Hutchinson-Gilford syndrome oor Frans
Hutchinson-Gilford syndrome
Vertalings in die woordeboek Engels - Frans
progérie
progeria
syndrome d'Hutchinson-Gilford
syndrome de Gilford
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voorbeelde
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One out of eight million kids develops Hutchinson-Gilford progeria syndrome.
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Lmna gene and its involvement in hutchinson-gilford progeria syndrome (hgps) and arteriosclerosis
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The present application describes the therapeutic effect of hypothalamic neuropeptide Y overexpression against age related pathologies progression and progeroid syndromes, namely the Hutchinson-Gilford progeria syndrome.
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Hastings Gilford (1861–1941) was an English surgeon, best known for his description of Hutchinson–Gilford progeria syndrome in 1897.
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hutchinson-gilford, de barsy syndrome, cockayne, gottron's.
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The compounds are able to inhibit excessive or inappropriate bone resorption and for the treatment of other diseases which are caused by excessive prenylation of target proteins, such as Hutchinson-Gilford progeria syndrome.
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The invention relates to the use of a hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor and of a farnesyl-pyrophosphate synthase inhibitor, or of one of their associated physiologically acceptable salts, in the preparation of a composition, particularly a pharmaceutical composition, for use in the treatment of human or animal, pathological or nonpathological situations related to the accumulation and/or the persistence of prenylated proteins in cells, such as during progeria (Hutchinson-Gilford syndrome), restrictive dermopathy or physiological ageing.
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Nearly all subjects affected with Hutchinson Gilford progeria syndrome (HGPS) carry mutation LMNA G608G (GGC>GGT), within exon 11 of LMNA activating a splicing donor site which leads to a deletion of 50 amino acids at the carboxyl-terminal of prelamin A.
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Hypoacetylation of H4K16 appears to cause delayed recruitment of DNA repair proteins to sites of DNA damage in a mouse model of the premature aging syndrome Hutchinson Gilford progeria.
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Progeria, also known as Hutchinson-Gilford syndrome (HGPS), is a genetic disease leading to a premature aging phenotype.
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This company is credited with the discovery of the genetic mutation involved in the triggering of Progeria (Hutchinson-Gilford syndrome).
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In Hutchinson-Gilford syndrome and Werner syndrome, the central nervous system and therefore the ability to do many daily activities are largely unaffected unless a stroke occurs.
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Hutchinson-Gilford progeria syndrome is a rare genetic disease which causes accelerating aging to children.
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Lonafarnib is currently considered an investigational treatment for Hutchinson-Gilford Progeria Syndrome and Progeroid Laminopathies.
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Hutchinson Gilford progeria syndrome (HGPS) is an extremely rare and severe genetic disease that causes precocious and accelerated ageing in children.
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The main differential diagnosis is the Ehlers-Danlos syndromes (see these terms) but similar skin manifestations may also occur in patients with Williams syndrome, pseudoxanthoma elasticum, Hutchinson Gilford syndrome, Barber Say syndrome, Costello syndrome, Cardio-Facio-Cutaneous syndrome and Kabuki syndrome (see these terms).
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"Unique preservation of neural cells in Hutchinson-Gilford Progeria Syndrome (HGPS) is due to the expression of the neural-specific miR-9 microRNA"
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At the same time, an iPSC senescence control was performed from cells of a Hutchinson-Gilford Progeria syndrome patient. iPSCs were characterized for pluripotency.
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Hemophilia A Hutchinson–Gilford progeria syndrome adrenoleukodystrophy (CCALD), skin fibroblasts have been used as source cells and retroviral integration has been used for generation of iPSCs.
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Progeria (also known as Hutchinson–Gilford progeria syndrome) is an extremely rare genetic condition wherein symptoms resembling aspects of aging are manifested at an early age.
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The purpose of this MAP is to allow eligible patients with Hutchinson-Gilford Progeria Syndrome (HGPS or Progeria) or a Progeroid Laminopathy (PL) to gain access to treatment with Lonafarnib.
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Hutchinson-Gilford progeria syndrome (HGPS) is caused by a point mutation in the LMNA gene that activates a cryptic donor splice site and yields a truncated form of prelamin A called progerin.
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The relationships of laminopathies with accelerated aging syndrome, Hutchinson-Gilford progeria, or progeroid syndromes, which are also related to A/C lamin anomalies, could provide new avenues of research on the pathogenesis of the metabolic syndrome.
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Premature aging syndromes (e.g., Werner’s, Hutchinson-Gilford, ataxia telangiectasia, Cockayne’s) also offer compelling evidence.
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A study by Xavier Nissan’s research team from I-Stem, in collaboration with Pr Nicolas Lévy’s (Aix-Marseille University – INSERM UMR_S910, Faculté de Médecine de Marseille), Dr Lino Ferreira’s (Coimbra University, Portugal) teams enabled to show the therapeutic potential of retinoic acid (Vitamin A) in the treatment of progeria. Hutchinson-Gilford progeria syndrome is a rare genetic disease which causes accelerating aging to children.
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