Example of Skeletal Muscle format
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Example of Skeletal Muscle format Example of Skeletal Muscle format Example of Skeletal Muscle format Example of Skeletal Muscle format Example of Skeletal Muscle format Example of Skeletal Muscle format Example of Skeletal Muscle format Example of Skeletal Muscle format Example of Skeletal Muscle format Example of Skeletal Muscle format Example of Skeletal Muscle format Example of Skeletal Muscle format Example of Skeletal Muscle format Example of Skeletal Muscle format Example of Skeletal Muscle format Example of Skeletal Muscle format Example of Skeletal Muscle format Example of Skeletal Muscle format
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open access Open Access
recommended Recommended

Skeletal Muscle — Template for authors

Publisher: Springer
Categories Rank Trend in last 3 yrs
Orthopedics and Sports Medicine #20 of 262 down down by 9 ranks
Molecular Biology #127 of 382 down down by 18 ranks
Cell Biology #102 of 279 down down by 7 ranks
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 132 Published Papers | 863 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 02/07/2020
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Related Journals

open access Open Access
recommended Recommended

Taylor and Francis

Quality:  
High
CiteRatio: 15.1
SJR: 3.934
SNIP: 2.351
open access Open Access

Nature

Quality:  
High
CiteRatio: 6.7
SJR: 1.542
SNIP: 1.216
open access Open Access
recommended Recommended

American Association for the Advancement of Science

Quality:  
High
CiteRatio: 10.6
SJR: 3.659
SNIP: 1.504
open access Open Access
recommended Recommended

Springer

Quality:  
High
CiteRatio: 12.8
SJR: 2.928
SNIP: 1.815

Journal Performance & Insights

CiteRatio

SCImago Journal Rank (SJR)

Source Normalized Impact per Paper (SNIP)

A measure of average citations received per peer-reviewed paper published in the journal.

Measures weighted citations received by the journal. Citation weighting depends on the categories and prestige of the citing journal.

Measures actual citations received relative to citations expected for the journal's category.

6.5

4% from 2019

CiteRatio for Skeletal Muscle from 2016 - 2020
Year Value
2020 6.5
2019 6.8
2018 7.2
2017 6.5
2016 5.1
graph view Graph view
table view Table view

1.816

5% from 2019

SJR for Skeletal Muscle from 2016 - 2020
Year Value
2020 1.816
2019 1.732
2018 2.185
2017 2.32
2016 2.021
graph view Graph view
table view Table view

1.352

24% from 2019

SNIP for Skeletal Muscle from 2016 - 2020
Year Value
2020 1.352
2019 1.088
2018 1.227
2017 1.164
2016 0.921
graph view Graph view
table view Table view

insights Insights

  • CiteRatio of this journal has decreased by 4% in last years.
  • This journal’s CiteRatio is in the top 10 percentile category.

insights Insights

  • SJR of this journal has increased by 5% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has increased by 24% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

Skeletal Muscle

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Springer

Skeletal Muscle

Approved by publishing and review experts on SciSpace, this template is built as per for Skeletal Muscle formatting guidelines as mentioned in Springer author instructions. The current version was created on and has been used by 827 authors to write and format their manuscripts to this journal.

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Last updated on
02 Jul 2020
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ISSN
1606-8610
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Open Access
Yes
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Sherpa RoMEO Archiving Policy
White faq
i
Plagiarism Check
Available via Turnitin
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Endnote Style
Download Available
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Citation Type
Numbered
[25]
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Bibliography Example
Blonder, G.E., Tinkham, M., Klapwijk, T.M.: Transition from metallic to tunneling regimes in superconducting microconstrictions: Excess current, charge imbalance, and supercurrent conversion. Phys. Rev. B 25(7), 4515–4532 (1982)

Top papers written in this journal

open accessOpen access Journal Article DOI: 10.1186/2044-5040-1-21
Aberrant repair and fibrosis development in skeletal muscle
04 May 2011 - Skeletal Muscle

Abstract:

The repair process of damaged tissue involves the coordinated activities of several cell types in response to local and systemic signals. Following acute tissue injury, infiltrating inflammatory cells and resident stem cells orchestrate their activities to restore tissue homeostasis. However, during chronic tissue damage, suc... The repair process of damaged tissue involves the coordinated activities of several cell types in response to local and systemic signals. Following acute tissue injury, infiltrating inflammatory cells and resident stem cells orchestrate their activities to restore tissue homeostasis. However, during chronic tissue damage, such as in muscular dystrophies, the inflammatory-cell infiltration and fibroblast activation persists, while the reparative capacity of stem cells (satellite cells) is attenuated. Abnormal dystrophic muscle repair and its end stage, fibrosis, represent the final common pathway of virtually all chronic neurodegenerative muscular diseases. As our understanding of the pathogenesis of muscle fibrosis has progressed, it has become evident that the muscle provides a useful model for the regulation of tissue repair by the local microenvironment, showing interplay among muscle-specific stem cells, inflammatory cells, fibroblasts and extracellular matrix components of the mammalian wound-healing response. This article reviews the emerging findings of the mechanisms that underlie normal versus aberrant muscle-tissue repair. read more read less

Topics:

Skeletal muscle fibrosis (61%)61% related to the paper, Fibrosis (59%)59% related to the paper, Stem cell (59%)59% related to the paper, Tissue homeostasis (58%)58% related to the paper, Muscular dystrophy (56%)56% related to the paper
View PDF
661 Citations
open accessOpen access Journal Article DOI: 10.1186/2044-5040-1-4
Regulation of skeletal muscle growth by the IGF1-Akt/PKB pathway: insights from genetic models.
Stefano Schiaffino, Cristina Mammucari1
24 Jan 2011 - Skeletal Muscle

Abstract:

A highly conserved signaling pathway involving insulin-like growth factor 1 (IGF1), and a cascade of intracellular components that mediate its effects, plays a major role in the regulation of skeletal muscle growth. A central component in this cascade is the kinase Akt, also called protein kinase B (PKB), which controls both ... A highly conserved signaling pathway involving insulin-like growth factor 1 (IGF1), and a cascade of intracellular components that mediate its effects, plays a major role in the regulation of skeletal muscle growth. A central component in this cascade is the kinase Akt, also called protein kinase B (PKB), which controls both protein synthesis, via the kinases mammalian target of rapamycin (mTOR) and glycogen synthase kinase 3β (GSK3β), and protein degradation, via the transcription factors of the FoxO family. In this paper, we review the composition and function of this pathway in skeletal muscle fibers, focusing on evidence obtained in vivo by transgenic and knockout models and by muscle transient transfection experiments. Although this pathway is essential for muscle growth during development and regeneration, its role in adult muscle response to mechanical load is less clear. A full understanding of the operation of this pathway could help to design molecularly targeted therapeutics aimed at preventing muscle wasting, which occurs in a variety of pathologic contexts and in the course of aging. read more read less

Topics:

Akt/PKB signaling pathway (65%)65% related to the paper, PI3K/AKT/mTOR pathway (62%)62% related to the paper, Skeletal muscle (62%)62% related to the paper, Protein kinase B (61%)61% related to the paper, Protein degradation (55%)55% related to the paper
View PDF
617 Citations
open accessOpen access Journal Article DOI: 10.1186/S13395-015-0046-6
Developmental myosins: expression patterns and functional significance
Stefano Schiaffino, Alberto C. Rossi1, Vika Smerdu2, Leslie A. Leinwand1, Carlo Reggiani3
15 Jul 2015 - Skeletal Muscle

Abstract:

Developing skeletal muscles express unique myosin isoforms, including embryonic and neonatal myosin heavy chains, coded by the myosin heavy chain 3 (MYH3) and MYH8 genes, respectively, and myosin light chain 1 embryonic/atrial, encoded by the myosin light chain 4 (MYL4) gene These myosin isoforms are transiently expressed dur... Developing skeletal muscles express unique myosin isoforms, including embryonic and neonatal myosin heavy chains, coded by the myosin heavy chain 3 (MYH3) and MYH8 genes, respectively, and myosin light chain 1 embryonic/atrial, encoded by the myosin light chain 4 (MYL4) gene These myosin isoforms are transiently expressed during embryonic and fetal development and disappear shortly after birth when adult fast and slow myosins become prevalent However, developmental myosins persist throughout adult stages in specialized muscles, such as the extraocular and jaw-closing muscles, and in the intrafusal fibers of the muscle spindles These myosins are re-expressed during muscle regeneration and provide a specific marker of regenerating fibers in the pathologic skeletal muscle Mutations in MYH3 or MYH8 are responsible for distal arthrogryposis syndromes, characterized by congenital joint contractures and orofacial dysmorphisms, supporting the importance of muscle contractile activity and body movements in joint development and in shaping the form of the face during fetal development The biochemical and biophysical properties of developmental myosins have only partially been defined, and their functional significance is not yet clear One possibility is that these myosins are specialized in contracting against low loads, and thus, they may be adapted to the prenatal environment, when fetal muscles contract against a very low load compared to postnatal muscles read more read less

Topics:

Myosin (64%)64% related to the paper, Myosin light-chain kinase (62%)62% related to the paper, MYH7 (58%)58% related to the paper, Skeletal muscle (54%)54% related to the paper
View PDF
339 Citations
open accessOpen access Journal Article DOI: 10.1186/2044-5040-1-11
Aging impairs contraction-induced human skeletal muscle mTORC1 signaling and protein synthesis
02 Mar 2011 - Skeletal Muscle

Abstract:

Sarcopenia, the loss of skeletal muscle mass during aging, increases the risk for falls and dependency. Resistance exercise (RE) training is an effective treatment to improve muscle mass and strength in older adults, but aging is associated with a smaller amount of training-induced hypertrophy. This may be due in part to an i... Sarcopenia, the loss of skeletal muscle mass during aging, increases the risk for falls and dependency. Resistance exercise (RE) training is an effective treatment to improve muscle mass and strength in older adults, but aging is associated with a smaller amount of training-induced hypertrophy. This may be due in part to an inability to stimulate muscle-protein synthesis (MPS) after an acute bout of RE. We hypothesized that older adults would have impaired mammalian target of rapamycin complex (mTORC)1 signaling and MPS response compared with young adults after acute RE. We measured intracellular signaling and MPS in 16 older (mean 70 ± 2 years) and 16 younger (27 ± 2 years) subjects. Muscle biopsies were sampled at baseline and at 3, 6 and 24 hr after exercise. Phosphorylation of regulatory signaling proteins and MPS were determined on successive muscle biopsies by immunoblotting and stable isotopic tracer techniques, respectively. Increased phosphorylation was seen only in the younger group (P 0.05). After exercise, MPS increased from baseline only in the younger group (P< 0.05), with MPS being significantly greater than that in the older group (P < 0.05). We conclude that aging impairs contraction-induced human skeletal muscle mTORC1 signaling and protein synthesis. These age-related differences may contribute to the blunted hypertrophic response seen after resistance-exercise training in older adults, and highlight the mTORC1 pathway as a key therapeutic target to prevent sarcopenia. read more read less

Topics:

Sarcopenia (58%)58% related to the paper, Skeletal muscle (57%)57% related to the paper, Muscle hypertrophy (56%)56% related to the paper
View PDF
319 Citations
open accessOpen access Journal Article DOI: 10.1186/2044-5040-1-34
Immortalized pathological human myoblasts: towards a universal tool for the study of neuromuscular disorders
01 Nov 2011 - Skeletal Muscle

Abstract:

Investigations into both the pathophysiology and therapeutic targets in muscle dystrophies have been hampered by the limited proliferative capacity of human myoblasts. Isolation of reliable and stable immortalized cell lines from patient biopsies is a powerful tool for investigating pathological mechanisms, including those as... Investigations into both the pathophysiology and therapeutic targets in muscle dystrophies have been hampered by the limited proliferative capacity of human myoblasts. Isolation of reliable and stable immortalized cell lines from patient biopsies is a powerful tool for investigating pathological mechanisms, including those associated with muscle aging, and for developing innovative gene-based, cell-based or pharmacological biotherapies. Using transduction with both telomerase-expressing and cyclin-dependent kinase 4-expressing vectors, we were able to generate a battery of immortalized human muscle stem-cell lines from patients with various neuromuscular disorders. The immortalized human cell lines from patients with Duchenne muscular dystrophy, facioscapulohumeral muscular dystrophy, oculopharyngeal muscular dystrophy, congenital muscular dystrophy, and limb-girdle muscular dystrophy type 2B had greatly increased proliferative capacity, and maintained their potential to differentiate both in vitro and in vivo after transplantation into regenerating muscle of immunodeficient mice. Dystrophic cellular models are required as a supplement to animal models to assess cellular mechanisms, such as signaling defects, or to perform high-throughput screening for therapeutic molecules. These investigations have been conducted for many years on cells derived from animals, and would greatly benefit from having human cell models with prolonged proliferative capacity. Furthermore, the possibility to assess in vivo the regenerative capacity of these cells extends their potential use. The innovative cellular tools derived from several different neuromuscular diseases as described in this report will allow investigation of the pathophysiology of these disorders and assessment of new therapeutic strategies. read more read less

Topics:

Muscular dystrophy (63%)63% related to the paper, Duchenne muscular dystrophy (60%)60% related to the paper, Facioscapulohumeral muscular dystrophy (60%)60% related to the paper, Congenital muscular dystrophy (59%)59% related to the paper, Oculopharyngeal muscular dystrophy (55%)55% related to the paper
View PDF
244 Citations
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Frequently asked questions

1. Can I write Skeletal Muscle in LaTeX?

Absolutely not! Our tool has been designed to help you focus on writing. You can write your entire paper as per the Skeletal Muscle guidelines and auto format it.

2. Do you follow the Skeletal Muscle guidelines?

Yes, the template is compliant with the Skeletal Muscle guidelines. Our experts at SciSpace ensure that. If there are any changes to the journal's guidelines, we'll change our algorithm accordingly.

3. Can I cite my article in multiple styles in Skeletal Muscle?

Of course! We support all the top citation styles, such as APA style, MLA style, Vancouver style, Harvard style, and Chicago style. For example, when you write your paper and hit autoformat, our system will automatically update your article as per the Skeletal Muscle citation style.

4. Can I use the Skeletal Muscle templates for free?

Sign up for our free trial, and you'll be able to use all our features for seven days. You'll see how helpful they are and how inexpensive they are compared to other options, Especially for Skeletal Muscle.

5. Can I use a manuscript in Skeletal Muscle that I have written in MS Word?

Yes. You can choose the right template, copy-paste the contents from the word document, and click on auto-format. Once you're done, you'll have a publish-ready paper Skeletal Muscle that you can download at the end.

6. How long does it usually take you to format my papers in Skeletal Muscle?

It only takes a matter of seconds to edit your manuscript. Besides that, our intuitive editor saves you from writing and formatting it in Skeletal Muscle.

7. Where can I find the template for the Skeletal Muscle?

It is possible to find the Word template for any journal on Google. However, why use a template when you can write your entire manuscript on SciSpace , auto format it as per Skeletal Muscle's guidelines and download the same in Word, PDF and LaTeX formats? Give us a try!.

8. Can I reformat my paper to fit the Skeletal Muscle's guidelines?

Of course! You can do this using our intuitive editor. It's very easy. If you need help, our support team is always ready to assist you.

9. Skeletal Muscle an online tool or is there a desktop version?

SciSpace's Skeletal Muscle is currently available as an online tool. We're developing a desktop version, too. You can request (or upvote) any features that you think would be helpful for you and other researchers in the "feature request" section of your account once you've signed up with us.

10. I cannot find my template in your gallery. Can you create it for me like Skeletal Muscle?

Sure. You can request any template and we'll have it setup within a few days. You can find the request box in Journal Gallery on the right side bar under the heading, "Couldn't find the format you were looking for like Skeletal Muscle?”

11. What is the output that I would get after using Skeletal Muscle?

After writing your paper autoformatting in Skeletal Muscle, you can download it in multiple formats, viz., PDF, Docx, and LaTeX.

12. Is Skeletal Muscle's impact factor high enough that I should try publishing my article there?

To be honest, the answer is no. The impact factor is one of the many elements that determine the quality of a journal. Few of these factors include review board, rejection rates, frequency of inclusion in indexes, and Eigenfactor. You need to assess all these factors before you make your final call.

13. What is Sherpa RoMEO Archiving Policy for Skeletal Muscle?

SHERPA/RoMEO Database

We extracted this data from Sherpa Romeo to help researchers understand the access level of this journal in accordance with the Sherpa Romeo Archiving Policy for Skeletal Muscle. The table below indicates the level of access a journal has as per Sherpa Romeo's archiving policy.

RoMEO Colour Archiving policy
Green Can archive pre-print and post-print or publisher's version/PDF
Blue Can archive post-print (ie final draft post-refereeing) or publisher's version/PDF
Yellow Can archive pre-print (ie pre-refereeing)
White Archiving not formally supported
FYI:
  1. Pre-prints as being the version of the paper before peer review and
  2. Post-prints as being the version of the paper after peer-review, with revisions having been made.

14. What are the most common citation types In Skeletal Muscle?

The 5 most common citation types in order of usage for Skeletal Muscle are:.

S. No. Citation Style Type
1. Author Year
2. Numbered
3. Numbered (Superscripted)
4. Author Year (Cited Pages)
5. Footnote

15. How do I submit my article to the Skeletal Muscle?

It is possible to find the Word template for any journal on Google. However, why use a template when you can write your entire manuscript on SciSpace , auto format it as per Skeletal Muscle's guidelines and download the same in Word, PDF and LaTeX formats? Give us a try!.

16. Can I download Skeletal Muscle in Endnote format?

Yes, SciSpace provides this functionality. After signing up, you would need to import your existing references from Word or Bib file to SciSpace. Then SciSpace would allow you to download your references in Skeletal Muscle Endnote style according to Elsevier guidelines.

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