China
Africa
Explore chapters and articles related to this topic
AI and Chronic Inflammation
Published in Louis J. Catania, AI for Immunology, 2021
Kynurenine pathway enzymes have been identified as key regulators of cancer immunity. An artificial intelligence (AI) with deep learning technology was employed to rationally design and discover a novel kynurenine pathway regulator with potent immunotherapeutic efficacy. The study demonstrated that AI modeling with deep learning is a valid strategy for a rational and effective development of an immunotherapeutic drug. This AI-based platform can be applied to other molecular targets to speed up the immuno-oncologic drug development.37
Emotional Health and Stress Management
Published in James M. Rippe, Lifestyle Medicine, 2019
Neil Nedly, Francisco E Ramirez
Exercise is an integral part of stress management as well. It is understood that general health is improved by a regular and sustainable exercise routine and that excessive exercise can lead to fatigue, injury, and decrease the ability to maintain the program in the long term. Exercise is also important for general brain health (stimulating Brain-derived Neurotrophic Factor, etc.) and it is protective against chronic stress effects. Exercise training induces changes at the level of the muscle gene expression that can increase kynurenine aminotransferases, enhancing the conversion of kynurenine into kynurenic acid, which protects the brain from stress-induced changes associated with depression.86 Moderate exercise not only decreases current stress but research shows that the effect lasts for extended periods post-workout.87
Food and drugs
Published in Richard Lawson, Jonathon Porritt, Bills of Health, 2018
Richard Lawson, Jonathon Porritt
Further studies support the idea that caffeine may contribute to anxiety/stress states. Kynurenine, a neurotransmitter related to anxiety, was found in the plasma of volunteers after a large dose of caffeine.28 In a survey of 293 Japanese medical students, caffeine consumption was significantly and positively related with anxiety symptoms in males.29
Increased tryptophan, but not increased glucose metabolism, predict resistance of pembrolizumab in stage III/IV melanoma
Published in OncoImmunology, 2023
Jorge D. Oldan, Benjamin C. Giglio, Eric Smith, Weiling Zhao, Deeanna M. Bouchard, Marija Ivanovic, Yueh Z. Lee, Frances A. Collichio, Michael O. Meyers, Diana E. Wallack, Amber Abernethy-Leinwand, Patricia K. Long, Dimitri G. Trembath, Paul B. Googe, Madeline H. Kowalski, Anastasia Ivanova, Jennifer A. Ezzell, Nana Nikolaishvili-Feinberg, Nancy E. Thomas, Terence Z. Wong, David W. Ollila, Zibo Li, Stergios J. Moschos
L-tryptophan (Trp) is an essential amino acid in translation and protein synthesis. However, the majority (>95%) of Trp serves as a biochemical precursor of metabolites with critical physiologic roles (reviewed in6) in gut homeostasis, immunity, and neuronal function. Under normal physiologic conditions, 95% of the absorbed Trp is metabolized via the kynurenine pathway by the action of indolamine 2,3-dioxygenases 1 and 2 (IDO1/IDO2) and Trp 2,3-dioxygenase (TDO2). The resultant kynurenines are biologically active metabolites involved in inflammation, immunoregulation, excitatory neurotransmission, and gut homeostasis. Dysregulation of kynurenine metabolism can lead to various conditions, such as cancer, diabetes, mood, and psychiatric disorders (reviewed in7).
The interplay between aryl hydrocarbon receptor, H. pylori, tryptophan, and arginine in the pathogenesis of gastric cancer
Published in International Reviews of Immunology, 2022
Marzieh Pirzadeh, Nastaran Khalili, Nima Rezaei
Kynurenine, a metabolite of the amino acid tryptophan, is a natural ligand for AHR [13]. Tryptophan dioxygenase, a liver enzyme that drives tryptophan consumption, is upregulated by many cancers, indicating that increased tryptophan consumption might be a possible mechanism of tumors to defeat immune barriers and continue progression [14]. Xanthurenic acid, which is a metabolite of the kynurenine pathway, acts as a potent inhibitor of a terminal enzyme in the synthetic pathway of tetrahydrobiopterin (BH4) named sepiapterin reductase (SPR) [15]. BH4 is a cofactor that is involved in the conversion of amino acids such as phenylalanine, tyrosine, and tryptophan to monoamine neurotransmitters such as dopamine and serotonin [16]. It has been shown that BH4 ameliorates immune response and prevents tumor progression [17]. Thus, the decreased production of BH4 impairs antitumor immune responses and T cell proliferation, resulting in immune suppression. Moreover, BH4 is a cofactor for NO synthesis from arginine [18]. Different studies have implicated that arginine can induce apoptosis in gastric epithelial cells and also mediate NO-induced H. pylori killing[19]. However, being a precursor for NO, a substance which contributes to tumor progression through angiogenesis, suggests a controversial role for BH4 in tumor progression.
δEPCD: the electrophysiologic coefficient of depressiveness
Published in Biomarkers, 2021
Rami Bou Khalil, Rhéa El Khoury
From another perspective, a sufficient amount of evidence links the metabolism of tryptophan to the occurrence of depressive symptoms via disturbances in the serotonin synthesis pathway. However, the vast majority of metabolised tryptophan is converted by the two heme-containing enzymes indoleamine 2,3-dioxygenase (IDO) and tryptophan 2,3-dioxygenase (TDO) into N-formylkynurenine. The activation of IDO by stressful life events, among other factors, is considered to be responsible for the production of neuroprotective substances such as Kynurenic acid (KYNA) as well as neurotoxic substances such quinolinic acid (QUIN) (Savitz et al. 2015a, 2015b). Recent studies have shown that this kynurenine pathway plays an important role in depression as well as in other psychiatric diseases, such as schizophrenia and bipolar disorder. However, the neurobiological effects found in the kynurenine pathway seem to be different in these diseases and depression. While a pathologic shift towards KYNA and away from QUIN production has been found in schizophrenia and bipolar disorder patients, the contrary has been established in the depression model in which KYNA is neuroprotective and QUIN is neurotoxic (Réus et al. 2015).