International journal of biological sciences (INT J BIOL SCI)

Publisher: Ivyspring International Publisher

Journal description

International Journal of Biological Sciences publishes peer-reviewed scientific papers of significance in all areas of biological sciences. The Journal targets wide ranges of international audiences of researchers and biotechnology company employees. The scope of the Journal includes cell biology, developmental biology, structural biology, microbiology, molecular biology & genetics, biochemistry, biotechnology, biodiversity, ecology, marine biology, plant biology, and bioinformatics. Articles of cross-disciplined research between biology and mathematics, physics, information science, material science and others are also considered. Selected papers from scientific meetings may be published as special issues of the Journal.

Current impact factor: 4.37

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 4.372
2012 Impact Factor 3.168
2011 Impact Factor 2.699
2010 Impact Factor 3.215
2009 Impact Factor 2.865

Impact factor over time

Impact factor
Year

Additional details

5-year impact 3.44
Cited half-life 3.20
Immediacy index 0.77
Eigenfactor 0.01
Article influence 0.95
Website International Journal of Biological Sciences website
ISSN 1449-2288
OCLC 57564437
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Ivyspring International Publisher

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Non-commercial use
    • On author's personal website or institutional website
    • Publisher copyright and source must be acknowledged
    • Publisher's version/PDF may be used
  • Classification
    ​ green

Publications in this journal

  • International journal of biological sciences 07/2015; 11(10):1140-1149. DOI:10.7150/ijbs.12657
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    ABSTRACT: Cardiovascular diseases (CVDs) are still a major cause of people deaths worldwide, and mesenchymal stem cells (MSCs) transplantation holds great promise due to its capacity to differentiate into cardiovascular cells and secrete protective cytokines, which presents an important mechanism of MSCs therapy for CVDs. Although the capability of MSCs to differentiate into cardiomyocytes (CMCs), endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) has been well recognized in massive previous experiments both in vitro and in vivo, low survival rate of transplanted MSCs in recipient hearts suggests that therapeutic effects of MSCs transplantation might be also correlated with other underlying mechanisms. Notably, recent studies uncovered that MSCs were able to secret cholesterol-rich, phospholipid exosomes which were enriched with microRNAs (miRNAs). The released exosomes from MSCs acted on hearts and vessels, and then exerted anti-apoptosis, cardiac regeneration, anti-cardiac remodeling, anti-inflammatory effects, neovascularization and anti-vascular remodeling, which are considered as novel molecular mechanisms of therapeutic potential of MSCs transplantation. Here we summarized recent advances about the role of exosomes in MSCs therapy for CVDs, and discussed exosomes as a novel approach in the treatment of CVDs in the future.
    International journal of biological sciences 01/2015; 11(2):238-245. DOI:10.7150/ijbs.10725
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    ABSTRACT: The forkhead box M1 (FOXM1) transcription factor is one of the key genes inducing tumor invasion and metastasis by an unknown mechanism. In this study, we set out to investigate the effects of FOXM1 overexpression on metastatic human lung adenocarcinoma and the underlying mechanism. FOXM1 expression was analyzed in 78 frozen lung adenocarcinoma tissue samples using an Affymetrix microarray and a 155-paraffin-embedded lung adenocarcinoma tissue microarray with immunohistochemical detection. FOXM1 was found to be overexpressed in lung adenocarcinoma, particularly in metastatic patients, compared to non-metastatic patients. Knockdown of FOXM1 by a specific siRNA significantly suppressed EMT progression, migration and invasion of lung adenocarcinoma cells in vitro, and tumor growth and metastasis in vivo, whereas restored expression of FOXM1 had the opposite effect. FOXM1 binds directly to the SNAIL promoter through two specific binding sites and constitutively transactivates it. Collectively, our findings indicate that FOXM1 may play an important role in advancing lung adenocarcinoma progression. Aberrant FOXM1 expression directly and constitutively activates SNAIL, thereby promoting lung adenocarcinoma metastasis. Inhibition of FOXM1-SNAIL signaling may present an ideal target for future treatment.
    International journal of biological sciences 01/2015; 11(2):186-98. DOI:10.7150/ijbs.10634
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    ABSTRACT: Excessive inflammatory response may delay the regeneration and damage the normal muscle fibers upon myoinjury. It would be important to be able to attenuate the inflammatory response and decrease inflammatory cells infiltration in order to improve muscle regeneration formation, resulting in better muscle functional recovery after myoinjury. This study was undertaken to explore the role of Nitric oxide (NO) during skeletal muscle inflammatory process, using a mouse model of Notexin induced myoinjury. Intramuscular injection (tibialis anterior, TA) of Notexin was performed for preparing mice myoinjury. NO synthase inhibitor (L-NAME) or NO donor (SNP) was intraperitoneally injected into model mice. On day 4 and 7 post-injury, expression of muscle-autoantigens and toll-like receptors (TLRs) was evaluated from muscle tissue by qRT-PCR and Western Blot; the intramuscular infiltration of monocytes/macrophage (CD11b(+) or F4/80(+) cells), CD8(+) T cell (CD3ε(+)CD8α(+)), apoptotic cell (CD11b(+)caspase3(+)), and MHC-I molecule H-2K(b)-expressing myofibers in damaged muscle were assessed by imunoflourecence analysis; the mRNAs expression of cytokines and chemokines associated with the preferential biological role during the muscle damage-induced inflammation response, were assessed by qRT-PCR. We detected the reduced monocytes/macrophages infiltration, and increased apoptotic cells in the damaged muscle treated with SNP comparing to untreatment. As well, SNP treatment down-regulated mRNA and protein levels of muscle autoantigens, TLR3, and mRNA levels of TNF-α, IL-6, MCP-1, MCP-3, and MIP-1α in damaged muscle. On the contrary, L-NAME induced more severe intramuscular infiltration of inflammatory cells, and mRNA level elevation of the above inflammatory mediators. Notably, we observed an increased number of MHC-I (H2-K(b)) positive new myofibers, and of the infiltrated CD8(+) T cells in damaged muscle at the day 7 after L-NAME treatment. The result herein shows that, NO can act as an endogenous anti-inflammatory molecule during the ongoing muscle inflammation. Our finding may provide new insight to optimize NO-based therapies for improving muscle regeneration after myoinjury.
    International journal of biological sciences 01/2015; 11(2):156-67. DOI:10.7150/ijbs.10283