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"... A geographic survey, which requires much of working hours in the digital mapping process, is consisted with the complementary survey and the attribute survey of topography and topographic features, and depended on the field survey. In previous research, using the location-based image had been recomm ..."
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A geographic survey, which requires much of working hours in the digital mapping process, is consisted with the complementary survey and the attribute survey of topography and topographic features, and depended on the field survey. In previous research, using the location-based image had been recommended for diminishing the workload of field survey and post processing. For this research, we have developed the hardware and software for gathering and processing the location-based images with referencing results from the previous research. Those Geographic surveys were performed using developed system on 1/5,000 map sheets for Si and Gun area, respectively. The results have been evaluated as the mobile geographic survey system were able to replace the large part of field survey, and also the working hours were decreased by 37.5 % at Si area. However, the complementary survey was needed for the attributes of topography and topographic features that were occluded
Inaugural Editors Comments
- MIS Quarterly
, 1999
"... DIK. 2013 A role for epigenetic inheritance in Author for correspondence: A role for epigenetic inheritance in genetic variant. This form of inheritance requires that a variant epigenetic state on September 18, ..."
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Cited by 29 (0 self)
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DIK. 2013 A role for epigenetic inheritance in Author for correspondence: A role for epigenetic inheritance in genetic variant. This form of inheritance requires that a variant epigenetic state on September 18,
S-J: Quadrupling muscle mass in mice by targeting TGFbeta signaling pathways. PLoS ONE 2007, 2(8):e789. et al
- Skeletal Muscle 2012, 2:3 http://www.skeletalmusclejournal.com/content/2/1/3 Page 14 of 14
"... Myostatin is a transforming growth factor-ß family member that normally acts to limit skeletal muscle growth. Mice genetically engineered to lack myostatin activity have about twice the amount of muscle mass throughout the body, and similar effects are seen in cattle, sheep, dogs, and a human with n ..."
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Myostatin is a transforming growth factor-ß family member that normally acts to limit skeletal muscle growth. Mice genetically engineered to lack myostatin activity have about twice the amount of muscle mass throughout the body, and similar effects are seen in cattle, sheep, dogs, and a human with naturally occurring loss-of-function mutations in the myostatin gene. Hence, there is considerable interest in developing agents capable of inhibiting myostatin activity for both agricultural and human therapeutic applications. We previously showed that the myostatin binding protein, follistatin, can induce dramatic increases in muscle mass when overexpressed as a transgene in mice. In order to determine whether this effect of follistatin results solely from inhibition of myostatin activity, I analyzed the effect of this transgene in myostatin-null mice. Mstn 2/2 mice carrying a follistatin transgene had about four times the muscle mass of wild type mice, demonstrating the existence of other regulators of muscle mass with similar activity to myostatin. The greatest effect on muscle mass was observed in offspring of mothers homozygous for the Mstn mutation, raising the possibility that either myostatin itself or a downstream regulator may normally be transferred from the maternal to fetal circulations. These findings demonstrate that the capacity for increasing muscle growth by manipulating TGF-ß signaling pathways is much more extensive than previously appreciated and suggest that muscle mass may be controlled at least in part by a systemic mode of action of myostatin.
A mutation in the myostatin gene increases muscle mass and enhances racing performance in heterozygote dogs
- J. Cell Biol
, 2007
"... Double muscling is a trait previously described in several mammalian species including cattle and sheep and is caused by mutations in the myostatin (MSTN) gene (previously referred to as GDF8). Here we describe a new mutation inMSTN found in the whippet dog breed that results in a double-muscled phe ..."
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Double muscling is a trait previously described in several mammalian species including cattle and sheep and is caused by mutations in the myostatin (MSTN) gene (previously referred to as GDF8). Here we describe a new mutation inMSTN found in the whippet dog breed that results in a double-muscled phenotype known as the ‘‘bully’ ’ whippet. Individuals with this phenotype carry two copies of a two-base-pair deletion in the third exon ofMSTN leading to a premature stop codon at amino acid 313. Individuals carrying only one copy of the mutation are, on average, more muscular than wild-type individuals (p 7.43 3 106; Kruskal-Wallis Test) and are significantly faster than individuals carrying the wild-type genotype in competitive racing events (Kendall’s nonparametric measure, s 0.3619; p ’ 0.00028). These results highlight the utility of performance-enhancing polymorphisms, marking the first time a mutation in MSTN has been quantitatively linked to increased athletic performance.
Modulation of myostatin expression during modified muscle use
- FASEB Journal
, 2000
"... ABSTRACT Previous findings have provided strong evidence that myostatin functions as a negative regulator of muscle mass during development and growth. In the present study, we test the hypothesis that myostatin may serve a similar function in fully differentiated muscle experiencing modified loadin ..."
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ABSTRACT Previous findings have provided strong evidence that myostatin functions as a negative regulator of muscle mass during development and growth. In the present study, we test the hypothesis that myostatin may serve a similar function in fully differentiated muscle experiencing modified loading. Our findings show that myostatin expression can be modulated in fully differentiated, nonpathological skeletal muscle in a manner that is inversely related to changes in muscle mass. Atrophy of rat hind limb muscles induced by 10 days of unloading resulted in a 16 % decrease in plantaris mass, a 110 % increase in myostatin mRNA, and a 37 % increase in myostatin protein. Immunohistochemical observations showed a detectable increase in myostatin concentration at myotendinous junctions during muscle unloading. The concentration of myostatin mRNA and protein returned to values not significantly different from ambulatory controls after 4 days of reloading, during which time plantaris mass also returned to control values. However, the results also show that periods of 30 min of daily muscle loading during the unloading period were sufficient to prevent significant losses of muscle mass caused by unloading, although myostatin mRNA still showed a 55 % increase in concentration. Thus, significant increases in myostatin expression are not sufficient for muscle mass loss, although muscle mass loss during unloading is accompanied by increases in myostatin.—Wehling, M., Cai, B., Tidball, J. G. Modulation of myostatin expression during modified muscle use. FASEB J. 14, 103–110
Meat tenderness and muscle growth: is there any relationship
- Meat Science
, 2002
"... Our objectives for this manuscript are to review the mechanisms of muscle growth, the biological basis of meat tenderness, and the relationship between these two processes. Muscle growth is determined by hyperplasia and hypertrophy. Muscle cell size is determined by the balance between the amount of ..."
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Our objectives for this manuscript are to review the mechanisms of muscle growth, the biological basis of meat tenderness, and the relationship between these two processes. Muscle growth is determined by hyperplasia and hypertrophy. Muscle cell size is determined by the balance between the amount of muscle protein synthesized and the amount of muscle protein degraded. Current evidence suggests that the calpain proteolytic system is a major regulator of muscle protein degradation. Sarcomere length, con-nective tissue content, and proteolysis of myofibrils and associated proteins account for most, if not all, of the explainable variation in tenderness of meat after postmortem storage. The relative contribution of each of the above components is muscle dependent. The calpain proteolytic system is a key regulator of postmortem proteolysis. While changes in muscle protein degradation affect meat tenderization/tenderness, changes in muscle protein synthesis are not expected to affect meat tenderization/tenderness.
The molecular bases of training adaptation
- Sports Med
, 2007
"... Publications arising from this thesis This thesis is based on the following publications: ..."
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Cited by 16 (0 self)
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Publications arising from this thesis This thesis is based on the following publications:
Excitation-transcription coupling in skeletal muscle: the molecular pathways of exercise
"... Muscle fibres have different properties with respect to force, contraction speed, endurance, oxidative/glycolytic capacity etc. Although adult muscle fibres are normally post-mitotic with little turnover of cells, the physiological properties of the pre-existing fibres can be changed in the adult an ..."
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Cited by 15 (1 self)
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Muscle fibres have different properties with respect to force, contraction speed, endurance, oxidative/glycolytic capacity etc. Although adult muscle fibres are normally post-mitotic with little turnover of cells, the physiological properties of the pre-existing fibres can be changed in the adult animal upon changes in usage such as after exercise. The signal to change is mainly conveyed by alterations in the patterns of nerve-evoked electrical activity, and is to a large extent due to switches in the expression of genes. Thus, an excitation-transcription coupling must exist. It is suggested that changes in nerve-evoked muscle activity lead to a variety of activity correlates such as increases in free intracellular Ca 2+ levels caused by influx across the cell membrane and/or release from the sarcoplasmatic reticulum, concentrations of metabolites such as lipids and ADP, hypoxia and mechanical stress. Such correlates are detected by sensors such as protein kinase C (PKC), calmodulin, AMP-activated kinase (AMPK), peroxisome proliferator-activated receptor δ (PPARδ), and oxygen dependent prolyl hydroxylases that trigger intracellular signaling cascades. These complex cascades involve several transcription factors such as nuclear factor of activated T-cells (NFAT), myocyte enhancer factor 2 (MEF2), myogenic differentiation factor (myoD), myogenin, PPARδ, and sine oculis homeobox 1/eyes absent 1 (Six1/Eya1). These factors might act indirectly by inducing gene products that act back on the cascade, or as ultimate transcription factors binding to and transactivating/repressing genes for the fast and slow isoforms of various contractile
A differential wiring analysis of expression data correctly identifies the gene containing the causal mutation
- PLoS Comput. Biol
, 2009
"... Transcription factor (TF) regulation is often post-translational. TF modifications such as reversible phosphorylation and missense mutations, which can act independent of TF expression level, are overlooked by differential expression analysis. Using bovine Piedmontese myostatin mutants as proof-of-c ..."
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Transcription factor (TF) regulation is often post-translational. TF modifications such as reversible phosphorylation and missense mutations, which can act independent of TF expression level, are overlooked by differential expression analysis. Using bovine Piedmontese myostatin mutants as proof-of-concept, we propose a new algorithm that correctly identifies the gene containing the causal mutation from microarray data alone. The myostatin mutation releases the brakes on Piedmontese muscle growth by translating a dysfunctional protein. Compared to a less muscular non-mutant breed we find that myostatin is not differentially expressed at any of ten developmental time points. Despite this challenge, the algorithm identifies the myostatin ‘smoking gun ’ through a coordinated, simultaneous, weighted integration of three sources of microarray information: transcript abundance, differential expression, and differential wiring. By asking the novel question ‘‘which regulator is cumulatively most differentially wired to the abundant most differentially expressed genes?’ ’ it yields the correct answer, ‘‘myostatin’’. Our new approach identifies causal regulatory changes by globally contrasting co-expression network dynamics. The entirely data-driven ‘weighting ’ procedure emphasises regulatory movement relative to the phenotypically relevant part of the network. In contrast to other published methods that compare co-expression networks, significance testing is not used to eliminate connections.
Regulation of Myostatin in Vivo by Growth and Differentiation Factor-Associated Serum Protein-1: A Novel Protein with Protease Inhibitor and Follistatin
"... Myostatin, a member of the TGF � superfamily, is a potent and specific negative regulator of skeletal muscle mass. In serum, myostatin circulates as part of a latent complex containing myostatin propeptide and/or follistatin-related gene (FLRG). Here, we report the identification of an additional pr ..."
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Cited by 12 (0 self)
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Myostatin, a member of the TGF � superfamily, is a potent and specific negative regulator of skeletal muscle mass. In serum, myostatin circulates as part of a latent complex containing myostatin propeptide and/or follistatin-related gene (FLRG). Here, we report the identification of an additional protein associated with endogenous myostatin in normal mouse and human serum, discovered by affinity purification and mass spectrometry. This protein, which we have named growth and differentiation factor-associated serum protein-1 (GASP-1), contains multiple domains associated with protease-inhibitory proteins, including a whey acidic protein domain, a Kazal domain, two Kunitz domains, and a netrin domain. GASP-1 also contains
