Example of Clinical Genetics format
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Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical Genetics format
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Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical Genetics format Example of Clinical 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

Clinical Genetics — Template for authors

Publisher: Wiley
Categories Rank Trend in last 3 yrs
Genetics #60 of 325 up up by 29 ranks
Genetics (clinical) #19 of 87 up up by 8 ranks
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 713 Published Papers | 5204 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 18/06/2020
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General info
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FAQ

Related Journals

open access Open Access
recommended Recommended

PLOS

Quality:  
High
CiteRatio: 9.0
SJR: 3.587
SNIP: 1.457
open access Open Access

Springer

Quality:  
High
CiteRatio: 7.7
SJR: 1.945
SNIP: 0.996
open access Open Access
recommended Recommended

Springer

Quality:  
High
CiteRatio: 15.2
SJR: 5.564
SNIP: 2.245
open access Open Access
recommended Recommended

Springer

Quality:  
High
CiteRatio: 9.5
SJR: 2.351
SNIP: 1.869

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.

3.578

13% from 2018

Impact factor for Clinical Genetics from 2016 - 2019
Year Value
2019 3.578
2018 4.104
2017 3.512
2016 3.326
graph view Graph view
table view Table view

7.3

3% from 2019

CiteRatio for Clinical Genetics from 2016 - 2020
Year Value
2020 7.3
2019 7.1
2018 6.2
2017 6.1
2016 6.4
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has decreased by 13% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

insights Insights

  • CiteRatio of this journal has increased by 3% 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.

1.543

0% from 2019

SJR for Clinical Genetics from 2016 - 2020
Year Value
2020 1.543
2019 1.539
2018 1.679
2017 1.522
2016 1.582
graph view Graph view
table view Table view

1.52

12% from 2019

SNIP for Clinical Genetics from 2016 - 2020
Year Value
2020 1.52
2019 1.363
2018 1.285
2017 1.172
2016 1.178
graph view Graph view
table view Table view

insights Insights

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

insights Insights

  • SNIP of this journal has increased by 12% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

Clinical Genetics

Guideline source: View

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Wiley

Clinical Genetics

Clinical Genetics links research to the clinic, translating advances in our understanding of the molecular basis of genetic disease for the practising clinical geneticist. The journal publishes high quality research papers, short reports, reviews and mini-reviews that connect ...... Read More

Genetics

Genetics(clinical)

Biochemistry, Genetics and Molecular Biology

i
Last updated on
18 Jun 2020
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ISSN
0009-9163
i
Impact Factor
High - 1.302
i
Acceptance Rate
66%
i
Open Access
Yes
i
Sherpa RoMEO Archiving Policy
Yellow faq
i
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

Journal Article DOI: 10.1111/J.1399-0004.1974.TB00638.X
Genetic and clinical aspects of Charcot‐Marie‐Tooth's disease
H. Skre1
23 Apr 2008 - Clinical Genetics

Abstract:

The prevalence of Charcot-Marie-Tooth's disease (CMT) was studied in Western Norway, an area with several isolated districts with a population of 725,000 (1968). Three hereditary types were distinguished in the area: autosomal dominant CMT with an estimated prevalence of 36/100,000; X-linked recessive CMT with a prevalence of... The prevalence of Charcot-Marie-Tooth's disease (CMT) was studied in Western Norway, an area with several isolated districts with a population of 725,000 (1968). Three hereditary types were distinguished in the area: autosomal dominant CMT with an estimated prevalence of 36/100,000; X-linked recessive CMT with a prevalence of 3.6/100,000; and autosomal recessive CMT with a prevalence of 1.4/100,00. Gene frequencies were 3 · 7. 10-4, 1 · 9. 10-4, and 4 · 8. 10-4 in autosomal dominant, X-linked, and autosomal recessive CMT, respectively, while the corresponding mutation rates were 13 · 0, 5 · 5, and 3 · 5 per million gametes per generation. The penetrance was almost complete for all three variants of CMT. Strict diagnostic criteria were followed in the selection of the 37 index cases. A family investigation was carried out with 238 subjects, during which 69 secondary cases were detected. Another 57 subjects had unspecific neuropathy (Un), which did not fit a diagnosis of CMT or other neurological disease. In the diagnosis of Un, a score system was used, with age and sex corrections based on findings in a normal population. Generally, the most severe disease course was found in the recessive CMT types, but there was also more clinical variation, suggesting CNS involvement in some cases (upper motor neuron affection, cerebellar signs). Scoliosis and spinal ataxia were not infrequent, even in cases with autosomal dominant CMT. The prevalence cf Un was highest in the relatives of recessive CMT cases, with a ratio of affected to normal in sibs compatible with a hypothesis of several cases of heterozygous manifestation. In the relatives of autosomal dominant CMT cases, Un prevalence was also higher than in the population, but lower in 2nd degree relatives than in 1st degree; the ratios fitted a hypothesis of polygenic Un inheritance. Significant differences were found in the score patterns of Un in the recessive CMT families and in the autosomal dominant families, suggesting their difference of origin. The reason for clustering of Un cases in autosomal dominant CMT families is obscure, since it can be only partly attributed to early manifestation of CMT. It is suggested that Un and CMT, mainly in autosomal dominant CMT, interact to form a spectrum of differing phenotypes, so explaining the problem of “transitional forms” between CMT and other hereditary nervous disorders. Recessive CMT, being a more generalized nervous disease, attains, through differing expressivity, phenotypes which vary between individual cases. read more read less

Topics:

Penetrance (53%)53% related to the paper, Population (52%)52% related to the paper
814 Citations
Journal Article DOI: 10.1034/J.1399-0004.2000.570103.X
The molecular regulation of myogenesis.
Luc A. Sabourin1, Michael A. Rudnicki1
01 Jan 2000 - Clinical Genetics

Abstract:

Over the past years, several studies have unraveled important mechanisms by which the four myogenic regulatory factors (MRFs: MyoD, Myf-5, myogenin, and MRF4) control the specification and the differentiation of the muscle lineage. Early experiments led to the hypothesis that these factors were redundant and could functionall... Over the past years, several studies have unraveled important mechanisms by which the four myogenic regulatory factors (MRFs: MyoD, Myf-5, myogenin, and MRF4) control the specification and the differentiation of the muscle lineage. Early experiments led to the hypothesis that these factors were redundant and could functionally replace one another. However, recent experiments using in vivo and in vitro models have demonstrated that in fact different aspects of the myogenic program are controlled by different factors in vivo, suggesting that these factors play distinct roles during myogenesis. The activity of the MRFs during proliferation and differentiation of muscle precursor cells has clearly been demonstrated to be dependent on specific cell-cycle control mechanisms as well as distinct interactions with other regulatory molecules, such as the ubiquitously expressed E proteins and several other transcription factors. Furthermore, the observation that the MRFs can recruit chromatin remodeling proteins has shed some light on the mechanisms by which the MRFs activate gene expression. Recently, a functional role for MyoD during satellite cell activation and muscle repair has been identified in vivo, which cannot be substituted for by the other MRFs. This has put forward the hypothesis that these factors also play specific biological roles following muscle injury and repair. read more read less

Topics:

Myogenic regulatory factors (66%)66% related to the paper, MyoD (63%)63% related to the paper, Myogenesis (60%)60% related to the paper, Myogenin (59%)59% related to the paper, Chromatin remodeling (53%)53% related to the paper
754 Citations
Journal Article DOI: 10.1111/J.1399-0004.2004.00241.X
A new model for prediction of the age of onset and penetrance for Huntington's disease based on CAG length.
Douglas R. Langbehn1, Ryan R. Brinkman2, Daniel Falush3, Jane S. Paulsen1, Michael R. Hayden
01 Apr 2004 - Clinical Genetics

Abstract:

Huntington's disease (HD) is a neurodegenerative disorder caused by an unstable CAG repeat. For patients at risk, participating in predictive testing and learning of having CAG expansion, a major unanswered question shifts from "Will I get HD?" to "When will it manifest?" Using the largest cohort of HD patients analyzed to da... Huntington's disease (HD) is a neurodegenerative disorder caused by an unstable CAG repeat. For patients at risk, participating in predictive testing and learning of having CAG expansion, a major unanswered question shifts from "Will I get HD?" to "When will it manifest?" Using the largest cohort of HD patients analyzed to date (2913 individuals from 40 centers worldwide), we developed a parametric survival model based on CAG repeat length to predict the probability of neurological disease onset (based on motor neurological symptoms rather than psychiatric onset) at different ages for individual patients. We provide estimated probabilities of onset associated with CAG repeats between 36 and 56 for individuals of any age with narrow confidence intervals. For example, our model predicts a 91% chance that a 40-year-old individual with 42 repeats will have onset by the age of 65, with a 95% confidence interval from 90 to 93%. This model also defines the variability in HD onset that is not attributable to CAG length and provides information concerning CAG-related penetrance rates. read more read less

Topics:

Age of onset (58%)58% related to the paper, Penetrance (53%)53% related to the paper
745 Citations
open accessOpen access Journal Article DOI: 10.1111/J.1399-0004.2009.01230.X
Review of the Lynch syndrome: history, molecular genetics, screening, differential diagnosis, and medicolegal ramifications
Henry T. Lynch1, Patrick M. Lynch, Stephen J. Lanspa1, Carrie Snyder1, Jane F. Lynch1, C. R. Boland2
01 Jul 2009 - Clinical Genetics

Abstract:

More than one million patients will manifest colorectal cancer (CRC) this year of which, conservatively, approximately 3% (~30,700 cases) will have Lynch syndrome (LS), the most common hereditary CRC predisposing syndrome. Each case belongs to a family with clinical needs that require genetic counseling, DNA testing for misma... More than one million patients will manifest colorectal cancer (CRC) this year of which, conservatively, approximately 3% (~30,700 cases) will have Lynch syndrome (LS), the most common hereditary CRC predisposing syndrome. Each case belongs to a family with clinical needs that require genetic counseling, DNA testing for mismatch repair genes (most frequently MLH1 or MSH2) and screening for CRC. Colonoscopy is mandated, given CRC’s proximal occurrence (70–80% proximal to the splenic flexure). Due to its early age of onset (average 45 years of age), colonoscopy needs to start by age 25, and because of its accelerated carcinogenesis, it should be repeated every 1 to 2 years through age 40 and then annually thereafter. Should CRC occur, subtotal colectomy may be necessary, given the marked frequency of synchronous and metachronous CRC. Because 40–60% of female patients will manifest endometrial cancer, tailored management is essential. Additional extracolonic cancers include ovary, stomach, small bowel, pancreas, hepatobiliary tract, upper uroepithelial tract, brain (Turcot variant) and sebaceous adenomas/carcinomas (Muir-Torre variant). LS explains only 10–25% of familial CRC. read more read less

Topics:

Lynch syndrome (62%)62% related to the paper, Splenic flexure (55%)55% related to the paper, Mass screening (52%)52% related to the paper, Colorectal cancer (52%)52% related to the paper, Endometrial cancer (50%)50% related to the paper
View PDF
741 Citations
Journal Article DOI: 10.1034/J.1399-0004.2002.610402.X
Gene/environment causes of cleft lip and/or palate
Jeffrey C. Murray1
01 Apr 2002 - Clinical Genetics

Abstract:

Craniofacial anomalies, and in particular cleft lip and palate, are major human birth defects with a worldwide frequency of 1 in 700 and substantial clinical impact. A wide range of studies in developmental biology has contributed to a better knowledge of how both genes and environmental exposures impact head organogenesis. S... Craniofacial anomalies, and in particular cleft lip and palate, are major human birth defects with a worldwide frequency of 1 in 700 and substantial clinical impact. A wide range of studies in developmental biology has contributed to a better knowledge of how both genes and environmental exposures impact head organogenesis. Specific causes have now been identified for some forms of cleft lip and palate, and we are at the beginning of a time in which the common nonsyndromic forms may also have specific etiologies identified. Mouse models have an especially important role in disclosing cleft etiologies and providing models for environmental cotriggers or interventions. An overview of the gene-environment contributions to nonsyndromic forms of clefting and their implications for developmental biology and clinical counseling is presented. read more read less

Topics:

IRF6 (68%)68% related to the paper, Environmental exposure (53%)53% related to the paper
709 Citations
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With SciSpace, you do not need a word template for Clinical Genetics.

It automatically formats your research paper to Wiley formatting guidelines and citation style.

You can download a submission ready research paper in pdf, LaTeX and docx formats.

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Clinical Genetics format uses apa citation style.

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Frequently asked questions

1. Can I write Clinical Genetics in LaTeX?

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

2. Do you follow the Clinical Genetics guidelines?

Yes, the template is compliant with the Clinical Genetics 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 Clinical Genetics?

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 Clinical Genetics citation style.

4. Can I use the Clinical Genetics 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 Clinical Genetics.

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

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

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

7. Where can I find the template for the Clinical Genetics?

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

SciSpace's Clinical Genetics 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 Clinical Genetics?

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 Clinical Genetics?”

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

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

12. Is Clinical Genetics'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 Clinical Genetics?

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 Clinical Genetics. 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 Clinical Genetics?

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

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

16. Can I download Clinical Genetics 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 Clinical Genetics 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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