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tryptophan/infarction

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Reliable methods for the determination of tryptophan and its metabolites are vital to the monitoring of biochemical states during the initiation and progression of cardiovascular disease. In the present study, a single-run liquid chromatography-tandem mass spectrometry (LC-MS/MS) method was
In this study, we investigated the relationship between tryptophan-5-hydroxytryptamine metabolism, depressive disorder, and gastrointestinal dysfunction in rats after myocardial infarction. Our goal was to elucidate the physiopathologic bases of somatic/psychiatric depression symptoms after

[Tryptophan and tyrosine in blood and cerebrospinal fluid in patients with recent cerebral infarct].

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The determinations were carried out in the blood and cerebrospinal fluid of 40 patients with recent cerebral infarction and 30 controls. Tryptophan concentration was determined by the fluorimetric method of Denckla and Dewey, and tyrosine concentration by the method of Waalkes and Udenfried. A

[Tryptophan in the blood in the acute phase of myocardial infarct].

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The present study was performed to evaluate the cardioprotective effects of KR-33028, a novel Na+/H+ exchanger subtype 1 (NHE-1) inhibitor, in rat and dog models of coronary artery occlusion and reperfusion. In anesthetized rats subjected to a 45-min coronary occlusion and a 90-min reperfusion,

Safe cross-clamp time using Custodiol®-histidine-tryptophan-ketoglutarate cardioplegia in the adult.

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INTRODUCTION
Safe cross-clamp time using single-dose Custodiol®-histidine-tryptophan-ketoglutarate cardioplegia has not been established conclusively.

Immediate post-operative outcomes of 1,420 non-consecutive, cardiac surgery patients were reviewed

Disturbance of serotonergic neurotransmission in patients with postmyocardial infarction and depression.

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The objective of this study was to assess the hypothesis that patients who develop depression after myocardial infarction (MI) have a lower level of brain serotonergic neurotransmission through measurement of plasma free fraction of L-tryptophan and intensity-dependence auditory-evoked potentials
Homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA) and tryptophan (TRP) were measured in the CSF obtained from the basal cistern of 20 patients, who had undergone surgical obliteration of bleeding aneurysms within 3 days after subarachnoid haemorrhage (SAH). The concentrations of these

Hypochlorous acid oxidizes methionine and tryptophan residues in myoglobin.

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After acute myocardial infarction (AMI), infiltrating proinflammatory cells generate two-electron oxidants such as hypochlorous acid (HOCl). Myoglobin (Mb) is present at approximately 0.3 mM in cardiomyocytes and, therefore, represents a significant target for oxidation. Exposure of horse Mb (50

Decreased plasma tryptophan associated with deep white matter lesions in elderly subjects.

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The aim was to identify potentially treatable risk factors for cerebral white matter lesions often found on MRI in elderly persons. findings were assessed on 1.0 T MRI of 178 subjects living in the community and aged 60 years or older. Participants underwent standardised evaluations including

Changes of some putative neurotransmitters in human cerebral infarction.

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Dopamine (DA), serotonin (5-HT), tryptophan (TRP), 5-hydroxyindole acetic acid (5-HIAA), and GABA were assayed spectrofluorometrically in various regions of 16 human post-mortem brains with acute and old cerebral infarction. In both recent and older strokes a total depletion of DA and 5-HT in the
OBJECTIVE Currently available cardioplegic solutions provide excellent protection in patients with normal surgical risk; in high-risk patients, however, such as in emergency coronary artery bypass surgery, there is still room for improvement. As most of the cardioplegic solutions primarily protect

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

Neurotransmitter precursor amino acids in the treatment of multi-infarct dementia and Alzheimer's disease.

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Ten patients with severe dementia due to Alzheimer's disease (AD) or multi-infarct dementia (MID) or both, were treated with the precursor amino acids of the neurotransmitters serotonin and dopamine. The precursor amino acids (PAA) were given orally in a preparation that included tyrosine (4 gm
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