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ribonucleic acid/atrofija

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There are two insulin receptor (IR) isoforms (designated type A and type B), derived from alternative splicing of exon 11 of the IR gene. Recently, we reported (Huang Z., Bodkin N.L., Ortmeyer H.K., Hansen B.C., Shuldiner A. R., 1994, J Clin Invest, 94:1289-1296) that an increase in the exon 11-

[Degeneration of transfer ribonucleic acids in the course of specific interaction with aminoacyl-RNA-synthetases].

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Ribonucleic acid in experimental neurofibrillary degeneration studied by quantitative cytochemical methods.

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Asymmetric parietal and temporal lobe atrophy due to the variant m.8363G>A in transfer ribonucleic acid (Lysine)

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The Effects of TWEAK, Fn14, and TGF-beta1 on Degeneration of Human Intervertebral Disc.

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OBJECTIVE The purpose of this study is to explain the effect and reciprocal action among tumor necrosis factor (TNF) like weak inducer of apoptosis (TWEAK), fibroblast growth factor-inducible 14 (Fn14), and transforming growth factor-beta1 (TGF-beta1) on degeneration of human intervertebral disc

Fatty degeneration and wnt10b expression in the supraspinatus muscle after surgical repair of torn rotator cuff tendon.

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In the torn rotator cuff muscles, decreased expression of wnt10b prior to elevation of peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα) has previously been reported. The purpose of this study is to elucidate the expression profiles of
METHODS An external compression model was used to evaluate gene and protein expression in intervertebral discs with moderate disc degeneration. OBJECTIVE To determine messenger ribonucleic acid and protein expression levels of relevant disc components. BACKGROUND An animal model of mechanically

An empty E1, E3, E4 adenovirus vector protects photoreceptors from light-induced degeneration.

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We have previously identified a neuroprotective effect associated with empty (E1(-), E3(-), E4(-)) adenovirus vector delivery in a model of light-induced, photoreceptor cell death. In this study, we further characterize this protective effect in light-injured retina and investigate its molecular

SMN transcript stability: could modulation of messenger RNA degradation provide a novel therapy for spinal muscular atrophy?

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Proximal spinal muscular atrophy is caused by deletion or mutation of the survival motor neuron 1 gene, SMN1. Rentention of a nearly identical copy gene, SMN2, enables survival but is unable to fully compensate for the loss of SMN1. The SMN1 and SMN2 genes differ by a single nucleotide that results

[Spinal muscular atrophy: disappearance of RNA fluorescence of degenerating motor neurons. An acridine orange study].

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The histochemical distribution of nucleic acids has been studied in degenerating motor neurons of 9 children who died with spinal muscular atrophy, using the fluorochrome acridine orange. Ribonucleic acid (RNA) fluorescence disappeared abruptly from involved motor neurons without chromatolysis,

[Elucidation of the mechanism of retinal degeneration and regeneration and the prospects for its clinical application].

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In order to obtain the basic knowledge necessary to develop therapeutical intervention for blindness due to the damaged retina and optic nerve, the mechanism of retinal degeneration and regeneration in an amphibian model, Cynops pyrrhogaster, was studied. In the retinal degenerative process
METHODS Bovine caudal intervertebral discs (IVDs) were exposed to free axial vibration for 10 to 60 minutes at 0 to 0.5 g and 0 to 200 Hz. Expression of messenger ribonucleic acid for aggrecan, collagen type I, collagen type II, biglycan, decorin, and versican were assayed, as was

Experimental and clinical studies on toxicity of xenogeneic tumor-specific immune ribonucleic acid.

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To learn the toxicity of xenogeneic tumor-specific immune ribonucleic acid (I-RNA), experimental and clinical studies were carried out. Experimentally, doses of 30 mg/kg, 15 mg/kg, 7.5 mg/kg or 3.75 mg/kg of xenogeneic I-RNA extracted from lymphoid tissues of rabbits sensitized with 105,000 Xg
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