taxol/atrophy

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Avian axons undergo Wallerian degeneration after injury and stress.

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The integrity of long axons is essential for neural communication. Unfortunately, relatively minor stress to a neuron can cause extensive loss of this integrity. Axon degeneration is the cell-intrinsic program that actively deconstructs an axon after injury or damage. Although ultrastructural

Calpain inhibition protects against Taxol-induced sensory neuropathy.

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Taxol is a highly effective anticancer agent that causes peripheral neuropathy as its major toxic side effect. The neuropathy is characterized by degeneration of sensory axons that may be severe enough to be dose limiting. Axonal degeneration involves the activation of the calcium-activated

Protection against beta-amyloid toxicity in primary neurons by paclitaxel (Taxol).

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Neurofibrillary tangles in Alzheimer's disease contain aggregates of abnormally phosphorylated microtubule-associated protein tau, indicating that microtubule breakdown is a primary event in the neurodegenerative cascade. Recent studies have shown that addition to neuronal cultures of amyloid

Taxol Improves Pre-Implantation Development Potential of Mouse Embryos.

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The objective of the present study was to investigate the development of mouse embryos and the chromosomal status after the pre-implantation treatment with paclitaxel (Taxol) based on the reports that indicate Taxol improves the developmental potential of vitrified human and mouse

A model of toxic neuropathy in Drosophila reveals a role for MORN4 in promoting axonal degeneration.

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Axonal degeneration is a molecular self-destruction cascade initiated following traumatic, toxic, and metabolic insults. Its mechanism underlies a number of disorders including hereditary and diabetic neuropathies and the neurotoxic side effects of chemotherapy drugs. Molecules that promote axonal

Investigational new drug-directed, 5-day repeat dose toxicity study of 4-[3-(2-nitro-1-imidazolyl)-propylamino]-7-chloroquinoline hydrochloride (NLCQ-1, NSC 709257) administered with or without Taxol in Sprague-Dawley rats.

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In pre-clinical studies, 4-[3-(2-nitro-1-imidazolyl)-propylamino]-7-chloroquinoline hydrochloride (NLCQ-1, NSC 709257) is a weak DNA-intercalating, hypoxia-selective cytotoxin with a promising profile as an adjuvant to radio/chemotherapy and it is about to enter phase I clinical trials. The present

The acute effects of taxol upon regenerating axons after nerve crush.

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The effects of taxol, a compound renowned for its ability to promote microtubule assembly, were studied upon axons after its injection into rat sciatic nerve immediately following a local nerve crush injury. The single injection of taxol was delivered into the lesion site and the animals were

Taxol-induced neuropathy: chronic effects of local injection.

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The long-term neurotoxic effects of taxol, a compound known to promote microtubule protein polymerization, injected subepineurially into rat sciatic nerve were studied up to 10 weeks post-injection. At the site of injection, taxol caused local axonal reactions and degeneration which were causally

Effect of taxol on the expression of FoxM1 ovarian cancer-associated gene.

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The incidence of ovarian cancer in women has been on the increase in recent years. The aim of the present study was to examine the effects of taxol on the expression of ovarian cancer-associated gene forkhead box transcription factor M1 (FoxM1) and its therapeutic effects for ovarian cancer. The

Fractionated stereotactic radiosurgery and concurrent taxol in recurrent glioblastoma multiforme: a preliminary report.

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OBJECTIVE Surgery and systemic chemotherapy offer modest benefit to patients with recurrent glioblastoma multiforme. These tumors are associated with rapid growth and progressive neurological deterioration. Radiosurgery offers a rational alternative treatment, delivering intensive local therapy. A

Taxol-induced neuropathy after nerve crush: long-term effects on regenerating axons.

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Previous studies have shown that newly derived axonal sprouts are sensitive to the effect of taxol. Taxol induced an accumulation of microtubules in axonal sprouts, which resulted in giant axonal bulbs with the subsequent excessive proliferation of distorted axonal twigs from the distal end of

Schwann cells and collagen synthesis in taxol-treated nerve crush. An electron microscopic study.

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The effect of nerve crush on collagen synthesis in rat sciatic nerve was studied by electron microscope. The crushed nerves were treated with taxol which is known to increase the amount of cytoplasmic microtubules at the expense of other cell organelles such as rough endoplasmic reticulum and Golgi

Effect of nerve growth factor on peptide neurons in dorsal root ganglia after taxol or cisplatin treatment and in diabetic (db/db) mice.

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In our study we have used morphological and radio-immunological methods for the investigation of calcitonin gene-related peptide (CGRP) and substance P in cervical dorsal root ganglia (DRGs) in mice after administration of taxol or cisplatin and in spontaneously diabetic animals (db/db mice). The

Changes of fast axonal transport by taxol injected subepineurally into the rat sciatic nerve.

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In contrast to the complete and long-lasting inhibition of tubulin transport, taxol has no effect on fast axonal transport examined immediately after its sub-epineural application to rat sciatic nerve. However, a significant accumulation of rapidly migrating radioactivity appears at the site

Microtubule-dependent processes precede pathological calcium influx in excitotoxin-induced axon degeneration.

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Axon degeneration and axonal loss is a feature of neurodegenerative disease and injury and occurs via programmed pathways that are distinct from cell death pathways. While the pathways of axonal loss following axon severing are well described, less is known about axonal loss following other

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