Gotowe bibliografie tematyczne / Quinolinic acid

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Gotowa bibliografia na temat „Quinolinic acid”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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Artykuły w czasopismach na temat "Quinolinic acid"

Sundberg, Markku, Rolf Uggla, Reijo Sillanpää, et al. "Adduct formed by chromium trioxide and zwitterionic quinolinic acid." Open Chemistry 8, no. 3 (2010): 486–93. http://dx.doi.org/10.2478/s11532-010-0033-z.

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AbstractChromium trioxide forms an adduct with zwitterionic quinolinic acid. The structure of the product was found to be (quinolinium-3-carboxylato-O)trioxidochromium(VI), determined by single-crystal X-ray diffraction methods. To evaluate the bonding properties of the compound, its structure was optimized at the B3LYP/6-311G* level of theory. The electronic characteristics were investigated by topological methods applied to the total charge density in various model compounds including the title compound, title compound with a HF molecule presenting a hydrogen bonding and anionic moiety. Calc

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Sinz, Elizabeth H., Patrick M. Kochanek, Melvyn P. Heyes, et al. "Quinolinic Acid is Increased in CSF and Associated with Mortality after Traumatic Brain Injury in Humans." Journal of Cerebral Blood Flow & Metabolism 18, no. 6 (1998): 610–15. http://dx.doi.org/10.1097/00004647-199806000-00002.

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We tested the hypothesis that quinolinic acid, a tryptophan-derived N-methyl-d-aspartate agonist produced by macrophages and microglia, would be increased in CSF after severe traumatic brain injury (TBI) in humans, and that this increase would be associated with outcome. We also sought to determine whether therapeutic hypothermia reduced CSF quinolinic acid after injury. Samples of CSF ( n = 230) were collected from ventricular catheters in 39 patients (16 to 73 years old) during the first week after TBI, (Glasgow Coma Scale [GCS] < 8). As part of an ongoing study, patients were randomized

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HEYES, Melvyn P., Cristian L. ACHIM, Clayton A. WILEY, Eugene O. MAJOR, Kuniaki SAITO, and Sanford P. MARKEY. "Human microglia convert l-tryptophan into the neurotoxin quinolinic acid." Biochemical Journal 320, no. 2 (1996): 595–97. http://dx.doi.org/10.1042/bj3200595.

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Immune activation leads to accumulations of the neurotoxin and kynurenine pathway metabolite quinolinic acid within the central nervous system of human patients. Whereas macrophages can convert l-tryptophan to quinolinic acid, it is not known whether human brain microglia can synthesize quinolinic acid. Human microglia, peripheral blood macrophages and cultures of human fetal brain cells (astrocytes and neurons) were incubated with [13C6]l-tryptophan in the absence or presence of interferon γ. [13C6]Quinolinic acid was identified and quantified by gas chromatography and electron-capture negati

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Ohashi, Kazuto, Shigeyuki Kawai, and Kousaku Murata. "Secretion of Quinolinic Acid, an Intermediate in the Kynurenine Pathway, for Utilization in NAD + Biosynthesis in the Yeast Saccharomyces cerevisiae." Eukaryotic Cell 12, no. 5 (2013): 648–53. http://dx.doi.org/10.1128/ec.00339-12.

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ABSTRACT NAD + is synthesized from tryptophan either via the kynurenine ( de novo ) pathway or via the salvage pathway by reutilizing intermediates such as nicotinic acid or nicotinamide ribose. Quinolinic acid is an intermediate in the kynurenine pathway. We have discovered that the budding yeast Saccharomyces cerevisiae secretes quinolinic acid into the medium and also utilizes extracellular quinolinic acid as a novel NAD + precursor. We provide evidence that extracellular quinolinic acid enters the cell via Tna1, a high-affinity nicotinic acid permease, and thereby helps to increase the int

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Niwa, Toshlmitsu, Hldeo Yoshizumi, Yutaka Emoto, et al. "Accumulation of quinolinic acid in uremic serum and its removal by hemodialysis." Clinical Chemistry 37, no. 2 (1991): 159–61. http://dx.doi.org/10.1093/clinchem/37.2.159.

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Abstract Quinolinic acid was first identified in uremic serum by use of gas chromatography/mass spectrometry. Quantification by selected ion monitoring revealed that the serum concentration of quinolinic acid was markedly increased in chronic hemodialysis patients, and that the acid could be removed by conventional hemodialysis. The serum concentration of quinolinic acid was weakly but significantly correlated with the serum uric acid concentration. Accumulation of quinolinic acid in uremic blood may be involved in the pathogenesis of anemia, suppressed immune system, and uremic encephalopathy

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Guillemin, Gilles J. "Quinolinic acid: neurotoxicity." FEBS Journal 279, no. 8 (2012): 1355. http://dx.doi.org/10.1111/j.1742-4658.2012.08493.x.

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Heyes, Melvyn P., and Thaddeus S. Nowak. "Delayed Increases in Regional Brain Quinolinic Acid Follow Transient Ischemia in the Gerbil." Journal of Cerebral Blood Flow & Metabolism 10, no. 5 (1990): 660–67. http://dx.doi.org/10.1038/jcbfm.1990.119.

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Excessive activity or release of excitatory amino acids has been implicated in the neuronal injury that follows transient cerebral ischemia. To investigate the metabolism of the endogenous excitotoxin, quinolinic acid, and its potential for mediating cell loss following ischemia, the concentrations of quinolinic acid, L-tryptophan, 5-hydroxytryptamine, and 5-hydroxyindoleacetic acid were quantified in gerbil brain regions at different times after 5 or 15 min of ischemia induced by bilateral carotid artery occlusion. Significant elevation of brain tryptophan levels, accompanied by increased 5-h

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Saito, K., C. Y. Chen, M. Masana, J. S. Crowley, S. P. Markey та M. P. Heyes. "4-Chloro-3-hydroxyanthranilate, 6-chlorotryptophan and norharmane attenuate quinolinic acid formation by interferon-γ-stimulated monocytes (THP-1 cells)". Biochemical Journal 291, № 1 (1993): 11–14. http://dx.doi.org/10.1042/bj2910011.

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Accumulation of quinolinic acid and L-kynurenine occurs in the brain and/or blood following immune activation, and may derive from L-tryptophan following induction of indoleamine 2,3-dioxygenase and other kynurenine-pathway enzymes. In the present study a survey of various cell lines derived from either brain or systemic tissues showed that, while all cells examined responded to interferon-gamma by increased conversion of L-[13C6]tryptophan into L-kynurenine (human: B-lymphocytes, neuroblastoma, glioblastoma, lung, liver, kidney; rat brain: microglia, astrocytes and oligodendrocytes), only mac

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Heyes, Melvyn P. "Hypothesis: A Role for Quinolinic Acid in the Neuropathology of Glutaric Aciduria Type I." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 14, S3 (1987): 441–43. http://dx.doi.org/10.1017/s0317167100037872.

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ABSTRACT:Glutaric aciduria type I is an autosomal recessive metabolic disorder of children associated with severe dystonic motor disturbances and degeneration in the cerebral cortex, striatum and cerebellum. Biochemical studies demonstrate a deficiency in the enzyme glutaryl-CoA dehydrogenase. This enzyme metabolizes substrate derived from dietary tryptophan that could otherwise be converted to quinolinic acid within the brain. The law of mass action predicts that the production of quinolinic acid should be increased in glutaric aciduria type I. Quinolinic acid is a potent neurotoxin and convu

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Egashira, Sato, Saito, and Sanada. "Dietary Protein Level and Dietary Interaction Affect Quinolinic Acid Concentration in Rats." International Journal for Vitamin and Nutrition Research 77, no. 2 (2007): 142–48. http://dx.doi.org/10.1024/0300-9831.77.2.142.

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During tryptophan-niacin conversion, hepatic α-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD) [EC4.1.1.45] plays a key role in regulating NAD biosynthesis. ACMSD activity is greatly affected by many factors such as nutritional status and disease. The tryptophan catabolite quinolinic acid has been reported to be associated with the pathogenesis of various disorders and is a potential endogenous toxin. However the effects of dietary protein levels or dietary interaction between protein levels and fatty acid type to this process have not been investigated and are still unknown. In t

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Rozprawy doktorskie na temat "Quinolinic acid"

Allsebrook, Andrew M. "QPRTase : quinolinic acid analogue synthesis and non-enzymic decarboxylation of N-alkylquinolinic acids." Thesis, University of St Andrews, 1998. http://hdl.handle.net/10023/14376.

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Quinolinate phosphoribosyltransferase (QPRTase, E.C. 2.4.2.19) is considered to be a unique enzyme in that it is thought to catalyse two distinct chemical reactions. Both the transfer of a phosphoribosyl group from 5-phosphoribosyl-1- pyrophosphate onto the nitrogen of quinolinic acid and the subsequent decarboxylation of the intermediate to form nicotinic acid mononucleotide are thought to be catalysed by the QPRTase system. Analogues of quinolinic acid were designed as potential inhibitors of QPRTase. These contain acidic groups at the 2- and 3- positions but are unable to decarboxylate. How

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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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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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Morgan, Elaine M. "The role of nitric oxide in N-methyl-D-aspartate receptor-mediated neurotoxicity." Thesis, University of Southampton, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243084.

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Catton, Gemma R. "Mechanistic studies on quinolinate phosphoribosyltransferase /." St Andrews, 2007. http://hdl.handle.net/10023/485.

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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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Heron, Paula Michelle. "An investigation of the neuroprotective effects of estrogen in a model of quinolinic acid-induced neurodegeneration." Thesis, Rhodes University, 2002. http://hdl.handle.net/10962/d1003237.

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The hippocampus, located in the medial temporal lobe, is an important region of the brain responsible for the formation of memory. Thus, any agent that induces stress in this area has detrimental effects and could lead to various types of dementia. Such agents include the neurotoxin, Quinolinic acid. Quinolinic acid (QUIN) is a neurotoxic metabolite of the tryptophan-kynurenine pathway and is an endogenous glutamate agonist that selectively injures and kills vulnerable neurons via the activation of the NMDA class of excitatory amino acid receptors. Estrogen is a female hormone that is responsi

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Thian, Stefanie. "The quinolinic acid lesion of the neostriatum examined in the context of neuronal transplantation." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624769.

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Ting, Ka Ka Clinical School St Vincent's Hospital Faculty of Medicine UNSW. "Quinolinic acid and its effect on the astrocyte with relevance to the pathogenesis of Alzheimer??s disease." Publisher:University of New South Wales. Clinical School - St Vincent's Hospital, 2008. http://handle.unsw.edu.au/1959.4/41288.

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There is evidence that the excitotoxin quinolinic acid (QUIN) synthesized through the kynurenine pathway (KP) by activated microglia may play a role in the pathogenesis of several major neuroinflammatory diseases and more particularly in Alzheimer??s disease (AD). The hypothesis of this project is QUIN affects the function and morphology of astrocytes. In this study I used human foetal astrocytes stimulated with AD associated cytokines including IFN-gamma, TNF-alpha, TGF-alpha and different concentrations of QUIN ranging from low physiological to high excitotoxic concentrations. I found that Q

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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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Książki na temat "Quinolinic acid"

W, Stone T., ed. Quinolinic acid and the kynurenines. CRC Press, 1989.

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Armstrong, Sally Fiona. Concentrations of quinolinic and kynuretic acid in patients with Alzheimer's disease and controls and their relationship to restlessness and mood states. University of Surrey Roehampton, 2000.

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Erickson, W. Randal. Studies on advanced intermediates in the biosynthesis of streptonigrin. 1987.

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Części książek na temat "Quinolinic acid"

Goda, K., R. Kishimoto, S. Shimizu, Y. Hamane, and M. Ueda. "Quinolinic Acid and Active Oxygens." In Advances in Experimental Medicine and Biology. Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0381-7_38.

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Schwarcz, R., E. Okuno, and C. Köhler. "Endogenous Excitotoxins: Focus on Quinolinic Acid." In Excitatory Amino Acids. Palgrave Macmillan UK, 1986. http://dx.doi.org/10.1007/978-1-349-08479-1_25.

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Schwarcz, R., and F. Du. "Quinolinic Acid and Kynurenic Acid in the Mammalian Brain." In Advances in Experimental Medicine and Biology. Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4684-5952-4_17.

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Schwarcz, R., C. Speciale, E. Okuno, E. D. French, and C. Köhler. "Quinolinic Acid: A Pathogen in Seizure Disorders?" In Advances in Experimental Medicine and Biology. Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-7971-3_53.

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Vezzani, A., J. B. P. Gramsbergen, C. Speciale, and R. Schwarcz. "Production of Quinolinic Acid and Kynurenic Acid by Human Glioma." In Advances in Experimental Medicine and Biology. Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4684-5952-4_95.

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Stone, T. W., J. H. Connick, J. I. Addae, D. A. S. Smith, and P. A. Brooks. "The Neuropharmacology of Quinolinic Acid and the Kynurenines." In Excitatory Amino Acids. Palgrave Macmillan UK, 1986. http://dx.doi.org/10.1007/978-1-349-08479-1_24.

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Guillemin, Gilles J., Kieran R. Williams, Danielle G. Smith, George A. Smythe, Juliana Croitoru-Lamoury, and Bruce J. Brew. "QUINOLINIC ACID IN THE PATHOGENESIS OF ALZHEIMER’S DISEASE." In Advances in Experimental Medicine and Biology. Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0135-0_19.

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Heyes, Melvyn P., Eugene O. Major, Kuniaki Sato, and Sanford M. Markey. "Quantification of Quinolinic Acid Metabolism by Macrophages and Astrocytes." In Technical Advances in AIDS Research in the Human Nervous System. Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1949-2_23.

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Mawatari, K., K. Oshida, F. Iinuma, and M. Watanabe. "Determination of Quinolinic Acid by Liquid Chromatography with Fluorimetric Detection." In Advances in Experimental Medicine and Biology. Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0381-7_112.

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Bergqvist, P. B. F., M. P. Heyes, and F. Bengtsson. "Is Quinolinic Acid Involed in the Pathogenesis of Hepatic Encephalopathy?" In Advances in Experimental Medicine and Biology. Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0381-7_61.

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Streszczenia konferencji na temat "Quinolinic acid"

Kopecky, Sarah E. "Investigation of Substituent Effects on the Corrosion Inhibition of Pyridine Derivatives with Acetylenic Alcohols on Steel in Acid Media." In CORROSION 2015. NACE International, 2015. https://doi.org/10.5006/c2015-05569.

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Abstract The corrosion inhibition of substituted pyridine derivatives and quaternized pyridines in the presence and absence of acetylenic alcohol synergists is reported. Electrochemical Frequency Modulation (EFM) was used as a method of monitoring corrosion rates of steel in acidic environments. Early stage pitting was evaluated via scanning electron microscope (SEM) for comparison of measured corrosion rates to observed pit formation. EFM was found to be a reliable and accurate method of monitoring general corrosion rates over time, and causality factor data was found to depend heavily on the

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Lukovits, I., T. Kosztolányi, E. Kálmán, and G. Pálinkás. "Corrosion Inhibitors: Correlation between Chemical Structure and Efficiency." In CORROSION 1999. NACE International, 1999. https://doi.org/10.5006/c1999-99242.

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Abstract Corrosion inhibition efficiencies of heterocyclic, aromatic or partially saturated aromatic compounds (pyrimidines, benzothiazole derivatives, amino-acids containing an aromatic part, pyridines and quinolines) were correlated with quantum chemical indices of the respective molecules. Inhibition efficiencies measured in acidic solutions containing 0.001 and 0.01 mol/L of the inhibitor, respectively, were collected. The quantum chemical calculations were done by using the simple Hückel method. Comparison of inhibition efficiencies and the differences between energies of the highest occu

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PAMART, Guillaume, Odile Poulain Godefroy, Philippe Gosset, and Olivier Le Rouzic. "Quinolinic Acid modulates pulmonary inflammatory response to influenza infection." In ERS Congress 2024 abstracts. European Respiratory Society, 2024. http://dx.doi.org/10.1183/13993003.congress-2024.pa892.

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Zhang, Ying, Weixin Liu, Chi Chun Wong, et al. "IDDF2025-ABS-0356 Catenibacterium mitsuokai promotes hepatocellular carcinogenesis by binding to hepatocyte and generating quinolinic acid." In Abstracts of the International Digestive Disease Forum (IDDF), Hong Kong, 5 – 6 July 2025. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2025. https://doi.org/10.1136/gutjnl-2025-iddf.7.

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Yang, Zhen, Yefei Wang, Matjaž Finšgar, Jiajia Wu, and Wengang Ding. "Novel High-Efficient Key Component of Steel Corrosion Inhibitors Formulation for Acidification: Indolizine Derivatives of the Conventional N-Heterocyclic Quaternary Ammonium Salts." In SPE International Conference on Oilfield Chemistry. SPE, 2023. http://dx.doi.org/10.2118/213814-ms.

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Abstract Acidizing, the widely used technique for well stimulation, requires a great consumption of effective Corrosion Inhibitors (CIs), due to the severe and fast corrosion of metallic equipment caused by strong hot acid as soon as the acidizing fluids are pumping down to reservoir. This paper presents a new concept of indolizine derivative inhibitors with remarkable inhibition effectiveness for steel under acidizing condition, which will reduce the cost and environmental burden of acidizing CIs significantly. Indolizine derivatives of several quinolinium salts (serves as main component of c

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Pattanayak, Subrat Kumar. "Quantum chemical study on the NLO and NBO properties of 4-hydroxy quinoline-2-carboxylic acid." In 2ND INTERNATIONAL CONFERENCE ON CONDENSED MATTER AND APPLIED PHYSICS (ICC 2017). Author(s), 2018. http://dx.doi.org/10.1063/1.5032823.

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Luo, Ya-Nan, Zhi-Chen Liu, Hui-Ying Jiang, Li-Ying Yu, and Xiao-Yang Yu. "A NEW NICKEL COORDINATION POLYMER CONSTRUCTED FROM 4-[(8-HYDROX -Y 5-QUINOLINYL) AZO]-BENZENESULFONIC ACID: SYNTHESIS, STRUCTURE AND PROPERTY." In International Conference on New Materials and Intelligent Manufacturing (ICNMIM). Volkson Press, 2018. http://dx.doi.org/10.26480/icnmim.01.2018.323.325.

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Manabe, S., H. Yanagisawa, S. Ishikawa, et al. "TRYPTOPHAN PYROLYSIS PRODUCTS FOUND IN COOKED FOODS INHIBIT HUMAN PLATELET AGGREGATION BY INHIBITING CYCLOOXYGENASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643402.

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Humans are exposed to numerous toxic compounds in foods. During the past decade, several carcinogenic heterocyclic amines have been reported to be present in the cooked foods. Recently, we reported that some of the carcinogenic heterocyclic amines isolated from foods were present in human plasma. In order to know the effects of the carcinogens isolated from foods on the cell function, we investigated the effects of the carcinogenic heterocyclic amines including Trp-P-1(3-amino-l,4-dimethyl-5H-pyrido❘4,3-b❘indole) and Trp-P-2(3-amino-1-methyl-5H-pyrido❘4,3-b❘indole) on human platelet aggregatio

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