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tryptophan/atrophy
Врската е зачувана во таблата со исечоци
Страница 1 од 400 резултати
The alpha2 type IX collagen tryptophan polymorphism is associated with the severity of disc degeneration in younger patients with herniated nucleus pulposus of the lumbar spine.
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Tryptophan alleles in COL9A2 (Trp2) and COL9A3 (Trp3) have been linked to lumbar disc diseases in the Finnish population. Although such diseases consist of various pathogenetically different conditions, detailed analysis of each has not been well documented. The aim of this study was to clarify
Behavioral and biochemical effects of L-tryptophan and buspirone in a model of cerebellar atrophy.
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The Lurcher mutant mouse can be considered an adequate model of autosomal dominant spinocerebellar atrophy because of the severe degeneration of its cerebellar cortex and inferior olive. The purpose of this study was to determine whether the motor coordination deficits of Lurcher mutants could be
Low Levels of Serum Tryptophan Underlie Skeletal Muscle Atrophy.
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Sarcopenia is a poor prognosis factor in some cancer patients, but little is known about the mechanisms by which malignant tumors cause skeletal muscle atrophy. Tryptophan metabolism mediated by indoleamine 2,3-dioxygenase is one of the most important amino acid changes associated with cancer
Kynurenine, a Tryptophan Metabolite That Increases with Age, Induces Muscle Atrophy and Lipid Peroxidation.
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The cellular and molecular mechanisms underlying loss of muscle mass with age (sarcopenia) are not well-understood; however, heterochronic parabiosis experiments show that circulating factors are likely to play a role. Kynurenine (KYN) is a circulating tryptophan metabolite that is known to increase
Rapid deterioration in patients with parkinsonism following tryptophan-pyridoxine administration.
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Cerebrospinal fluid tryptophan and brain atrophy in patients with chronic schizophrenia.
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Ultrafast Quantum Interference in the Charge Migration of Tryptophan.
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Extreme-ultraviolet-induced charge migration in bio-relevant molecules is a fundamental step in the complex path leading to photo-damage. In this work we propose a simple interpretation of the charge migration recently observed in an attosecond pump--probe experiment on the amino acid Tryptophan. We
Cerebrospinal fluid biogenic amines depletion and brain atrophy in adult patients with phenylketonuria.
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Biogenic amines synthesis in phenylketonuria (PKU) patients with high phenylalanine (Phe) concentration is thought to be impaired due to inhibition of tyrosine and tryptophan hydroxylases and competition with amino acids at the blood-brain barrier. Dopamine and serotonin deficits might explain brain
Noncovalent PEGylation: different effects of dansyl-, L-tryptophan-, phenylbutylamino-, benzyl- and cholesteryl-PEGs on the aggregation of salmon calcitonin and lysozyme.
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Protein aggregation is a major instability that can occur during all stages of protein drug production and development. Protein aggregates may compromise the safety and efficacy of the final protein formulation. In this paper, various new excipients [phenylbutylamino-, benzyl-, and
3,4-Methylenedioxymethamphetamine induces differential regulation of tryptophan hydroxylase 2 protein and mRNA levels in the rat dorsal raphe nucleus.
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Previous investigations with 3,4-methylenedioxymethamphetamine (MDMA) have suggested that administration of this drug results in a degeneration of 5-HT nerve terminals and subsequent alterations in 5-HT neurotransmission. However, only limited investigations have examined the effects of MDMA on the
Ultrastructural characterization of tryptophan hydroxylase 2-specific cortical serotonergic fibers and dorsal raphe neuronal cell bodies after MDMA treatment in rat.
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BACKGROUND
3,4-Methylenedioxymethamphetamine (MDMA, "ecstasy") is a widely used recreational drug known to cause selective long-term serotonergic damage.
OBJECTIVE
The aim of this study was to characterize the ultrastructure of serotonergic pericarya and proximal neurites in the dorsal raphe nucleus
Magnetic resonance imaging findings in relation to the COL9A2 tryptophan allele among patients with sciatica.
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METHODS
The phenotype of patients with sciatica who have the Trp2 allele is characterized cross-sectionally.
OBJECTIVE
To determine whether it is possible to differentiate patients with the Trp2 allele clinically or by magnetic resonance imaging.
BACKGROUND
Several studies have indicated a positive
State of the art. Four easy pieces: interconnections between tissue injury, intermediary metabolism, autoimmunity, and chronic degeneration.
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Four questions are posed: (1) Can tissue damage itself provoke autoimmunity? (2) Can genetic mutations of key structures produce tissue pathology and thus provoke autoimmunity? (3) Can acute immune damage produce tissue degeneration without further hallmarks of an immune response? (4) Can
L-tryptophan and the eosinophilia-myalgia syndrome: pathologic findings in eight patients.
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Pathologic findings in eight patients with the eosinophilia-myalgia syndrome, secondary to L-tryptophan ingestion, are reported. Tissue was obtained by biopsy alone in six patients, by biopsy and autopsy in the seventh patient, and by autopsy alone in the eighth patient. Muscle biopsies in five
Alpha-[11C] methyl-L-tryptophan and glucose metabolism in patients with temporal lobe epilepsy.
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OBJECTIVE
To determine whether metabolism in the brain serotonergic system, including the kynurenine pathway, is involved in temporal lobe epilepsy (TLE).
METHODS
The authors studied 14 patients with intractable TLE by PET using alpha-[11C] methyl-L-tryptophan (alpha-MTrp) and
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