Example of Respiratory Research format
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Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format
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Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format Example of Respiratory Research format
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open access Open Access

Respiratory Research — Template for authors

Publisher: Springer
Categories Rank Trend in last 3 yrs
Pulmonary and Respiratory Medicine #20 of 133 down down by 1 rank
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 1045 Published Papers | 6849 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 14/06/2020
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Related Journals

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Quality:  
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SNIP: 2.902

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.

3.924

2% from 2018

Impact factor for Respiratory Research from 2016 - 2019
Year Value
2019 3.924
2018 3.829
2017 3.751
2016 3.841
graph view Graph view
table view Table view

6.6

25% from 2019

CiteRatio for Respiratory Research from 2016 - 2020
Year Value
2020 6.6
2019 5.3
2018 5.3
2017 6.3
2016 6.7
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has increased by 2% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

insights Insights

  • CiteRatio of this journal has increased by 25% 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.

1.846

29% from 2019

SJR for Respiratory Research from 2016 - 2020
Year Value
2020 1.846
2019 1.436
2018 1.409
2017 1.644
2016 1.649
graph view Graph view
table view Table view

1.501

32% from 2019

SNIP for Respiratory Research from 2016 - 2020
Year Value
2020 1.501
2019 1.137
2018 1.182
2017 1.161
2016 1.261
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has increased by 29% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has increased by 32% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

Respiratory Research

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Springer

Respiratory Research

Approved by publishing and review experts on SciSpace, this template is built as per for Respiratory Research formatting guidelines as mentioned in Springer author instructions. The current version was created on and has been used by 883 authors to write and format their manuscripts to this journal.

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Last updated on
14 Jun 2020
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ISSN
1465-993X
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Open Access
Yes
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Sherpa RoMEO Archiving Policy
Green 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: 10.1186/1465-9921-11-122
Characterisation of COPD heterogeneity in the ECLIPSE cohort
10 Sep 2010 - Respiratory Research

Abstract:

Chronic obstructive pulmonary disease (COPD) is a complex condition with pulmonary and extra-pulmonary manifestations. This study describes the heterogeneity of COPD in a large and well characterised and controlled COPD cohort (ECLIPSE). We studied 2164 clinically stable COPD patients, 337 smokers with normal lung function an... Chronic obstructive pulmonary disease (COPD) is a complex condition with pulmonary and extra-pulmonary manifestations. This study describes the heterogeneity of COPD in a large and well characterised and controlled COPD cohort (ECLIPSE). We studied 2164 clinically stable COPD patients, 337 smokers with normal lung function and 245 never smokers. In these individuals, we measured clinical parameters, nutritional status, spirometry, exercise tolerance, and amount of emphysema by computed tomography. COPD patients were slightly older than controls and had more pack years of smoking than smokers with normal lung function. Co-morbidities were more prevalent in COPD patients than in controls, and occurred to the same extent irrespective of the GOLD stage. The severity of airflow limitation in COPD patients was poorly related to the degree of breathlessness, health status, presence of co-morbidity, exercise capacity and number of exacerbations reported in the year before the study. The distribution of these variables within each GOLD stage was wide. Even in subjects with severe airflow obstruction, a substantial proportion did not report symptoms, exacerbations or exercise limitation. The amount of emphysema increased with GOLD severity. The prevalence of bronchiectasis was low (4%) but also increased with GOLD stage. Some gender differences were also identified. The clinical manifestations of COPD are highly variable and the degree of airflow limitation does not capture the heterogeneity of the disease. read more read less

Topics:

COPD (58%)58% related to the paper, Spirometry (57%)57% related to the paper, Population (50%)50% related to the paper
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1,021 Citations
open accessOpen access Journal Article DOI: 10.1186/1465-9921-6-56
TGF-β1 induces human alveolar epithelial to mesenchymal cell transition (EMT)
Hidenori Kasai1, Jeremy T. Allen2, Roger M. Mason3, Takashi Kamimura, Zhi Zhang1
09 Jun 2005 - Respiratory Research

Abstract:

Fibroblastic foci are characteristic features in lung parenchyma of patients with idiopathic pulmonary fibrosis (IPF). They comprise aggregates of mesenchymal cells which underlie sites of unresolved epithelial injury and are associated with progression of fibrosis. However, the cellular origins of these mesenchymal phenotype... Fibroblastic foci are characteristic features in lung parenchyma of patients with idiopathic pulmonary fibrosis (IPF). They comprise aggregates of mesenchymal cells which underlie sites of unresolved epithelial injury and are associated with progression of fibrosis. However, the cellular origins of these mesenchymal phenotypes remain unclear. We examined whether the potent fibrogenic cytokine TGF-β1 could induce epithelial mesenchymal transition (EMT) in the human alveolar epithelial cell line, A549, and investigated the signaling pathway of TGF-β1-mediated EMT. A549 cells were examined for evidence of EMT after treatment with TGF-β1. EMT was assessed by: morphology under phase-contrast microscopy; Western analysis of cell lysates for expression of mesenchymal phenotypic markers including fibronectin EDA (Fn-EDA), and expression of epithelial phenotypic markers including E-cadherin (E-cad). Markers of fibrogenesis, including collagens and connective tissue growth factor (CTGF) were also evaluated by measuring mRNA level using RT-PCR, and protein by immunofluorescence or Western blotting. Signaling pathways for EMT were characterized by Western analysis of cell lysates using monoclonal antibodies to detect phosphorylated Erk1/2 and Smad2 after TGF-β1 treatment in the presence or absence of MEK inhibitors. The role of Smad2 in TGF-β1-mediated EMT was investigated using siRNA. The data showed that TGF-β1, but not TNF-α or IL-1β, induced A549 cells with an alveolar epithelial type II cell phenotype to undergo EMT in a time-and concentration-dependent manner. The process of EMT was accompanied by morphological alteration and expression of the fibroblast phenotypic markers Fn-EDA and vimentin, concomitant with a downregulation of the epithelial phenotype marker E-cad. Furthermore, cells that had undergone EMT showed enhanced expression of markers of fibrogenesis including collagens type I and III and CTGF. MMP-2 expression was also evidenced. TGF-β1-induced EMT occurred through phosphorylation of Smad2 and was inhibited by Smad2 gene silencing; MEK inhibitors failed to attenuate either EMT-associated Smad2 phosphorylation or the observed phenotypic changes. Our study shows that TGF-β1 induces A549 alveolar epithelial cells to undergo EMT via Smad2 activation. Our data support the concept of EMT in lung epithelial cells, and suggest the need for further studies to investigate the phenomenon. read more read less

Topics:

Epithelial–mesenchymal transition (61%)61% related to the paper, A549 cell (58%)58% related to the paper, Cellular differentiation (53%)53% related to the paper, CTGF (53%)53% related to the paper, Vimentin (53%)53% related to the paper
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711 Citations
open accessOpen access Journal Article DOI: 10.1186/RR36
Alveolar epithelial type II cell: defender of the alveolus revisited
Heinz Fehrenbach1
15 Jan 2001 - Respiratory Research

Abstract:

In 1977, Mason and Williams developed the concept of the alveolar epithelial type II (AE2) cell as a defender of the alveolus. It is well known that AE2 cells synthesise, secrete, and recycle all components of the surfactant that regulates alveolar surface tension in mammalian lungs. AE2 cells influence extracellular surfacta... In 1977, Mason and Williams developed the concept of the alveolar epithelial type II (AE2) cell as a defender of the alveolus. It is well known that AE2 cells synthesise, secrete, and recycle all components of the surfactant that regulates alveolar surface tension in mammalian lungs. AE2 cells influence extracellular surfactant transformation by regulating, for example, pH and [Ca2+] of the hypophase. AE2 cells play various roles in alveolar fluid balance, coagulation/fibrinolysis, and host defence. AE2 cells proliferate, differentiate into AE1 cells, and remove apoptotic AE2 cells by phagocytosis, thus contributing to epithelial repair. AE2 cells may act as immunoregulatory cells. AE2 cells interact with resident and mobile cells, either directly by membrane contact or indirectly via cytokines/growth factors and their receptors, thus representing an integrative unit within the alveolus. Although most data support the concept, the controversy about the character of hyperplastic AE2 cells, reported to synthesise profibrotic factors, proscribes drawing a definite conclusion today. read more read less

Topics:

A549 cell (60%)60% related to the paper, Stem cell (54%)54% related to the paper, Alveolar Epithelium (53%)53% related to the paper
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692 Citations
open accessOpen access Journal Article DOI: 10.1186/1465-9921-7-135
IL-17 mRNA in sputum of asthmatic patients: linking T cell driven inflammation and granulocytic influx?
Dominique Bullens1, Els Truyen1, Liesbeth Coteur1, Ellen Dilissen1, Peter Hellings1, Lieven Dupont1, Jan Ceuppens1
03 Nov 2006 - Respiratory Research

Abstract:

The role of Th2 cells (producing interleukin (IL-)4, IL-5 and IL-13) in allergic asthma is well-defined. A distinct proinflammatory T cell lineage has recently been identified, called Th17 cells, producing IL-17A, a cytokine that induces CXCL8 (IL-8) and recruits neutrophils. Neutrophilic infiltration in the airways is promin... The role of Th2 cells (producing interleukin (IL-)4, IL-5 and IL-13) in allergic asthma is well-defined. A distinct proinflammatory T cell lineage has recently been identified, called Th17 cells, producing IL-17A, a cytokine that induces CXCL8 (IL-8) and recruits neutrophils. Neutrophilic infiltration in the airways is prominent in severe asthma exacerbations and may contribute to airway gland hypersecretion, bronchial hyper-reactivity and airway wall remodelling in asthma. to study the production of IL-17 in asthmatic airways at the mRNA level, and to correlate this with IL-8 mRNA, neutrophilic inflammation and asthma severity. We obtained airway cells by sputum induction from healthy individuals (n = 15) and from asthmatic patients (n = 39). Neutrophils were counted on cytospins and IL-17A and IL-8 mRNA expression was quantified by real-time RT-PCR (n = 11 controls and 33 asthmatics). Sputum IL-17A and IL-8 mRNA levels are significantly elevated in asthma patients compared to healthy controls. IL-17 mRNA levels are significantly correlated with CD3γ mRNA levels in asthmatic patients and mRNA levels of IL-17A and IL-8 correlated with each other and with sputum neutrophil counts. High sputum IL-8 and IL-17A mRNA levels were also found in moderate-to-severe (persistent) asthmatics on inhaled steroid treatment. The data suggest that Th17 cell infiltration in asthmatic airways links T cell activity with neutrophilic inflammation in asthma. read more read less

Topics:

Sputum (56%)56% related to the paper, Interleukin 17 (52%)52% related to the paper, Asthma (51%)51% related to the paper, Proinflammatory cytokine (51%)51% related to the paper, T cell (50%)50% related to the paper
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575 Citations
open accessOpen access Journal Article DOI: 10.1186/RR25
Epithelial antimicrobial peptides in host defense against infection
Robert Bals1
20 Oct 2000 - Respiratory Research

Abstract:

One component of host defense at mucosal surfaces seems to be epithelium-derived antimicrobial peptides. Antimicrobial peptides are classified on the basis of their structure and amino acid motifs. Peptides of the defensin, cathelicidin, and histatin classes are found in humans. In the airways, α-defensins and the cathelicidi... One component of host defense at mucosal surfaces seems to be epithelium-derived antimicrobial peptides. Antimicrobial peptides are classified on the basis of their structure and amino acid motifs. Peptides of the defensin, cathelicidin, and histatin classes are found in humans. In the airways, α-defensins and the cathelicidin LL-37/hCAP-18 originate from neutrophils. β-Defensins and LL-37/hCAP-18 are produced by the respiratory epithelium and the alveolar macrophage and secreted into the airway surface fluid. Beside their direct antimicrobial function, antimicrobial peptides have multiple roles as mediators of inflammation with effects on epithelial and inflammatory cells, influencing such diverse processes as proliferation, immune induction, wound healing, cytokine release, chemotaxis, protease-antiprotease balance, and redox homeostasis. Further, antimicrobial peptides qualify as prototypes of innovative drugs that might be used as antibiotics, anti-lipopolysaccharide drugs, or modifiers of inflammation. read more read less

Topics:

Antimicrobial peptides (72%)72% related to the paper, Cathelicidin (69%)69% related to the paper, Beta defensin (66%)66% related to the paper, Defensin (58%)58% related to the paper, Antimicrobial (56%)56% related to the paper
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500 Citations
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Frequently asked questions

1. Can I write Respiratory Research in LaTeX?

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

2. Do you follow the Respiratory Research guidelines?

Yes, the template is compliant with the Respiratory Research 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 Respiratory Research?

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 Respiratory Research citation style.

4. Can I use the Respiratory Research 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 Respiratory Research.

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

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

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

7. Where can I find the template for the Respiratory Research?

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

SciSpace's Respiratory Research 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 Respiratory Research?

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 Respiratory Research?”

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

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

12. Is Respiratory Research'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 Respiratory Research?

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 Respiratory Research. 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 Respiratory Research?

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

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

16. Can I download Respiratory Research 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 Respiratory Research Endnote style according to Elsevier guidelines.

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