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Page 1 de 23 résultats
Histological and magnetic resonance analysis of sciatic nerves in the tellurium model of neuropathy.
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Ingestion of tellurium (Te), a toxic element, produces paralysis of the hind limbs in weanling rats that is due to temporary, segmental demyelination of the sciatic nerves bilaterally. Weanling rats were fed a 1.1% elemental Te diet and sacrificed at various time points for histological and magnetic
Primary demyelination induced by exposure to tellurium alters Schwann cell gene expression: a model for intracellular targeting of NGF receptor.
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Exposure of developing rats to tellurium results in a highly synchronous segmental demyelination of peripheral nerves with sparing of axons; this demyelination is followed closely by a period of rapid remyelination. Demyelination occurs subsequent to a tellurium-induced block in the synthesis of
Hypomyelination in the neonatal rat central and peripheral nervous systems following tellurium intoxication.
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Neonatal rats were exposed to Tellurium (Te), via the mother's milk, from the day of birth until sacrifice at 7, 14, 21, and 28 days of age. Light and electron microscopy revealed Schwann cell and myelin degeneration in the sciatic nerves at each age studied. These changes were similar to those
Strain tuning of electronic properties of various dimension elemental tellurium with broken screw symmetry.
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We present a systematical study of atomic structures and electronic properties of various dimension tellurium (Te) with broken intrinsical screw symmetry by applying reasonable strain. It is demonstrated that (i) bulk trigonal Te has degenerate Weyl nodes around the H point near the Fermi energy,
Ultrafast photoinduced band splitting and carrier dynamics in chiral tellurium nanosheets
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Trigonal tellurium (Te) is a chiral semiconductor that lacks both mirror and inversion symmetries, resulting in complex band structures with Weyl crossings and unique spin textures. Detailed time-resolved polarized reflectance spectroscopy is used to investigate its band structure and carrier
Activation of the autophagy, c-FOS and ubiquitin expression, and nucleolar alterations in Schwann cells precede demyelination in tellurium-induced neuropathy.
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We have used an experimental model of tellurium (Te)-induced demyelinating neuropathy in the rat to study cellular mechanisms involved in the early response of myelinating Schwann cells (SCs) to injury, prior to demyelination. Starting at postnatal day 21, weaned rats were fed a diet containing 1.1%
Lipid droplets in Schwann cells during tellurium neuropathy are derived from newly synthesized lipid.
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Exposure of weanling rats to a diet containing elemental tellurium results in a peripheral neuropathy characterized by segmental demyelination and minimal axonal degeneration. One of the earliest ultrastructural abnormalities in tellurium neuropathy is an increased number of cytoplasmic lipid
Gene expression during tellurium-induced primary demyelination.
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A compound may be "developmentally neurotoxic" because it interferes with a metabolic step exclusively or preferentially expressed during development in a particular class of neural cells. The initial metabolic specificity is often complicated by: (1) secondary responses in the affected cells, (2)
Necrosis of schwann cells during tellurium-induced primary demyelination: DNA fragmentation, reorganization of splicing machinery, and formation of intranuclear rods of actin.
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We present a cytological, immunocytochemical, and biochemical study of the cell death of mature myelinating Schwann cells (SCs) in the primary demyelinating neuropathy induced by tellurium (Te). Weaned rats were fed a diet containing 1.1% elemental Te. The animals were killed daily within the first
Tellurium as a high-performance elemental thermoelectric.
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High-efficiency thermoelectric materials require a high conductivity. It is known that a large number of degenerate band valleys offers many conducting channels for improving the conductivity without detrimental effects on the other properties explicitly, and therefore, increases thermoelectric
Cloning and base sequence analysis of a cDNA encoding mouse lung thioether S-methyltransferase.
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Thioether S-methyltransferase catalyzes transfer of the methyl group from S-adenosylmethionine to X in compounds of the structure R-X-R', where X may be sulfur, selenium, or tellurium, and R and R' may be various organic groups. To obtain a cDNA clone of thioether S-methyltransferase, a mouse lung
Carbon disulfide neurotoxicity in rats: IV. Increased mRNA expression of low-affinity nerve growth factor receptor--a sensitive and early indicator of PNS damage.
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Expression of the low-affinity nerve growth factor receptor (NGF-R) in the peripheral nervous system is regulated by Schwann cell-axonal contact. Steady-state mRNA levels for NGF-R are very low in the mature peripheral nervous system, but are markedly upregulated in sciatic nerve during both primary
Schwann cells as targets for neurotoxicants.
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Schwann cells subserve a variety of roles in the peripheral nervous system (PNS), including ionic homeostasis, and protection and possible metabolic support of axons. It is, however, the myelinating subtype of these glia which appear most sensitive to toxic insults. Myelinating Schwann cells must
Carrier-Type Modulation and Mobility Improvement of Thin MoTe2.
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A systematic modulation of the carrier type in molybdenum ditelluride (MoTe2 ) field-effect transistors (FETs) is described, through rapid thermal annealing (RTA) under a controlled O2 environment (p-type modulation) and benzyl viologen (BV) doping (n-type modulation). Al2 O3 capping is then
Apolipoprotein E is released by rat sciatic nerve during segmental demyelination and remyelination.
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Apolipoprotein E (apo E) is synthesized and released in greatly increased amounts by peripheral nerve following Wallerian degeneration; it has been suggested that this protein may function in the transport of degenerated myelin lipid. The purpose of this study was to determine if the amount of apo E
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