Absence of dystrophin in mice reduces NO-dependent vascular function and vascular density: total recovery after a treatment with the aminoglycoside gentamicin.
about
Aminoglycosides and other nonsense suppression therapies for the treatment of dystrophinopathyFluorescence-based force/tension sensors: a novel tool to visualize mechanical forces in structural proteins in live cellsDirect isolation, culture and transplant of mouse skeletal muscle derived endothelial cells with angiogenic potential.New trends in aminoglycosides use.Aminoglycoside-induced mutation suppression (stop codon readthrough) as a therapeutic strategy for Duchenne muscular dystrophyNonsense-mediated decay in genetic disease: friend or foe?A new series of small molecular weight compounds induce read through of all three types of nonsense mutations in the ATM gene.Making sense of nonsense GABA(A) receptor mutations associated with genetic epilepsies.The decrease of expression of ryanodine receptor sub-type 2 is reversed by gentamycin sulphate in vascular myocytes from mdx mice.The role of shear stress in the pathogenesis of atherosclerosis.Blood flow modulation of vascular dynamics.ANG1 treatment reduces muscle pathology and prevents a decline in perfusion in DMD mice.Absence of Dystrophin Disrupts Skeletal Muscle Signaling: Roles of Ca2+, Reactive Oxygen Species, and Nitric Oxide in the Development of Muscular Dystrophy.Hypoxia-induced cardiac injury in dystrophic mice.Role of the cytoskeleton in flow (shear stress)-induced dilation and remodeling in resistance arteries.Mice with missense and nonsense NF1 mutations display divergent phenotypes compared with human neurofibromatosis type I.Mechanotransduction gone awry.Nonaminoglycoside compounds induce readthrough of nonsense mutations.Angiogenesis as a novel therapeutic strategy for Duchenne muscular dystrophy through decreased ischemia and increased satellite cells.Skeletal Muscle Microvasculature: A Highly Dynamic Lifeline.Central Arterial Function Measured by Non-invasive Pulse Wave Analysis is Abnormal in Patients with Duchenne Muscular Dystrophy.Time-related alteration in flow- (shear stress-) mediated remodeling in resistance arteries from spontaneously hypertensive rats.Increased plasma lipid levels exacerbate muscle pathology in the mdx mouse model of Duchenne muscular dystrophyQuantification of the mechanical behavior of carotid arteries from wild-type, dystrophin-deficient, and sarcoglycan-delta knockout mice.Implications for Cardiac Function Following Rescue of the Dystrophic Diaphragm in a Mouse Model of Duchenne Muscular Dystrophy.Altered biomechanical properties of carotid arteries in two mouse models of muscular dystrophy.Contractile efficiency of dystrophic mdx mouse muscle: in vivo and ex vivo assessment of adaptation to exercise of functional end points.Dual effects of resveratrol on arterial damage induced by insulin resistance in aged mice.Supplementation with a selective amino acid formula ameliorates muscular dystrophy in mdx mice
P2860
Q24240721-7048264C-E425-4709-B0D5-CD5504664B87Q27693233-09B5F46C-7975-4082-8D77-24F3853F2A4DQ33323355-FF013A9E-B971-4264-9319-2413F508608BQ33951177-9651B810-4FF1-42D3-BCC7-E9C92AF73C43Q34409434-19EA07FF-EA8D-432C-8E2E-BE28F4E54481Q34658988-B929E35B-F697-4F88-ABE2-2483543A1E69Q34775214-03DD38F8-53CE-4826-A0DD-D5F70A6F3A46Q34789999-65198C91-55F1-49F3-B0BF-82D589077844Q35893242-6011FFBE-A194-40A7-8201-F25B957FF8F5Q35965518-1138C5DC-F96C-4F8F-B899-EE048F24171DQ36224629-61698F83-6C08-40D9-885A-A4846F0A8216Q36320134-D0B17FD6-372B-4EC4-A12E-94BDA30357E0Q36422465-EB2A43A0-1E26-4D10-A96B-F09606A20C65Q36895785-9C294149-FEC3-4B11-9922-4D4CA9B5A057Q36935093-061FF825-74D9-4C37-885C-D2F7C66CCD23Q37120427-D1CD3E81-5DDF-497C-8650-4B3B761B3EABQ37158222-13E3FC6F-2BAB-4954-8876-5256C813F3A7Q37377461-DFA46DAB-DE63-4C0B-85D1-E08A5E2575ACQ38193799-000E1278-61B5-468C-9C74-A9B3AF1C4D6CQ38622645-E087E60C-7576-44E4-9607-93FD1697BDD1Q38714542-B212FA1B-855E-478D-B1F2-F83C314EAD1FQ39963141-60A50D2B-DC91-483B-8118-568811794CB1Q41151043-8F34EC5A-3A5C-46E3-99B7-5E1EFB5143C8Q41820296-60C66953-D716-4A5D-B3AF-D1A204DC53CCQ41949953-7735E5B3-AFB4-4397-9D82-730D854A5076Q42513141-A8E8593D-7E0D-4C39-9C2A-E3FFDABCC146Q45050237-36E2DD45-FDA7-417B-8850-005709F81539Q50884915-72A3637E-9F4F-4E54-B8B1-0DE74FC733B9Q57050163-C17B78A6-647A-470D-A2BE-9BB8F15C1985
P2860
Absence of dystrophin in mice reduces NO-dependent vascular function and vascular density: total recovery after a treatment with the aminoglycoside gentamicin.
description
2004 nî lūn-bûn
@nan
2004年の論文
@ja
2004年論文
@yue
2004年論文
@zh-hant
2004年論文
@zh-hk
2004年論文
@zh-mo
2004年論文
@zh-tw
2004年论文
@wuu
2004年论文
@zh
2004年论文
@zh-cn
name
Absence of dystrophin in mice ...... the aminoglycoside gentamicin.
@en
type
label
Absence of dystrophin in mice ...... the aminoglycoside gentamicin.
@en
prefLabel
Absence of dystrophin in mice ...... the aminoglycoside gentamicin.
@en
P2093
P2860
P1476
Absence of dystrophin in mice ...... the aminoglycoside gentamicin
@en
P2093
Bernard Levy
Caroline Dubroca
Denise Paulin
Laurent Loufrani
P2860
P304
P356
10.1161/01.ATV.0000118683.99628.42
P407
P577
2004-01-29T00:00:00Z