BioFactors (BIOFACTORS)

Publisher: International Society of Vitamins and Related Biofactors; International Union of Biochemistry and Molecular Biology

Journal description

BioFactors is an international journal aimed at identifying and increasing our understanding of the precise biochemical effects and roles of the large number of trace substances that are required by living organisms. These include vitamins and trace elements, as well as growth factors and regulatory substances made by cells themselves. The elucidation, in a particular organism or cell line, of the roles of substances active in trace quantities, is frequently applicable directly to many other forms of life. In keeping with this unified view of biochemistry, BioFactors publishes articles dealing with the identification of new substances and the elucidation of their functions at the basic biochemical level as well as those revealing novel functions of trace substances already known.

Current impact factor: 3.00

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 3
2012 Impact Factor 3.088
2011 Impact Factor 4.933
2010 Impact Factor 2.793
2009 Impact Factor 0.912
2008 Impact Factor 1.23
2007 Impact Factor 1.451
2006 Impact Factor 1.095
2005 Impact Factor 1.162
2004 Impact Factor 1.273
2003 Impact Factor 1.852
2002 Impact Factor 1.815
2001 Impact Factor 1.273

Impact factor over time

Impact factor
Year

Additional details

5-year impact 3.03
Cited half-life 7.20
Immediacy index 0.45
Eigenfactor 0.00
Article influence 0.81
Website Biofactors website
Other titles BioFactors (Online)
ISSN 0951-6433
OCLC 41948746
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Colorectal cancer (CRC) is the third most common malignancy in males and the second most common cancer worldwide. Chronic colonic inflammation is a known risk factor for CRC. Cocoa contains many polyphenolic compounds that have beneficial effects in humans. The objective of this study is to explore the antioxidant properties of cocoa in the mouse model of azoxymethane (AOM)/dextran sulfate sodium (DSS)- induced colitis-associated cancer, focusing on the activation of Nrf2 signaling. Mice were treated with AOM/DSS and randomized to receive either a control diet or a 5 and 10% cocoa diet during the study period. On day 62 of the experiment, the entire colon was processed for biochemical and histopathological examination and further evaluations. Increased levels of malondialdehyde (MDA) were observed in AOM/DSS-induced mice; however, subsequent administration of cocoa decreased the MDA. Enzymatic and nonenzymatic antioxidants, such as superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, were decreased in the AOM/DSS mice. Cocoa treatment increases the activities/levels of enzymatic and nonenzymatic antioxidants. Inflammatory mediators, such as inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, were elevated during AOM/DSS-induction, and treatment with 5 and 10% cocoa effectively decreases the expression of iNOS and COX-2. The NF-E2-related factor 2 and its downstream targets, such as NQO1 and UDP-GT, were increased by cocoa treatment. The results of our study suggest that cocoa may merit further clinical investigation as a chemopreventive agent that helps prevent CAC.
    BioFactors 01/2015; 41(1). DOI:10.1002/biof.1195
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    ABSTRACT: Thy-1 or CD90 is a glycophosphatidylinositol-linked glycoprotein expressed on the surface of neurons, thymocytes, subsets of fibroblasts, endothelial cells, mesangial cells and some hematopoietic cells. Thy-1 is evolutionarily conserved, developmentally regulated, and often has dramatic effects on cell phenotype; however, the effects vary between and in some cases within cell types and tissues, and between similar tissues in different species, indicating that the biological role of Thy-1 is context-dependent. Thy-1 exists in soluble form in some body fluids; however, the mechanisms of its shedding are unknown. In addition, Thy-1 expression can be regulated by epigenetic silencing. Because Thy-1 modulates many basic cellular processes and is involved in the pathogenesis of a number of diseases, it is important to better understand its regulation.
    BioFactors 05/2009; 35(3):258-65. DOI:10.1002/biof.41
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    ABSTRACT: Although apolipoprotein E (apoE) is the most common genetic risk factor for Alzheimer's Disease (AD), how apoE participates in AD pathogenesis remains incompletely understood. ApoE is also the major carrier of lipids in the brain. Here, we review studies showing that the lipidation status of apoE influences the metabolism of Abeta peptides, which accumulate as amyloid deposits in the neural parenchyma and cerebrovasculature. One effect of apoE is to inhibit the transport of Abeta across the blood-brain-barrier (BBB), particularly when apoE is lipidated. A second effect is to facilitate the proteolytic degradation of Abeta by neprilysin and insulin degrading enzyme (IDE), which is enhanced when apoE is lipidated. We also describe how apoE becomes lipidated and how this impacts Abeta metabolism. Specifically, genetic loss of the cholesterol transporter ABCA1 impairs apoE lipidation and promotes amyloid deposition in AD mouse models. ABCA1 catalyses the ATP-dependent transport of cholesterol and phospholipids from the plasma membrane to lipid-free apolipoproteins including apoE. Conversely, selective overexpression of ABCA1 increases apoE lipidation in the central nervous system (CNS) and eliminates the formation of amyloid plaques in vivo. Deficiency of Liver-X-Receptors (LXRs), transcription factors that stimulate ABCA1 and apoE expression, exacerbates AD pathogenesis in vivo, whereas treatment of AD mice with synthetic LXR agonists reduces amyloid load and improves cognitive performance. These studies provide new insights into the mechanisms by which apoE affects Abeta metabolism, and offer opportunities to develop novel therapeutic approaches to reduce the leading cause of dementia in the elderly.
    BioFactors 05/2009; 35(3):239-248. DOI:10.1002/biof.37
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    ABSTRACT: Current intakes of very long chain omega-3 fatty acids, eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) are low in most individuals living in Western countries. A good natural source of these fatty acids is seafood, especially oily fish. Fish oil capsules contain these fatty acids too. Very long chain omega-3 fatty acids are readily incorporated from capsules into transport, functional, and storage pools. This incorporation is dose-dependent and follows a kinetic pattern that is characteristic for each pool. At sufficient levels of incorporation, EPA and DHA influence the physical nature of cell membranes and membrane protein-mediated responses, eicosanoid generation, cell signaling and gene expression in many different cell types. Through these mechanisms, EPA and DHA influence cell and tissue physiology, and the way cells and tissues respond to external signals. In most cases, the effects seen are compatible with improvements in disease biomarker profiles or in health-related outcomes. As a result, very long chain omega-3 fatty acids play a role in achieving optimal health and in protection against disease. Long chain omega-3 fatty acids protect against cardiovascular morbidity and mortality, and might be beneficial in rheumatoid arthritis, inflammatory bowel diseases, childhood learning, and behavior, and adult psychiatric and neurodegenerative illnesses. DHA has an important structural role in the eye and brain, and its supply early in life is known to be of vital importance. On the basis of the recognized health improvements brought about by long chain omega-3 fatty acids, recommendations have been made to increase their intake.
    BioFactors 05/2009; 35(3):266-72. DOI:10.1002/biof.42
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    ABSTRACT: It has been demonstrated that vitamin E deficiency from birth increases anxiety-related behavior using knockout animals with no vitamin E transfer proteins. The current study was undertaken to elucidate the effect of dietary vitamin E deficiency on anxiety-related behavior of rats in different housing conditions. Male Wistar strain rats were divided into two groups during the weaning period and fed a control or vitamin E-deficient diet. All rats were housed in groups (three rats per cage) for 3 weeks. In the fourth week, half of the rats in each dietary treatment were kept in social housing and the other half were kept in individual housing. Before sacrifice, rota-rod and elevated plus-maze (EPM) tests were performed to measure motor coordination and anxiety, respectively. The EPM test revealed that vitamin E-deficient rats spent less time in the open arms and showed more stretch-out posture than the control rats, showing that anxiety increased with dietary vitamin E deficiency. Furthermore, vitamin E deficiency-induced anxiety behavior was observed more prominent in individual housed rats than in social housed rats. On the basis of these results, we conclude that dietary vitamin E deficiency induces anxiety in rats especially under stress of social isolation.
    BioFactors 05/2009; 35(3):273-8. DOI:10.1002/biof.33
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    ABSTRACT: Studies in animals and humans indicate that diets containing diacylglycerol (DAG) oil (containing >80% DAG) decrease body weight gain and body fat accumulation, especially visceral fat. Body weight and body fat are controlled by energy expenditure, fat oxidation, fat storage capacity, and appetite control. Recent researches indicate that DAG oil, compared with conventional oils, has distinct metabolic effects. We review the evidence concerning the effects of DAG oil intake on fat oxidation and energy expenditure. In humans, dietary DAG is more susceptible to oxidation, and in animals 1,3-DAG, a major component of DAG oil, is rapidly oxidized. Short-term human studies with indirect calorimetry demonstrate greater fat oxidation with DAG oil consumption compared with triacylglycerol (TAG) oil consumption. Furthermore, DAG oil consumption for 14 days stimulates energy expenditure. Based on these reports, enhanced fat oxidation and energy expenditure by daily DAG oil intake could contribute to long-term reductions in body weight and fat accumulation. The literature provides support for the notion that dietary DAG is more rapidly oxidized than dietary TAG, and that, compared with TAG oil, DAG oil consumption increases whole body fat oxidation. The effects of DAG oil consumption on energy expenditure, however, remain inconclusive. (c) 2009 International Union of Biochemistry and Molecular Biology, Inc.
    BioFactors 04/2009; 35(2):175-7. DOI:10.1002/biof.25
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    ABSTRACT: During HIV infection, the perturbation of the adaptive and innate immune responses contributes to the progressive immunosuppression leading to an increased susceptibility to opportunistic infections and neoplastic diseases. Several impairments observed in HIV-infected patients include a gradual loss of CD4(+) T cells, CD8(+) T cell dysfunction, and a decreased number and function of natural killer (NK) cells. Moreover, a functional impairment and variation in the number of DC and B cells were observed during HIV infection. HIV-1 codes for proteins, including the accessory Nef proteins, that interacting with immune cells may contribute to AIDS pathogenesis. Here, we review the recent progress on the immunomodulatory effect of the accessory Nef protein and its role in the pathogenesis of HIV-1 infection. (c) 2009 International Union of Biochemistry and Molecular Biology, Inc.
    BioFactors 04/2009; 35(2):169-74. DOI:10.1002/biof.28
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    ABSTRACT: The role of the transcription factor CCATT/enhancer binding protein alpha (C/EBPalpha) as a lineage instructive determinant in myelopoiesis is widely accepted. Furthermore, early mutational events ultimately leading to acute myeloid leukemia (AML) often involve abrogation of C/EBPalpha expression and/or function. The main focus of this review is the progression from a preclinical state to AML, and which preleukemic cell population(s) might-in general and in particular in patients with CEBPA mutations-be a target for the secondary genetic and epigenetic events leading to this progression.
    BioFactors 04/2009; 35(3):227-31. DOI:10.1002/biof.36
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    ABSTRACT: Melatonin acts both as a hormone of the pineal gland and as a local regulator molecule in various tissues. Quantities of total tissue melatonin exceed those released from the pineal. With regard to this dual role, to the orchestrating, systemic action on various target tissues, melatonin is highly pleiotropic. Numerous secondary effects result from the control of the circadian pacemaker and, in seasonal breeders, of the hypothalamic/pituitary hormonal axes. In mammals, various binding sites for melatonin have been identified, the membrane receptors MT(1) and MT(2), which are of utmost chronobiological importance, ROR and RZR isoforms as nuclear receptors from the retinoic acid receptor superfamily, quinone reductase 2, calmodulin, calreticulin, and mitochondrial binding sites. The G protein-coupled receptors (GPCRs) MT(1) and MT(2) are capable of parallel or alternate signaling via different Galpha subforms, in particular, Galpha(i) (2/) (3) and Galpha(q), and via Gbetagamma, as well. Multiple signaling can lead to the activation of different cascades and/or ion channels. Melatonin frequently decreases cAMP, but also activates phospholipase C and protein kinase C, acts via the MAP kinase and PI3 kinase/Akt pathways, modulates large conductance Ca(2+)-activated K(+) and voltage-gated Ca(2+) channels. MT(1) and MT(2) can form homo and heterodimers, and MT(1) interacts with other proteins in the plasma membrane, such as an orphan GPCR, GPR50, and the PDZ domain scaffolding protein MUPP1, effects which negatively or positively influence signaling capacity. Cross-talks between different signaling pathways, including influences of the membrane receptors on nuclear binding sites, are discussed. (c) 2009 International Union of Biochemistry and Molecular Biology, Inc.
    BioFactors 03/2009; 35(2):183-92. DOI:10.1002/biof.23