Results 91 to 100 of about 5,015,403 (283)

Can IDO activity predict primary resistance to anti-PD-1 treatment in NSCLC?

open access: yesJournal of Translational Medicine, 2018
Background Immune checkpoint inhibitors have revolutionized the treatment paradigm of highly lethal malignancies like advanced non-small cell lung cancer (NSCLC), demonstrating long-term tumour control and extended patient survival.
Andrea Botticelli   +9 more
doaj   +1 more source

Increased indoleamine-2,3-dioxygenase activity is associated with poor clinical outcome in adults hospitalized with influenza in the INSIGHT FLU003Plus study [PDF]

open access: yes, 2017
BACKGROUND: Indoleamine-2,3-dioxygenase (IDO) mediated tryptophan (TRP) depletion has antimicrobial and immuno-regulatory effects. Increased kynurenine (KYN)-to-TRP (KT) ratios, reflecting increased IDO activity, have been associated with poorer ...
Aagaard, B   +99 more
core   +2 more sources

Phosphorylation of ITIM motifs drives the structural transition of indoleamine 2,3‐dioxygenase 1 between enzymatic and non‐enzymatic states

open access: yesProtein Science, Volume 34, Issue 6, June 2025.
Abstract Indoleamine 2,3‐dioxygenase 1 (IDO1) is the rate‐limiting enzyme in tryptophan metabolism that plays a central role in immune regulation across a range of diseases, including cancer. Beyond its enzymatic role, IDO1 has a non‐enzymatic function that remains poorly understood.
Gyula Hoffka   +3 more
wiley   +1 more source

Beta-trace Protein as a new non-invasive immunological Marker for Quinolinic Acid-induced impaired Blood-Brain Barrier Integrity

open access: yesScientific Reports, 2017
Quinolinic acid, a macrophage/microglia-derived excitotoxin fulfills a plethora of functions such as neurotoxin, gliotoxin, and proinflammatory mediator, and it alters the integrity and cohesion of the blood-brain barrier in several pathophysiological ...
A. Baranyi   +9 more
semanticscholar   +1 more source

Hyperammonemia-induced toxicity for the developing central nervous system [PDF]

open access: yes, 2007
In pediatric patients, hyperammonemia can be caused by various acquired or inherited disorders such as urea cycle deficiencies or organic acidemias. The brain is much more susceptible to the deleterious effects of ammonium during development than in ...
Braissant, O., Cagnon, L.
core   +1 more source

Is quinolinic acid involved in etiopathogenesis of schizophrenia? [PDF]

open access: yesJournal of Neurochemistry, 2003
Retroviruses have been proposed as one of the infectious agents involved in the pathogenesis of schizophrenia. They can cause neuronal death by endogenous toxin(s), such as quinolinic acid (QUIN), released by virus‐activated brain macrophages/microglia. QUIN is an endogenous excitotoxin, with an affinity at specific NMDA‐R heteromers.
Hana Tejkalová   +4 more
openaire   +2 more sources

Multi‐Omic Analysis of Glutamate Excitotoxicity in Primary Neuronal Cultures

open access: yesJournal of Neurochemistry, Volume 169, Issue 6, June 2025.
Our study on rat neuron cells found 250 μM glutamate to be toxic, causing neuron death. We identified genes in pathways linked to apoptosis, neuron plasticity, and cell signaling, along with proteins regulating the cell cycle and tumor proliferation.
Jennifer H. Nguyen   +13 more
wiley   +1 more source

High Kynurenine (a Tryptophan Metabolite) Predicts Remission in Patients with Major Depression to Add-on Treatment with Celecoxib [PDF]

open access: yes, 2017
Background: Signs of an inflammatory process have been described in major depression. Methods: In a double-blind, randomized study of celecoxib or placebo add-on to reboxetine in 40 depressed patients, celecoxib treatment has beneficial effects. In order
Anja Cerovecki   +9 more
core   +2 more sources

Kynurenine pathway metabolite alterations in Down syndrome and Alzheimer's disease

open access: yesAlzheimer's &Dementia, Volume 21, Issue 5, May 2025.
Abstract INTRODUCTION Down syndrome (DS) is a genetic disorder that leads to intellectual disability and accelerated aging, increasing the risk of Alzheimer's disease (AD). The pathophysiology of AD and DS is multifactorial, involving amyloid precursor protein overexpression, neuroinflammation, and oxidative stress.
Rafaela Gomes dos Reis   +4 more
wiley   +1 more source

In vivo evidence for NMDA receptor mediated excitotoxicity in a murine genetic model of Huntington Disease [PDF]

open access: yes, 2008
N-methyl-D-aspartate receptor (NMDAR) mediated excitotoxicity is implicated as a proximate cause of neurodegeneration in Huntington Disease (HD). However, this hypothesis has not been tested rigorously in vivo. NMDAR NR2B-subunits are the predominant NR2
Joe Tsien   +4 more
core   +1 more source

Home - About - Disclaimer - Privacy