Example of Inflammation format
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Example of Inflammation format Example of Inflammation format Example of Inflammation format Example of Inflammation format Example of Inflammation format Example of Inflammation format Example of Inflammation format Example of Inflammation format Example of Inflammation format Example of Inflammation format Example of Inflammation format Example of Inflammation format Example of Inflammation format Example of Inflammation format Example of Inflammation format Example of Inflammation format Example of Inflammation format Example of Inflammation format
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open access Open Access

Inflammation — Template for authors

Publisher: Springer
Categories Rank Trend in last 3 yrs
Immunology and Allergy #67 of 182 down down by 1 rank
Immunology #85 of 202 down down by 2 ranks
journal-quality-icon Journal quality:
Good
calendar-icon Last 4 years overview: 821 Published Papers | 4901 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 03/07/2020
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Related Journals

open access Open Access

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Frontiers Media

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American Association for the Advancement of Science

Quality:  
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CiteRatio: 17.8
SJR: 8.83
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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.

3.212

9% from 2018

Impact factor for Inflammation from 2016 - 2019
Year Value
2019 3.212
2018 2.939
2017 2.884
2016 2.955
graph view Graph view
table view Table view

6.0

9% from 2019

CiteRatio for Inflammation from 2016 - 2020
Year Value
2020 6.0
2019 5.5
2018 5.1
2017 5.6
2016 4.8
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has increased by 9% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

insights Insights

  • CiteRatio of this journal has increased by 9% 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.

1.027

11% from 2019

SJR for Inflammation from 2016 - 2020
Year Value
2020 1.027
2019 0.927
2018 0.874
2017 1.023
2016 0.942
graph view Graph view
table view Table view

0.982

4% from 2019

SNIP for Inflammation from 2016 - 2020
Year Value
2020 0.982
2019 0.94
2018 0.895
2017 0.956
2016 0.959
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has increased by 11% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

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

Inflammation

Guideline source: View

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Springer

Inflammation

Inflammation presents the latest international advances in experimental and clinical research on the physiology, biochemistry, cell biology, and pharmacology of inflammation. Published items include full-length scientific reports, short definitive articles, and papers from mee...... Read More

Immunology and Allergy

Medicine

i
Last updated on
03 Jul 2020
i
ISSN
0360-3997
i
Impact Factor
Medium - 0.749
i
Acceptance Rate
50%
i
Open Access
Yes
i
Sherpa RoMEO Archiving Policy
Green faq
i
Plagiarism Check
Available via Turnitin
i
Endnote Style
Download Available
i
Bibliography Name
SPBASIC
i
Citation Type
Author Year
(Blonder et al, 1982)
i
Bibliography Example
Beenakker CWJ (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

Journal Article DOI: 10.1007/S10753-004-6641-Z
Hypothesis: The Humoral Immune Response to Oral Bacteria Provides a Stimulus for the Development of Rheumatoid Arthritis
Elliot D. Rosenstein, Robert A. Greenwald1, Laura J. Kushner, Gerald Weissmann2
01 Dec 2004 - Inflammation

Abstract:

Rheumatoid arthritis (RA) and adult periodontitis share common pathogenetic mechanisms and immunologic and pathological findings. One oral pathogen strongly implicated in the pathogenesis of periodontal disease, Porphyromonas gingivalis, possesses a unique microbial enzyme, peptidylarginine deiminase (PAD), the human equivale... Rheumatoid arthritis (RA) and adult periodontitis share common pathogenetic mechanisms and immunologic and pathological findings. One oral pathogen strongly implicated in the pathogenesis of periodontal disease, Porphyromonas gingivalis, possesses a unique microbial enzyme, peptidylarginine deiminase (PAD), the human equivalent of which has been identified as a susceptibility factor for RA. We suggest that individuals predisposed to periodontal infection are exposed to antigens generated by PAD, with deiminated fibrin as a likely candidate, which become systemic immunogens and lead to intraarticular inflammation. PAD engendered antigens lead to production of rheumatoid factor-containing immune complexes and provoke local inflammation, both in gingiva and synovium via Fc and C5a receptors. read more read less

Topics:

Porphyromonas gingivalis (53%)53% related to the paper, Immune system (52%)52% related to the paper, Periodontitis (52%)52% related to the paper, Rheumatoid arthritis (51%)51% related to the paper, Pathogenesis (51%)51% related to the paper
356 Citations
Journal Article DOI: 10.1007/BF00920471
Mechanisms of acute and chronic intestinal inflammation induced by indomethacin
01 Dec 1993 - Inflammation

Abstract:

The objective of this study was to characterize the mechanisms of acute and chronic intestinal mucosal injury and inflammation induced by subcutaneously injected indomethacin (Indo). One injection of Indo (7.5 mg/kg) produced acute injury and inflammation in the distal jejunum and proximal ileum that were maximal at three day... The objective of this study was to characterize the mechanisms of acute and chronic intestinal mucosal injury and inflammation induced by subcutaneously injected indomethacin (Indo). One injection of Indo (7.5 mg/kg) produced acute injury and inflammation in the distal jejunum and proximal ileum that were maximal at three days and completely resolved within one week. Two daily subcutaneous injections of Indo produced a more extensive and chronic inflammation that lasted in an active form in more than 75% of the rats for at least two weeks. Epithelial injury, as measured by enhanced mucosal permeability, was significantly elevated only at one day in the acute model (one injection) but was persistently elevated in the chronic model (two injections). Bile duct ligation completely attenuated increased mucosal permeability in the acute model, however, depletion of circulating neutrophils had no effect. Neither Indo (0-0.1 mg/ml) nor normal bile was cytotoxic to cultured rat intestinal epithelial cells; however, they synergistically promoted significant cytotoxicity. Bile collected from rats treated with Indo was cytotoxic towards the epithelial cells in a dose-dependent manner. Sulfasalazine and metronidazole (100 mg/kg/day, both) attenuated enhanced mucosal permeability in the chronic model. Massive bacterial translocation into the mesenteric lymph nodes, liver, and spleen following two injections of Indo was significantly attenuated by metronidazole. We conclude that: (1) a single injection of Indo produces acute intestinal mucosal injury and inflammation that resolve completely within three to seven days, whereas two daily injections of Indo produce both acute and chronic injury and inflammation, (2) enterohepatic circulation of Indo is important in promoting the acute phases of injury and inflammation, (3) circulating neutrophils do not play a role in the pathogenesis of this model, and (4) endogenous bacteria play an important role in exacerbating and/or perpetuating the chronic phases of injury and inflammation. read more read less

Topics:

Pathogenesis (51%)51% related to the paper, Inflammation (50%)50% related to the paper, Enterohepatic circulation (50%)50% related to the paper
314 Citations
Journal Article DOI: 10.1007/S10753-016-0447-7
Indirubin Inhibits LPS-Induced Inflammation via TLR4 Abrogation Mediated by the NF-kB and MAPK Signaling Pathways.
Jin-lun Lai1, Yu-hui Liu1, Chang Liu1, Mingpu Qi1, Rui-ning Liu1, Xifang Zhu1, Qiu-ge Zhou1, Yingyu Chen1, Aizhen Guo1, Changmin Hu1
01 Feb 2017 - Inflammation

Abstract:

Indirubin plays an important role in the treatment of many chronic diseases and exhibits strong anti-inflammatory activity. However, the molecular mode of action during mastitis prophylaxis remains poorly understood. In this study, a lipopolysaccharide (LPS)-induced mastitis mouse model showed that indirubin attenuated histop... Indirubin plays an important role in the treatment of many chronic diseases and exhibits strong anti-inflammatory activity. However, the molecular mode of action during mastitis prophylaxis remains poorly understood. In this study, a lipopolysaccharide (LPS)-induced mastitis mouse model showed that indirubin attenuated histopathological changes in the mammary gland, local tissue necrosis, and neutrophil infiltration. Moreover, indirubin significantly downregulated the production of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α). We explored the mechanism whereby indirubin exerts protective effects against LPS-induced inflammation of mouse mammary epithelial cells (MMECs). The addition of different concentrations of indirubin before exposure of cells to LPS for 1 h significantly attenuated inflammation and reduced the concentrations of the three inflammatory cytokines in a dose-dependent manner. Indirubin downregulated LPS-induced cyclooxygenase-2 (COX-2) and Toll-like receptor 4 (TLR4) expression, inhibited phosphorylation of the LPS-induced nuclear transcription factor-kappa B (NF-kB) P65 protein and its inhibitor IkBα of the NF-kB signaling pathway. Furthermore, indirubin suppressed phosphorylation of P38, extracellular signal-regulated kinase (ERK), and c-Jun NH2-terminal kinase (JNK) of the mitogen-activated protein kinase (MAPK) signal pathways. Thus, indirubin effectively suppressed LPS-induced inflammation via TLR4 abrogation mediated by the NF-kB and MAPK signaling pathways and may be useful for mastitis prophylaxis. read more read less

Topics:

Indirubin (67%)67% related to the paper, MAPK/ERK pathway (53%)53% related to the paper, Proinflammatory cytokine (53%)53% related to the paper, TLR4 (52%)52% related to the paper, Tumor necrosis factor alpha (52%)52% related to the paper
286 Citations
open accessOpen access Journal Article DOI: 10.1007/S10753-013-9621-3
The Adenosine-Dependent Angiogenic Switch of Macrophages to an M2-Like Phenotype is Independent of Interleukin-4 Receptor Alpha (IL-4Rα) Signaling
17 Mar 2013 - Inflammation

Abstract:

Murine macrophages are activated by interferon-γ (IFN-γ) and/or Toll-like receptor (TLR) agonists such as bacterial endotoxin (lipopolysaccharide [LPS]) to express an inflammatory (M1) phenotype characterized by the expression of nitric oxide synthase-2 (iNOS) and inflammatory cytokines such as tumor necrosis factor-α (TNF-α)... Murine macrophages are activated by interferon-γ (IFN-γ) and/or Toll-like receptor (TLR) agonists such as bacterial endotoxin (lipopolysaccharide [LPS]) to express an inflammatory (M1) phenotype characterized by the expression of nitric oxide synthase-2 (iNOS) and inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin (IL)-12. In contrast, Th2 cytokines IL-4 and IL-13 activate macrophages by inducing the expression of arginase-1 and the anti-inflammatory cytokine IL-10 in an IL-4 receptor-α (IL-4Rα)-dependent manner. Macrophages activated in this way are designated as "alternatively activated" (M2a) macrophages. We have shown previously that adenosine A2A receptor (A(2A)R) agonists act synergistically with TLR2, TLR4, TLR7, and TLR9 agonists to switch macrophages into an "M2-like" phenotype that we have termed "M2d." Adenosine signaling suppresses the TLR-dependent expression of TNF-α, IL-12, IFN-γ, and several other inflammatory cytokines by macrophages and induces the expression of vascular endothelial growth factor (VEGF) and IL-10. We show here using mice lacking a functional IL-4Rα gene (IL-4Rα(-/-) mice) that this adenosine-mediated switch does not require IL-4Rα-dependent signaling. M2d macrophages express high levels of VEGF, IL-10, and iNOS, low levels of TNF-α and IL-12, and mildly elevated levels of arginase-1. In contrast, M2d macrophages do not express Ym1, Fizz1 (RELM-α), or CD206 at levels greater than those induced by LPS, and dectin-1 expression is suppressed. The use of these markers in vivo to identify "M2" macrophages thus provides an incomplete picture of macrophage functional status and should be viewed with caution. read more read less

Topics:

Macrophage-activating factor (66%)66% related to the paper, Macrophage inflammatory protein (63%)63% related to the paper, Interleukin 10 (62%)62% related to the paper, Adipose tissue macrophages (61%)61% related to the paper, Interleukin-4 receptor (59%)59% related to the paper
252 Citations
Journal Article DOI: 10.1007/BF00916097
Host response to Bothrops asper snake venom. Analysis of edema formation, inflammatory cells, and cytokine release in a mouse model.
Bruno Lomonte1, Andrej Tarkowski1, Lars Å. Hanson1
01 Apr 1993 - Inflammation

Abstract:

As part of the characterization of the host reactivity to the venom ofBothrops asper, we investigated the inflammatory responses in the mouse footpad model. The subcutaneously injected venom induced a rapid increase of serum IL-6 concentration, which peaked between 3 and 6 h and returned to normal values at 12 h. In contrast,... As part of the characterization of the host reactivity to the venom ofBothrops asper, we investigated the inflammatory responses in the mouse footpad model. The subcutaneously injected venom induced a rapid increase of serum IL-6 concentration, which peaked between 3 and 6 h and returned to normal values at 12 h. In contrast, serum TNF-α and IL-1α were not detectable at any time point studied. A myotoxic phospholipase A2 isoform purified from this venom, myotoxin II, was also able to induce a systemic IL-6 release when injected into the footpad. Both venom and myotoxin induced local edema and a leukocyte infiltrate accumulating in the muscle and subdermal tissue within 6 h. The infiltrate consisted predominantly of neutrophils at 6 and 24 h, but at later times, mononuclear cells also appeared. The edema, leukocyte infiltration, and IL-6 responses did not depend on the hemorrhagic activity of venom, since all three effects were seen after injection of (1) preneutralized venom, devoid of hemorrhagic activity, and (2) purified myotoxin II. Circulating platelet numbers were significantly decreased 30 min after venom injection and returned to normal after 12 h. The venom also induced a rapid inversion in the ratio of neutrophils to lymphocytes in peripheral blood, which did not normalize until 12 h later. The present observations suggest that venom, besides its cytotoxic properties, induces early hematologic and immunologic alterations. These findings may be of relevance in future treatment modalities. read more read less

Topics:

Venom (56%)56% related to the paper, Myotoxin (54%)54% related to the paper, Snake venom (54%)54% related to the paper
239 Citations
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Inflammation format uses SPBASIC citation style.

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Frequently asked questions

1. Can I write Inflammation in LaTeX?

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

2. Do you follow the Inflammation guidelines?

Yes, the template is compliant with the Inflammation 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 Inflammation?

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 Inflammation citation style.

4. Can I use the Inflammation 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 Inflammation.

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

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

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

7. Where can I find the template for the Inflammation?

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

SciSpace's Inflammation 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 Inflammation?

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 Inflammation?”

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

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

12. Is Inflammation'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 Inflammation?

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 Inflammation. 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 Inflammation?

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

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

16. Can I download Inflammation 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 Inflammation Endnote style according to Elsevier guidelines.

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