Disease relevance of Mice, Inbred mdx

• Combinatorial blockade of calcineurin and CD28 signaling facilitates primary and secondary therapeutic gene transfer by adenovirus vectors in dystrophic (mdx) mouse muscles [1].
• Muscles affected by muscular dystrophy undergo severe muscle damage; therefore, the hypothesis was tested that muscles of dystrophic (mdx) mice contain elevated levels of albumin [2].
• Genetically normal (C57BL/10) and dystrophic (mdx) mice underwent a 15 week endurance swimming programme (2 hours per day, 5 days per week) where animals were weighted (5% body weight) during most sessions [3].

Psychiatry related information on Mice, Inbred mdx

• We use dystrophin-deficient mice (mdx), an animal model of DMD, to evaluate the effect of chinese herbal medicines on locomotor activity [4].

High impact information on Mice, Inbred mdx

• Dystrophin-deficient mice (mdx) expressing a truncated (trc) utrophin transgene show amelioration of the dystrophic phenotype [5].
• Fibroblast growth factor in the extracellular matrix of dystrophic (mdx) mouse muscle [6].
• Increased calcium influx is responsible for the sustained mechanical tone in colon from dystrophic (mdx) mice [7].
• Mdx mice lacking myostatin were stronger and more muscular than their mdx counterparts [8].
• Mdx mouse muscle, which shows characteristic dystrophic damage and regeneration, demonstrated mononuclear cells containing myogenin and bFGF transcripts in similar regions of adjacent sections of focal degeneration and repair, particularly near recent segmental fiber damage [9].

Chemical compound and disease context of Mice, Inbred mdx

• C57BL/10SNJ (control) and dystrophic (mdx) mice were given clenbuterol (1.0-1.5 mg/kg body weight/day) in the drinking water [10].

Biological context of Mice, Inbred mdx

• Dissection of temporal gene expression signatures of affected and spared muscle groups in dystrophin-deficient (mdx) mice [11].
• Dystrophin distribution in heterozygote MDX mice [12].
• Serum creatine kinase (CK) activity, calcium (Ca) and magnesium (Mg) contents of skeletal muscle and isolated mitochondria, as well as oxidative phosphorylation of X-linked muscular dystrophic (mdx) mice were compared with normal control animals at ages 5, 10, and 23 weeks [13].
• Dystrophin cDNAs have been introduced into skeletal muscle fibers of dystrophin-deficient mice (mdx) through direct DNA injection in plasmid expression vectors and by replication-defective recombinant adenovirus vectors [14].
• The results revealed that total and basal energy expenditure, as well as spontaneous activity, energetic cost of activity, and, therefore, energy expended in relation to activity were not significantly different in C57B1/10 (control) and in dystrophic (mdx) mice [15].

Anatomical context of Mice, Inbred mdx

• Involvement of TRPC in the abnormal calcium influx observed in dystrophic (mdx) mouse skeletal muscle fibers [16].
• In the present study, myotubes from DMD patients and murine X-linked muscular dystrophic mice (mdx) were used to measure their adhesive force to the physiological laminin-alpha2 substrate, and it was found that the dystrophic myotubes were selectively unable to sustain adhesion [17].
• We have previously described a method for the derivation of long term cultures of undifferentiated myoblasts from the skeletal muscle of dystrophic (mdx) mice (J. Smith and P. N. Schofield, Exp. Cell Res., 210: 86-93, 1994) [18].
• Global/temporal gene expression in diaphragm and hindlimb muscles of dystrophin-deficient (mdx) mice [19].
• Altered electrical activity in colonic smooth muscle cells from dystrophic (mdx) mice [20].

Associations of Mice, Inbred mdx with chemical compounds

• Plasma creatine kinase levels were slightly increased in ADR-MDX, but significantly lower when compared to MDX mice [21].
• 2. Normal (C57BL/10) and dystrophic (mdx) mice were administered clenbuterol (2 mg/kg per day) for 15 weeks [22].
• Mdx mice had significantly elevated values for o-tyrosine, succinat-phenacinmetosulfat oxidoreductase [23].
• Prostaglandin metabolism in dystrophin-deficient MDX mouse muscle [24].
• Strength and endurance in the therapeutic evaluation of prednisolone-treated MDX mice [25].

Gene context of Mice, Inbred mdx

• Extensive but coordinated reorganization of the membrane skeleton in myofibers of dystrophic (mdx) mice [26].
• To test this hypothesis in vivo, we bred a double mutant mouse that combines two genetic defects: the dystrophin-deficiency of the MDX mouse and the Cl- channel myotonia of the arrested development of righting response (ADR) mouse [21].
• Our results suggest that histopathologies associated with Mdx mice did not diminish gross temporalis structure or function, whilst the force-frequency changes associated with Mstn(-/-) mice were reflected in an elevation of type IIx/b fibres [27].
• A developmental change in the content of parvalbumin in normal and dystrophic mouse (mdx) muscle [28].
• Mdx mice may be tolerant due to the presence of rare 'revertant' dystrophin-positive fibres in their skeletal muscles [29].

Analytical, diagnostic and therapeutic context of Mice, Inbred mdx

• On Western blots of normal mouse muscle extracts, the antibodies bind specifically to a 400,000 Mr protein which is absent from dystrophic mouse (mdx) muscle [30].
• Both Mstn(-/-) and Mdx mice showed significant elevation in bite force and muscle mass [27].

References