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Страна 1 од 326 резултати
Carbon disulfide effects on the visual system. II. Retinogeniculate degeneration.
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We examined the morphological effects of carbon disulfide exposure on neurons and vasculature of the visual system of macaque monkeys. Five monkeys were exposed to 256 ppm carbon disulfide (CS2) by inhalation for 6 hr a day, 5 days a week. One monkey, sacrificed immediately after exposure, had
Dynamic thiol/disulfide homeostasis in patients with age-related macular degeneration.
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UNASSIGNED
We evaluated dynamic thiol/disulfide homeostasis (TDH), malondialdehyde (MDA) levels, and catalase (CAT) activity in patients with age-related macular degeneration (AMD). All analyzes were conducted on plasma samples.
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Thirty-two patients with AMD and 38 age-matched healthy
Thiol-disulfide Oxidoreductases TRX1 and TMX3 Decrease Neuronal Atrophy in a Lentiviral Mouse Model of Huntington's Disease.
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Huntington's disease (HD) is caused by a trinucleotide CAG repeat in the huntingtin gene (HTT) that results in expression of a polyglutamine-expanded mutant huntingtin protein (mHTT). N-terminal fragments of mHTT accumulate in brain neurons and glia as soluble monomeric and oligomeric species as
X-ray-induced deterioration of disulfide bridges at atomic resolution.
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Overall and site-specific X-ray-induced damage to porcine pancreatic elastase was studied at atomic resolution at temperatures of 100 and 15 K. The experiments confirmed that irradiation causes small movements of protein domains and bound water molecules in protein crystals. These structural changes
Do Beta 2-Glycoprotein I Disulfide Bonds Protect the Human Retina in the Setting of Age-Related Macular Degeneration?
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Age-related macular degeneration (AMD) affects the region of the retina that is responsible for high-resolution vision. It is a major cause of blindness in the aging population. This is the first study that examines the association of redox-modified, cysteine-based, post-translational forms of beta
Multiple system atrophy following chronic carbon disulfide exposure.
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Carbon disulfide toxicity is well characterized. The principal target organ is the nervous system, although cardiovascular, reproductive, ophthalmologic, and other effects are also recognized. The neurotoxicity manifests in three ways: encephalopathy, peripheral and cranial nerve dysfunction, and
Cerebellar atrophy as a delayed manifestation of chronic carbon disulfide poisoning.
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A 70-year-old man developed a slowly progressive cerebellar syndrome after having been exposed to carbon disulfide (CS2) in a viscose rayon plant for 27 years. Ataxia, dysmetria, dysarthria and adiadochokinesia appeared 7 years after retirement from work (at age 54), and were later accompanied by
Nitric oxide mediates selective degeneration of hypothalamic orexin neurons through dysfunction of protein disulfide isomerase.
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We addressed the role of nitric oxide (NO) in orexin neuron degeneration that has been observed under various pathological conditions. Administration of an NO donor NOC18 (50 nmol) into the third ventricle of mice resulted in a significant decrease of orexin-immunoreactive (-IR) neurons, in contrast
A Novel Tool for the Assessment Oxidative Stress in Age-Related Macular Degeneration: Thiol/Disulfide Homeostasis Revisited.
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To investigate thiol/disulfide status using a novel automated assay in patients with age-related macular degeneration (AMD) compared to age-matched healthy controls.
A total of 64 AMD patients [51 (79%) non-exudative, 13 (21%) exudative AMD] and 21 age-matched healthy control subjects were enrolled
Protein disulfide isomerase immunopositive glial cytoplasmic inclusions in patients with multiple system atrophy.
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BACKGROUND
Glial cytoplasmic inclusions (GCIs) are the pathological hallmarks of multiple system atrophy (MSA) and α-synuclein is abnormally deposited in GCIs. Protein disulfide isomerase (PDI) is a member of the thioredoxin superfamily and is believed to accelerate the folding of disulfide-bonded
Differential requirements for retinal degeneration slow intermolecular disulfide-linked oligomerization in rods versus cones.
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It is commonly assumed that the ultrastructural organization of the rim region of outer segment (OS) discs in rods and lamellae in cones requires functional retinal degeneration slow/rod outer segment membrane protein 1 (Rds/Rom-1) complexes. Cysteine-150 (C150) in Rds has been implicated in
Femtosecond degenerate four-wave mixing of carbon disulfide: high-accuracy rotational constants.
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Femtosecond degenerate four-wave mixing (fs-DFWM) rotational coherence spectroscopy (RCS) has been used to determine the rotational and centrifugal distortion constants of the 00 (0)0 ground and 01 (1)0 vibrationally excited states of gas-phase CS(2). RCS transients were recorded over the 0-3300 ps
Disulfide-mediated oligomerization of Peripherin/Rds and Rom-1 in photoreceptor disk membranes. Implications for photoreceptor outer segment morphogenesis and degeneration.
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Peripherin/Rds is a tetraspanning membrane protein that has been implicated in photoreceptor outer segment morphogenesis and inherited retinal degenerative diseases. Together with the structurally related protein, Rom-1, it forms a complex along the rims of rod and cone disc membranes. We have
Carbon disulfide neuropathy in rats. A morphological and ultrastructural study of degeneration and regeneration.
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The aim of this study was to elucidate the site and detailed nature of peripheral nerve damage induced in the rat by chronic CS2 inhalation exposure in the light of the relationship between pathological and neurophysiological data. Adult male rats were exposed to 700 ppm of CS2 2 h/d, 5 d/week for
Degeneration of the basal ganglia in monkeys from chronic carbon disulfide poisoning.
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