Example of Journal of Medical Genetics format
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Example of Journal of Medical Genetics format Example of Journal of Medical Genetics format Example of Journal of Medical Genetics format Example of Journal of Medical Genetics format Example of Journal of Medical Genetics format Example of Journal of Medical Genetics format
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Example of Journal of Medical Genetics format Example of Journal of Medical Genetics format Example of Journal of Medical Genetics format Example of Journal of Medical Genetics format Example of Journal of Medical Genetics format Example of Journal of Medical Genetics format
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This content is only for preview purposes. The original open access content can be found here.
open access Open Access ISSN: 222593 e-ISSN: 14686244
recommended Recommended

Journal of Medical Genetics — Template for authors

Categories Rank Trend in last 3 yrs
Genetics (clinical) #7 of 87 up up by 2 ranks
Genetics #33 of 325 down down by 4 ranks
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 407 Published Papers | 3968 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 16/06/2020
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FAQ

Journal Performance & Insights

  • Impact Factor
  • CiteRatio
  • SJR
  • SNIP

Impact factor 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.

4.943

16% from 2018

Impact factor for Journal of Medical Genetics from 2016 - 2019
Year Value
2019 4.943
2018 5.899
2017 5.751
2016 5.451
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has decreased by 16% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

CiteRatio is a measure of average citations received per peer-reviewed paper published in the journal.

9.7

4% from 2019

CiteRatio for Journal of Medical Genetics from 2016 - 2020
Year Value
2020 9.7
2019 10.1
2018 10.7
2017 10.4
2016 10.6
graph view Graph view
table view Table view

insights Insights

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

SCImago Journal Rank (SJR) measures weighted citations received by the journal. Citation weighting depends on the categories and prestige of the citing journal.

2.439

0% from 2019

SJR for Journal of Medical Genetics from 2016 - 2020
Year Value
2020 2.439
2019 2.45
2018 3.017
2017 3.304
2016 3.252
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has decreased by 0% in last years.
  • This journal’s SJR is in the top 10 percentile category.

Source Normalized Impact per Paper (SNIP) measures actual citations received relative to citations expected for the journal's category.

1.883

1% from 2019

SNIP for Journal of Medical Genetics from 2016 - 2020
Year Value
2020 1.883
2019 1.906
2018 1.829
2017 1.799
2016 1.815
graph view Graph view
table view Table view

insights Insights

  • SNIP of this journal has decreased by 1% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

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Journal of Medical Genetics

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BMJ Publishing Group

Journal of Medical Genetics

Journal of Medical Genetics is a leading international publication covering original research in human genetics, including reviews of and opinion on the latest developments. Articles cover the genetic basis of human disease including germline cancer genetics, the clinical mani...... Read More

Genetics(clinical)

Medicine

i
Last updated on
16 Jun 2020
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ISSN
0022-2593
i
Impact Factor
High - 2.079
i
Acceptance Rate
17%
i
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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Bibliography Name
unsrt
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Citation Type
Numbered
[25]
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Bibliography Example
C. W. J. Beenakker. Specular andreev reflection in graphene. Phys. Rev. Lett., 97(6):067007, 2006.

Top papers written in this journal

open accessOpen access Journal Article DOI: 10.1136/JMG.16.2.101
Genetic heterogeneity in osteogenesis imperfecta.
D. O. Sillence, Alison Senn, D. M. Danks

Abstract:

An epidemiological and genetical study of osteogenesis imperfecta (OI) in Victoria, Australia confirmed that there are at least four distinct syndromes at present called OI. The largest group of patients showed autosomal dominant inheritance of osteoporosis leading to fractures and distinctly blue sclerae. A large proportion ... An epidemiological and genetical study of osteogenesis imperfecta (OI) in Victoria, Australia confirmed that there are at least four distinct syndromes at present called OI. The largest group of patients showed autosomal dominant inheritance of osteoporosis leading to fractures and distinctly blue sclerae. A large proportion of adults had presenile deafness or a family history of presenile conductive hearing loss. A second group, who comprised the majority of newborns with neonatal fractures, all died before or soon after birth. These had characteristic broad, crumpled femora and beaded ribs in skeletal x-rays. Autosomal recessive inheritance was likely for some, if not all, of these cases. A third group, two thirds of whom had fractures at birth, showed severe progressive deformity of limbs and spine. The density of scleral blueness appeared less than that seen in the first group of patients and approximated that seen in normal children and adults. Moreover, the blueness appeared to decrease with age. All patients in this group were sporadic cases. The mode of inheritance was not resolved by the study, but it is likely that the group is heterogeneous with both dominant and recessive genotypes responsible for the syndrome. The fourth group of patients showed dominant inheritance of osteoporosis leading to fractures, with variable deformity of long bones, but normal sclerae. read more read less

Topics:

Osteogenesis Imperfecta Type II (57%)57% related to the paper, Osteogenesis imperfecta (56%)56% related to the paper, Osteogenesis Imperfecta Type III (55%)55% related to the paper, Bruck syndrome (52%)52% related to the paper, Dentinogenesis imperfecta (51%)51% related to the paper
View PDF
1,772 Citations
open accessOpen access Journal Article DOI: 10.1136/JMG.2009.072785
The revised Ghent nosology for the Marfan syndrome

Abstract:

The diagnosis of Marfan syndrome (MFS) relies on defined clinical criteria (Ghent nosology), outlined by international expert opinion to facilitate accurate recognition of this genetic aneurysm syndrome and to improve patient management and counselling. These Ghent criteria, comprising a set of major and minor manifestations ... The diagnosis of Marfan syndrome (MFS) relies on defined clinical criteria (Ghent nosology), outlined by international expert opinion to facilitate accurate recognition of this genetic aneurysm syndrome and to improve patient management and counselling. These Ghent criteria, comprising a set of major and minor manifestations in different body systems, have proven to work well since with improving molecular techniques, confirmation of the diagnosis is possible in over 95% of patients. However, concerns with the current nosology are that some of the diagnostic criteria have not been sufficiently validated, are not applicable in children or necessitate expensive and specialised investigations. The recognition of variable clinical expression and the recently extended differential diagnosis further confound accurate diagnostic decision making. Moreover, the diagnosis of MFS—whether or not established correctly—can be stigmatising, hamper career aspirations, restrict life insurance opportunities, and cause psychosocial burden. An international expert panel has established a revised Ghent nosology, which puts more weight on the cardiovascular manifestations and in which aortic root aneurysm and ectopia lentis are the cardinal clinical features. In the absence of any family history, the presence of these two manifestations is sufficient for the unequivocal diagnosis of MFS. In absence of either of these two, the presence of a bonafide FBN1 mutation or a combination of systemic manifestations is required. For the latter a new scoring system has been designed. In this revised nosology, FBN1 testing, although not mandatory, has greater weight in the diagnostic assessment. Special considerations are given to the diagnosis of MFS in children and alternative diagnoses in adults. We anticipate that these new guidelines may delay a definitive diagnosis of MFS but will decrease the risk of premature or misdiagnosis and facilitate worldwide discussion of risk and follow-up/management guidelines. read more read less

Topics:

Life insurance (52%)52% related to the paper, Nosology (52%)52% related to the paper, Medical diagnosis (51%)51% related to the paper
View PDF
1,408 Citations
open accessOpen access Journal Article DOI: 10.1136/JMG.34.10.798
Spectrum of clinical features associated with interstitial chromosome 22q11 deletions: a European collaborative study.

Abstract:

We present clinical data on 558 patients with deletions within the DiGeorge syndrome critical region of chromosome 22q11. Twenty-eight percent of the cases where parents had been tested had inherited deletions, with a marked excess of maternally inherited deletions (maternal 61, paternal 18). Eight percent of the patients had... We present clinical data on 558 patients with deletions within the DiGeorge syndrome critical region of chromosome 22q11. Twenty-eight percent of the cases where parents had been tested had inherited deletions, with a marked excess of maternally inherited deletions (maternal 61, paternal 18). Eight percent of the patients had died, over half of these within a month of birth and the majority within 6 months. All but one of the deaths were the result of congenital heart disease. Clinically significant immunological problems were very uncommon. Nine percent of patients had cleft palate and 32% had velopharyngeal insufficiency, 60% of patients were hypocalcaemic, 75% of patients had cardiac problems, and 36% of patients who had abdominal ultrasound had a renal abnormality. Sixty-two percent of surviving patients were developmentally normal or had only mild learning problems. The majority of patients were constitutionally small, with 36% of patients below the 3rd centile for either height or weight parameters. read more read less

Topics:

DiGeorge syndrome (52%)52% related to the paper
View PDF
1,033 Citations
open accessOpen access Journal Article DOI: 10.1136/JMG.2007.053959
Hirschsprung disease, associated syndromes and genetics: a review
Jeanne Amiel1, Stanislas Lyonnet2

Abstract:

Hirschsprung disease (HSCR, aganglionic megacolon) represents the main genetic cause of functional intestinal obstruction with an incidence of 1/5000 live births. This developmental disorder is a neurocristopathy and is characterised by the absence of the enteric ganglia along a variable length of the intestine. In the last d... Hirschsprung disease (HSCR, aganglionic megacolon) represents the main genetic cause of functional intestinal obstruction with an incidence of 1/5000 live births. This developmental disorder is a neurocristopathy and is characterised by the absence of the enteric ganglia along a variable length of the intestine. In the last decades, the development of surgical approaches has importantly decreased mortality and morbidity which allowed the emergence of familial cases. Isolated HSCR appears to be a non-Mendelian malformation with low, sex-dependent penetrance, and variable expression according to the length of the aganglionic segment. While all Mendelian modes of inheritance have been described in syndromic HSCR, isolated HSCR stands as a model for genetic disorders with complex patterns of inheritance. The tyrosine kinase receptor RET is the major gene with both rare coding sequence mutations and/or a frequent variant located in an enhancer element predisposing to the disease. Hitherto, 10 genes and five loci have been found to be involved in HSCR development. read more read less

Topics:

Hirschsprung's disease (55%)55% related to the paper, Neurocristopathy (52%)52% related to the paper, Penetrance (52%)52% related to the paper
View PDF
1,024 Citations
open accessOpen access Journal Article DOI: 10.1136/JMG.39.5.311
Malignant peripheral nerve sheath tumours in neurofibromatosis 1
D G R Evans1, Michael E. Baser, Julie McGaughran2, S Sharif2, E Howard2, A Moran2

Abstract:

Background: Cross sectional studies have shown that 1-2% of patients with neurofibromatosis 1 (NF1) develop malignant peripheral nerve sheath tumours (MPNST). However, no population based longitudinal studies have assessed lifetime risk. Methods: NF1 patients with MPNST were ascertained from two sources for our north west Eng... Background: Cross sectional studies have shown that 1-2% of patients with neurofibromatosis 1 (NF1) develop malignant peripheral nerve sheath tumours (MPNST). However, no population based longitudinal studies have assessed lifetime risk. Methods: NF1 patients with MPNST were ascertained from two sources for our north west England population of 4.1 million in the 13 year period 1984-1996: the North West Regional NF1 Register and review of notes of patients with MPNST in the North West Regional Cancer Registry. Results: Twenty-one NF1 patients developed MPNST, equivalent to an annual incidence of 1.6 per 1000 and a lifetime risk of 8-13%. There were 37 patients with sporadic MPNST. The median age at diagnosis of MPNST in NF1 patients was 26 years, compared to 62 years in patients with sporadic MPNST (p Conclusion: The lifetime risk of MPNST in NF1 is much higher than previously estimated and warrants careful surveillance and a low threshold for investigation. read more read less

Topics:

Malignant peripheral nerve sheath tumor (66%)66% related to the paper, Nerve sheath neoplasm (55%)55% related to the paper, Population (52%)52% related to the paper
View PDF
911 Citations
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Journal of Medical Genetics format uses unsrt citation style.

Automatically format and order your citations and bibliography in a click.

SciSpace allows imports from all reference managers like Mendeley, Zotero, Endnote, Google Scholar etc.

Frequently asked questions

Absolutely not! With our tool, you can freely write without having to focus on LaTeX. You can write your entire paper as per the Journal of Medical Genetics guidelines and autoformat it.

Yes. The template is fully compliant as per the guidelines of this journal. Our experts at SciSpace ensure that. Also, if there's any update in the journal format guidelines, we take care of it and include that in our algorithm.

Sure. We support all the top citation styles like APA style, MLA style, Vancouver style, Harvard style, Chicago style, etc. For example, in case of this journal, when you write your paper and hit autoformat, it will automatically update your article as per the Journal of Medical Genetics citation style.

You can avail our Free Trial for 7 days. I'm sure you'll find our features very helpful. Plus, it's quite inexpensive.

Yup. You can choose the right template, copy-paste the contents from the word doc and click on auto-format. You'll have a publish-ready paper that you can download at the end.

A matter of seconds. Besides that, our intuitive editor saves a load of your time in writing and formating your manuscript.

One little Google search can get you the Word template for any journal. However, why do you need a Word template when you can write your entire manuscript on SciSpace, autoformat it as per Journal of Medical Genetics's guidelines and download the same in Word, PDF and LaTeX formats? Try us out!.

Absolutely! You can do it using our intuitive editor. It's very easy. If you need help, you can always contact our support team.

SciSpace is an online tool for now. We'll soon release a desktop version. You can also request (or upvote) any feature that you think might be helpful for you and the research community in the feature request section once you sign-up with us.

Sure. You can request any template and we'll have it up and running within a matter of 3 working days. You can find the request box in the Journal Gallery on the right sidebar under the heading, "Couldn't find the format you were looking for?".

After you have written and autoformatted your paper, you can download it in multiple formats, viz., PDF, Docx and LaTeX.

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 those factors the review board, rejection rates, frequency of inclusion in indexes, Eigenfactor, etc. You must assess all the factors and then take the final call.

SHERPA/RoMEO Database

We have extracted this data from Sherpa Romeo to help our researchers understand the access level of this journal. The following table indicates the level of access a journal has as per Sherpa Romeo 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.

The 5 most common citation types in order of usage are:.

S. No. Citation Style Type
1. Author Year
2. Numbered
3. Numbered (Superscripted)
4. Author Year (Cited Pages)
5. Footnote

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After uploading your paper on SciSpace, you would see a button to request a journal submission service for Journal of Medical Genetics.

Each submission service is completed within 4 - 5 working days.

Yes. SciSpace provides this functionality.

After signing up, you would need to import your existing references from Word or .bib file.

SciSpace would allow download of your references in Journal of Medical Genetics Endnote style, according to bmj-publishing-group guidelines.

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