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tryptophan/hemorragia

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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

Alterations of monoamine metabolites and of tryptophan in the basal cisternal CSF of patients after subarachnoid haemorrhage.

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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

Hypotensive but not normotensive haemorrhage increases tryptophan hydroxylase-2 mRNA in caudal midline medulla.

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Severe blood loss triggers shock, a precipitous hypotension and bradycardia. The integrity of (i) neurons in the vasodepressor region of the caudal midline medulla and (ii) central 5-HT neurotransmission are critical for the expression of haemorrhagic shock. This study investigated whether

The effect of L-tryptophan on hemorrhagic shock induced bacterial translocation.

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Hemorrhagic shock causes mucosal damage in intestine and it results in translocation of bacteria to distant organs. In this study, effects of various doses of L-Tryptophan on the prevention of bacterial translocation in hemorrhagic shock induced rabbits were investigated. This study was carried out

[Some aspects of the metabolism and balance of tryptophan in patients with Far Eastern hemorrhagic fever with renal syndrome].

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Cerebrospinal fluid untargeted metabolomic profiling of aneurysmal subarachnoid hemorrhage: an exploratory study.

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Despite advancements in medical and surgical therapies, clinical outcomes of aneurysmal subarachnoid hemorrhage (aSAH) continue to be poor. Currently, aSAH pathophysiology remains poorly understood. No aSAH biomarkers are commonly used in the clinical setting. This exploratory study

Mechanism of metabolic stroke and spontaneous cerebral hemorrhage in glutaric aciduria type I.

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BACKGROUND Metabolic stroke is the rapid onset of lasting central neurological deficit associated with decompensation of an underlying metabolic disorder. Glutaric aciduria type I (GA1) is an inherited disorder of lysine and tryptophan metabolism presenting with metabolic stroke in infancy. The

Serotonin neurons of the caudal raphe nuclei contribute to sympathetic recovery following hypotensive hemorrhage.

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Serotonin is thought to contribute to the syncopal-like response that develops during severe blood loss by inhibiting presympathetic neurons of the rostroventrolateral medulla (RVLM). Here, we tested whether serotonin cells activated during hypotensive hemorrhage, i.e., express the protein product

Tryptophan catabolism restricts IFN-γ-expressing neutrophils and Clostridium difficile immunopathology.

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The interplay between Clostridium difficile and the host's metabolome is believed to influence the severity of infection. However, the mechanism for this phenomenon remains unclear. In this study, we model one of these metabolic pathways by focusing on tryptophan metabolism in the host. We found

[Removal ability of anti-ganglioside antibodies in immunoadsorption using a modified tryptophan-immobilized column].

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Guillain-Barré syndrome (GBS) patients are often treated by immunoadsorption using a tryptophan-immobilized column (TR) in Japan. To reduce adsorption of fibrinogens, a modified TR (TR-S) was developed. In this study, we compared removal ability of antiganglioside antibodies among TR-S, TR and a

Comparison of the adsorption ability between tryptophan and modified tryptophan columns.

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Immunoadsorption therapy (IAT) using the tryptophan column (TR:TR-350, Asahi Medical Co., Tokyo, Japan) is used for patients with Guillain-Barré syndrome or Fisher's syndrome. Recently, a modified tryptophan column (modified TR:TR-350S, Asahi) was developed to reduce adsorption of fibrinogens.

Eosinophilia-myalgia syndrome in association with L-tryptophan ingestion.

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The association between the recently described eosinophilia-myalgia syndrome and L-tryptophan is now well established. We describe a patient with eosinophilia-myalgia syndrome who developed incapacitating myalgias and peripheral eosinophilia responsive only to high dose corticosteroids. When massive
OBJECTIVE To compare histopathological findings and the degree of apoptosis among rat lungs preserved with low-potassium dextran (LPD) solution, histidine-tryptophan-ketoglutarate (HTK) solution, or normal saline (NS) at two ischemia periods (6 h and 12 h) using an experimental rat model of ex vivo

[A disorder of serotonin metabolism in patients in the acute period of nontraumatic intracranial hemorrhages].

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The indices of serotonin metabolism in cerebrospinal fluid (CSF) and blood were studied in 43 patients with nontraumatic intracerebral hemorrhage in the interval from 1 - 2 to 28 days after the onset of the disease. The considerable increase of tryptophan, serotonin and its main metabolite

The use of antiserotonergic agents for the treatment of acute hemorrhagic shock of cats.

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In cats anesthetized with pentobarbitone sodium the effect of two types of antiserotonergic agents on cardiovascular recuperation after acute hemorrhage was examined. Methysergide, a competitive inhibitor for 5-HT receptors and p-chlorophenylalanine (PCPA), an inhibitor of tryptophan-5-hydroxylase,
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