Contribution of Histochemistry to the Diagnosis of Muscle Pathology

2015 ◽  
pp. 42-46
Author(s):  
Victor Dubowitz
Keyword(s):  
Muscle Pathology

Skeletal Muscle Pathology

Pathology ◽  
1983 ◽  
Vol 15 (4) ◽  
pp. 511
Author(s):  
J.G. McLeod
Keyword(s):  
Skeletal Muscle ◽  
Muscle Pathology

scholarly journals Enhanced Ca2+ influx from STIM1–Orai1 induces muscle pathology in mouse models of muscular dystrophy

2014 ◽  
Vol 23 (14) ◽  
pp. 3706-3715 ◽  
Author(s):  
Sanjeewa A. Goonasekera ◽  
Jennifer Davis ◽  
Jennifer Q. Kwong ◽  
Federica Accornero ◽  
Lan Wei-LaPierre ◽  
...  
Keyword(s):  
Muscular Dystrophy ◽  
Mouse Models ◽  
Muscle Pathology

scholarly journals Myosin VI Localization and Expression in Striated Muscle Pathology

2014 ◽  
Vol 297 (9) ◽  
pp. 1706-1713 ◽  
Author(s):  
Justyna Karolczak ◽  
Serge Weis ◽  
Elisabeth Ehler ◽  
Biruta Kierdaszuk ◽  
Mariusz Berdyński ◽  
...  
Keyword(s):  
Striated Muscle ◽  
Muscle Pathology ◽  
Myosin Vi

scholarly journals Treatment with rGDF11 does not improve the dystrophic muscle pathology of mdx mice

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Fabrizio Rinaldi ◽  
Yu Zhang ◽  
Ricardo Mondragon-Gonzalez ◽  
Jeffrey Harvey ◽  
Rita C. R. Perlingeiro
Keyword(s):  
Muscle Pathology ◽  
Mdx Mice ◽  
Dystrophic Muscle

Amniotic Stem Cell-Conditioned Media for the Treatment of Nerve and Muscle Pathology: A Systematic Review

2021 ◽  
Author(s):  
Chukwuweike Gwam ◽  
Ahmed Emara ◽  
Nequesha Mohamed ◽  
Noor Chughtai ◽  
Johannes Plate ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Tissue Regeneration ◽  
Cell Damage ◽  
Conditioned Media ◽  
Nerve Tissue ◽  
Muscle Pathology ◽  
Loss Of Function ◽  
Cell Based Therapy

Muscle and nerve tissue damage can elicit a significant loss of function and poses as a burden for patients and healthcare providers. Even for tissues, such as the peripheral nerve and skeletal muscle, that harbor significant regenerative capacity, innate regenerative processes often lead to less than optimal recovery and residual loss of function. The reasons for poor regeneration include significant cell damage secondary to oxidative stress, poor recruitment of resident stem cells, and an unfavorable microenvironment for tissue regeneration. Stem cell-based therapy was once thought as a potential therapy in tissue regeneration, due to its self-renewal and multipotent capabilities. Early advocates for cellular-based therapy pointed to the pluripotent nature of stem cells, thus eluding to its ability to differentiate into resident cells as the source of its regenerative capability. However, increasing evidence has revealed a lack of engraftment and differentiation of stem cells, thereby pointing to stem cell paracrine activity as being responsible for its regenerative potential. Stem cell-conditioned media houses biomolecular factors that portray significant regenerative potential. Amniotic-derived stem cell-conditioned media (AFS-CM) has been of particular interest because of its ease of allocation and in vitro culture. The purpose of this review is to report the results of studies that assess the role of AFS-CM for nerve and muscle conditions. In this review, we will cover the effects of AFS-CM on cellular pathways, genes, and protein expression for different nerve and muscle cell types.

MRI diagnosis of occult ganglion compression of the posterior interosseous nerve and associated supinator muscle pathology

2005 ◽  
Vol 29 (5) ◽  
pp. 362-363 ◽  
Author(s):  
Justin Q. Ly ◽  
Terrence J. Barrett ◽  
Douglas P. Beall ◽  
Reono Bertagnolli
Keyword(s):  
Muscle Pathology ◽  
Posterior Interosseous Nerve ◽  
Supinator Muscle ◽  
Mri Diagnosis

scholarly journals Reinvestigation of the dysbindin subunit of BLOC-1 (biogenesis of lysosome-related organelles complex-1) as a dystrobrevin-binding protein

2006 ◽  
Vol 395 (3) ◽  
pp. 587-598 ◽  
Author(s):  
Ramin Nazarian ◽  
Marta Starcevic ◽  
Melissa J. Spencer ◽  
Esteban C. Dell'Angelica
Keyword(s):  
Recombinant Proteins ◽  
Binding Protein ◽  
Coiled Coil ◽  
Direct Interaction ◽  
Muscle Pathology ◽  
Binding Assays ◽  
Genetic Studies ◽  
Binding Interface ◽  
Lysosome Related Organelles

Dysbindin was identified as a dystrobrevin-binding protein potentially involved in the pathogenesis of muscular dystrophy. Subsequently, genetic studies have implicated variants of the human dysbindin-encoding gene, DTNBP1, in the pathogeneses of Hermansky–Pudlak syndrome and schizophrenia. The protein is a stable component of a multisubunit complex termed BLOC-1 (biogenesis of lysosome-related organelles complex-1). In the present study, the significance of the dystrobrevin–dysbindin interaction for BLOC-1 function was examined. Yeast two-hybrid analyses, and binding assays using recombinant proteins, demonstrated direct interaction involving coiled-coil-forming regions in both dysbindin and the dystrobrevins. However, recombinant proteins bearing the coiled-coil-forming regions of the dystrobrevins failed to bind endogenous BLOC-1 from HeLa cells or mouse brain or muscle, under conditions in which they bound the Dp71 isoform of dystrophin. Immunoprecipitation of endogenous dysbindin from brain or muscle resulted in robust co-immunoprecipitation of the pallidin subunit of BLOC-1 but no specific co-immunoprecipitation of dystrobrevin isoforms. Within BLOC-1, dysbindin is engaged in interactions with three other subunits, named pallidin, snapin and muted. We herein provide evidence that the same 69-residue region of dysbindin that is sufficient for dystrobrevin binding in vitro also contains the binding sites for pallidin and snapin, and at least part of the muted-binding interface. Functional, histological and immunohistochemical analyses failed to detect any sign of muscle pathology in BLOC-1-deficient, homozygous pallid mice. Taken together, these results suggest that dysbindin assembled into BLOC-1 is not a physiological binding partner of the dystrobrevins, likely due to engagement of its dystrobrevin-binding region in interactions with other subunits.

Sign in / Sign up

Export Citation Format

Share Document