Gene Regulation and Systems Biology
Synopsis: An open access, peer reviewed electronic journal that covers regulation of genes and proteins they encode and the broader field of systems biology.
Indexing: 7 major databases. Pubmed indexing for NIH-funded research.
Processing time: Decision in 2 weeks for 90% of papers.
Visibility: Most popular article read 7600+ times.
About this journal
Aims and scope:
Gene Regulation and Systems Biology is concerned with the regulation of genes and the proteins they encode and the relationship between gene regulation and the wider field of systems biology.
The regulation of genes and the proteins they encode is at the core of systems biology. Understanding the role of gene regulation in the context of the entire system as it relates to disease processes will aid therapeutic development. Therefore, combining our knowledge of gene expression and promoter control, improving gene and protein networks, and determining the role of signal transduction will enhance our ability to treat complex diseases.
Systems biology is concerned with the integration of different levels of information to understand how complex biological systems function. By studying the relationships and interactions between various parts of a biological system (including gene and protein networks involved in cell signaling) it may be possible to create an understandable model of the whole system. Mathematical, analytic, and particularly computer simulation and heuristics are used as research methods.
Editorial standards and procedures:
Submissions, excluding editorials, letters to the editor and dedications, will be peer reviewed by two reviewers. Reviewers are required to provide fair, balanced and constructive reports.
Under our Fairness in Peer Review Policy authors may appeal against reviewers' recommendations which are ill-founded, unobjective or unfair. Appeals are considered by the Editor in Chief or Associate Editor.
Papers are not sent to peer reviewers following submission of a revised manuscript. Editorial decisions on re-submitted papers are based on the author's response to the initial peer review report.
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This journal is indexed by the following services:
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As of April 7 2008, the US NIH Public Access Policy requires that all peer reviewed articles resulting from research carried out with NIH funding be deposited in the Pubmed Central archive.
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Call for papers:
The Editor in Chief welcomes submissions. Submissions of the following types are invited:
- Original research articles.
- Reviews: comprehensive, authoritative, descriptions of any subject within the journal's scope. They may cover basic science and clinical reviews, ethics, pro/con debates, and equipment reviews.
- Commentaries: focused and opinionated articles on any subject within the journal's scope. These articles are usually related to a contemporary issue.
- Hypotheses: articles that present an original hypothesis backed solely by previously published results rather than any new evidence. They should outline significant progress in thinking that would also be testable.
- Letters to the Editor: these can be either a re-analysis of a previously published article, or a response to such a re-analysis from the authors of the original publication.
- Methodology articles: these discuss a new experimental method, test or procedure. The article must describe a demonstrable advance on what is currently available. The method needs to have been well tested and ideally, but not necessarily, used in a way that proves its value.
- Short reports: brief reports of data from original research.
- Meeting reports: a report pertaining to activity at a meeting or conference Articles published in this journal are immediately available without delay upon publication and enjoy substantial visibility.
- Case reports: reports of clinical cases that can be educational, describe a diagnostic or therapeutic dilemma, suggest an association, or present an important adverse reaction. Case reports must meet appropriate ethical standards.
All submissions are subject to prompt, objective and fair peer review in compliance with our Fairness in Peer Review Policy. Copyright in published articles remains with the author(s). Authors are continually informed of the progress of their paper and our staff are friendly and responsive.
One author recently wrote: "I would like to say that this is the most author-friendly editing process I have experienced in over 150 publications. Thank you most sincerely."
Criteria for publication:
Publication is dependent on peer reviewers' judgement of papers. Reviewers are asked to provide thoughtful and unbiased feedback to authors to ensure that the conclusions of papers are valid and manuscripts achieve reasonable standards of scholarliness and intelligibility.
Previous work in the field must be acknowledged and papers should read without unreasonable difficulty. Papers should fit comfortably within the scope of the journal.
Reviewers are asked to act in a fair, objective and constructive manner which maintains quality standards and helps authors to communicate their research. They are instructed that in areas of genuinely novel research issues may be raised which cannot immediately be resolved and that absolutely rigorous validation of data may therefore not be possible.
More information on the role of peer reviewers is available on the information for reviewers page. Where authors consider that reviewers have made recommendations which are unreasonable, unobjective or ill-founded they may appeal them to the Editor in Chief or Associate Editor under our Fairness in Peer Review Policy.
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We are willing to consider papers which have been peer reviewed by other journals but not accepted for publication.
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Prior to peer review of your paper we can:
- Have your paper's reference style revised to meet our requirements,
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After peer review of your paper we can:
- Have your paper revised in accordance with peer reviewer's recommendations and have a summary of responses to the reviewers created by our specialist external substantive editors,
- Provide bound reprints of your article in colour or black and white ,
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Read an interview with the Editor in Chief.
Role of Cytokines During Epileptogenesis and in the Transition from the Interictal to the Ictal State in the Epileptic Mutant EL Mouse
Yoshiya L. Murashima, Jiro Suzuki and Mitsunobu Yoshii
Division of Psychobiology, Tokyo Institute of Psychiatry, Tokyo, Japan.
Abstract
Purpose: Epileptic mutant EL mice show secondary generalized seizures. Seizure discharges initiate in the parietal cortex and generalize through the hippocampus. We have previously demonstrated an increase in the activity of inducible nitric oxide synthetase (iNOS) as well as a decrease in the activity of superoxide dismutase (SOD) in the hippocampus of EL mice, suggesting that cell toxic free radicals are increased in the brain of EL mice. In parallel with this, neurotrophic factors were significantly increased in the hippocampus of EL mice in earlier developmental stages before exhibiting frequent seizures. These findings were no longer present after frequent seizures, suggesting that these events may trigger ictogenesis. On the other hand, it is reported that limbic seizures rapidly induce cytokines and related inflammatory mediators. It remains to be seen, however, whether cytokines contribute to the transition from interictal to ictal state. The present study was designed to address this issue using EL mice.
Methods: EL mice at the age from 4 to 23 weeks and their control animal, DDY mice at the age of 10 and 20 weeks were used. Seizures were induced in EL mice once every week since 5 weeks. Cytokines, such as interleukin-1 alpha (IL-1a), interleukin 1-beta (IL-1b), IL-6, IL-1 receptor (IL-1r), IL-1 receptor antagonist (IL-ra) and tumor necrosis factor alpha (TNF-a) were examined by Western blotting in the ‘focus complex’ of brain (namely, in the parietal cortex and hippocampus) of EL mice in the interictal period at different developmental stages. In 15 week old EL mice, which show seizures once a week, these cytokines were similarly determined 5 min, 2 hr, 4 hr, 11 hr, 24 hr, 3 days and 6 days after the last seizure induced.
Results: A significant increase in the level of cytokines was observed in the brain of EL mice at any stages during development, compared with the level of cytokines in the brain of control DDY. Cytokines were increased predominantly before experiencing frequent seizures. In EL mice at the age of 15 weeks, the level of cytokines in the hippocampus was highest 6 days after seizures. In the parietal cortex, cytokines were most highly expressed 2 hr after seizures. The results indicate that cytokines were kept up-regulated until next seizures in the hippocampus, whereas they were transiently up-regulated immediately after seizures in the parietal cortex.
Conclusion: It is concluded that in the brain of EL mice, pro-inflammatory cytokines are increased progressively and periodically in association with the development and the seizure activity, respectively. A periodic increase of cytokines prior to the next seizure episode may play a role in triggering the ictal activity. Namely, alteration of region-specific cytokines may induce ictal activities from the interictal state. It is conceivable that inflammatory cytokines may work together with neuronal factors during epileptogenesis and in the transition from interictal to ictal state.
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