Example of Acta Physiologica format
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Example of Acta Physiologica format Example of Acta Physiologica format Example of Acta Physiologica format Example of Acta Physiologica format Example of Acta Physiologica format Example of Acta Physiologica format Example of Acta Physiologica format
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Acta Physiologica — Template for authors

Publisher: Wiley
Categories Rank Trend in last 3 yrs
Physiology #17 of 169 down down by 1 rank
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 422 Published Papers | 4327 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 05/06/2020
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SJR: 1.596
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Journal Performance & Insights

Impact Factor

CiteRatio

Determines the importance of a journal by taking a measure of frequency with which the average article in a journal has been cited in a particular year.

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

5.542

6% from 2018

Impact factor for Acta Physiologica from 2016 - 2019
Year Value
2019 5.542
2018 5.868
2017 5.93
2016 4.867
graph view Graph view
table view Table view

10.3

21% from 2019

CiteRatio for Acta Physiologica from 2016 - 2020
Year Value
2020 10.3
2019 8.5
2018 9.2
2017 9.3
2016 7.9
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has decreased by 6% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

insights Insights

  • CiteRatio of this journal has increased by 21% in last years.
  • This journal’s CiteRatio is in the top 10 percentile category.

SCImago Journal Rank (SJR)

Source Normalized Impact per Paper (SNIP)

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.

1.591

9% from 2019

SJR for Acta Physiologica from 2016 - 2020
Year Value
2020 1.591
2019 1.457
2018 1.751
2017 1.542
2016 1.654
graph view Graph view
table view Table view

1.463

16% from 2019

SNIP for Acta Physiologica from 2016 - 2020
Year Value
2020 1.463
2019 1.258
2018 1.306
2017 1.219
2016 1.073
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has increased by 9% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has increased by 16% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

Acta Physiologica

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Wiley

Acta Physiologica

Acta Physiologica is an important forum for the publication of high quality original research in physiology and related areas by authors from all over the world. Acta Physiologica is a leading journal in human/translational physiology while promoting all aspects of the science...... Read More

Physiology

Biochemistry, Genetics and Molecular Biology

i
Last updated on
05 Jun 2020
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ISSN
1748-1708
i
Impact Factor
High - 1.058
i
Open Access
Yes
i
Sherpa RoMEO Archiving Policy
Yellow faq
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Plagiarism Check
Available via Turnitin
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Endnote Style
Download Available
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Bibliography Name
apa
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Citation Type
Numbered
[25]
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Bibliography Example
Beenakker, C.W.J. (2006) Specular andreev reflection in graphene.Phys. Rev. Lett., 97 (6), 067 007. URL 10.1103/PhysRevLett.97.067007.

Top papers written in this journal

open accessOpen access Journal Article DOI: 10.1111/J.1748-1716.2009.01964.X
Endothelial dysfunction and vascular disease
Paul M. Vanhoutte1, Hiroaki Shimokawa2, E. H. C. Tang3, Michel Félétou
01 Jun 2009 - Acta Physiologica

Abstract:

The endothelium can evoke relaxations (dilatations) of the underlying vascular smooth muscle, by releasing vasodilator substances. The best characterized endothelium-derived relaxing factor (EDRF) is nitric oxide (NO). The endothelial cells also evoke hyperpolarization of the cell membrane of vascular smooth muscle (endotheli... The endothelium can evoke relaxations (dilatations) of the underlying vascular smooth muscle, by releasing vasodilator substances. The best characterized endothelium-derived relaxing factor (EDRF) is nitric oxide (NO). The endothelial cells also evoke hyperpolarization of the cell membrane of vascular smooth muscle (endothelium-dependent hyperpolarizations, EDHF-mediated responses). Endothelium-dependent relaxations involve both pertussis toxin-sensitive G(i) (e.g. responses to serotonin and thrombin) and pertussis toxin-insensitive G(q) (e.g. adenosine diphosphate and bradykinin) coupling proteins. The release of NO by the endothelial cell can be up-regulated (e.g. by oestrogens, exercise and dietary factors) and down-regulated (e.g. oxidative stress, smoking and oxidized low-density lipoproteins). It is reduced in the course of vascular disease (e.g. diabetes and hypertension). Arteries covered with regenerated endothelium (e.g. following angioplasty) selectively loose the pertussis toxin-sensitive pathway for NO release which favours vasospasm, thrombosis, penetration of macrophages, cellular growth and the inflammatory reaction leading to atherosclerosis. In addition to the release of NO (and causing endothelium-dependent hyperpolarizations), endothelial cells also can evoke contraction (constriction) of the underlying vascular smooth muscle cells by releasing endothelium-derived contracting factor (EDCF). Most endothelium-dependent acute increases in contractile force are due to the formation of vasoconstrictor prostanoids (endoperoxides and prostacyclin) which activate TP receptors of the vascular smooth muscle cells. EDCF-mediated responses are exacerbated when the production of NO is impaired (e.g. by oxidative stress, ageing, spontaneous hypertension and diabetes). They contribute to the blunting of endothelium-dependent vasodilatations in aged subjects and essential hypertensive patients. read more read less

Topics:

Vascular smooth muscle (63%)63% related to the paper, Endothelium (58%)58% related to the paper, Endothelial dysfunction (58%)58% related to the paper, Vasodilation (56%)56% related to the paper, Endothelial stem cell (55%)55% related to the paper
View PDF
730 Citations
open accessOpen access Journal Article DOI: 10.1111/J.1748-1716.2009.01972.X
LKB1 and AMP‐activated protein kinase control of mTOR signalling and growth
Reuben J. Shaw1
01 May 2009 - Acta Physiologica

Abstract:

The AMP-activated serine/threonine protein kinase (AMPK) is a sensor of cellular energy status found in all eukaryotes that is activated under conditions of low intracellular ATP following stresses such as nutrient deprivation or hypoxia. In the past 5 years, work from a large number of laboratories has revealed that one of t... The AMP-activated serine/threonine protein kinase (AMPK) is a sensor of cellular energy status found in all eukaryotes that is activated under conditions of low intracellular ATP following stresses such as nutrient deprivation or hypoxia. In the past 5 years, work from a large number of laboratories has revealed that one of the major downstream signalling pathways regulated by AMPK is the mammalian target-of-rapamycin [mammalian target of rapamycin (mTOR) pathway]. Interestingly, like AMPK, the mTOR serine/threonine kinase plays key roles not only in growth control and cell proliferation but also in metabolism. Recent work has revealed that across eukaryotes mTOR orthologues are found in two biochemically distinct complexes and only one of those complexes (mTORC1 in mammals) is acutely sensitive to rapamycin and regulated by nutrients and AMPK. Many details of the molecular mechanism by which AMPK inhibits mTORC1 signalling have also been decoded in the past 5 years. AMPK directly phosphorylates at least two proteins to induce rapid suppression of mTORC1 activity, the TSC2 tumour suppressor and the critical mTORC1 binding subunit raptor. Here we explore the molecular connections between AMPK and mTOR signalling pathways and examine the physiological processes in which AMPK regulation of mTOR is critical for growth or metabolic control. The functional conservation of AMPK and TOR in all eukaryotes, and the sequence conservation around the AMPK phosphorylation sites in raptor across all eukaryotes examined suggest that this represents a fundamental cell growth module connecting nutrient status to the cell growth machinery. These findings have broad implications for the control of cell growth by nutrients in a number of cellular and organismal contexts. read more read less

Topics:

AMPK (76%)76% related to the paper, RPTOR (59%)59% related to the paper, mTORC1 (57%)57% related to the paper, PI3K/AKT/mTOR pathway (55%)55% related to the paper, TOR Serine-Threonine Kinases (54%)54% related to the paper
View PDF
599 Citations
Journal Article DOI: 10.1111/APHA.12646
Endothelial dysfunction and vascular disease – a 30th anniversary update
Paul M. Vanhoutte1, Hiroaki Shimokawa2, Michel Félétou, Eva Hoi Ching Tang1
01 Jan 2017 - Acta Physiologica

Abstract:

The endothelium can evoke relaxations of the underlying vascular smooth muscle, by releasing vasodilator substances. The best-characterized endothelium-derived relaxing factor (EDRF) is nitric oxide (NO) which activates soluble guanylyl cyclase in the vascular smooth muscle cells, with the production of cyclic guanosine monop... The endothelium can evoke relaxations of the underlying vascular smooth muscle, by releasing vasodilator substances. The best-characterized endothelium-derived relaxing factor (EDRF) is nitric oxide (NO) which activates soluble guanylyl cyclase in the vascular smooth muscle cells, with the production of cyclic guanosine monophosphate (cGMP) initiating relaxation. The endothelial cells also evoke hyperpolarization of the cell membrane of vascular smooth muscle (endothelium-dependent hyperpolarizations, EDH-mediated responses). As regards the latter, hydrogen peroxide (H2 O2 ) now appears to play a dominant role. Endothelium-dependent relaxations involve both pertussis toxin-sensitive Gi (e.g. responses to α2 -adrenergic agonists, serotonin, and thrombin) and pertussis toxin-insensitive Gq (e.g. adenosine diphosphate and bradykinin) coupling proteins. New stimulators (e.g. insulin, adiponectin) of the release of EDRFs have emerged. In recent years, evidence has also accumulated, confirming that the release of NO by the endothelial cell can chronically be upregulated (e.g. by oestrogens, exercise and dietary factors) and downregulated (e.g. oxidative stress, smoking, pollution and oxidized low-density lipoproteins) and that it is reduced with ageing and in the course of vascular disease (e.g. diabetes and hypertension). Arteries covered with regenerated endothelium (e.g. following angioplasty) selectively lose the pertussis toxin-sensitive pathway for NO release which favours vasospasm, thrombosis, penetration of macrophages, cellular growth and the inflammatory reaction leading to atherosclerosis. In addition to the release of NO (and EDH, in particular those due to H2 O2 ), endothelial cells also can evoke contraction of the underlying vascular smooth muscle cells by releasing endothelium-derived contracting factors. Recent evidence confirms that most endothelium-dependent acute increases in contractile force are due to the formation of vasoconstrictor prostanoids (endoperoxides and prostacyclin) which activate TP receptors of the vascular smooth muscle cells and that prostacyclin plays a key role in such responses. Endothelium-dependent contractions are exacerbated when the production of nitric oxide is impaired (e.g. by oxidative stress, ageing, spontaneous hypertension and diabetes). They contribute to the blunting of endothelium-dependent vasodilatations in aged subjects and essential hypertensive and diabetic patients. In addition, recent data confirm that the release of endothelin-1 can contribute to endothelial dysfunction and that the peptide appears to be an important contributor to vascular dysfunction. Finally, it has become clear that nitric oxide itself, under certain conditions (e.g. hypoxia), can cause biased activation of soluble guanylyl cyclase leading to the production of cyclic inosine monophosphate (cIMP) rather than cGMP and hence causes contraction rather than relaxation of the underlying vascular smooth muscle. read more read less

Topics:

Vascular smooth muscle (65%)65% related to the paper, Soluble guanylyl cyclase (60%)60% related to the paper, Endothelium (58%)58% related to the paper, Endothelial dysfunction (57%)57% related to the paper, Cyclic guanosine monophosphate (57%)57% related to the paper
599 Citations
Journal Article DOI: 10.1111/J.1748-1716.2007.01713.X
Effects of dietary nitrate on oxygen cost during exercise
Filip J. Larsen1, Eddie Weitzberg1, Jon O. Lundberg1, Björn Ekblom1
01 Sep 2007 - Acta Physiologica

Abstract:

AIM: Nitric oxide (NO), synthesized from l-arginine by NO synthases, plays a role in adaptation to physical exercise by modulating blood flow, muscular contraction and glucose uptake and in the con AIM: Nitric oxide (NO), synthesized from l-arginine by NO synthases, plays a role in adaptation to physical exercise by modulating blood flow, muscular contraction and glucose uptake and in the con read more read less

Topics:

Nitric oxide (51%)51% related to the paper, Glucose uptake (51%)51% related to the paper
589 Citations
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Acta Physiologica format uses apa citation style.

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Frequently asked questions

1. Can I write Acta Physiologica in LaTeX?

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

2. Do you follow the Acta Physiologica guidelines?

Yes, the template is compliant with the Acta Physiologica 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 Acta Physiologica?

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 Acta Physiologica citation style.

4. Can I use the Acta Physiologica 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 Acta Physiologica.

5. Can I use a manuscript in Acta Physiologica 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 Acta Physiologica that you can download at the end.

6. How long does it usually take you to format my papers in Acta Physiologica?

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

7. Where can I find the template for the Acta Physiologica?

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 Acta Physiologica'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 Acta Physiologica'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. Acta Physiologica an online tool or is there a desktop version?

SciSpace's Acta Physiologica 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 Acta Physiologica?

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 Acta Physiologica?”

11. What is the output that I would get after using Acta Physiologica?

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

12. Is Acta Physiologica'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 Acta Physiologica?

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 Acta Physiologica. 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 Acta Physiologica?

The 5 most common citation types in order of usage for Acta Physiologica 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 Acta Physiologica?

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 Acta Physiologica's guidelines and download the same in Word, PDF and LaTeX formats? Give us a try!.

16. Can I download Acta Physiologica 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 Acta Physiologica Endnote style according to Elsevier guidelines.

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I spent hours with MS word for reformatting. It was frustrating - plain and simple. With SciSpace, I can draft my manuscripts and once it is finished I can just submit. In case, I have to submit to another journal it is really just a button click instead of an afternoon of reformatting.

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