actinomycin d/atrofija

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[Wallerian degeneration of the rat sciatic nerve. Lack of effect of cycloheximide and of actinomycin D on the increase of radiophosphate incorporation in acid soluble phosphates observed after section of the nerve].

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Plasma inorganic phosphate incorporation into inorganic and organic acid-soluble phosphate fractions of the rat sciatic nerve increases markedly during Wallerian degeneration. Administration of cycloheximide and actinomycin D remains without effect on this specific increase which appears thus

Inhibitory effect of actinomycin D on tail atrophy in Xenopus larvae at metamorphosis.

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Effects of actinomycin D on developing hamster molar tooth germs in vitro.

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The aim of this study was to evaluate the toxic effects of actinomycin D on the developing hamster tooth germ in organ culture. Hamster tooth germs during early secretory amelogenesis were exposed in vitro for 24 h to 10(-9) M-5 x 10(-5) M actinomycin D. Actinomycin D dose-dependently (> or = 10(-7)

Caspase Inhibitor z-VAD-FMK Increases the Survival of Hair Cells After Actinomycin-D-induced Damage in Vitro

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Actinomycin-D (Act-D) is a highly effective chemotherapeutic agent that induces apoptosis in systemic tissues. Act-D combined with other chemotherapeutic agents exhibits ototoxic effects and causes hearing impairment. To investigate the potential toxic effects of Act-D in the inner ear, we treated

The differential sensitivity of cultured chick mesodermal cells to actinomycin D.

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Cells were isolated from the somite mesoderm and from the unsegmented (presomite) mesoderm of early chick embryos and exposed to actinomycin D in single cell culture. Actinomycin D inhibited proliferation in cell cultures derived from the unsegmented mesoderm, although the same concentrations of

[Postnatal growth inhibition in the rat retina after actinomycin D adminstration].

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The effects of actinomycin D on the development of the rats retina were observed. At the day of birth the inner neurons and the inner cells of the bipolar layer are vulnerable. The pale degeneration of these neurons accompanied by a dilatation of the endoplasmatic reticulum and the dark degeneration

Is actinomycin D suitable for the investigation of memory processes?

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The influence of Actinomycin D (AMD) applied intrahippocampally at doses of 1-6 mug/animal, on the acquisition and retention of a shock-motivated brightness discrimination was studied on rats in a semiautomatic Y-maze. The injection of AMD 4 hr prior to training did not influence the acquisition,

Nerve regeneration in Wld(s) mice is normalized by actinomycin D.

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Injured nerves of Wld(s) mice neither degenerate nor regenerate for several weeks. We have conjectured that Wld(s) axons have the ability to regenerate but its expression is impaired by the Schwann cells of the undegenerated distal stump. To test this conjecture, transcription was locally arrested

Neuronal chromatin changes in layer V pyramidal cells of somatomotor cortex after pyramidal tract lesions as demonstrated by [3H]actinomycin D binding.

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Changes in chromatin structure of pyramidal tract neurons after medullary pyramidal tract lesions were examined autoradiographically utilizing [3H]actinomycin D (Act D) binding to nuclei in frozen sections of brain. After a right pyramidal tract lesion, the binding of Act D to nuclei of axotomized

Downregulation of inhibitor of apoptosis proteins in apoptotic human chondrocytes treated with tumor necrosis factor-alpha and actinomycin D.

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OBJECTIVE Apoptosis of chondrocytes plays a pivotal role in cartilage degeneration. Tumor necrosis factor-alpha (TNF-alpha) is a proinflammatory cytokine and has been assumed to cause the degradation of human cartilage. To investigate the mechanisms of TNF-alpha-mediated apoptosis of human

Fibroblast growth factor and glutamate: opposing roles in the generation and degeneration of hippocampal neuroarchitecture.

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Neuritic regression and cell death (neurodegeneration) are common features of both normal nervous system development and neurodegenerative disorders. Growth factors and excitatory amino acid neurotransmitters have been suggested independently to play roles in neurodegenerative processes. The present

On the differential cytotoxicity of actinomycin D.

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Actinomycin D (AMD) at concentrations that inhibit cellular RNA synthesis by 85% or more causes an acute phase of lethal cell degeneration in HeLa cultures beginning as early as 3 hr after drug exposure, resulting in the nearly complete loss of viable cells by 12 hr. The loss of cells during this

Inhibitory effects of actinomycin D and cycloheximide on neuronal death in adult Manduca sexta.

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A decline in circulating 20-hydroxyecdysone permits the emergence of the adult Manduca sexta moth; this endocrine signal also triggers the death of approximately half of the neurons in the unfused abdominal ganglia of the moth central nervous system. This programmed death of neurons was markedly

Staurosporine-induced cell death in Tetrahymena thermophila has mixed characteristics of both apoptotic and autophagic degeneration.

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Staurosporine blocks signal transduction associated with cell survival, proliferation and chemosensory behaviour in the ciliated protozoan, Tetrahymena thermophila. Staurosporine inhibits cell proliferation and in vivo protein phosphorylation induced by phorbol ester. It also reduces the in vitro

The role of glucagon-like peptide-2 on apoptosis, cell proliferation, and oxidant-antioxidant system at a mouse model of intestinal injury induced by tumor necrosis factor-alpha/actinomycin D.

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Tumor necrosis factor-alpha (TNF-α) is a multifunctional cytokine, which has the ability to produce cytotoxicity via induction of cell death and cell cycle arrest. Blocking the synthesis of protective proteins through a transcriptional inhibitor such as actinomycin D (Act D) sensitizes many cell

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