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UV radiation-induced photochemical damage of tryptophan in peptides, proteins and ocular lensesHibbard, Lisa B. 05 1900 (has links)
No description available.
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Tryptophan metabolism in insectsColes, B. G. January 1971 (has links)
No description available.
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Tryptophan binding to mouse brain cell membranesMcLean, Milton Ray 12 1900 (has links)
No description available.
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The development and application of a liquid chromatographic-fluorometric method for the analysis of tryptophan matabolites in physiological samples /Anderson, George Magruder. January 1978 (has links)
No description available.
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Some studies in connection with indolesDearnaley, D. P. January 1964 (has links)
No description available.
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The development and application of a liquid chromatographic-fluorometric method for the analysis of tryptophan matabolites in physiological samples /Anderson, George Magruder January 1978 (has links)
No description available.
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Electronic spectroscopy as a probe of heterogeneity in the local environment of polar aromatic chromophores in proteins and free solution.Purkey, Robert Michael. January 1972 (has links)
No description available.
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Electronic spectroscopy as a probe of heterogeneity in the local environment of polar aromatic chromophores in proteins and free solution.Purkey, Robert Michael. January 1972 (has links)
No description available.
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Activation of the kynurenine pathway and increased production of the excitotoxin quinolinic acid following traumatic brain injury in humansYan, Edwin B., Frugier, Tony, Lim, Chai K., Heng, Benjamin, Sundaram, Gayathri, Tan, May, Rosenfeld, Jeffrey V., Walker, David W., Guillemin, Gilles J., Morganti-Kossmann, Maria C. January 2015 (has links)
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 QUIN levels were further correlated with outcome scores to explore its prognostic value in TBI recovery. METHODS: Twenty-eight patients with severe TBI (GCS ≤ 8, three patients had initial GCS = 9-10, but rapidly deteriorated to ≤8) were recruited. CSF was collected from admission to day 5 post-injury. TRP, kynurenine (KYN), kynurenic acid (KYNA), QUIN, anthranilic acid (AA) and 3-hydroxyanthranilic acid (3HAA) were measured in CSF. The Glasgow Outcome Scale Extended (GOSE) score was assessed at 6 months post-TBI. Post-mortem brains were obtained from the Australian Neurotrauma Tissue and Fluid Bank and used in qPCR for quantitating expression of KP enzymes (indoleamine 2,3-dioxygenase-1 (IDO1), kynurenase (KYNase), kynurenine amino transferase-II (KAT-II), kynurenine 3-monooxygenase (KMO), 3-hydroxyanthranilic acid oxygenase (3HAO) and quinolinic acid phosphoribosyl transferase (QPRTase) and IDO1 immunohistochemistry. RESULTS: In CSF, KYN, KYNA and QUIN were elevated whereas TRP, AA and 3HAA remained unchanged. The ratios of QUIN:KYN, QUIN:KYNA, KYNA:KYN and 3HAA:AA revealed that QUIN levels were significantly higher than KYN and KYNA, supporting increased neurotoxicity. Amplified IDO1 and KYNase mRNA expression was demonstrated on post-mortem brains, and enhanced IDO1 protein coincided with overt tissue damage. QUIN levels in CSF were significantly higher in patients with unfavourable outcome and inversely correlated with GOSE scores. CONCLUSION: TBI induced a striking activation of the KP pathway with sustained increase of QUIN. The exceeding production of QUIN together with increased IDO1 activation and mRNA expression in brain-injured areas suggests that TBI selectively induces a robust stimulation of the neurotoxic branch of the KP pathway. QUIN's detrimental roles are supported by its association to adverse outcome potentially becoming an early prognostic factor post-TBI.
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The chromatography and detection of various metabolites along the tryptophan-kynurenine-nicotinic acid pathway with application to plasma and homogenized rat kidney and liver /Markus, George Eugene. January 1982 (has links)
No description available.
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