Example of Journal of Molecular Histology format
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Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format
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Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format Example of Journal of Molecular Histology format
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open access Open Access

Journal of Molecular Histology — Template for authors

Publisher: Springer
Categories Rank Trend in last 3 yrs
Histology #17 of 60 up up by 1 rank
Physiology #98 of 169 down down by 28 ranks
Cell Biology #182 of 279 down down by 33 ranks
journal-quality-icon Journal quality:
Good
calendar-icon Last 4 years overview: 196 Published Papers | 751 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 02/07/2020
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FAQ

Related Journals

open access Open Access

American Chemical Society

Quality:  
High
CiteRatio: 6.5
SJR: 1.158
SNIP: 1.002
open access Open Access
recommended Recommended

Springer

Quality:  
High
CiteRatio: 7.5
SJR: 1.64
SNIP: 1.281
open access Open Access
recommended Recommended

Springer

Quality:  
High
CiteRatio: 6.9
SJR: 1.107
SNIP: 0.923

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.

2.531

14% from 2018

Impact factor for Journal of Molecular Histology from 2016 - 2019
Year Value
2019 2.531
2018 2.937
2017 2.412
2016 2.362
graph view Graph view
table view Table view

3.8

12% from 2019

CiteRatio for Journal of Molecular Histology from 2016 - 2020
Year Value
2020 3.8
2019 4.3
2018 4.3
2017 4.6
2016 4.4
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has decreased by 14% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

insights Insights

  • CiteRatio of this journal has decreased by 12% 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.

0.665

16% from 2019

SJR for Journal of Molecular Histology from 2016 - 2020
Year Value
2020 0.665
2019 0.792
2018 0.928
2017 0.981
2016 0.921
graph view Graph view
table view Table view

0.779

5% from 2019

SNIP for Journal of Molecular Histology from 2016 - 2020
Year Value
2020 0.779
2019 0.823
2018 0.769
2017 0.785
2016 0.829
graph view Graph view
table view Table view

insights Insights

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

insights Insights

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

Journal of Molecular Histology

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Springer

Journal of Molecular Histology

The Journal of Molecular Histology publishes results of original research on the localization and expression of molecules in animal cells, tissues and organs. Coverage includes studies describing novel cellular or ultrastructural distributions of molecules which provide insigh...... Read More

Medicine

i
Last updated on
01 Jul 2020
i
ISSN
1567-2379
i
Impact Factor
Medium - 0.703
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: 10.1023/B:HIJO.0000032355.66152.B8
CXCR4-SDF-1 signalling, locomotion, chemotaxis and adhesion.

Abstract:

Chemokines, small pro-inflammatory chemoattractant cytokines, that bind to specific G-protein-coupled seven-span transmembrane receptors present on plasma membranes of target cells are the major regulators of cell trafficking. In addition some chemokines have been reported to modulate cell survival and growth. Moreover, compe... Chemokines, small pro-inflammatory chemoattractant cytokines, that bind to specific G-protein-coupled seven-span transmembrane receptors present on plasma membranes of target cells are the major regulators of cell trafficking. In addition some chemokines have been reported to modulate cell survival and growth. Moreover, compelling evidence is accumulating that cancer cells may employ several mechanisms involving chemokine–chemokine receptor axes during their metastasis that also regulate the trafficking of normal cells. Of all the chemokines, stromal-derived factor-1 (SDF-1), an α-chemokine that binds to G-protein-coupled CXCR4, plays an important and unique role in the regulation of stem/progenitor cell trafficking. First, SDF-1 regulates the trafficking of CXCR4+ haemato/lymphopoietic cells, their homing/retention in major haemato/lymphopoietic organs and accumulation of CXCR4+ immune cells in tissues affected by inflammation. Second, CXCR4 plays an essential role in the trafficking of other tissue/organ specific stem/progenitor cells expressing CXCR4 on their surface, e.g., during embryo/organogenesis and tissue/organ regeneration. Third, since CXCR4 is expressed on several tumour cells, these CXCR4 positive tumour cells may metastasize to the organs that secrete/express SDF-1 (e.g., bones, lymph nodes, lung and liver). SDF-1 exerts pleiotropic effects regulating processes essential to tumour metastasis such as locomotion of malignant cells, their chemoattraction and adhesion, as well as plays an important role in tumour vascularization. This implies that new therapeutic strategies aimed at blocking the SDF-1–CXCR4 axis could have important applications in the clinic by modulating the trafficking of haemato/lymphopoietic cells and inhibiting the metastatic behaviour of tumour cells as well. In this review, we focus on a role of the SDF-1–CXCR4 axis in regulating the metastatic behaviour of tumour cells and discuss the molecular mechanisms that are essential to this process. read more read less

Topics:

Cancer cell (58%)58% related to the paper, Homing (hematopoietic) (56%)56% related to the paper, Progenitor cell (56%)56% related to the paper, Chemotaxis (54%)54% related to the paper, Chemokine (53%)53% related to the paper
707 Citations
Journal Article DOI: 10.1023/B:HIJO.0000032354.94213.69
CD44 in cancer progression: adhesion, migration and growth regulation.
Rachid Marhaba1, Margot Zöller1, Margot Zöller2

Abstract:

It is well established that the large array of functions that a tumour cell has to fulfil to settle as a metastasis in a distant organ requires cooperative activities between the tumour and the surrounding tissue and that several classes of molecules are involved, such as cell-cell and cell-matrix adhesion molecules and matri... It is well established that the large array of functions that a tumour cell has to fulfil to settle as a metastasis in a distant organ requires cooperative activities between the tumour and the surrounding tissue and that several classes of molecules are involved, such as cell-cell and cell-matrix adhesion molecules and matrix degrading enzymes, to name only a few. Furthermore, metastasis formation requires concerted activities between tumour cells and surrounding cells as well as matrix elements and possibly concerted activities between individual molecules of the tumour cell itself. Adhesion molecules have originally been thought to be essential for the formation of multicellular organisms and to tether cells to the extracellular matrix or to neighbouring cells. CD44 transmembrane glycoproteins belong to the families of adhesion molecules and have originally been described to mediate lymphocyte homing to peripheral lymphoid tissues. It was soon recognized that the molecules, under selective conditions, may suffice to initiate metastatic spread of tumour cells. The question remained as to how a single adhesion molecule can fulfil that task. This review outlines that adhesion is by no means a passive task. Rather, ligand binding, as exemplified for CD44 and other similar adhesion molecules, initiates a cascade of events that can be started by adherence to the extracellular matrix. This leads to activation of the molecule itself, binding to additional ligands, such as growth factors and matrix degrading enzymes, complex formation with additional transmembrane molecules and association with cytoskeletal elements and signal transducing molecules. Thus, through the interplay of CD44 with its ligands and associating molecules CD44 modulates adhesiveness, motility, matrix degradation, proliferation and cell survival, features that together may well allow a tumour cell to proceed through all steps of the metastatic cascade. read more read less

Topics:

Cell adhesion (65%)65% related to the paper, Cell adhesion molecule (64%)64% related to the paper, Lymphocyte homing receptor (59%)59% related to the paper, Extracellular matrix (56%)56% related to the paper, CD44 (52%)52% related to the paper
436 Citations
Journal Article DOI: 10.1007/S10735-007-9145-Y
Expression of the short-chain fatty acid receptor, GPR43, in the human colon.

Abstract:

Short-chain fatty acids (SCFAs), 2-4 carbon monocarboxylates including acetate, propionate and butyrate, are known to have a variety of physiological and pathophysiological effects on the intestine. Previously, we reported that the SCFA receptor, G-protein coupled receptor 43 (GPR43), is expressed by enteroendocrine and mucos... Short-chain fatty acids (SCFAs), 2-4 carbon monocarboxylates including acetate, propionate and butyrate, are known to have a variety of physiological and pathophysiological effects on the intestine. Previously, we reported that the SCFA receptor, G-protein coupled receptor 43 (GPR43), is expressed by enteroendocrine and mucosal mast cells in the rat intestine. In the present study, expression and localization of GPR43 were investigated in the human large intestine. Gene and protein expression of GPR43 in the human ascending colon was analyzed by reverse transcriptase/polymerase chain reaction and Western blotting, respectively. In addition, localization of GPR43 was investigated by immunohistochemistry. In RT-PCR analysis, GPR43 mRNA was detected in whole wall mRNA samples. Western blotting analysis revealed the expression of GPR43 protein in whole wall and scraped mucosa protein samples, but not in muscle or submucosa. GPR43 immunoreactivity was observed in the intracellularly in enterocytes and in the peptide YY-immunoreactive enteroendocrine cells. These results indicate that the short chain fatty acid receptor, GPR43 is expressed by enteroendocrine L cells containing peptide YY in the human large intestine. read more read less

Topics:

Free fatty acid receptor 2 (60%)60% related to the paper, Enteroendocrine cell (59%)59% related to the paper, Short-chain fatty acid (56%)56% related to the paper, Butyrate (55%)55% related to the paper, Peptide YY (54%)54% related to the paper
302 Citations
Journal Article DOI: 10.1023/B:HIJO.0000032357.16261.C5
Tumour biological aspects of CD24, a mucin-like adhesion molecule.
G Kristiansen1, Marei Sammar2, Peter Altevogt2

Abstract:

CD24 is a molecule that recently has raised considerable attention in tumour biology. It is involved in cell adhesion and metastatic tumour spread. It has also been described as a new diagnostic marker of tumours, of neuroendocrine differentiation and, possibly most intriguing of all, of patient prognosis. High rates of CD24 ... CD24 is a molecule that recently has raised considerable attention in tumour biology. It is involved in cell adhesion and metastatic tumour spread. It has also been described as a new diagnostic marker of tumours, of neuroendocrine differentiation and, possibly most intriguing of all, of patient prognosis. High rates of CD24 expression detected by immunohistochemistry have been found in epithelial ovarian cancer (83%), breast cancer (85%), non-small cell lung cancer (45%), prostate cancer (48%) and pancreatic cancer (72%). With the exception of pancreatic cancer, high rates of CD24 are significantly associated with a more aggressive course of the disease, a finding that remains significant in a multivariate analysis. The aim of this review is to summarize relevant work covering these aspects of CD24. read more read less

Topics:

Cancer (65%)65% related to the paper, CA19-9 (63%)63% related to the paper, CA15-3 (62%)62% related to the paper, Pancreatic cancer (60%)60% related to the paper, Tumor-associated glycoprotein 72 (59%)59% related to the paper
296 Citations
open accessOpen access Journal Article DOI: 10.1007/S10735-020-09915-3
COVID-19 and multiorgan failure: A narrative review on potential mechanisms.

Abstract:

The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) in December 2019 form Wuhan, China leads to coronavirus disease 2019 (COVID-19) pandemic. While the common cold symptoms are observed in mild cases, COVID-19 is accompanied by multiorgan failure in severe patients. The involvement of different organs ... The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) in December 2019 form Wuhan, China leads to coronavirus disease 2019 (COVID-19) pandemic. While the common cold symptoms are observed in mild cases, COVID-19 is accompanied by multiorgan failure in severe patients. The involvement of different organs in severe patients results in lengthening the hospitalization duration and increasing the mortality rate. In this review, we aimed to investigate the involvement of different organs in COVID-19 patients, particularly in severe cases. Also, we tried to define the potential underlying mechanisms of SARS-CoV2 induced multiorgan failure. The multi-organ dysfunction is characterized by acute lung failure, acute liver failure, acute kidney injury, cardiovascular disease, and as well as a wide spectrum of hematological abnormalities and neurological disorders. The most important mechanisms are related to the direct and indirect pathogenic features of SARS-CoV2. Although the presence of angiotensin-converting enzyme 2, a receptor of SARS-CoV2 in the lung, heart, kidney, testis, liver, lymphocytes, and nervous system was confirmed, there are controversial findings to about the observation of SARS-CoV2 RNA in these organs. Moreover, the organ failure may be induced by the cytokine storm, a result of increased levels of inflammatory mediators, endothelial dysfunction, coagulation abnormalities, and infiltration of inflammatory cells into the organs. Therefore, further investigations are needed to detect the exact mechanisms of pathogenesis. Since the involvement of several organs in COVID-19 patients is important for clinicians, increasing their knowledge may help to improve the outcomes and decrease the rate of mortality and morbidity. read more read less

Topics:

Acute kidney injury (54%)54% related to the paper, Cytokine storm (51%)51% related to the paper
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281 Citations
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Frequently asked questions

1. Can I write Journal of Molecular Histology in LaTeX?

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

2. Do you follow the Journal of Molecular Histology guidelines?

Yes, the template is compliant with the Journal of Molecular Histology 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 Journal of Molecular Histology?

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 Journal of Molecular Histology citation style.

4. Can I use the Journal of Molecular Histology 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 Journal of Molecular Histology.

5. Can I use a manuscript in Journal of Molecular Histology 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 Journal of Molecular Histology that you can download at the end.

6. How long does it usually take you to format my papers in Journal of Molecular Histology?

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7. Where can I find the template for the Journal of Molecular Histology?

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 Journal of Molecular Histology'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 Journal of Molecular Histology'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.

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SciSpace's Journal of Molecular Histology 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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11. What is the output that I would get after using Journal of Molecular Histology?

After writing your paper autoformatting in Journal of Molecular Histology, you can download it in multiple formats, viz., PDF, Docx, and LaTeX.

12. Is Journal of Molecular Histology'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 Journal of Molecular Histology?

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 Journal of Molecular Histology. 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 Journal of Molecular Histology?

The 5 most common citation types in order of usage for Journal of Molecular Histology 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 Journal of Molecular Histology?

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

16. Can I download Journal of Molecular Histology 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 Journal of Molecular Histology Endnote style according to Elsevier guidelines.

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