Example of Therapeutic Advances in Musculoskeletal Disease format
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Example of Therapeutic Advances in Musculoskeletal Disease format Example of Therapeutic Advances in Musculoskeletal Disease format Example of Therapeutic Advances in Musculoskeletal Disease format Example of Therapeutic Advances in Musculoskeletal Disease format
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Example of Therapeutic Advances in Musculoskeletal Disease format Example of Therapeutic Advances in Musculoskeletal Disease format Example of Therapeutic Advances in Musculoskeletal Disease format Example of Therapeutic Advances in Musculoskeletal Disease format
Sample paper formatted on SciSpace - SciSpace
This content is only for preview purposes. The original open access content can be found here.
open access Open Access

Therapeutic Advances in Musculoskeletal Disease — Template for authors

Publisher: SAGE
Categories Rank Trend in last 3 yrs
Orthopedics and Sports Medicine #27 of 262 down down by 3 ranks
Rheumatology #17 of 56 down down by None rank
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 144 Published Papers | 789 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 06/06/2020
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Related Journals

open access Open Access
recommended Recommended

Elsevier

Quality:  
High
CiteRatio: 9.0
SJR: 1.974
SNIP: 1.97
open access Open Access

Springer

Quality:  
Good
CiteRatio: 3.0
SJR: 0.837
SNIP: 1.396
open access Open Access
recommended Recommended

Taylor and Francis

Quality:  
High
CiteRatio: 5.3
SJR: 1.287
SNIP: 2.109
open access Open Access

Taylor and Francis

Quality:  
High
CiteRatio: 4.8
SJR: 1.811
SNIP: 1.877

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.

5.5

31% from 2019

CiteRatio for Therapeutic Advances in Musculoskeletal Disease from 2016 - 2020
Year Value
2020 5.5
2019 8.0
2018 6.1
2017 5.1
2016 7.7
graph view Graph view
table view Table view

1.387

6% from 2019

SJR for Therapeutic Advances in Musculoskeletal Disease from 2016 - 2020
Year Value
2020 1.387
2019 1.475
2018 1.566
2017 1.118
2016 1.245
graph view Graph view
table view Table view

2.262

52% from 2019

SNIP for Therapeutic Advances in Musculoskeletal Disease from 2016 - 2020
Year Value
2020 2.262
2019 1.488
2018 1.701
2017 1.506
2016 1.775
graph view Graph view
table view Table view

insights Insights

  • CiteRatio of this journal has decreased by 31% in last years.
  • This journal’s CiteRatio is in the top 10 percentile category.

insights Insights

  • SJR of this journal has decreased by 6% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has increased by 52% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

Therapeutic Advances in Musculoskeletal Disease

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SAGE

Therapeutic Advances in Musculoskeletal Disease

Approved by publishing and review experts on SciSpace, this template is built as per for Therapeutic Advances in Musculoskeletal Disease formatting guidelines as mentioned in SAGE author instructions. The current version was created on 05 Jun 2020 and has been used by 884 authors to write and format their manuscripts to this journal.

Medicine

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Last updated on
05 Jun 2020
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ISSN
1759-720X
i
Impact Factor
High - 1.263
i
Open Access
No
i
Sherpa RoMEO Archiving Policy
Green faq
i
Plagiarism Check
Available via Turnitin
i
Endnote Style
Download Available
i
Bibliography Name
SageV
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Citation Type
Numbered (Superscripted)
25
i
Bibliography Example
Blonder GE, Tinkham M and Klapwijk TM. Transition from metallic to tunneling regimes in superconducting microconstrictions: Excess current, charge imbalance, and supercurrent conversion. Phys. Rev. B 1982; 25(7): 4515–4532. URL 10.1103/PhysRevB.25.4515.

Top papers written in this journal

open accessOpen access Journal Article DOI: 10.1177/1759720X12467868
Role of inflammation in the pathogenesis of osteoarthritis: latest findings and interpretations
Jeremy Sokolove1, Christin M. Lepus1

Abstract:

Osteoarthritis (OA) has traditionally been classified as a noninflammatory arthritis; however, the dichotomy between inflammatory and degenerative arthritis is becoming less clear with the recognition of a plethora of ongoing immune processes within the OA joint and synovium. Synovitis is defined as inflammation of the synovi... Osteoarthritis (OA) has traditionally been classified as a noninflammatory arthritis; however, the dichotomy between inflammatory and degenerative arthritis is becoming less clear with the recognition of a plethora of ongoing immune processes within the OA joint and synovium. Synovitis is defined as inflammation of the synovial membrane and is characteristic of classical inflammatory arthritidies. Increasingly recognized is the presence of synovitis in a significant proportion of patients with primary OA, and based on this observation, further studies have gone on to implicate joint inflammation and synovitis in the pathogenesis of OA. However, clinical OA is not one disease but a final common pathway secondary to many predisposing factors, most notably age, joint trauma, altered biomechanics, and obesity. How such biochemical and mechanical processes contribute to the progressive joint failure characteristic of OA is tightly linked to the interplay of joint damage, the immune response to perceived damage, and the subsequent state of chronic inflammation resulting in propagation and progression toward the phenotype recognized as clinical OA. This review will discuss a wide range of evolving data leading to our current hypotheses regarding the role of immune activation and inflammation in OA onset and progression. Although OA can affect any joint, most commonly the knee, hip, spine, and hands, this review will focus primarily on OA of the knee as this is the joint most well characterized by epidemiologic, imaging, and translational studies investigating the association of inflammation with OA. read more read less

Topics:

Synovitis (56%)56% related to the paper, Arthritis (55%)55% related to the paper, Osteoarthritis (53%)53% related to the paper
View PDF
754 Citations
open accessOpen access Journal Article DOI: 10.1177/1759720X12448454
Chondrogenesis, chondrocyte differentiation, and articular cartilage metabolism in health and osteoarthritis.
Mary B. Goldring1

Abstract:

Chondrogenesis occurs as a result of mesenchymal cell condensation and chondroprogenitor cell differentiation. Following chondrogenesis, the chondrocytes remain as resting cells to form the articular cartilage or undergo proliferation, terminal differentiation to chondrocyte hypertrophy, and apoptosis in a process termed endo... Chondrogenesis occurs as a result of mesenchymal cell condensation and chondroprogenitor cell differentiation. Following chondrogenesis, the chondrocytes remain as resting cells to form the articular cartilage or undergo proliferation, terminal differentiation to chondrocyte hypertrophy, and apoptosis in a process termed endochondral ossification, whereby the hypertrophic cartilage is replaced by bone. Human adult articular cartilage is a complex tissue of matrix proteins that varies from superficial to deep layers and from loaded to unloaded zones. A major challenge to efforts to repair cartilage by stem cell-based and other tissue-engineering strategies is the inability of the resident chondrocytes to lay down a new matrix with the same properties as it had when it was formed during development. Thus, understanding and comparing the mechanisms of cartilage remodeling during development, osteoarthritis (OA), and aging may lead to more effective strategies for preventing cartilage damage and promoting repair. The pivotal proteinase that marks OA progression is matrix metalloproteinase 13 (MMP-13), the major type II collagen-degrading collagenase, which is regulated by both stress and inflammatory signals. We and other investigators have found that there are common mediators of these processes in human OA cartilage. We also observe temporal and spatial expression of these mediators in early through late stages of OA in mouse models and are analyzing the consequences of knockout or transgenic overexpression of critical genes. Since the chondrocytes in adult human cartilage are normally quiescent and maintain the matrix in a low turnover state, understanding how they undergo phenotypic modulation and promote matrix destruction and abnormal repair in OA may to lead to identification of critical targets for therapy to block cartilage damage and promote effective cartilage repair. read more read less

Topics:

Chondrogenesis (71%)71% related to the paper, Chondrocyte (64%)64% related to the paper, Cartilage (62%)62% related to the paper, Stem cell transplantation for articular cartilage repair (62%)62% related to the paper, Endochondral ossification (57%)57% related to the paper
View PDF
362 Citations
open accessOpen access Journal Article DOI: 10.1177/1759720X11430858
Aging and bone loss: new insights for the clinician:

Abstract:

It is well known that the underlying mechanisms of osteoporosis in older adults are different than those associated with estrogen deprivation. Age-related bone loss involves a gradual and progressive decline, which is also seen in men. Markedly increased bone resorption leads to the initial fall in bone mineral density. With ... It is well known that the underlying mechanisms of osteoporosis in older adults are different than those associated with estrogen deprivation. Age-related bone loss involves a gradual and progressive decline, which is also seen in men. Markedly increased bone resorption leads to the initial fall in bone mineral density. With increasing age, there is also a significant reduction in bone formation. This is mostly due to a shift from osteoblastogenesis to predominant adipogenesis in the bone marrow, which also has a lipotoxic effect that affects matrix formation and mineralization. We review new evidence on the pathophysiology of age-related bone loss with emphasis upon the mechanism of action of current osteoporosis treatments. New potential treatments are also considered, including therapeutic approaches to osteoporosis in the elderly that focus on the pathophysiology and potential reversal of adipogenic shift in bone. read more read less

Topics:

Osteoporosis (62%)62% related to the paper, Bone mineral (60%)60% related to the paper, Osteoclast (53%)53% related to the paper, Osteoblast (52%)52% related to the paper
View PDF
359 Citations
open accessOpen access Journal Article DOI: 10.1177/1759720X16670154
Bone modeling and remodeling: potential as therapeutic targets for the treatment of osteoporosis.
Bente L. Langdahl1, Serge Ferrari2, David W. Dempster3

Abstract:

The adult skeleton is renewed by remodeling throughout life. Bone remodeling is a process where osteoclasts and osteoblasts work sequentially in the same bone remodeling unit. After the attainment of peak bone mass, bone remodeling is balanced and bone mass is stable for one or two decades until age-related bone loss begins. ... The adult skeleton is renewed by remodeling throughout life. Bone remodeling is a process where osteoclasts and osteoblasts work sequentially in the same bone remodeling unit. After the attainment of peak bone mass, bone remodeling is balanced and bone mass is stable for one or two decades until age-related bone loss begins. Age-related bone loss is caused by increases in resorptive activity and reduced bone formation. The relative importance of cortical remodeling increases with age as cancellous bone is lost and remodeling activity in both compartments increases. Bone modeling describes the process whereby bones are shaped or reshaped by the independent action of osteoblast and osteoclasts. The activities of osteoblasts and osteoclasts are not necessarily coupled anatomically or temporally. Bone modeling defines skeletal development and growth but continues throughout life. Modeling-based bone formation contributes to the periosteal expansion, just as remodeling-based resorption is responsible for the medullary expansion seen at the long bones with aging. Existing and upcoming treatments affect remodeling as well as modeling. Teriparatide stimulates bone formation, 70% of which is remodeling based and 20-30% is modeling based. The vast majority of modeling represents overflow from remodeling units rather than de novo modeling. Denosumab inhibits bone remodeling but is permissive for modeling at cortex. Odanacatib inhibits bone resorption by inhibiting cathepsin K activity, whereas modeling-based bone formation is stimulated at periosteal surfaces. Inhibition of sclerostin stimulates bone formation and histomorphometric analysis demonstrated that bone formation is predominantly modeling based. The bone-mass response to some osteoporosis treatments in humans certainly suggests that nonremodeling mechanisms contribute to this response and bone modeling may be such a mechanism. To date, this has only been demonstrated for teriparatide, however, it is clear that rediscovering a phenomenon that was first observed more half a century ago will have an important impact on our understanding of how new antifracture treatments work. read more read less

Topics:

Bone remodeling period (79%)79% related to the paper, Bone remodeling (76%)76% related to the paper, Bone cell (73%)73% related to the paper, Bone resorption (66%)66% related to the paper, Bone healing (64%)64% related to the paper
View PDF
271 Citations
open accessOpen access Journal Article DOI: 10.1177/1759720X12466608
Wnt signaling in bone formation and its therapeutic potential for bone diseases

Abstract:

The Wnt signaling pathway plays an important role not only in embryonic development but also in the maintenance and differentiation of the stem cells in adulthood. In particular, Wnt signaling has been shown as an important regulatory pathway in the osteogenic differentiation of mesenchymal stem cells. Induction of the Wnt si... The Wnt signaling pathway plays an important role not only in embryonic development but also in the maintenance and differentiation of the stem cells in adulthood. In particular, Wnt signaling has been shown as an important regulatory pathway in the osteogenic differentiation of mesenchymal stem cells. Induction of the Wnt signaling pathway promotes bone formation while inactivation of the pathway leads to osteopenic states. Our current understanding of Wnt signaling in osteogenesis elucidates the molecular mechanisms of classic osteogenic pathologies. Activating and inactivating aberrations of the canonical Wnt signaling pathway in osteogenesis results in sclerosteosis and osteoporosis respectively. Recent studies have sought to target the Wnt signaling pathway to treat osteogenic disorders. Potential therapeutic approaches attempt to stimulate the Wnt signaling pathway by upregulating the intracellular mediators of the Wnt signaling cascade and inhibiting the endogenous antagonists of the pathway. Antibodies against endogenous antagonists, such as sclerostin and dickkopf-1, have demonstrated promising results in promoting bone formation and fracture healing. Lithium, an inhibitor of glycogen synthase kinase 3β, has also been reported to stimulate osteogenesis by stabilizing β catenin. Although manipulating the Wnt signaling pathway has abundant therapeutic potential, it requires cautious approach due to risks of tumorigenesis. The present review discusses the role of the Wnt signaling pathway in osteogenesis and examines its targeted therapeutic potential. read more read less

Topics:

LRP5 (70%)70% related to the paper, LRP6 (70%)70% related to the paper, Wnt signaling pathway (68%)68% related to the paper, Catenin (55%)55% related to the paper, Regulatory Pathway (54%)54% related to the paper
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265 Citations
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Frequently asked questions

1. Can I write Therapeutic Advances in Musculoskeletal Disease in LaTeX?

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

2. Do you follow the Therapeutic Advances in Musculoskeletal Disease guidelines?

Yes, the template is compliant with the Therapeutic Advances in Musculoskeletal Disease 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 Therapeutic Advances in Musculoskeletal Disease?

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 Therapeutic Advances in Musculoskeletal Disease citation style.

4. Can I use the Therapeutic Advances in Musculoskeletal Disease 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 Therapeutic Advances in Musculoskeletal Disease.

5. Can I use a manuscript in Therapeutic Advances in Musculoskeletal Disease 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 Therapeutic Advances in Musculoskeletal Disease that you can download at the end.

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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.

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SciSpace's Therapeutic Advances in Musculoskeletal Disease 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.

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12. Is Therapeutic Advances in Musculoskeletal Disease'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 Therapeutic Advances in Musculoskeletal Disease?

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 Therapeutic Advances in Musculoskeletal Disease. 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 Therapeutic Advances in Musculoskeletal Disease?

The 5 most common citation types in order of usage for Therapeutic Advances in Musculoskeletal Disease 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 Therapeutic Advances in Musculoskeletal Disease?

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16. Can I download Therapeutic Advances in Musculoskeletal Disease 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 Therapeutic Advances in Musculoskeletal Disease Endnote style according to Elsevier guidelines.

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