Example of Pathophysiology format
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Example of Pathophysiology format Example of Pathophysiology format Example of Pathophysiology format Example of Pathophysiology format Example of Pathophysiology format Example of Pathophysiology format Example of Pathophysiology format Example of Pathophysiology format Example of Pathophysiology format
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Example of Pathophysiology format Example of Pathophysiology format Example of Pathophysiology format Example of Pathophysiology format Example of Pathophysiology format Example of Pathophysiology format Example of Pathophysiology format Example of Pathophysiology format Example of Pathophysiology format
Sample paper formatted on SciSpace - SciSpace
This content is only for preview purposes. The original open access content can be found here.
open access Open Access

Pathophysiology — Template for authors

Publisher: Elsevier
Categories Rank Trend in last 3 yrs
Pathology and Forensic Medicine #27 of 191 up up by 22 ranks
Physiology (medical) #27 of 98 up up by 20 ranks
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 100 Published Papers | 597 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 08/06/2020
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Journal Performance & Insights

CiteRatio

SCImago Journal Rank (SJR)

Source Normalized Impact per Paper (SNIP)

A measure of average citations received per peer-reviewed paper published in the journal.

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.

6.0

58% from 2019

CiteRatio for Pathophysiology from 2016 - 2020
Year Value
2020 6.0
2019 3.8
2018 3.7
2017 3.8
2016 4.1
graph view Graph view
table view Table view

0.758

27% from 2019

SJR for Pathophysiology from 2016 - 2020
Year Value
2020 0.758
2019 0.595
2018 0.686
2017 0.67
2016 0.809
graph view Graph view
table view Table view

1.154

41% from 2019

SNIP for Pathophysiology from 2016 - 2020
Year Value
2020 1.154
2019 0.816
2018 1.31
2017 1.096
2016 0.891
graph view Graph view
table view Table view

insights Insights

  • CiteRatio of this journal has increased by 58% in last years.
  • This journal’s CiteRatio is in the top 10 percentile category.

insights Insights

  • SJR of this journal has increased by 27% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has increased by 41% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

Pathophysiology

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Elsevier

Pathophysiology

Pathophysiology is an international journal which publishes papers in English which address the etiology, development, and elimination of pathological processes. Contributions on the basic mechanisms underlying these processes, model systems and interdisciplinary approaches ar...... Read More

Medicine

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Last updated on
08 Jun 2020
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ISSN
0928-4680
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Impact Factor
High - 1.026
i
Open Access
No
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Sherpa RoMEO Archiving Policy
Green faq
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Plagiarism Check
Available via Turnitin
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Endnote Style
Download Available
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Bibliography Name
elsarticle-num
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Citation Type
Numbered
[25]
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Bibliography Example
G. E. Blonder, M. Tinkham, T. M. Klapwijk, Transition from metallic to tunneling regimes in superconducting microconstrictions: Excess current, charge imbalance, and supercurrent conversion, Phys. Rev. B 25 (7) (1982) 4515–4532. URL 10.1103/PhysRevB.25.4515

Top papers written in this journal

Journal Article DOI: 10.1016/S0928-4680(00)00053-5
Oxidative stress and apoptosis
Krishnaswamy Kannan1, Sushil K. Jain1
01 Sep 2000 - Pathophysiology

Abstract:

Apoptosis or programmed cell death, is essential for the normal functioning and survival of most multi-cellular organisms. The morphological and biochemical characteristics of apoptosis, however, are highly conserved during the evolution. It is currently believed that apoptosis can be divided into at least three functionally ... Apoptosis or programmed cell death, is essential for the normal functioning and survival of most multi-cellular organisms. The morphological and biochemical characteristics of apoptosis, however, are highly conserved during the evolution. It is currently believed that apoptosis can be divided into at least three functionally distinct phases, i.e. induction, effector and execution phase. Recent studies have demonstrated that reactive oxygen species (ROS) and the resulting oxidative stress play a pivotal role in apoptosis. Antioxidants and thiol reductants, such as N-acetylcysteine, and overexpression of manganese superoxide (MnSOD) can block or delay apoptosis. Bcl-2, an endogenously produced protein, has been shown to prevent cells from dying of apoptosis apparently by an antioxidative mechanism. Taken together ROS, and the resulting cellular redox change, can be part of signal transduction pathway during apoptosis. It is now established that mitochondria play a prominent role in apoptosis. During mitochondrial dysfunction, several essential players of apoptosis, including pro-caspases, cytochrome C, apoptosis-inducing factor (AIF), and apoptotic protease-activating factor-1 (APAF-1) are released into the cytosol. The multimeric complex formation of cytochrome C, APAF-1 and caspase 9 activates downstream caspases leading to apoptotic cell death. All the three functional phases of apoptosis are under the influence of regulatory controls. Thus, increasing evidences provide support that oxidative stress and apoptosis are closely linked physiological phenomena and are implicated in pathophysiology of some of the chronic diseases including AIDS, autoimmunity, cancer, diabetes mellitus, Alzheimer's and Parkinson's and ischemia of heart and brain. read more read less

Topics:

Intrinsic apoptosis (69%)69% related to the paper, Apoptosome (63%)63% related to the paper, XIAP (62%)62% related to the paper, Programmed cell death (60%)60% related to the paper, Apoptosis-inducing factor (58%)58% related to the paper
880 Citations
Journal Article DOI: 10.1016/J.PATHOPHYS.2006.05.007
Oxidative stress in autism
01 Aug 2006 - Pathophysiology

Abstract:

Autism is a severe developmental disorder with poorly understood etiology. Oxidative stress in autism has been studied at the membrane level and also by measuring products of lipid peroxidation, detoxifying agents (such as glutathione), and antioxidants involved in the defense system against reactive oxygen species (ROS). Lip... Autism is a severe developmental disorder with poorly understood etiology. Oxidative stress in autism has been studied at the membrane level and also by measuring products of lipid peroxidation, detoxifying agents (such as glutathione), and antioxidants involved in the defense system against reactive oxygen species (ROS). Lipid peroxidation markers are elevated in autism, indicating that oxidative stress is increased in this disease. Levels of major antioxidant serum proteins, namely transferrin (iron-binding protein) and ceruloplasmin (copper-binding protein), are decreased in children with autism. There is a positive correlation between reduced levels of these proteins and loss of previously acquired language skills in children with autism. The alterations in ceruloplasmin and transferrin levels may lead to abnormal iron and copper metabolism in autism. The membrane phospholipids, the prime target of ROS, are also altered in autism. The levels of phosphatidylethanolamine (PE) are decreased, and phosphatidylserine (PS) levels are increased in the erythrocyte membrane of children with autism as compared to their unaffected siblings. Several studies have suggested alterations in the activities of antioxidant enzymes such as superoxide dismutase, glutathione peroxidase, and catalase in autism. Additionally, altered glutathione levels and homocysteine/methionine metabolism, increased inflammation, excitotoxicity, as well as mitochondrial and immune dysfunction have been suggested in autism. Furthermore, environmental and genetic factors may increase vulnerability to oxidative stress in autism. Taken together, these studies suggest increased oxidative stress in autism that may contribute to the development of this disease. A mechanism linking oxidative stress with membrane lipid abnormalities, inflammation, aberrant immune response, impaired energy metabolism and excitotoxicity, leading to clinical symptoms and pathogenesis of autism is proposed. read more read less

Topics:

Autism (63%)63% related to the paper, Oxidative stress (57%)57% related to the paper, Glutathione peroxidase (53%)53% related to the paper, Lipid peroxidation (52%)52% related to the paper, Superoxide dismutase (52%)52% related to the paper
View PDF
524 Citations
Journal Article DOI: 10.1016/J.PATHOPHYS.2006.05.002
Oxidative stress and atherosclerosis.
Uma Singh1, Ishwarlal Jialal1
01 Aug 2006 - Pathophysiology

Abstract:

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the Western world. Its incidence has been increasing lately in developing countries. Several lines of evidence support a role for oxidative stress in atherogenesis. Growing evidence indicates that chronic and acute overproduction of reactive oxyge... Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the Western world. Its incidence has been increasing lately in developing countries. Several lines of evidence support a role for oxidative stress in atherogenesis. Growing evidence indicates that chronic and acute overproduction of reactive oxygen species (ROS) under pathophysiologic conditions is integral in the development of cardiovascular diseases (CVD). ROS mediate various signaling pathways that underlie vascular inflammation in atherogenesis from the initiation of fatty streak development through lesion progression to ultimate plaque rupture. Various animal models of oxidative stress support the notion that ROS have a causal role in atherosclerosis and other cardiovascular diseases. Human investigations also support the oxidative stress hypothesis of atherosclerosis. Oxidative stress is the unifying mechanism for many CVD risk factors, which additionally supports its central role in CVD. A main source of ROS in vascular cells is the reduced nicotinamide adenine dinucleotide/nicotinamide adenine dinucleotide phosphate (NAD(P)H) oxidase system. This is a membrane-associated enzyme, composed of five subunits, catalyzing the one-electron reduction of oxygen, using NADH or NADPH as the electron donor. This system is an important target for genetic investigations. Identification of groups of patients with genetically prone or resistant of oxidative stress is therefore an obvious target of investigation. A better understanding of the complexity of cellular redox reactions, development of a new class of antioxidants targeted to specific subcellular sites, and the phenotype-genotype linkage analysis for oxidative stress will likely be avenues for future research with regards to the broader use of pharmacological therapies in the treatment and prevention of CVD. read more read less

Topics:

Oxidative stress (57%)57% related to the paper, NAD(P)H oxidase (54%)54% related to the paper, Nicotinamide adenine dinucleotide phosphate (52%)52% related to the paper
443 Citations
Journal Article DOI: 10.1016/J.PATHOPHYS.2009.12.001
Pathophysiologic mechanisms of acute ischemic stroke: An overview with emphasis on therapeutic significance beyond thrombolysis
Prabal Deb1, Suash Sharma2, Hassan Km
01 Jun 2010 - Pathophysiology

Abstract:

Stroke is a serious neurological disease, and constitutes a major cause of death and disability throughout the world. The pathophysiology of stroke is complex, and involves excitotoxicity mechanisms, inflammatory pathways, oxidative damage, ionic imbalances, apoptosis, angiogenesis and neuroprotection. The ultimate result of ... Stroke is a serious neurological disease, and constitutes a major cause of death and disability throughout the world. The pathophysiology of stroke is complex, and involves excitotoxicity mechanisms, inflammatory pathways, oxidative damage, ionic imbalances, apoptosis, angiogenesis and neuroprotection. The ultimate result of ischemic cascade initiated by acute stroke is neuronal death along with an irreversible loss of neuronal function. Therapeutic strategies in stroke have been developed with two main aims: restoration of cerebral flow and the minimization of the deleterious effects of ischemia on neurons. Intense research spanning over the last two decades has witnessed significant therapeutic advances in the form of carotid endarterectomy, thrombolytics, anticoagulant therapy, antiplatelet agents, neuroprotective agents, and treating associated risk factors such as hypertension and hyperlipidemia. However, the search for an effective neuroprotectant remains frustrating, and the current therapeutic protocols remain suboptimal. Till date only one FDA-approved drug is available for ischemic stroke; i.e., the serine protease tissue-type plasminogen activator (tPA), utility of which is limited by short therapeutic window. The objective of this review is to critically evaluate the major mechanisms underlying stroke pathophysiology, with emphasis on potential novel targets for designing newer therapeutic modalities. read more read less

Topics:

Ischemic cascade (63%)63% related to the paper, Stroke (58%)58% related to the paper, Neuroprotection (54%)54% related to the paper
422 Citations
Journal Article DOI: 10.1016/J.PATHOPHYS.2006.05.004
Oxidative stress in Alzheimer's disease
01 Aug 2006 - Pathophysiology

Abstract:

Oxidative damage is a major feature in the pathophysiology of Alzheimer's disease (AD). In this review, we discuss free radical-mediated damage to the biochemical components involved in the pathology and clinical symptoms of AD. We explain how amyloid beta-protein (Abeta), microtubule-associated protein tau, presenilins, apol... Oxidative damage is a major feature in the pathophysiology of Alzheimer's disease (AD). In this review, we discuss free radical-mediated damage to the biochemical components involved in the pathology and clinical symptoms of AD. We explain how amyloid beta-protein (Abeta), microtubule-associated protein tau, presenilins, apolipoprotein E, mitochondria and proteases play a role in increasing oxidative stress in AD. Abeta not only can induce oxidative stress, but its generation is also increased as a result of oxidative stress. Finally, a hypothetical model linking oxidative stress with beta-amyloid and neurofibrillary tangle pathology in AD is proposed. read more read less

Topics:

Oxidative stress (58%)58% related to the paper, Neurofibrillary tangle (57%)57% related to the paper, Presenilin (52%)52% related to the paper
285 Citations
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With SciSpace, you do not need a word template for Pathophysiology.

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Pathophysiology format uses elsarticle-num citation style.

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Frequently asked questions

1. Can I write Pathophysiology in LaTeX?

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

2. Do you follow the Pathophysiology guidelines?

Yes, the template is compliant with the Pathophysiology 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 Pathophysiology?

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 Pathophysiology citation style.

4. Can I use the Pathophysiology 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 Pathophysiology.

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

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

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

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

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

SciSpace's Pathophysiology 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 Pathophysiology?

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 Pathophysiology?”

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

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

12. Is Pathophysiology'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 Pathophysiology?

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 Pathophysiology. 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 Pathophysiology?

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

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

16. Can I download Pathophysiology 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 Pathophysiology 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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