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Regulation of blood pressure and glucose metabolism induced by L-tryptophan in stroke-prone spontaneously hypertensive rats.

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BACKGROUND Amino acids have been reported to act as modulators of various regulatory processes and to provide new therapeutic applications for either the prevention or treatment of metabolic disorders. The purpose of the present study is to investigate the effects of single oral dose administration

Inflammation-induced catabolism of tryptophan and tyrosine in acute ischemic stroke.

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Whether the inflammatory response that accompanies acute ischemic stroke induces the kynurenine pathway is currently a matter of conjecture. Activation of this pathway may disturb active metabolites. The aim of this study was thus to characterize the catabolism of tryptophan and tyrosine in acute

Variation of Genes Encoding Tryptophan Catabolites Pathway Enzymes in Stroke.

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The abnormal activation of the tryptophan catabolites pathway (TRYCATs) is observed in patients suffering from cerebrovascular disease, including stroke. A previous study confirmed that lower bioavailability of tryptophan for serotonin synthesis was characterized in the patients during the acute

The role of tryptophan catabolism along the kynurenine pathway in acute ischemic stroke.

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Post-stroke inflammation may induce upregulation of the kynurenine (KYN) pathway for tryptophan (TRP) oxidation, resulting in neuroprotective (kynurenic acid, KA) and neurotoxic metabolites (3-hydroxyanthranillic acid, 3-HAA). We investigated whether activity of the kynurenine pathway in acute

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

A substance P antagonist improves outcome when administered 4 h after onset of ischaemic stroke.

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Previous studies have suggested that substance P (SP) plays a critical role in the development of brain oedema and functional deficits following traumatic brain injury and that SP receptor antagonism may improve outcome. No studies have described such a role in ischemic stroke. The present study

Tryptophan hydroxylase 2 gene polymorphisms and poststroke anxiety disorders.

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BACKGROUND Anxiety is common in stroke survivors and may adversely affect recovery. Polymorphisms of tryptophan hydroxylase2 (THP2) gene have been shown to be associated with anxiety disorders and other affective disorders. This study was aimed to investigate the association of two polymorphisms of

Clinical features of the pathogenic m.5540G>A mitochondrial transfer RNA tryptophan gene mutation.

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Mitochondrial DNA disease is one of the most common groups of inherited neuromuscular disorders and frequently associated with marked phenotypic and genotypic heterogeneity. We describe an adult patient who initially presented with childhood-onset ataxia without a family history and an unremarkable

The effect of F-actin on the relay helix position of myosin II, as revealed by tryptophan fluorescence, and its implications for mechanochemical coupling.

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The fluorescence properties of Dictyostelium discoideum (Dd) myosin II constructs containing a single tryptophan residue have revealed detailed information regarding nucleotide binding and hydrolysis steps. Here we extend these studies to investigate the influence of actin on nucleotide-induced

The relationship between indoleamine 2,3-dioxygenase activity and post-stroke cognitive impairment.

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BACKGROUND Activation of indoleamine 2,3-dioxygenase (IDO) and higher concentrations of several kynurenine metabolites have been observed post-stroke, where they have been associated with increased mortality. While lower tryptophan or a higher ratio of kynurenine/tryptophan (K/T) in peripheral blood

Tertiary structural changes in the cleft containing the ATP sensitive tryptophan and reactive thiol are consistent with pivoting of the myosin heavy chain at Gly699.

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The conformation of myosin subfragment 1 (S1) in the vicinity of the ATP sensitive tryptophan (Trp510) and the highly reactive thiol (SH1), both residing in the "probe-binding" cleft at the junction of the catalytic and lever arm domains, was studied to ascertain its role in the mechanism of energy

Involvement of kynurenines in Huntington's disease and stroke-induced brain damage.

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Several components of the kynurenine pathway of tryptophan metabolism are now recognised to have actions of profound biological importance. These include the ability to modulate the activation of glutamate and nicotinic receptors, to modify the responsiveness of the immune system to inflammation and

Selective perturbation of the myosin recovery stroke by point mutations at the base of the lever arm affects ATP hydrolysis and phosphate release.

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After ATP binding the myosin head undergoes a large structural rearrangement called the recovery stroke. This transition brings catalytic residues into place to enable ATP hydrolysis, and at the same time it causes a swing of the myosin lever arm into a primed state, which is a prerequisite for the

Combined tissue plasminogen activator and an NK1 tachykinin receptor antagonist: an effective treatment for reperfusion injury following acute ischemic stroke in rats.

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We have recently reported on the efficacy of an NK1 tachykinin receptor antagonist in improving outcome following stroke, including reduced blood-brain barrier (BBB) disruption, reduced cerebral edema and improved functional outcome. The clinically approved stroke treatment, tissue plasminogen

Mechanoenergetic function and troponin T release following cardioplegic arrest induced by St Thomas' and histidine-tryptophan-ketoglutarate cardioplegia--an experimental comparative study in pigs.

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The study compares the single dose histidine-tryptophan-ketoglutarate (HTK) cardioplegia to the repeatedly delivered St Thomas' Hospital Solution (STHS) with respect to preservation of left ventricular mechanoenergetics and leakage of troponin T in a porcine experimental model. Fourteen pigs were

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