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Your search keyword '"Galli, Ricardo A."' showing total 20 results
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20 results on '"Galli, Ricardo A."'

1. Tirasemtiv enhances submaximal muscle tension in an Acta1:p.Asp286Gly mouse model of nemaline myopathy

Author

Galli, Ricardo A., primary, Borsboom, Tamara C., additional, Gineste, Charlotte, additional, Brocca, Lorenza, additional, Rossi, Maira, additional, Hwee, Darren T., additional, Malik, Fady I., additional, Bottinelli, Roberto, additional, Gondin, Julien, additional, Pellegrino, Maria-Antonietta, additional, de Winter, Josine M., additional, and Ottenheijm, Coen A.C., additional

Published
2024
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2. El informe NERA analizado

Author

Galli, Ricardo

Subjects
Computer Science - Computers and Society, K.4.1, K.4.4
Abstract

This is a review of the article "Government Preferences for Promoting Open-Source Software: A Solution in Search of A Problem" by David Evans and Bernard J. Reddy. This report was paid for by Microsoft and put together at its request. Now Microsoft is using it as part of their lobbying campaign in Europe against governments' promotion of Open Source Software. As expected, this article is strongly biased and most of the conclusions are based upon false hypotheses and evidence., Comment: Spanish

Published
2003

4. KBTBD13 is a novel cardiomyopathy gene

Author

de Winter, Josine M., primary, Bouman, Karlijn, additional, Strom, Joshua, additional, Methawasin, Mei, additional, Jongbloed, Jan D. H., additional, van der Roest, Wilma, additional, Wijngaarden, Jan van, additional, Timmermans, Janneke, additional, Nijveldt, Robin, additional, van den Heuvel, Frederik, additional, Kamsteeg, Erik‐Jan, additional, van Engelen, Baziel G., additional, Galli, Ricardo, additional, Bogaards, Sylvia J. P., additional, Boon, Reinier A., additional, van der Pijl, Robbert J., additional, Granzier, Henk, additional, Koeleman, Bobby, additional, Amin, Ahmad S., additional, van der Velden, Jolanda, additional, van Tintelen, J. Peter, additional, van den Berg, Maarten P., additional, van Spaendonck‐Zwarts, Karin Y., additional, Voermans, Nicol C., additional, and Ottenheijm, Coen A. C., additional

Published
2022
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5. Actin maturation requires the ACTMAP/C19orf54 protease

Author

Haahr, Peter, primary, Galli, Ricardo A., additional, van den Hengel, Lisa G., additional, Bleijerveld, Onno B., additional, Kazokaitė-Adomaitienė, Justina, additional, Song, Ji-Ying, additional, Kroese, Lona J., additional, Krimpenfort, Paul, additional, Baltissen, Marijke P., additional, Vermeulen, Michiel, additional, Ottenheijm, Coen A. C., additional, and Brummelkamp, Thijn R., additional

Published
2022
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6. Lack of Tgfbr1 and Acvr1b synergistically stimulates myofibre hypertrophy and accelerates muscle regeneration

Author

Hillege, Michele M. G., Shi, Andi, Galli, Ricardo A., Wu, Gang, Bertolino, Philippe, Hoogaars, Willem M. H., Jaspers, Richard T., Huang, Christopher L-H, Physiology, Maxillofacial Surgery (VUmc), Oral Implantology, AMS - Rehabilitation & Development, and AMS - Tissue Function & Regeneration

Subjects
Cardiotoxin, TGF-β, Type I receptor, EXPRESSION, Mouse, injury, FACTOR-BETA, FACTOR-I, Skeletal muscle, Injury, MYOSTATIN, General Biochemistry, Genetics and Molecular Biology, type I receptor, TRANSFORMING-GROWTH-FACTOR, CONNECTIVE-TISSUE FIBROBLASTS, FIBER SIZE, TGF-beta, skeletal muscle, Inflammation, General Immunology and Microbiology, General Neuroscience, INHIBITS MYOBLAST DIFFERENTIATION, General Medicine, Hypertrophy, Myostatin, Fibrosis, SKELETAL-MUSCLE, SATELLITE CELL-PROLIFERATION, hypertrophy
Abstract

In skeletal muscle, transforming growth factor-β (TGF-β) family growth factors, TGF-β1 and myostatin, are involved in atrophy and muscle wasting disorders. Simultaneous interference with their signalling pathways may improve muscle function; however, little is known about their individual and combined receptor signalling. Here, we show that inhibition of TGF-β signalling by simultaneous muscle-specific knockout of TGF-β type I receptors Tgfbr1 and Acvr1b in mice, induces substantial hypertrophy, while such effect does not occur by single receptor knockout. Hypertrophy is induced by increased phosphorylation of Akt and p70S6K and reduced E3 ligases expression, while myonuclear number remains unaltered. Combined knockout of both TGF-β type I receptors increases the number of satellite cells, macrophages and improves regeneration post cardiotoxin-induced injury by stimulating myogenic differentiation. Extra cellular matrix gene expression is exclusively elevated in muscle with combined receptor knockout. Tgfbr1 and Acvr1b are synergistically involved in regulation of myofibre size, regeneration, and collagen deposition.

Published
2022

7. Actin maturation requires the ACTMAP/C19orf54 protease

Author

Haahr, Peter, Galli, Ricardo A., van den Hengel, Lisa G., Bleijerveld, Onno B., Kazokaitė-Adomaitienė, Justina, Song, Ji Ying, Kroese, Lona J., Krimpenfort, Paul, Baltissen, Marijke P., Vermeulen, Michiel, Ottenheijm, Coen A.C., Brummelkamp, Thijn R., Haahr, Peter, Galli, Ricardo A., van den Hengel, Lisa G., Bleijerveld, Onno B., Kazokaitė-Adomaitienė, Justina, Song, Ji Ying, Kroese, Lona J., Krimpenfort, Paul, Baltissen, Marijke P., Vermeulen, Michiel, Ottenheijm, Coen A.C., and Brummelkamp, Thijn R.

Abstract

Protein synthesis generally starts with a methionine that is removed during translation. However, cytoplasmic actin defies this rule because its synthesis involves noncanonical excision of the acetylated methionine by an unidentified enzyme after translation. Here, we identified C19orf54, named ACTMAP (actin maturation protease), as this enzyme. Its ablation resulted in viable mice in which the cytoskeleton was composed of immature actin molecules across all tissues. However, in skeletal muscle, the lengths of sarcomeric actin filaments were shorter, muscle function was decreased, and centralized nuclei, a common hallmark of myopathies, progressively accumulated. Thus, ACTMAP encodes the missing factor required for the synthesis of mature actin and regulates specific actin-dependent traits in vivo.

Published
2022

8. KBTBD13 is a novel cardiomyopathy gene

Author

Genetica Groep Koeleman, Brain, Cancer, Child Health, Circulatory Health, Genetica, de Winter, Josine M, Bouman, Karlijn, Strom, Joshua, Methawasin, Mei, Jongbloed, Jan D H, van der Roest, Wilma, Wijngaarden, Jan van, Timmermans, Janneke, Nijveldt, Robin, van den Heuvel, Frederik, Kamsteeg, Erik-Jan, van Engelen, Baziel G, Galli, Ricardo, Bogaards, Sylvia J P, Boon, Reinier A, van der Pijl, Robbert J, Granzier, Henk, Koeleman, Bobby, Amin, Ahmad S, van der Velden, Jolanda, van Tintelen, J Peter, van den Berg, Maarten P, van Spaendonck-Zwarts, Karin Y, Voermans, Nicol C, Ottenheijm, Coen A C, Genetica Groep Koeleman, Brain, Cancer, Child Health, Circulatory Health, Genetica, de Winter, Josine M, Bouman, Karlijn, Strom, Joshua, Methawasin, Mei, Jongbloed, Jan D H, van der Roest, Wilma, Wijngaarden, Jan van, Timmermans, Janneke, Nijveldt, Robin, van den Heuvel, Frederik, Kamsteeg, Erik-Jan, van Engelen, Baziel G, Galli, Ricardo, Bogaards, Sylvia J P, Boon, Reinier A, van der Pijl, Robbert J, Granzier, Henk, Koeleman, Bobby, Amin, Ahmad S, van der Velden, Jolanda, van Tintelen, J Peter, van den Berg, Maarten P, van Spaendonck-Zwarts, Karin Y, Voermans, Nicol C, and Ottenheijm, Coen A C

Published
2022

13. MWorld: a multiuser 3D virtual environment

Author

Salles Dias, Jose Miguel, Galli, Ricardo, Almeida, Antonio Carlos, Belo, Carlos A.C., and Rebordao, Jose Manuel

Subjects
Work group computing -- Research, Virtual reality -- Research
Published
1996

18. Mu3D

Author

Galli, Ricardo, primary and Luo, Yuhua, additional

Published
2000
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19. Mworld: A multiuser 3D virtual environment.

Author

Dias, Jose Miguel Sal and Galli, Ricardo

Subjects
*COMPUTER software
Abstract

Discusses information about the mWorld, a 3D virtual environment system. How it immerses several users in the same world space; Where does consistency control applied; Its cooperative environment support; Communication aspects; Implementation of mWorld; Scene initialization and consistency; Deformable surface objects; Modeling of object; Visualization and interaction. INSETS: JESP Service Interface and Protocols.;The MLBlinker Class..

Published
1997
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20. Small molecule drugs to improve sarcomere function in those with acquired and inherited myopathies.

Author

Claassen WJ, Baelde RJ, Galli RA, de Winter JM, and Ottenheijm CAC

Subjects
Humans, Muscle Contraction physiology, Muscle Weakness, Myosins genetics, Troponin, Sarcomeres physiology, Calcium
Abstract

Muscle weakness is a hallmark of inherited or acquired myopathies. It is a major cause of functional impairment and can advance to life-threatening respiratory insufficiency. During the past decade, several small-molecule drugs that improve the contractility of skeletal muscle fibers have been developed. In this review, we provide an overview of the available literature and the mechanisms of action of small-molecule drugs that modulate the contractility of sarcomeres, the smallest contractile units in striated muscle, by acting on myosin and troponin. We also discuss their use in the treatment of skeletal myopathies. The first of three classes of drugs discussed here increase contractility by decreasing the dissociation rate of calcium from troponin and thereby sensitizing the muscle to calcium. The second two classes of drugs directly act on myosin and stimulate or inhibit the kinetics of myosin-actin interactions, which may be useful in patients with muscle weakness or stiffness. NEW & NOTEWORTHY During the past decade, several small molecule drugs that improve the contractility of skeletal muscle fibers have been developed. In this review, we provide an overview of the available literature and the mechanisms of action of small molecule drugs that modulate the contractility of sarcomeres, the smallest contractile units in striated muscle, by acting on myosin and troponin.

Published
2023
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