Dobih danas mailom neke novosti o distrofiji, na engleskom je pa nisam 100% sve razumeo ali može da se shvati ako se
koristi neki online rečnik, ja koristim:
www.tranexp.com, može za reč ili ceo tekst mada dosta brlja sa celim tekstom
ipak može da se prilično dobro iskombinuje.
Tekst glasi:
Royal Cells Institute
Dear Sir,
As you already know the aim of Royal Cells Institute www.musculardystrophy.gr is to delay the progress of Muscular Dystrophy
until the Medical Community will finally find a way to cure the disease.
Mean while informs you - in case of your interest - with the latest official results of experiments all over the world
Witth Regards
Royal Cells Institute
Department of Physiology and Pennsylvania Muscle Institute, University of Pennsylvania, A601 Richards Building, 3700 Hamilton Walk, Philadelphia, PA, 19104, USA, moorwood@mail.med.upenn.edu.
Syncoilin is a member of the intermediate filament protein family, highly expressed in skeletal and cardiac muscle. Syncoilin binds alpha-dystrobrevin, a component of the dystrophin associated protein complex (DAPC) located at the muscle cell membrane, and desmin, a muscle-specific intermediate filament protein, thus providing a link between the DAPC and the muscle intermediate filament network. This link may be important for muscle integrity and force transduction during contraction, a theory that is supported by the reduced force-generating capacity of muscles from syncoilin-null mice. Additionally, syncoilin is found at increased levels in the regenerating muscle fibres of patients with muscular dystrophies and mouse models of muscle disease. Therefore, syncoilin may be important for muscle regeneration in response to injury. The aims of this article are to review current knowledge about syncoilin and to discuss its possible functions in skeletal muscle.Royal Cells Institute
Dear Sir,
As you already know the aim of Royal Cells Institute
www.musculardystrophy.gr is to delay the progress of Muscular Dystrophy
until the Medical Community will finally find a way to cure the disease.
Mean while informs you - in case of your interest - with the latest official results of experiments all over the world
Witth Regards
Royal Cells Institute
A deficit of brain dystrophin impairs specific amygdala GABAergic transmission and enhances defensive behaviour in mice.
Sekiguchi M, Zushida K, Yoshida M, Maekawa M, Kamichi S, Yoshida M, Sahara Y, Yuasa S, Takeda S, Wada K.
Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Centre of Neurology and Psychiatry, 4-1-1 Ogawahigashi, Kodaira, Tokyo 187-8502, CREST, Japan Science and Technology Agency, Kawaguchi, Saitama 322-0012, Department of Molecular Therapy, Department of Ultrastructure Research and Department of Cell Biology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, 4-1-1 Ogawahigashi, Kodaira, Tokyo 187-8502, Japan.
Duchenne muscular dystrophy (DMD) is accompanied by cognitive deficits and psychiatric symptoms. In the brain, dystrophin, the protein responsible for DMD, is localized to a subset of GABAergic synapses, but its role in brain function has not fully been addressed. Here, we report that defensive behaviour, a response to danger or a threat, is enhanced in dystrophin-deficient mdx mice. Mdx mice consistently showed potent defensive freezing responses to a brief restraint that never induced such responses in wild-type mice. Unconditioned and conditioned defensive responses to electrical footshock were also enhanced in mdx mice. No outstanding abnormality was evident in the performances of mdx mice in the elevated plus maze test, suggesting that the anxiety state is not altered in mdx mice. We found that, in mdx mice, dystrophin is expressed in the amygdala, and that, in the basolateral nucleus (BLA), the numbers of GABA(A) receptor alpha2 subunit clusters are reduced. In BLA pyramidal neurons, the frequency of norepinephrine-induced GABAergic inhibitory synaptic currents was reduced markedly in mdx mice. Morpholino oligonucleotide-induced expression of truncated dystrophin in the brains of mdx mice, but not in the muscle, ameliorated the abnormal freezing response to restraint. These results suggest that a deficit of brain dystrophin induces an alteration of amygdala local inhibitory neuronal circuits and enhancement of fear-motivated defensive behaviours in mice.
Tema: Novine u lečenju (Pročitano 15043 puta)