Frontiers in Bioscience Journal Impact Factor & Information

Publisher: Frontiers in Bioscience

Journal description

The journal "Frontiers in Bioscience" is a modern forum for scientific communication. Data and information that are useful to investigators in any discipline in biology and medicine including biochemistry, microbiology, parasitology, virology, immunology, biotechnology, and bioinformatics will be published after they have been peer reviewed. This will include reviews and research articles in basic science and clinical science, as well as technical notes and protocols. Other materials that have not been traditionally published as peer reviewed articles will also be considered for publication. This will include, rare images,videos and sounds, and assimilated data in the form of a database on any subject in medicine. The journal will include useful search strategies of internet and databases related to biology and medicine, links to medically relevant journals and the guidelines to authors of scientific journals and as well as information regarding manufacturers' products and links to manufacturers' homepages. Other items that will be posted are book reviews, as well as a list of conferences.

Current impact factor: 3.52

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 3.523
2013 Impact Factor 4.249
2012 Impact Factor 3.286
2011 Impact Factor 3.52
2010 Impact Factor 4.048
2009 Impact Factor 3.736
2008 Impact Factor 3.308
2007 Impact Factor 2.989
2006 Impact Factor 2.771
2005 Impact Factor 2.623
2004 Impact Factor 3.226
2003 Impact Factor 3.603
2002 Impact Factor 3.063

Impact factor over time

Impact factor

Additional details

5-year impact 3.20
Cited half-life 6.90
Immediacy index 0.71
Eigenfactor 0.01
Article influence 1.01
Website Frontiers in Bioscience website
ISSN 1093-4715
OCLC 216615969
Material type Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Frontiers in Bioscience

  • Pre-print
    • Archiving status unclear
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors un-copyedited manuscript
    • Publisher's version/PDF cannot be used
    • Set statement to accompany (see policy)
    • Creative Commons Attribution License
    • If submission to PubMed Central is required authors must request in writing from publisher (see policy for details)
    • All titles are open access journals
  • Classification

Publications in this journal

  • Frontiers in Bioscience 01/2016;
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    ABSTRACT: Globally, greater than 30 million individuals are afflicted with disorders of the nervous system accompanied by tens of thousands of new cases annually with limited, if any, treatment options. Erythropoietin (EPO) offers an exciting and novel therapeutic strategy to address both acute and chronic neurodegenerative disorders. EPO governs a number of critical protective and regenerative mechanisms that can impact apoptotic and autophagic programmed cell death pathways through protein kinase B (Akt), sirtuins, mammalian forkhead transcription factors, and wingless signaling. Translation of the cytoprotective pathways of EPO into clinically effective treatments for some neurodegenerative disorders has been promising, but additional work is necessary. In particular, development of new treatments with erythropoiesis-stimulating agents such as EPO brings several important challenges that involve detrimental vascular outcomes and tumorigenesis. Future work that can effectively and safely harness the complexity of the signaling pathways of EPO will be vital for the fruitful treatment of disorders of the nervous system.
    Frontiers in Bioscience 11/2015; 21(3):561-596. DOI:10.2741/4408
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    ABSTRACT: The kynurenine (Kyn) pathway is the major route for tryptophan (Trp) metabolism, and it contributes to several fundamental biological processes. Trp is constitutively oxidized by tryptophan 2, 3-dioxygenase in liver cells. In other cell types, it is catalyzed by an alternative inducible indoleamine-pyrrole 2, 3-dioxygenase (IDO) under certain pathophysiological conditions, which consequently increases the formation of Kyn metabolites. IDO is up-regulated in response to inflammatory conditions as a novel marker of immune activation in early atherosclerosis. Besides, IDO and the IDO-related pathway are important mediators of the immunoinflammatory responses in advanced atherosclerosis. In particular, Kyn, 3-hydroxykynurenine, and quinolinic acid are positively associated with inflammation, oxidative stress (SOX), endothelial dysfunction, and carotid artery intima-media thickness values in end-stage renal disease patients. Moreover, IDO is a potential novel contributor to vessel relaxation and metabolism in systemic infections, which is also activated in acute severe heart attacks. The Kyn pathway plays a key role in the increased prevalence of cardiovascular disease by regulating inflammation, SOX, and immune activation.
    Frontiers in Bioscience 06/2015; 20(7):1116-1143.
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    ABSTRACT: Ventricular septal defect (VSD) is a common congenital heart malformation. Several factors lead to the development of VSD, including familial causes, exposure to certain drugs, infectious agents, and maternal metabolic disturbances. We hypothesized that induced pluripotent stem (iPS) cells can be obtained from VSD patients to generate cardiomyocytes. Here, we show the generation and cardiomyocyte differentiation of iPS cells from the thymic epithelial cells of a patient with VSD (TECs-VSD) by overexpressing four transcription factors: OCT4, SOX2, NANOG, and LIN28 using lentiviral vectors. The self-renewal capacity and pluripotency of iPS cells was verified in vitro by expression of pluripotency markers and formation of teratoma in vivo. The results show that iPS cells can be derived from patients with VSD and they can be differentiated into cardiomyocytes. These cells can be used for understanding the pathogenesis of defect that causes VSD.
    Frontiers in Bioscience 06/2015; 20(6):964-974.
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    ABSTRACT: At present, the identity of the proteins that participate in mechanical stimulation during the fracture healing process is not known. Here, we screened for and identified 299 proteins that are expressed in various stages of mechanically stimulated fracture healing. Among these biomarkers, 54 proteins were differentially expressed during all three recovery time points. Gene ontology (GO) analysis and selected biomarker candidates were used to determine their involvement in biological processes required for mechanically stimulated healing. The levels of cofilin-1 and A2HSG protein were significantly upregulated in the forth week after fracture suggesting that that they play a role in mechanically stimulated fracture healing.
    Frontiers in Bioscience 06/2015; 20(7):1036-1046.
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    ABSTRACT: Colorectal Cancer (CRC) is one of the most common malignant tumors of gastrointestinal tract. The occurrence, development, diagnosis and prognosis have become a hot topic in current clinical research. However, current diagnosis and treatment still depend on the results of tumor imaging or pathology test. Therefore, to reveal the biological pathogenesis of CRC and to discover specific biomarkers for early diagnosis and better prognosis assessment of CRC have become key roles in current studies. Recent literature has revealed that aberrant expression of microRNAs (miRNAs) could contribute to the development and progression of CRC through the regulation of several critical pathways, including apoptosis, epithelial-mesenchymal transition, angiogenesis and signal transduction. These findings have also indicated that miRNAs could be a novel biomarker for early clinical diagnosis and prognosis evaluation of CRC. In this review, we have summarized the recent studies of miRNAs on the diagnosis, treatment and prognosis clinical biomarker of CRC. We also discussed the regulatory mechanisms of miRNAs in CRC, which may guide the future treatment for CRC.
    Frontiers in Bioscience 06/2015; 20(7):1092-1103.
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    ABSTRACT: Glioma is the most common primary brain tumor, accounting for 30% to 40% of all intracranial tumors. About half of all gliomas in adults are glioblastomas. Patients with glioblastoma have a poor prognosis, with a median survival of one year despite aggressive therapy and a five year mortality of over 95%. Although considerable progress has been made in the technical proficiencies of surgical and radiation oncology, the overall impact of these advances on clinical outcomes has been disappointing. Recent elucidation of several biochemical and molecular markers associated with glioma may provide valuable insight into the underlying biological features of the disease, as well as illuminate possible new therapeutic targets. This review focuses on the current characteristics, classifications, and management of glioma.
    Frontiers in Bioscience 06/2015; 20(7):1104-1115.
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    ABSTRACT: BRAF is a cytoplasmic serine-threonine protein kinasethat plays a critical role in the MAPK signaling pathway. BRAF is the only member of the RAF family activated by mutation in human cancers. A single amino acid substitution (V600E) accounts for a multitude of human cancers, which causes constitutive kinase activity. In papillary thyroid cancer (PTC) and papillary-derived anaplastic thyroid cancer (ATC), the BRAFV600E mutation promotes follicular cell transformation. The BRAFV600E mutation could provide valuable prognostic information for thyroid cancer, because this mutation has been correlated with more aggressive and iodine-resistant phenotypes. Evidence has also shown that the detection of the BRAFV600E mutation in cancer is crucial in order to identify novel avenues for thyroid cancer treatment. Based on the BRAF kinase structure, novel drugs can potentially be designed to target oncogenic BRAF in cancer therapeutics. This review will focus on the recent progress in understandingthe functions of BRAF, the role of the BRAF mutations in thyroid carcinoma, and the correlation between BRAF mutations and cancer microenvironment.
    Frontiers in Bioscience 06/2015; 20(7):1068-1078.
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    ABSTRACT: Although quantal release provides a basic control of synaptic strength, its underlying mechanisms remain unclear. Here, we report a refined realistic 3D vesicle fusion model at calyx-type synapses. By refining the micro ultrastructure and combining updated parameters, our model is appropriate for simulating quantal release. First, we confirmed the existence of kiss-and-run fusion and gave a justified estimation of its percentage in spontaneous and stimulated release. Second, we found the location of AMPA receptors caused the huge variation in the mEPSC rise time. Third, glutamate spillover only slightly contributed to the mEPSC decay time in small vesicles but caused a dual-peak event in large vesicles. Fourth, mEPSC rise time increased with amplitude, suggesting the contribution of vesicle size, not glutamate concentration. We also applied our model to the analysis of KCl, CaCl2 and synaptotagmin-2 triggered exocytosis. KCl globally accelerated the mEPSCs, whereas mEPSCs were slowed down in high calcium treatments and synaptotagmin-2 knock-out mice, indicating more kiss-and-run release. In summary, our model provides a convenient method for exploring the detailed mechanism of vesicle fusion.
    Frontiers in Bioscience 06/2015; 20(7):1079-1091.
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    ABSTRACT: Development of inhibitors of (MMPs) has been fraught with challenges. Early compounds largely failed due to poor selectivity and bioavailability. Dose-limiting side effects, off-target interactions, and improperly designed clinical trials significantly impeded clinical success. As information becomes available and technology evolves, tools to combat these obstacles have been developed. Improved methods for high throughput screening and drug design have led to identification of compounds exhibiting high potency, binding affinity, and favorable pharmacokinetic profiles. Current research into MMP inhibitors employs innovative approaches for drug delivery methods and allosteric inhibitors. Such innovation is key for development of clinically successful compounds.
    Frontiers in Bioscience 06/2015; 20(7):1164-1178.
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    ABSTRACT: Although circulating histones were demonstrated as major mediators of death in septic mice models, their roles in septic patients are not clarified. The present study sought to evaluate the clinical relevance of the circulating histone levels in septic children, and the antagonizing effects of heparin on circulating histones. Histone levels in the plasma of septic children were significantly higher than healthy controls, and positively correlated with disease severity. Histone treatment could activate NF-κB pathway of the endothelial cells and induce the secretion of large amount of cytokines that further amplify inflammation, subsequently leading to organ damage. Co-injection of low dose heparin with lethal dose histones could protect mouse from organ damage and death by antagonizing circulating histones, and similar effects were also observed in other septic models. Collectively, these findings indicated that circulating histones might serve as key factors in the pathogenesis of sepsis and their levels in plasma might be a marker for disease progression and prognosis. Furthermore, low dose heparin might be an effective therapy to hamper sepsis progression and reduce the mortality.
    Frontiers in Bioscience 05/2015; 20:1259-70.
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    ABSTRACT: Pancreatic cancer (PC) is an aggressive malignancy with a high mortality rate and poor prognosis. Numerous investigations have shown that microRNA (miRNA) plays a vital role in PC. Thousands of miRNAs have been screened in PC and altered miRNAs, including circulating miRNAs, are associated with PC proliferation, apoptosis, metastasis, chemosensitivity, and radiosensitivity. Several studies have shown that miRNAs can act as potential diagnostic and prognostic markers. The present review focuses on recent advances regarding the roles of miRNAs in PC and their practical value.
    Frontiers in Bioscience 05/2015; 20(7):1017-28.
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    ABSTRACT: Extensive research has been carried out in the past two decades to provide insights into the molecular mechanisms by which the Nucleophosmin-Anaplastic Lymphoma Kinase (NPM-ALK) exerts its oncogenic effects. These studies led to the concept that NPM-ALK acts at the transcriptional level through the activation of several transcription factors downstream of many different signaling pathways including JAK3/STAT3, PI3K/AKT and RAS/ERK. Nevertheless, the discovery of several RNA-binding proteins (RBPs) within ALK interactome suggested an additional and complementary role of this oncogenic kinase at the post-transcriptional level. This review gives emerging views in ALK-mediated post-transcriptional regulation with a focus on RBPs that are associated with ALK. We will summarize the capacity of NPM-ALK in modulating the biological properties of RBPs and then discuss the role of cytoplasmic aggregates, called AGs for "ALK granules", which are observed in anaplastic large cell lymphoma (ALCL) expressing the ALK kinase. AGs contain polyadenylated mRNAs and numerous RBPs but are distinct from processing bodies (PBs) and stress granules (SGs), two well-known discrete cytoplasmic sites involved in mRNA fate.
    Frontiers in Bioscience 05/2015; 20:1250-8.