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Dissertations / Theses on the topic 'Kynurenine'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Milne, Gavin D. S. "Inhibition studies of kynurenine 3-monooxygenase." Thesis, University of St Andrews, 2013. http://hdl.handle.net/10023/4101.

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Kynurenine 3-monooxygenase (K3MO) lies on the kynurenine pathway, the major pathway for the catabolism of L-tryptophan. It converts kynurenine to 3-hydroxy kynurenine. Inhibition of K3MO is important in several neurological diseases and there is evidence that inhibition of K3MO could also be targeted for the prevention of multiple organ failure, secondary to acute pancreatitis. A structure activity relationship based upon the 1,2,4-oxadiazoles motif was carried out which revealed amide 207 as an inhibitor of P. fluorescens K3MO. Further structure activity relationships were developed based upo

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2

Thevandavakkam, Mathuravani Aaditiyaa. "Deciphering the kynurenine-3-monooxygenase interactome." Thesis, University of Leicester, 2011. http://hdl.handle.net/2381/10070.

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Kynurenine-3-monooxygenase (KMO) is a mitochondrial enzyme in the kynurenine pathway (KP) through which tryptophan is degraded to NAD+. The central KP is altered in neurodegenerative diseases and other CNS disorders. The causative role of KP metabolites has been particularly well studied in the neurodegenerative disorder Huntington’s disease (HD), a fatal adult onset condition inherited in an autosomal dominant manner. In HD, flux in the KP is perturbed such that neurotoxic metabolites (3-hydroxykynurenine and quinolinic acid) of the pathway are increased relative to a neuroprotective metaboli

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3

Bell, Helen Barbara. "Characterisation of the active site of kynurenine 3-monooxygenase." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/20397.

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Kynurenine 3-monooxygenase (KMO) is a flavoprotein which has been implicated in Huntington’s disease, Alzheimer’s disease and acute pancreatitis. Recently there has been important research published about this enzyme including the structure of a truncated Saccharomyces cerevisiae KMO enzyme and KMO inhibition studies in animal models of disease. In previous work from this research group the complete Pseudomonas fluorescens KMO enzyme has been successfully crystallised both with and without the substrate, L-kynurenine, from which significant insights were gained into function and the potential

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4

Wilkinson, Martin. "Structural dynamics and ligand binding in kynurenine-3-monooxygenase." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/7965.

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Kynurenine 3-monooxygenase is a FAD-dependent aromatic hydroxylase (FAH) which is a widely suggested therapeutic target for controlling the balance of bioactive metabolite levels produced by the mammalian kynurenine pathway (KP). Prior to starting this work no structural information was known for the enzyme, with studies of the human form complicated by the presence of a C-terminal transmembrane helix. The bacterial Pseudomonas fluorescens enzyme (PfKMO) lacks the transmembrane region and has been previously characterised by Crozier-Reabe and Moran [1, 2]. Therefore PfKMO, which shares 32 % se

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5

Owe-Young, Robert School of Medicine UNSW. "Kynurenine pathway metabolism at the blood-brain barrier." Awarded by:University of New South Wales. School of Medicine, 2006. http://handle.unsw.edu.au/1959.4/26183.

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A major product of HIV-infected and cytokine-stimulated monocytic-lineage cells is quinolinic acid (QUIN), a neurotoxic metabolite of the kynurenine pathway (KP) of L-tryptophan (L-Trp) metabolism. Despite the large number of neurotoxins found in HIV patients with AIDS Dementia Complex (ADC), only QUIN correlates with both the presence and severity of ADC. With treatment, cerebrospinal fluid (CSF) QUIN concentrations decrease proportionate to the degree of clinical and neuropsychological improvement. As endothelial cells (EC) of the blood-brain barrier (BBB) are the first brain-associated cell

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6

Taylor, Mark Robert Duncan. "High-resolution structural studies of kynurenine 3-monooxygenase." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/28913.

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The kynurenine pathway produces NAD+ from L-tryptophan. Metabolites known as the kynurenines are produced within the pathway. The effects of the kynurenines have been associated with a number of diseases including cancer, Alzheimer’s disease, Huntington’s disease, and acute pancreatitis. Kynurenine monooxygenase (KMO) is an enzyme that catalyses the conversion of L-kynurenine to 3-hydroxy-L-kynurenine, the downstream product of which is the neurotoxic quinolinic acid. L-kynurenine is positioned at a branching point within the pathway. Metabolism via KMO leads to quinolinic acid production wher

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7

Swaih, Aisha Mahmod O. "Functional and localization studies of human kynurenine 3-monooxygenase." Thesis, University of Leicester, 2016. http://hdl.handle.net/2381/37835.

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Kynurenine 3-monooxygensae (KMO) is an outer mitochondrial membrane protein which plays a critical regulatory role in the kynurenine pathway (KP), catalysing the production of 3-hydroxykynurenine (3-HK). Increased KMO activity likely contributes to the excitotoxicity seen in neurodegenerative disorders by elevating the levels of the neurotoxic KP metabolites 3-HK and quinolinic acid. Studies employing models of Huntington’s disease (HD) have shown that inhibition of KMO is neuroprotective, making KMO a potential therapeutic target for this disorder. This study interrogates the subcellular loca

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8

Kolodziej, Lukasz. "An investigation of the kynurenine pathway in experimental arthritis." Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/9641.

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The kynurenine pathway is a catabolic biochemical pathway responsible for degradation of tryptophan, an essential amino acid. As a consequence, biologically active molecules, kynurenines, are produced. These chemical entities can influence immune responses. Previously, it has been shown that pharmacological inhibition of the initial step on the pathway increases the severity of collagen-induced arthritis (CIA), an animal model of rheumatoid arthritis. In contrast, treatment with kynurenine, a major by product of tryptophan degradation, effectively ameliorated the disease. This project was base

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9

Skouras, Christos. "Kynurenine metabolism and organ dysfunction in human acute pancreatitis." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28898.

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BACKGROUND: Acute pancreatitis (AP) is a sterile initiator of systemic inflammation that can trigger multiple organ dysfunction syndrome (MODS). In the acute phase of AP, the kynurenine pathway of tryptophan metabolism plays an important role in the genesis of AP-MODS in experimental animal models, but it is unknown whether the pathway is activated in human AP. Human data are required to support the rationale for kynurenine 3- monooxygenase (KMO) inhibition as a treatment for AP-MODS and reinforce the translational potential. Additionally, as respiratory dysfunction is frequent in severe AP, t

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10

Urenjak, Jutta A., and Tihomir P. Obrenovitch. "Accumulation of quinolinic acid with euro-inflammation: does it mean excitotoxicity?" Thesis, Kluwer Academic, Plenum Publishers, New York, 2003. http://hdl.handle.net/10454/2833.

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11

Chen, Yiquan Medical Sciences Faculty of Medicine UNSW. "The involvement of the Kynurenine pathway in amyotrophic lateral sclerosis." Publisher:University of New South Wales. Medical Sciences, 2009. http://handle.unsw.edu.au/1959.4/43774.

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Amyotrophic lateral sclerosis (ALS) is a progressive and fatal motor neuron disease of unclear aetiology, although the general consensus is of a multifactorial disease. The kynurenine pathway (KP), activated during neuroinflammation, is emerging as a possible contributory factor in ALS. The KP is the major route for tryptophan (TRP) catabolism. The intermediates generated can be either neurotoxic, such as quinolinic acid (QUIN), or neuroprotective, such as picolinic acid (PIC), an important endogenous metal chelator. The first and inducible enzyme is indoleamine 2,3-dioxygenase (IDO). As the e

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12

Miranda, Allan F. "Modulation of quinolinic acid-induced excitotoxicity by endogenous kynurenine pathway intermediates." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/nq22484.pdf.

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13

Parker, Nicole Renee. "The role of kynurenine and UV light in lens protein modification." Access electronically, 2005. http://www.library.uow.edu.au/adt-NWU/public/adt-NWU20060720.111305/index.html.

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Thesis (Ph.D.)--University of Wollongong, 2005.<br>Typescript. EMBARGOED - This thesis is subject to a 12 month embargo (07/03/06 to 07/03/07) and may only be viewed and copied with the permission of the author. For further information please Contact the Archivist. Includes bibliographical references: leaf 236-266.

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14

Khalil, Omari S. "Effects on brain development of prenatal inhibition of Kynurenine-3-Monooxygenase." Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/5075/.

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Much is known about the disease pathology related to schizophrenia, however, little is known with regards to its aetiology. Recent evidences suggest a neurodevelopmental hypothesis for schizophrenia where environmental factors including: infection, stress and malnutrition, can adversely affect the pregnant mother thereby elevating the risk for schizophrenia developing in the offspring during adulthood (Meyer et al., 2008d; Meyer and Feldon, 2009; 2012; Forrest et al., 2012; Meyer, 2013). Since a variety of viral and bacterial infections in animal models have demonstrated to increase the risk i

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15

Kubo, Hisako. "Absence of kynurenine 3-monooxygenase reduces mortality of acute viral myocarditis in mice." 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225521.

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16

Bipath, Priyesh. "Tryptophan and the kynurenine pathway in chronic renal failure patients on dialysis." Diss., Pretoria : [s.n.], 2008. http://upetd.up.ac.za/thesis/available/etd-10212008-135418.

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17

Pershing, Michelle. "Acute elevations in kynurenic acid result in cognitive inflexibility in an attentinal set-shfiting task via an alpha 7-mediated mechanism." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1354032404.

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18

Pisar, Mazura Md. "The role of kynurenine metabolism in the development of the central nervous system." Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/5550/.

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Prenatal exposure to maternal infection has been thought as a major risk factor for neurodevelopmental brain damage and thus contributes to the pathophysiology of neurodegenerative diseases including schizophrenia and autism. The mechanisms of aberrant neurodevelopmental processes on the offspring, in which primary cerebral insults occur during early brain development, are not fully understood. In the present investigation, maternal infection was modelled in timed-pregnant rats at embryonic day (E) 14, 16 and 18 by administering intraperitoneal injections of polyriboinosinic-polyribocytidilic

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19

Kariyawasam, Sandhya Himani. "An investigation into the biochemical changes in Tourette syndrome and associated conditions with a potential for pharmacological manipulation." Thesis, Aston University, 1999. http://publications.aston.ac.uk/10977/.

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Kynurenine (KYN) is the first stable metabolite of the kynurenine pathway, which accounts for over 95% of tryptophan metabolism. Two previous studies by this research group reported elevated plasma KYN in Tourette syndrome (TS) patients when compared with age and sex matched controls and another study showed that KYN potentiated 5-HT2A-mediated head-shakes (HS) in rodents. These movements have been suggested to model tics in TS. This raised the questions how KYN acts in eliciting this response and whether it is an action of its own or of a further metabolite along the kynurenine pathway. In th

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20

Cobb, Christina. "A Link Between Gut Microbes & Depression: Microbial Activation of the Human Kynurenine Pathway." Scholarship @ Claremont, 2018. http://scholarship.claremont.edu/cmc_theses/1799.

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Our gut microbiota is involved in human development, nutrition, and the pathogenesis of gut disorders, but has more recently been implicated as a possible mechanism in the pathophysiology of several brain disorders, including disorders of mood and affect, such as depression. Researchers have referred to this dynamic, bidirectional signaling pathway between the gut and the brain as the “gut-brain axis.” However, most research on this axis has been limited to rodent studies, and there has been little insight into the mechanism behind it. I propose that the kynurenine pathway, where tryptophan is

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21

Jayawickrama, Gayan. "Study and Design of Kynurenine Aminotransferase-II Inhibitors for the Treatment of Neurological Conditions." Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/20270.

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The majority of tryptophan metabolism passes through the kynurenine pathway. Metabolic imbalances in this pathway are implicated disease. KYNA, transaminated by the kynurenine aminotransferase (KAT) enzymes, is elevated in patients with schizophrenia. Schizophrenia is a neuropsychiatric disease with limited treatment options and debilitating symptoms. Glutamatergic systems are thought to have a significant role in its pathogenesis, providing a basis by which KYNA, an endogenous glutamate antagonist, is implicated in the disease. Four pyridoxal 5’-phosphate-dependent homologues of KAT are repor

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22

Nematollahi, Alireza. "Kynurenine Aminotransferases as Novel Targets in Neurodegenerative and Cognitive Disorders using Rational Drug Discovery." Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/15985.

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This dissertation is premised on observations that kynurenine aminotransferase (KAT) isozymes play a role in neurodegenerative and cognitive disorders and has considered the probable mechanisms of action of inhibitors. This thesis used rational drug discovery in the design of novel reversible human KAT-2 inhibitors. This work is presented in publication format with six chapters. Chapter 1 includes two published papers of which the first article is about the evolution of antipsychotic drugs used in the clinic to overcome both positive and negative symptoms of schizophrenia with an emphasis on t

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23

Hara, Toshiaki, Fumiyuki Yamakura, Osamu Takikawa, et al. "Diazotization of kynurenine by acidified nitrite secreted from indoleamine 2,3-dioxygenase-expressing myeloid dendritic cells." Elsevier, 2008. http://hdl.handle.net/2237/11379.

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24

Akhouayri, Idir Georges. "Gene silencing of the kynurenine pathway and melanotic lesions in the malaria mosquito vector anopheles gambiae." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.445336.

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25

Laugeray, Anthony. "Etude du rôle de la voie de la kynurénine dans un modèle animale de dépression : le stress chronique imprédictible : approches biochimique et comportementale." Thesis, Tours, 2010. http://www.theses.fr/2010TOUR4013/document.

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Dans ce travail de thèse, nous nous sommes intéressés à mieux comprendre le rôle du métabolisme du tryptophane (TRP), et en particulier de la voie de la kynurénine (KYN), dans la physiopathologie des troubles dépressifs en utilisant un modèle murin de dépression - le stress chronique imprédictible modéré (Unpredictable Chronic Mild Stress = UCMS). Nous avons montré que 1) l'UCMS affecte de façon différentielle le métabolisme de la KYN selon qu'il se déroule en périphérie ou dans le SNC 2) l'UCMS induit l'accumulation de certains métabolites toxiques de la KYN en périphérie alors que dans le ce

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26

Sakurai, Masashi. "Serum Metabolic Profiles of the Tryptophan-Kynurenine Pathway in the high risk subjects of major depressive disorder." Kyoto University, 2020. http://hdl.handle.net/2433/259732.

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27

Wilson, Kris. "Novel screening techniques for the discovery of human KMO inhibitors." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/18743.

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Kynurenine 3-monooxygenase (KMO) is an enzyme central to the kynurenine pathway of tryptophan degradation. KMO is emerging as an increasingly important target for drug development. The enzyme is implicated in the development and progression of several neurodegenerative disorders, in the regulation of the immune response and in sterile systemic inflammation. Production of recombinant human enzyme is challenging due to the presence of transmembrane domains, which localise KMO to the outer mitochondrial membrane and render KMO insoluble in many in vitro expression systems. Although several in vit

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28

Yan, Edwin B., Tony Frugier, Chai K. Lim, et al. "Activation of the kynurenine pathway and increased production of the excitotoxin quinolinic acid following traumatic brain injury in humans." BioMed Central, 2015. http://hdl.handle.net/10150/610324.

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ABSTRACT: During inflammation, the kynurenine pathway (KP) metabolises the essential amino acid tryptophan (TRP) potentially contributing to excitotoxicity via the release of quinolinic acid (QUIN) and 3-hydroxykynurenine (3HK). Despite the importance of excitotoxicity in the development of secondary brain damage, investigations on the KP in TBI are scarce. In this study, we comprehensively characterised changes in KP activation by measuring numerous metabolites in cerebrospinal fluid (CSF) from TBI patients and assessing the expression of key KP enzymes in brain tissue from TBI victims. Acute

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Alexander, Kathleen Shannon. "Elevated Kynurenic Acid as an Animal Model of Schizophrenia." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1304691359.

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30

Bellac, Caroline. "Pathomechanisms of bacterial meningitis based on transcriptome analysis : role of kynurenine 3-hydroxylase and galectin-3/-9 in brain injury /." [S.l.] : [s.n.], 2007. http://www.zb.unibe.ch/download/eldiss/07bellac_c.pdf.

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31

Tan, Vanessa. "Identification of biomarkers for MND, and understanding the potential role of the cyanotoxin BMAA in neurodegeneration Involvement of Quinolinic Acid in the Neuropathogenesis of amyotrophic lateral sclerosis Detection of the Cyanotoxins L-BMAA Uptake and Accumulation in Primary Neurons and Astrocytes." Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS590.

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La Sclérose Latérale Amyotrophique (SLA) est une maladie neurodégénérative dévastatrice dont les causes sont inconnues et pour laquelle il n’existe aucun traitement ni marqueur spécifique. Dans ce contexte, nous avons étudié le rôle de la voie métabolique des kynurénines impliquée dans la production de métabolites neuroactifs qui peuvent être immunomodulateurs, neuroprotecteurs ou à l’inverse neurotoxiques. Dans une étude longitudinale du sérum de 66 patients atteints de SLA, nous avons évalué le profil de 10 métabolites de la voie des kynurénines par chromatographie HPLC et spectrographie GC/

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32

Hara, Toshiaki, Nanako Ogasawara, Hidetoshi Akimoto, et al. "High-affinity uptake of kynurenine and nitric oxide-mediated inhibition of indoleamine 2,3-dioxygenase in bone marrow-derived myeloid dendritic cells." Elsevier, 2008. http://hdl.handle.net/2237/11381.

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33

Favennec, Marie. "Etude de la voie des kynurénines dans l'obésité humaine." Thesis, Lille 2, 2015. http://www.theses.fr/2015LIL2S037/document.

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Le tryptophane, un acide aminé essentiel, est soit utilisé pour la synthèse protéique et la synthèse de sérotonine, soit dégradé en plusieurs métabolites appelés collectivement les kynurénines. L’expression et l’activité des enzymes de la voie des kynurénines sont stimulées par l’inflammation. La synthèse des kynurénines est donc susceptible d’être augmentée chez les individus obèses. En effet, l’obésité est caractérisée par une inflammation chronique à bas bruit du tissu adipeux, reflétée par l’augmentation de facteurs inflammatoires circulants qui contribuent à l’apparition de l’insulinorési

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34

Okada, Sabrina Sayori. "Regulação cruzada entre peroxidases e indolamina 2,3 dioxigenase no controle da metabolização do triptofano." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/9/9136/tde-21012011-151605/.

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Triptofano (TRP) é metabolizado por duas vias, a via serotonérgica e a via das quinureninas. Na via serotonérgica, TRP é metabolizado a serotonina (5-HT) e, em algumas células, à melatonina (MLT) que pode ser oxidada à N1-acetil-N2-formil-5- metoxiquinuramina (AFMK) e N1-acetil-5-metoxiquinuramina (AMK) por ação de peroxidases. Na via das quinureninas o TRP é diretamente metabolizado à N formilquinurenina (NFK) e em seguida a quinurenina (QUIN). A enzima indolamina 2, 3 dioxigenase (IDO) é uma das responsáveis por esta reação. Dada a importância da IDO na tolerância imunológica e pelo fato des

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Hang, Regina [Verfasser]. "ATP, HMGB1, and S100A4 promote immunosuppressive mesenchymal stromal cells by enhancing their kynurenine production : impact of necrosis on tumor-associated MSCs / Regina Hang." Ulm : Universität Ulm, 2019. http://d-nb.info/1186139927/34.

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Reis, Dênis Augusto Santana. "Ativação supraespinal da via das quinureninas contribui para a manutenção da dor neuropática." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/17/17133/tde-29052015-154850/.

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Introdução: Um fator que pode contribuir para o desenvolvimento da dor neuropática é a modulação negativa da via descendente da dor pelo aumento da degradação do triptofano pela ativação da enzima indoleamina 2,3-dioxigenase 1 (IDO1) ou a ativação da via descendente facilitatória da dor por um agonista glutamatérgicos produzido pela enzima quinurenina 3 monoxigenase (KMO). Objetivo: Foi avaliar a participação das enzimas IDO1 e a KMO presente na substância cinzenta periaquedutal (PAG) e no bulbo rostral ventromedial (RVM) no desenvolvimento da dor neuropática em camundongos induzida pelo model

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Marchi, Alexandre Froes. "Produção de quinurenina em modelos experimentais de restrição de sono e obesidade." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/9/9141/tde-03062015-165904/.

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A via das Quinureninas (Via Quin) representa a principal via catabólica do metabolismo do triptofano (Trp) e é essencial para diversos processos fisiológicos. No fígado, o Trp é catalisado por triptofano 2,3-dioxigenase (TDO) quinurenina (Quin). A mesma reação também pode ser catalisada pela enzima indolamina 2,3-dioxigenase (IDO), produzida por células imunológicas. Em alguns processos patológicos, há um aumento do consumo de Trp pela Via Quin, que gera compostos que estão relacionados ao processo de imunotolerância. No presente estudo, foram selecionados dois modelos que mimetizam situações

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Zmarowski, Amy L. "Astrocytes Regulate Cortical Ach Release Via Kynurenic Acid: Implications For Cognitive Impairments In Schizophrenia." Columbus, Ohio : Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1217199677.

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Tourino, Melissa Cavalheiro. "Estudo da ação inibitória da enzima indolamina 2,3-dioxigenase pelos compostos triptamina (TRY) e N,N-dimetiltriptamina (DMT)." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/9/9136/tde-02092013-123633/.

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A enzima indolamina 2,3-dioxigenase (IDO) é responsável pela degradação de triptofano (TRP) pela via das quinureninas. O aumento da expressão de IDO é a grande responsável pela resposta de tolerância imunológica e pode ser induzida por IFN-γ e lipopolissacarídeos (LPS). É conhecido que a IDO participa do mecanismo de imuno escape de células tumorais, sendo relatada como marcadora de progressão tumoral. Desta forma, a inibição da atividade da IDO para a restauração da imunidade anti-tumoral do hospedeiro tem sido considerada uma estratégia para a terapêutica antineoplásica. N,N-dimetiltrip

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Genestet, Charlotte. "Dialogue inter-règne entre Pseudomonas aeruginosa et les cellules de l'immunité innée. Rôle de la production de L-kynurénine par les bactéries." Thesis, Grenoble, 2014. http://www.theses.fr/2014GRENS026/document.

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Pseudomonas aeruginosa est responsable d'infections persistantes chez les patients atteints de mucoviscidose, suggérant une capacité à mettre en échec les défenses immunitaires innées. Par ailleurs, nous savons que les cellules de l'hôte produisent de la kynurénine, exerçant un contrôle sur l'homéostasie du système immunitaire. Or, la bactérie elle-même produit de la kynurénine. Des résultats préliminaires de notre équipe ont montré que lors d'une infection pulmonaire aiguë chez la souris par une souche de P. aeruginosa ne produisant pas de kynurénine, il y a une perte de virulence (diminution

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Phenis, David Anthony. "Performance of Adult Rats Exposed to Elevated Levels of Kynurenic Acid during Gestation in a Rodent Target Detection Task: A Translational Model for Studying the Effects of Cognitive Training." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu154211727456543.

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MARTIMIANO, Paula Honório de Melo. "Etude de l’impact à court et à long terme de la dénutrition périnatale sur le métabolisme du Trp cérébral." Universidade Federal de Pernambuco, 2016. https://repositorio.ufpe.br/handle/123456789/18023.

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Submitted by Fabio Sobreira Campos da Costa (fabio.sobreira@ufpe.br) on 2016-10-20T12:15:15Z No. of bitstreams: 2 license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) Thèse-Paula Honório de Melo Martimiano - para imprimir.pdf: 2048933 bytes, checksum: 7f54e2714049362a7394297a27060229 (MD5)<br>Made available in DSpace on 2016-10-20T12:15:15Z (GMT). No. of bitstreams: 2 license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) Thèse-Paula Honório de Melo Martimiano - para imprimir.pdf: 2048933 bytes, checksum: 7f54e2714049362a7394297a27060229 (MD5) Pr

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Souza, Fladjule Rejane Soares de. "An?lise de polimorfismos dos genes da rota quinurenina em pacientes com meningite bacteriana." Universidade Federal do Rio Grande do Norte, 2008. http://repositorio.ufrn.br:8080/jspui/handle/123456789/16756.

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Made available in DSpace on 2014-12-17T15:18:08Z (GMT). No. of bitstreams: 1 FladjuleRSS.pdf: 330062 bytes, checksum: 22e7d9836e1ea44b75c1f00b2ab22a60 (MD5) Previous issue date: 2008-03-28<br>Bacterial meningitis (BM) is still an important infectious disease causing death and disability. Invasive bacterial infections of the central nervous systems (CNS) generate some of the most powerful inflammatory responses known, which contributes to neuronal damage. The DNA microarray technology showed alterations in the kynurenine (KYN) pathway that is induced in

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Mizdrak, Jasminka. "Human lens chemistry: UV filters and age-related nuclear cataract." Australia : Macquarie University, 2007. http://hdl.handle.net/1959.14/16855.

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"A thesis submitted in partial fulfillment of the requirements for the award of the degree of Doctor of Philosophy".<br>Thesis (PhD) -- Macquarie University, Division of Environmental and Life Sciences, Dept. of Chemistry and Biomolecular Sciences, 2007.<br>Bibliography: p. 243-277.<br>Introduction -- A convenient synthesis of 30HKG -- Facile synthesis of the UV filter compounds 30HKyn and AHBG -- Synthesis, identification and quantification of novel human lens metabolites -- Modification of bovine lens protein with UV filters and related metabolites -- Effect of UV light on UV filter-treated

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Coutinho, Leonam Gomes. "Ativa??o local da rota da quinurenina por moduladores inflamat?rios durante a meningite bacteriana." Universidade Federal do Rio Grande do Norte, 2008. http://repositorio.ufrn.br:8080/jspui/handle/123456789/16760.

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Made available in DSpace on 2014-12-17T15:18:09Z (GMT). No. of bitstreams: 1 LeonamGC.pdf: 218692 bytes, checksum: 002840894937241c14e673ee875d7524 (MD5) Previous issue date: 2008-03-18<br>Conselho Nacional de Desenvolvimento Cient?fico e Tecnol?gico<br>Activation of the kynurenine (KYN) pathway (KP) by modulators of immune system has been observed during several neurological diseases. Here we assessed the association of chemo-/cytokine levels with the concentration of KP metabolites in cerebrospinal fluid (CSF) and plasma samples from patients with bacterial meningitis (BM). All

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Tutakhail, Abdulkarim. "Potential muscular doping effects of anti-depressants." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS513.

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Bien que l’effet psychotrope des antidépresseurs soit bien connu, afin de corriger les conséquences du stress et de renforcer la confiance en soi, de nombreux autres effets pharmacologiques, notamment périphériques, doivent encore être approfondis. Les antidépresseurs inhibiteurs de la recapture de la sérotonine (ISRS) peuvent avoir un effet bénéfique sur la performance physique en participant à une réparation et à une croissance plus rapides des muscles. Il a récemment été démontré que la sérotonine était impliquée dans la récupération de la force musculaire chez un modèle murin de myopathie

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Migliorini, Silene. "Metabolismo de triptofano na vigência de choque endotóxico induzido por LPS e hipertriptofanemia." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/9/9136/tde-15072011-104933/.

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Triptofano (TRP), um amino ácido essencial, é metabolizado por duas vias principais, a via das quinureninas e a via serotonérgica. Em ambas as vias há a possibilidade de formação de compostos ativos no sistema imune que se caracterizam pelas ações imunossupressoras e indutoras de tolerância. Na via serotonérgica há a formação de serotonina (5-HT) e em alguns tecidos de melatonina (MEL). Este composto pode ainda ser oxidado por ação de peroxidases aos seus produtos de abertura de anel indólico o AFMK (N1-acetil-n2-formil-5-metoxiquinuramina) e AMK (N1-acetil-5-metoxiquinuramina). Já na via das

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Mackay, Gillian Moira. "Kynurenines in neurological disorders." Thesis, University of Glasgow, 2007. http://theses.gla.ac.uk/39/.

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The kynurenine pathway is thought to be involved in neurological disorders but its precise role and the mechanisms involved have yet to be established. Tryptophan can be metabolised via this pathway to produce the neurotoxic N-methyl-D-aspartate (NMDA) receptor agonist, quinolinic acid (QUIN), and the direct generators of reactive oxygen species, 3-hydroxykynurenine (3HKYN) and 3-hydroxyanthranilic acid (3HANA), as well as the neuroprotective NMDA receptor antagonist, kynurenic acid (KYNA). High performance liquid chromatography (HPLC) methods were successfully developed and validated for meas

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Vallius, Laura I. "Modulating the immune system by amino acid depletion : IDO and beyond." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:eb1a1987-4121-4042-be82-2aafb67c9941.

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Amino acid availability plays an important role in modulating the activity of T-cells. One of the pathways employed by T-cells to sense nutrient levels is the “mammalian target of rapamycin” (mTOR) pathway that is inhibited in response to nutrient depletion. Indoleamine 2,3-dioxygenase (IDO) is the first and rate-limiting enzyme along the tryptophan catabolising kynurenine pathway. T-cells are very sensitive to lack of this essential amino acid in their microenvironment and this confers strong immunomodulatory properties to cells expressing active IDO. It therefore has a significant physiologi

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Lôbo, Patricia Rolim Mendonça. "Avaliação dos metabólitos do triptofano e do polimorfismo do gene da indoleamina 2,3-dioxigenase 1 (IDO1) na etiopatogênese da artrite reumatoide." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/17/17138/tde-13092018-151726/.

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A artrite reumatoide (AR) é a artropatia inflamatória mais prevalente no mundo, de etiologia multifatorial e fenótipos heterogêneos. Busca-se, além de definir fatores etiológicos, compreender as interações entre mecanismos envolvidos na fisiopatologia da AR. Entre estes, fatores genéticos, tanto genes do antígeno leucocitário humano (HLA), especialmente a presença do epítopo compartilhado (Shared epitope - SE) do HLA-DRB1, como genes não-HLA, e fatores ambientais e epigenéticos têm sido associados à doença. Assim, a identificação de novos fatores relacionados à etiopatogenia da AR e suas possí

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