injections. To circumvent this problem, two manipulations to the erythropoietin molecule were engineered. The first of these was to attach an extra two carbohydrate chains to the therapeutic protein hormone (to make darbepoetin alfa), and the second was to attach a large pegylation chain to make continuous erythropoietin receptor activator. Both of these strategies prolonged the circulating half-life of the erythropoietin analogue. The next erythropoietic agent to be produced was peginesatide, a peptide-based agent which had no structural homology with native or recombinant erythropoietin, but shared the same biological and functional characteristics. Future strategies include stabilization of hypoxia-inducible factor, by orally active inhibitors of the prolyl hydroxylase enzyme, and advanced clinical trials are underway. In the meantime, several large randomized controlled trials have highlighted the potential harm in targeting a near normal haemoglobin of 13–14 g/dL (with an increased risk of cardiovascular complications), and sub-normal correction of anaemia is now advised. Some patients may show mild or severe resistance to erythropoiesis-stimulating agent (ESA) therapy, and common causes include iron insufficiency, infection, and underlying inflammation. Very rarely, patients may produce antibodies against their ESA, which neutralize not only the ESA, but also endogenous erythropoietin, causing pure red cell aplasia.
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