BioFactors (BIOFACTORS )

Publisher: International Society of Vitamins and Related Biofactors; International Union of Biochemistry and Molecular Biology, John Wiley and Sons


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.

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  • Website
    Biofactors website
  • Other titles
    BioFactors (Online)
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  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

John Wiley and Sons

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    • Author can archive a post-print version
  • Conditions
    • See Wiley-Blackwell entry for articles after February 2007
    • On personal web site or secure external website at authors institution
    • Deposit in institutional repositories is not allowed
    • JASIST authors may deposit in an institutional repository
    • Non-commercial
    • Pre-print must be accompanied with set phrase (see individual journal copyright transfer agreements)
    • Published source must be acknowledged with set phrase (see individual journal copyright transfer agreements)
    • Publisher's version/PDF cannot be used
    • Articles in some journals can be made Open Access on payment of additional charge
    • 'John Wiley and Sons' is an imprint of 'Wiley'
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Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Endogenous morphine and its derivatives (morphine-6-glucuronide [M6G]; morphine-3-glucuronide [M3G]) are formed by mammalian cells from dopamine. Changes in the concentrations of endogenous morphine have been demonstrated in several pathologies (sepsis, Parkinson's disease, etc.), and they might be relevant as pathological markers. While endogenous morphine levels are detectable using enzyme-linked immunosorbant assay (ELISA), mass spectrometry (MS) analysis was, so far, the only approach to detect and quantify M6G. This study describes the preparation of a specific anti-M6G rabbit polyclonal antibody and its validation. The specificity of this antibody was assessed against 30 morphine-related compounds. Then, a M6G-specific ELISA-assay was tested to quantify M6G in the plasma of healthy donors, morphine-treated, and critically ill patients. The antibody raised against M6G displays a strong affinity for M6G, codeine-6-glucuronide, and morphine-3-6-glucuronide, whereas only weak cross-reactivities were observed for the other compounds. Both M6G-ELISA and LC-MS/MS approaches revealed the absence of M6G in the plasma of healthy donors (controls, n = 8). In all positive donors treated with morphine-patch (n = 5), M6G was detected using both M6G-ELISA and LC-MS/MS analysis. Finally, in a study on critically ill patients with circulating endogenous morphine (n = 26), LC-MS/MS analysis revealed that 73% of the positive-patients (19 of 26), corresponding to high M6G-levels in M6G-ELISA, contained M6G. In conclusion, we show that endogenous M6G can be found at higher levels than morphine in the blood of morphine-naive patients. With respect to the interest of measuring endogenous M6G in pathologies, we provide evidences that our ELISA procedure represents a powerful tool as it can easily and specifically detect endogenous M6G levels. © 2013 BioFactors, 2013.
    BioFactors 01/2014; 40(1):113-120.
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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 06/2009; 35(3):258-65.
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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.
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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.
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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.
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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.
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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 04/2009; 35(2):183-92.
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    ABSTRACT: It has been well-established that type-2 immunity, characterized by eosinophilia, goblet cell hyperplasia, mucus production, and B cell class switching to IgE, is highly dependent on the production of the type-2 cytokines, interleukin (IL)-4, IL-5, IL-9, and IL-13, by T helper 2 (Th2) cells. However, it is less clear how the type-2 cytokine effector response is induced and in addition what innate cell type produces the initiating factor. Recent reports highlight IL-25 as a type-2 inducing factor, with IL-25 administration resulting in severe gut and lung type-2 pathologies. The expression of IL-25 is also necessary for initiation of a robust type-2 response both at the genesis of the response, as with helminth infection, and during the response, as has been shown in experimental allergic asthma. It is also apparent that, as well as directly controlling type-2 immunity via IL-4, IL-5, and IL-13, IL-25 may also interact with other cytokines and their receptors, such as IL-17A and the IL-17RA receptor. Here, we review the role of IL-25 as an important factor in controlling the initiation and severity of the type-2 response, and as an alternative therapeutic target to the type-2 cytokine family, for the treatment of allergic asthma. (c) 2009 International Union of Biochemistry and Molecular Biology, Inc.
    BioFactors 04/2009; 35(2):178-82.