1,720,974 research outputs found
MicroRNA signature in mdx dystrophic mice overexpressing mIGF-1 in Abstracts of the XII annual meeting of the Interuniversity Institute of Myology | Reggio Emilia, Italy, October 1-4, 2015
No full textDuchenne muscular dystrophy (DMD) is a genetic disease in which loss of functional dystrophin protein results in progressive skeletal muscle degeneration. Although the genetic defect is widely known, the mechanisms by which the absence of dystrophin leads to the complex pathophisiology of the disease is not completely understood. MiRNAs are small non coding RNA that are important regulatory elements for muscle development and function [1]. Altered levels of specific miRNAs were found in several muscular disorders, including DMD [2, 3]. In particular it has been identified a specific DMD-signature miRNAs that may serve as a marker for therapeutic purposes [4]. Moreover, in a recent work it has been defined a specific group of miRNAs strictly correlated to dystrophin levels and whose deregulated expression could explain several pathogenetic features of DMD [5]. Previously we have demonstrated that the local expression of mIGF-1 in mdx mice ameliorates the dystrophic phenotype reducing myonecrosis and upregulating survival pathways such as AKT pathway [6]. In this work, we show that a specific group of miRNAs, dystrophin-indipendent, are modulated by mIGF-1 expression. In particular, local expression of mIGF-1 promotes the modulation of miR-206 and miR-24 as well as muscle specific genes associated with maturation of regenerating muscle fibers and differentiation. These results indicates that local overexpression of the anabolic factor mIGF-1 in mdx mice ameliorates the dystrophic microenviroment modulating the expression of a specific group of miRNAs and inducing a partial rescue of the characteristic DMD-signature
An overview about the biology of skeletal muscle satellite cells
Get PDFThe peculiar ability of skeletal muscle tissue to operate adaptive changes during post-natal de-velopment and adulthood has been associated with the existence of adult somatic stem cells. Satellite cells, occupying an exclusive niche within the adult muscle tissue, are considered bona fide stem cells with both stem-like properties and myogenic activities. Indeed, satellite cells retain the capability to both maintain the quiescence in uninjured muscles and to be promptly activated in response to growth or re-generative signals, re-engaging the cell cycle. Activated cells can undergo myogenic differentiation or self-renewal moving back to the quiescent state. Satellite cells behavior and their fate decision are finely controlled by mechanisms involving both cell-autonomous and external stimuli. Alterations in these regu-latory networks profoundly affect muscle homeostasis and the dynamic response to tissue damage, con-tributing to the decline of skeletal muscle that occurs under physio-pathologic conditions. Although the clear myogenic activity of satellite cells has been described and their pivotal role in muscle growth and regeneration has been reported, a comprehensive picture of inter-related mechanisms guiding muscle stem cell activity has still to be defined. Here, we reviewed the main regulatory networks determining satellite cell behavior. In particular, we focused on genetic and epigenetic mechanisms underlining satel-lite cell maintenance and commitment. Besides intrinsic regulations, we reported current evidences about the influence of environmental stimuli, derived from other cell populations within muscle tissue, on satel-lite cell biology
The role of Igf-1 on Muscle Wasting: a Therapeutic Approach
No full textWhile much has been learned about skeletal muscle formation in the embryo, less is known
about the molecular pathways controlling skeletal myocyte survival and plasticity in the
adult. Tissue remodelling is an important physiological process which allows skeletal
muscle to respond to environmental demands. In particular, the complex contractile
properties of skeletal muscle depend upon a heterogeneous population of myofibers that
confer the functional plasticity necessary to modulate responses to a wide range of external
factors, including physical activity, change in hormone levels and motor-neuron activity,
oxygen and nutrients supply. Fiber type is an essential determinant of muscle function and
alteration in fiber composition represents a major component in muscle wasting associated
with muscle diseases. In this context, the prolongation of skeletal muscle strength in aging
and neuromuscular disease has been the objective of numerous studies employing a variety
of approaches. To date however, efforts to prevent or attenuate age- or disease-related
muscle degeneration have been largely unsuccessful. In this context, where direct
therapeutic approaches to redress the primary disease are still sub-optimal, it may be more
effective to focus on strategies for improving skeletal muscle function. In this review we
will discuss the potential therapeutic role of Insulin-like Growth Factor 1 (IGF-1) in
treatment of muscle wasting associated with several muscle diseases
Going Beyond Counting First Authors in Author Co-citation Analysis
Get PDFThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Variations on the Author
Get PDF“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Appropriate Similarity Measures for Author Cocitation Analysis
Get PDFWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
Insights into the pathogenic secondary symptoms caused by the primary loss of dystrophin
Get PDFDuchenne muscular dystrophy (DMD) is an X-linked genetic disease in which the dystrophin gene is mutated, resulting in dysfunctional dystrophin protein. Without dystrophin, the dystrophin-glycoprotein complex (DGC) is unstable, leading to an increase in muscle damage. Moreover, the imbalance between muscle damage and repair leads to a chronic inflammatory response and an increase in the amount of fibrosis over time. The absence of dystrophin at the sarcolemma also delocalizes and downregulates nitric oxide synthase (nNOS) and alters enzymatic antioxidant responses, leading to an increase in oxidative stress. In this review, we analyze the pathogenic role of both inflammation and oxidative stress in muscular dystrophy
Dispelling the Myths Behind First-author Citation Counts
Get PDFWe conducted a full-scale evaluative citation analysis study of scholars in the XML research field to explore just how different from each other author rankings resulting from different citation counting methods actually are, and to demonstrate the capability of emerging data and tools on the Web in supporting more realistic citation counting methods. Our results contest some common arguments for the continued
use of first-author citation counts in the evaluation of scholars, such as high correlations between author rankings by first-author citation counts and other citation
counting methods, and high costs of using more realistic citation counting methods that are not well-supported by the ISI databases. It is argued that increasingly available digital full text research papers make it possible for citation analysis studies to go beyond what the ISI databases have directly supported and to employ more
sophisticated methods
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