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Biochemical studies on the cardioprotective effect of glutamine on tissue antioxidant defense system in isoprenaline-induced myocardial infarction in rats.
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Oxidative stress is one of the mechanisms with a central role involved in the pathogenesis of myocardial infarction. The protective effect of glutamine on myocardial antioxidant defense system was investigated during isoprenaline-induced myocardial infarction, an animal model of myocardial
Intestinal barrier function in patients with acute myocardial infarction and the therapeutic effect of glutamine.
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Mutations in long-chain 3-hydroxyacyl coenzyme a dehydrogenase are associated with placental maternal floor infarction/massive perivillous fibrin deposition.
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Maternal floor infarction/massive perivillous fibrin deposition (MFI/MPVFD) of the placenta has an unclear etiology. The placenta of an 8-month-old child diagnosed with long-chain 3-hydroxyacyl coenzyme A dehydrogenase (LCHAD) deficiency reportedly showed MFI, but no further evidence of a direct
Lubeluzole blocks increases in extracellular glutamate and taurine in the peri-infarct zone in rats.
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A microdialysis probe was positioned inside the peri-infarct zone of a photochemically induced neocortical infarct in rats. Extracellular glutamate rose within 20 min after the start of infarct induction and continued to increase during the 5 h observation period to 5.5-fold the pre-infarct baseline
Leiden factor V mutation in four patients with small bowel infarctions.
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The Leiden factor V mutation is observed in 20% of unexplained lower limb venous thromboses and involves substitution of the arginine residue at position 506 by glutamine (R506Q). It is known to decrease the anticoagulant activity of activated protein C. This case report describes 4 cases of small
Microdialysis patterns in subarachnoid hemorrhage patients with focus on ischemic events and brain interstitial glutamine levels.
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BACKGROUND
This observational microdialysis (MD) study of 33 subarachnoid hemorrhage patients explores brain interstitial levels of glutamine, glutamate, lactate and pyruvate, and their relationship to clinical status and clinical course at the neurointensive care unit.
METHODS
The focus was on
Glutamine is cardioprotective in patients with ischemic heart disease following cardiopulmonary bypass.
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BACKGROUND
The aim of the present study was to investigate the cardioprotective effects of the perioperative use of N(2)-L-alanyl-L-glutamine (GLN) in patients with ischemic heart disease (IHD) who undergo their operations under cardiopulmonary bypass (CPB).
METHODS
This double-blind,
Methionine sulfoximine reduces cortical infarct size in rats after middle cerebral artery occlusion.
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The methionine analogue methionine sulfoximine was administered to 10 rats 24 hours before occlusion of the proximal left middle cerebral artery. Three days later the rats were decapitated and the brain infarct volumes were compared with those in 10 control rats that received saline before middle
Close association between the reduction in myocardial energy metabolism and infarct size: dose-response assessment of cyclosporine.
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Cyclosporine protects the heart against ischemia/reperfusion injury, but its effect on cardiac metabolism is largely unknown. We assessed cyclosporine-induced metabolic changes in the rat heart prior to occlusion using magnetic resonance spectroscopy (MRS) and correlated effects with infarct size in
Intravenous glutamine enhances COX-2 activity giving cardioprotection.
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BACKGROUND
Preconditioning, a highly evolutionary conserved endogenous protective response, provides the most powerful form of anti-infarct protection known. We investigated whether acute intravenous glutamine, through an effect on cyclooxygenase (COX)-2 and heat shock protein (HSP) 72, might induce
Physiological levels of glutamine prevent morphine-induced preconditioning in the isolated rat heart.
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Morphine induces cardioprotection against ischaemia-reperfusion injury. While aiming to investigate the underlying signal transduction cascade of morphine preconditioning in isolated Langendorff-perfused rat hearts, the expected cardioprotection was not detectable. Thus, we investigated the
[Certain nitrogen-containing components of the heart, of the coronary-sinus blood and of the aorta in experimental myocardial infarct].
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Forty-two dogs were subjected to studies of nitrogen-containing metabolites in the blood of the aorta, coronary sinus and in various parts of the heart under normal conditions and 1, 24 hours and 3 days following the induction of myocardial infarction. In normal dogs the myocardium usually retains
Host-pathogen evolution: Implications for the prevention and treatment of malaria, myocardial infarction and AIDS.
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Humans have evolved complex immune systems to protect against infection by pathogens. However, pathogens possess a remarkable genetic versatility that allows them to gain new vigour and so escape such population immunity. Conflicting pathogen-host objectives, therefore, lead to the evolutionary
Metabolic Characterization of Myocardial Infarction Using GC-MS-Based Tissue Metabolomics.
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Understanding the metabolic features of myocardial infarction (MI) is critical to its prevention and treatment. Here, we aimed to characterize the metabolic features of early MI using a tissue metabolomics method based on gas chromatography-mass spectrometry (GC-MS). Thirty-four pairs of infarcted
Glutamate, glutamine, and GABA as substrates for the neuronal and glial compartments after focal cerebral ischemia in rats.
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OBJECTIVE
Even though the utilization of substrates alternative to glucose may play an important role in the survival of brain cells under ischemic conditions, evidence on changes in substrate selection by the adult brain in vivo during ischemic episodes remains very limited. This study investigates
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