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: 4.25

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 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
Year

Additional details

5-year impact 3.23
Cited half-life 5.30
Immediacy index 1.35
Eigenfactor 0.03
Article influence 1.06
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
    ​ blue

Publications in this journal

  • Frontiers in Bioscience 01/2015; 20:335-76. DOI:10.2741/4313
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    ABSTRACT: Tumor necrosis factor, a regulatory cytokine, is extremely important signaling protein in the immune system. Among TNF family, TNF-alpha, TNF-beta are most the significant family members. Receptor of TNF namely TNFR1 and TNFR2 stimulates two different signaling pathways. TNFR1 signaling induces apoptosis pathway. Conversely, TNFR2 signaling triggers cell survival pathways. In this paper, we discuss about the TNF family with special reference to TNF-alpha / TNF-beta, different hypothesis related to autoimmunity and role of TNF, structure of TNF-alpha / TNF-beta, distribution and normal activity in human body of TNF, receptors and signaling pathway for drug targeting. Finally, we also discuss about the therapy for autoimmune diseases and immune-mediated inflammatory diseases (IMIDs) using small molecules or therapeutic proteins.
    Frontiers in Bioscience 01/2014;
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    ABSTRACT: From an evolutionary viewpoint, readiness to engage in appropriate behavior toward a recognized person seems to be inherent in the human brain. In support of this hypothesis, functional neuroimaging studies have demonstrated activation in regions relevant to relationship-appropriate behavior during the recognition of personally familiar (PF) people. Recognition of friends and colleagues activates regions involved in real-time communication, including the regions for inference about the other's mental state, autobiographical memory retrieval, and self-referential processes. Recognition of people related by romantic love, maternal love, and lost love induces activation in regions involved in motivational, reward, and affective processes, reflecting behavioral readiness for mating, caretaking, and yearning, respectively. The involvement of motor-associated cortices during recognition of a personal enemy may reflect readiness for attack or defense. Self-recognition in a body-related modality uniquely activates sensory and motor association cortices reflecting the sensorimotor origin of the bodily self-concept, with social cognitive processes being suppressed or context dependent. Issues and future directions are also discussed.
    Frontiers in Bioscience 01/2014; 19:672-86. DOI:10.2741/4235
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    ABSTRACT: Extracellular matrix is one of the key environmental factors influencing cell survival and provides signals for cell morphological change, migration, proliferation and differentiation. However, the mechanism through which denatured collagen modulates the biological properties of fibroblasts, is unclear. We investigated the regulation of human fibroblast differentiation in vitro grown in collagen gels with different properties. The break modulus of collagen with denatured collagen and half-load normal collagen was reduced compared with that of normal collagen gel. Fibroblasts cultured in denatured collagen gels showed increased expression of matrix metalloproteinase9 ( MMP-9), tissue inhibitor of metalloproteinase 2 (TIMP2), α-smooth muscle actin (α-SMA), osteoblast cadherin, phosphorylated Myosin phosphatase target subunit1 (p-MYPT1), connective tissue growth factor, type I collagen, type III collagen, α-smooth muscle actin messenger RNA, RhoA, rho-associated protein kinase, and transforming growth factor β receptors 1 and 2 compared with that in cells cultured in normal collagen gel. But there was no significant difference regarding expression level between denatured collagen gel and half-load normal collagen gel .These findings suggest that the change in break modulus caused by decreasing normal collagen concentration may be the key factor inducing fibroblast differentiation.
    Frontiers in Bioscience 01/2014; 19:727-33.
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    ABSTRACT: Disrupting the regenerative capacity of tumorigenic cells is a major focus in medicine. These regenerative properties are carried by a subpopulation of cells within the tumor, termed cancer stem cells. Current therapies don't effectively tackle the disease suggesting these cells employ yet unidentified molecular mechanisms allowing them to evade targeting. Recent observations in neural stem cells reveal an extraordinary plasticity in the signaling pathways they utilize to grow. These findings are being extended to the cancer stem cell field, illuminating conceptually novel treatment strategies. Tumorigenic cells can make use of distinct, even opposing pathways, including JAK/STAT and the non-canonical STAT3-Ser/Hes3 signaling axis. This plasticity may not be confined to the cancer stem cell population, but may be shared by various cell types within the tumor, blurring the line distinguishing cancer stem cells from other tumor cell types. The implications to anti-cancer medicine are highly significant, since these findings demonstrate that inhibiting one cell growth pathway may actually enhance the activity of alternative ones. Drug discovery programs will also benefit from these concepts.
    Frontiers in Bioscience 01/2014; 19:718-26.
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    ABSTRACT: The present study investigated whether pharmacological postconditoning with netrin-1 is cardioprotective against ischemia reperfusion (I/R) injury, and the underlying signaling mechanisms. Langendorff perfused hearts isolated from wild-type (WT) C57BL/6 or DCC+/- mice underwent a 20-min of ischemia, followed by a 60-min of reperfusion, in the presence or absence of netrin-1, or netrin-1 in combination with U0126 (MEK1/2 inhibitor), or PTIO (nitric oxide/NO scavenger). In WT mice, netrin-1 postconditioning dramatically reduced infarct size to 17.0±2.5%, from 40.5±4.2% in the untreated I/R group. U0126 or PTIO alone had no effect on infarct size but abolished the effects of netrin-1. The protective effect of netrin-1 was markedly diminished in DCC+/- mice (44.5±2% vs. 15±2.6 % for infract size in DCC+/- vs. DCC+/+ group). Our results indicate that netrin-1, given as a pharmacological postconditioning agent, induces cardioprotection via a DCC-dependent mechanism that involves ERK1/2 activation and NO production. Combined with our previous findings, netrin-1 treatment proves to be extremely and consistently beneficial whenever delivered to the heart, establishing its substantial promises for being developed into a robust therapeutic strategy for acute myocardial infarction.
    Frontiers in Bioscience 01/2014; 19:566-70.
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    ABSTRACT: Acute Myeloid Leukemia (AML), a cancer of the myeloid line of blood cells, progresses rapidly and is typically fatal within weeks or months if left untreated. Asparaginases are a class of enzymatic anti-leukemia agents that induce apoptosis in leukemia cell lines; however, the role of L-asparaginase in the induction of apoptosis in AML cells has not been investigated. In this study, we investigated the apoptosis-inducing effect of L-asparaginase and its underlying mechanism in AML U937 cells. The results showed that L-asparaginase significantly inhibited the proliferation of U937 cells by inducing apoptosis. Furthermore, the low baseline expression level of asparaginase synthase (ASNS) demonstrated the sensitivity of U937 cells and AML M5, a rare subtype of AML, to L-asparaginase. Apoptosis induced by L-asparaginase is mediated by apoptosis-inducing factor (AIF). Our findings show the potential of L-asparaginase as an effective approach in treating AML via the induction of apoptosis mediated by AIF.
    Frontiers in Bioscience 01/2014; 19:515-27.
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    ABSTRACT: Prostate cancer is one of the leading causes of cancer death among men in the United States. Although, recent advancement in diagnostic tools has significantly increased early detection and decreased cases of advanced diseases, high numbers of patients who underwent treatment still experience recurrent disease at distant sites, after long periods of remission. Therefore, it is of paramount importance to elucidate the pathological mechanism of the tumor recurrence in order to identify better therapeutic targets and also to distinguish patients with indolent disease from patients with recurrent disease at the time of surgery for optimization of therapeutic intervention. Recurrent tumor cells disseminate at a very early stage even before diagnosis of localized disease and remain dormant as "residual disease" in patients for a long period of time. Colonization and recurrent growth at distant site requires acquisition of genetic and epigenetic alterations and remodeling of signaling pathways. This review focuses on recent advances on identification of biomarkers associated with early and late recurrent disease as well as mechanisms involved during recurrence of prostate cancer.
    Frontiers in Bioscience 01/2014; 19:339-51. DOI:10.2741/4211
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    ABSTRACT: The quality of life of patients with head and neck squamous cell carcinoma (HNSCC) has been improved because of advances in surgical and radiotherapeutic techniques as well as organ-preservation methods. Despite such progresses, survival rates are dismal because of frequent recurrences, distant metastases and the development of secondary primary tumors. Nanoparticles have distinct characteristics such as a high surface/volume ratio and surface charge and size that can be easily modified. Because of such inherent features, nanoparticles are used in imaging, adjuvant radiotherapy, and drug- or gene-delivery. Thus, nanomedicine holds great promise in the diagnosis and treatment of cancer. In the present review, we summarize recent advances in nanomedicine in the diagnosis and treatment of head and neck cancer. We first review the application of inorganic nanoparticles to photo-thermal and magneto-thermal radiotherapy. We also discuss the use of organic nanoparticles in drug- or gene-delivery during chemotherapy. We then review the application of inorganic nanoparticles as radiotherapy enhancers. Finally, we address the factors that influence the biodistribution of nanoparticles in vivo.
    Frontiers in Bioscience 01/2014; 19:783-8. DOI:10.2741/4245