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tryptophan/inflamación
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Tryptophan depletion in context of the inflammatory and general nutritional status of a low-income South African HIV-infected population.
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BACKGROUND
The essential amino acid tryptophan cannot be synthesised in the body and must be acquired through dietary intake. Oxidation of tryptophan, due to immune induction of the enzyme indoleamine 2,3-dioxygenase (IDO), is considered to be the main cause of tryptophan depletion in HIV infection
5-methoxyindole metabolites of L-tryptophan: control of COX-2 expression, inflammation and tumorigenesis.
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Cyclooxygenase-2(COX-2) overexpression promotes inflammation and tumorigenesis. COX-2 expression in response to diverse stimuli is tightly controlled to avoid persistent overexpression. 5-methoxyindole metabolites of L-tryptophan represent a new class of compounds that control COX-2 expression at
Possible role of cytokine-induced tryptophan degradation in anaemia of inflammation.
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Anaemia of inflammation (AI) is a frequent complication in patients suffering from chronic inflammatory disorders including infections, autoimmune and malignant disease. Cytokine imbalance with a shift towards T-helper (Th)1-type immune response seems to be important in the pathogenesis of this type
A synthetic tryptophan metabolite reduces hemorrhagic area and inflammation after pulmonary radiofrequency ablation in rabbit nonneoplastic lungs.
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OBJECTIVE
The purpose of this study was to determine the effect of a synthetic tryptophan metabolite, tranilast [N-(3,4-dimethoxycinnamoyl)-anthranilic acid], on inflammatory and hemorrhagic areas after pulmonary radiofrequency ablation (RFA) in rabbits.
METHODS
Percutaneous RFA using a 17-gauge
Is tryptophan catabolism increased under indoleamine 2,3 dioxygenase activity during chronic lung inflammation in pigs?
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In a preliminary study we observed that piglets suffering from chronic lung inflammation induced by an intravenous injection of complete Freund adjuvant showed a marked decrease in plasma tryptophan (Trp) concentration suggesting increased Trp utilisation. During the inflammatory process, a
Redox Regulation and the Autistic Spectrum: Role of Tryptophan Catabolites, Immuno-inflammation, Autoimmunity and the Amygdala.
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The autistic spectrum disorders (ASD) form a set of multi-faceted disorders with significant genetic, epigenetic and environmental determinants. Oxidative and nitrosative stress (O&NS), immuno-inflammatory pathways, mitochondrial dysfunction and dysregulation of the tryptophan catabolite (TRYCATs)
Comparison of fluoxetine and 1-methyl-L-tryptophan in treatment of depression-like illness in Bacillus Calmette-Guerin-induced inflammatory model of depression in mice.
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BACKGROUND
The inflammatory response system has been implicated in the pathophysiology of major depression. The pro-inflammatory cytokines like interferon-γ induce the enzyme indoleamine-2,3-dioxygenase (IDO) of the kynurenine pathway of tryptophan metabolism. The induction of IDO reduces the
Effects of chronic lung inflammation on tryptophan metabolism in piglets.
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A fundamental question in animal nutrition is the amino acid requirement induced by inflammation and immune response. The aim of the present experiment was to study the effect of chronic lung inflammation induced by injection of complete Freund adjuvant on amino acid metabolism in pigs. For 10 days,
Altered tryptophan metabolism as a paradigm for good and bad aspects of immune privilege in chronic inflammatory diseases.
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The term "immune privilege" was coined to describe weak immunogenicity (hypo-immunity) that manifests in some transplant settings. We extended this concept to encompass hypo-immunity that manifests at local sites of inflammation relevant to clinical diseases. Here, we focus on emerging evidence that
Relation of kynurenine/tryptophan with immune and inflammatory markers in coronary artery disease.
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BACKGROUND
Inflammation and immune activation have a crucial role in the pathogenesis of cardiovascular diseases. Indolamine 2,3-dioxygenase, a tryptophan catabolising enzyme, is up-regulated with various inflammatory stimuli. The aim of this study was to evaluate the relationship of tryptophan
Psychosocial stress and inflammation driving tryptophan breakdown in children and adolescents: A cross-sectional analysis of two cohorts.
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BACKGROUND
Tryptophan breakdown is an important mechanism in several diseases e.g. inflammation and stress-induced inflammation have been associated with the development of depression via enhanced tryptophan breakdown. Depression is a major public health problem which commonly starts during
Linking the biological underpinnings of depression: Role of mitochondria interactions with melatonin, inflammation, sirtuins, tryptophan catabolites, DNA repair and oxidative and nitrosative stress, with consequences for classification and cognition.
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The pathophysiological underpinnings of neuroprogressive processes in recurrent major depressive disorder (rMDD) are reviewed. A wide array of biochemical processes underlie MDD presentations and their shift to a recurrent, neuroprogressive course, including: increased immune-inflammation,
Associations Among Obesity, Inflammation, and Tryptophan Catabolism in Pregnancy.
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To evaluate relationships among obesity in pregnancy and plasma levels of tryptophan (TRP) and kynurenine (KYN), inflammatory markers, and depressed mood.
Pregnant women ( N = 374) were enrolled, and data were collected at a mean gestation of 20 weeks in this cross-sectional study. Plasma was
Revisiting the tryptophan-serotonin deficiency and the inflammatory hypotheses of major depression in a biopsychosocial approach.
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UNASSIGNED
The aim of this cross-sectional study was to identify important biopsychosocial correlates of major depression. Biological mechanisms, including the inflammatory and the tryptophan-serotonin deficiency hypotheses of major depression, were investigated alongside health-related quality of
Serotonin-immune interactions in detoxified chronic alcoholic patients without apparent liver disease: activation of the inflammatory response system and lower plasma total tryptophan.
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The aims of the present study were to examine (1) the inflammatory response system (IRS), through measurements of serum interleukin-6 (IL-6), soluble IL-6 receptor (sIL-6R), sgp130 (the soluble form of the IL-6 transducer signal protein), CC16 (Clara Cell protein; an endogenous anti-cytokine), IL-1R
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