Frontiers in Bioscience (Front Biosci )

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.

  • Impact factor
    3.29
  • 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

Publications in this journal

  • [Show abstract] [Hide abstract]
    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: Despite recent advances in individualised targeted therapy, gastric cancer remains one of the most challenging diseases in gastrointestinal oncology. Modern imaging techniques using endoscopic filter devices and in vivo molecular imaging are designed to enable early detection of the cancer and surveillance of patients at risk. Molecular characterisation of the tumour itself as well as of the surrounding inflammatory environment is more sophisticated in the view of tailored therapies and individual prognostic assessment. The broad application of high throughput techniques for the description of genome wide patterns of structural (copy number aberrations, single nucleotide polymorphisms, methylation pattern) and functional (gene expression profiling, proteomics, miRNA) alterations in the cancer tissue lead not only to a better understanding of the tumour biology but also to a description of gastric cancer subtypes independent from classical stratification systems. Biostatistical means are required for the interpretation of the massive amount of data generated by these approaches. In this review we give an overview on the current knowledge of diagnostic methods for detection, description and understanding of gastric cancer disease.
    Frontiers in Bioscience 01/2014; 19:312-38.
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    ABSTRACT: The Nek2 and Plk4 kinases serve as crucial regulators of mitotic processes such as the centrosome duplication cycle and spindle assembly. Deregulation of these processes can trigger chromosome instability and aneuploidy, which are hallmarks of many solid tumors, including breast cancer. Emerging data from the literature illustrated various functions of Nek2 in breast cancer models, with compelling evidence of its prognostic value in breast tumors. The two kinases control distinct steps in the centrosome-centriole cycle and their dysregulation lead to centrosome amplification, marked by the presence of more than two centrosomes within the cell. We found single or composite overexpression of these kinases in breast tumor samples, regardless of subtype, which strongly associated with poor prognosis. Interestingly, in a panel of established cell lines, both kinases are highly expressed in Her2-positive breast cancer cells exhibiting centrosome amplification and trastuzumab resistance. In summary, it appears that Nek2 and Plk4 might synergize to promote breast tumorigenesis and may also be involved in tamoxifen and trastuzumab resistance.
    Frontiers in Bioscience 01/2014; 19:352-65.
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    ABSTRACT: Since pancreatic carcinoma is largely refractory to conventional therapies, development of novel agents is required for the effective treatment of pancreatic cancer. The objective of this paper was to examine the molecular mechanisms by which embelin inhibited human pancreatic cancer growth in mice by modulating tumor immune microenvironment. Embelin inhibited PANC-1 tumor growth, angiogenesis, and metastasis which were associated with suppression of Akt and Sonic Hedgehog (Shh) pathways. Embelin inhibited the expression of Bcl-2, cyclin D1, CDK2 and CDK6, IL-6 and IL-8, and induced the expression of Bax in tumor tissues. Embelin also reversed epithelial-mesenchymal transition by up-regulating E-cadherin and inhibiting the expression of Snail, Slug and Zeb1. Embelin inhibited pancreatic cancer growth in Kras(G12D) mice by modulating tumor immune microenvironment where CTL, NKT, γδT, NK, and IFNγ (Th1 type) cells were up-regulated, and Th17, PMN-MDSC, IL-6 and IL-8 (Th2 type) immune cells were inhibited. These data suggest that embelin can inhibit pancreatic cancer growth by modulating tumor immune microenvironment and Akt and Shh pathways, and inhibiting inflammation. Embelin may offer therapeutic benefits for the treatment and/or prevention of pancreatic cancer.
    Frontiers in Bioscience 01/2014; 19:113-25.
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    ABSTRACT: Maternally inherited diabetes and deafness (MIDD), a mitochondrial disease first described in 1992, results from the mitochondrial DNA mutation and affects up to 1% of the patients with diabetes. This review discusses the biomedical mechanisms of MIDD patients; summarizes the recent improvement of clinical and genetic diagnosis of MIDD; outlines the advances of the clinical management of these patients and their families.
    Frontiers in Bioscience 01/2014; 19:777-82.
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    ABSTRACT: Since William Morton successfully demonstrated the use of inhaled ether for surgical anesthesia in 1846, the development of new anesthetics and safe general anesthesia techniques have contributed greatly to the advancement of surgery and other invasive procedures. However, the underlying neurocellular mechanisms by which the state of general anesthesia is achieved are only just beginning to be understood. The general anesthetic state comprises multiple components (amnesia, unconsciousness, analgesia, and immobility), each of which is mediated by effects on different neurotransmitter receptors and neuronal pathways. In this review, we focus on the mechanisms of action of inhaled and intravenous, and we describe the neuronal systems thought to be involved in mediating the clinically relevant actions of general anesthetics. We then describe the neurotransmitter receptors that are the principal targets of many general anesthetics, in particular ã-aminobutyric acid type A receptor subtypes.
    Frontiers in Bioscience 01/2014; 19:747-57.
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    ABSTRACT: H. pylori causes gastritis and increases the risk of gastric ulcer and gastric cancer. However, it was recently shown that H. pylori provides protection against inflammatory bowel diseases. To assess the molecular mechanism of such functions, we studied the role of DC-SIGN in H. pylori-infected gastrointestinal epithelial cells. DC-SIGN was found to be over-expressed in the gastric epithelial cells infected with H. pylori and mediated Th1 differentiation, which may be involved in H. pylori-induced gastric mucosal injury. In addition, DC-SIGN was also up-regulated in the intestinal epithelial cells derived from colitis mouse model, but the expression levels were blocked upon H. pylori infection, indicating that H. pylori infection may reduce both local and systemic inflammatory responses. In conclusion, we propose that gastrointestinal epithelial cells infected with H. pylori may lead to acquiring of immune properties via a trans-differentiation process, and regulate tissue-associated immune compartments under the control of DC-SIGN.
    Frontiers in Bioscience 01/2014; 19:825-34.
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    ABSTRACT: Prostate-specific membrane antigen (PSMA) is an integral, non-shed membrane glycoprotein that is a well-characterized and clinically validated marker of prostate cancer. The expression profile and other biological properties of PSMA make it an attractive target for antibody-drug conjugate (ADC) therapy of prostate cancer, as well as a broad range of other tumors in which PSMA is abundantly expressed within the tumor neovasculature. PSMA-targeted ADCs have been developed using auristatin and maytansinoid drugs, and each ADC has undergone extensive preclinical testing and has completed phase 1 testing in men with advanced prostate cancer. The preclinical and clinical findings have largely substantiated the promise of PSMA as an ADC target. This report summarizes the completed studies, current status, and potential future directions for ADCs that target PSMA.
    Frontiers in Bioscience 01/2014; 19:12-33.
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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.
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    ABSTRACT: MicroRNAs (miRNAs) are small noncoding RNA molecules present in all cell types, with sizes that vary from 18 to 28 nucleotides. miRNAs play significant roles in several biological processes, including development, differentiation, metabolism, initiation, and progression of cancer. In recent years, considerable research has been directed towards identifying miRNAs in peripheral blood from circulating tumor cells and disseminating tumor cells. Because these circulatory miRNAs are very stable and reproducible, their identification could be useful as prognostic markers as well as therapeutic agents for many cancers such as breast cancer. In this article, we review the role of specific circulatory miRNAs in breast cancer, with particular emphasis on their clinical importance.
    Frontiers in Bioscience 01/2014; 19:1-11.
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    ABSTRACT: Bone is continuously renewed through a dynamic balance between bone resorption and formation and is the fundamental basis for maintaining normal bone mass and architecture by osteoclasts (bone resorption) and osteoblasts (bone formation). Bone resorption is an elementary cellular activity in the modeling of the skeleton during growth and development. Later in life, bone remodeling occurs, and is locally initiated by resorption. During remodeling, bone resorption is coupled to new bone formation, that ensures bone renewal with only minor and temporary local bone loss. Osteoclasts play a crucial role in both physiological and pathological bone resorption, and receptor activator of nuclear factor-κB ligand is the key cytokine that induces osteoclastogenesis. At the same time, various factors produced during immune responses are capable of profoundly affecting bone regulation; bone and immune systems share an abundance of molecules and regulatory mechanisms. We summarize the new insights on the link between osteoclastogenesis and osteoimmunology.
    Frontiers in Bioscience 01/2014; 19:758-67.
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    ABSTRACT: Endothelial progenitor cells (EPCs) play a fundamental role in the maintenance and repair of damaged vascular endothelium, as well as in new blood vessel formation. Based on this function of EPCs, it has been hypothesized that transfusion of these cells could be an approach to treat vascular disease. While this concept has subsequently been proven in animal models clinical trials have not been encouraging. These discrepancies have limited translation of EPCs from bench to bedside. In this review, by analyzing the reported data from the animal models and clinical trials, we describe the main factors limiting the clinical effects of EPCs infusion and the unfavorable in vivo reactions of the receipts. To facilitate future clinical application of EPCs, a series of strategy to overcome the obstacles have been suggested.
    Frontiers in Bioscience 01/2014; 19:34-48.
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    ABSTRACT: Rapamycin, a macrolide antibiotic, has potent immunosuppressive properties as an antirejection therapy in organ transplantation. Studies show that dendritic cells (DC) are important targets for rapamycin, which can inhibit DC maturation and DC-induced allogeneic T cell proliferation. In this study, we investigated the effects of rapamycin on the expressions of DC-SIGN and transcription factor PU.1 and the function of DC. Treatment with rapamycin significantly reduced the expression of DC-SIGN in a dose-dependent manner associated with suppression of PU.1 gene expression and the ability of DC to migrate and stimulate T cell proliferation. The expression of DC-SIGN was significantly suppressed using PU.1 siRNA. Intriguingly, rapamycin treatment largely decreased the expressions of PU.1 and DC-SIGN in THP-1 cells. In addition, treatment with rapamycin down-regulated the promoter activity of DC-SIGN. In conclusion, rapamycin inhibits DC-SIGN expression and suppresses the ability of DC to migrate and stimulate T cell proliferation through the PU.1 gene transcription pathway.
    Frontiers in Bioscience 01/2014; 19:557-65.
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    ABSTRACT: The role of lymphocytes in eliminating lymphoma cells is based on the interaction between activating receptors on lymphocytes and target surface ligands on lymphoma cells. Stress-related immunity can be triggered both in Hodgkin's (HL) and non-Hodgkin lymphomas (NHL), through the activation of the NKG2D receptor on CD8+ T and gammadelta T lymphocytes, by NKG2D-ligands (NKG2D-L), as the MHC class-I related molecules MIC-A/B and the UL16-binding proteins 1-4 (ULBPs), expressed on lymphoma cells. Furthermore, NKG2D-L can be shed and interact with NKG2D on effector lymphocytes affecting the recognition of lymphoma cells. Proteolytic cleavage of MIC-A is known to depend on the thiol isomerase ERp5 and the disintegrins and metalloproteinases ADAM10 and ADAM17, which also cleave ULPBs. Mesenchymal stromal cells (MSC) are relevant in regulating effector T lymphocytes-mediated lymphoma surveillance. Indeed, MSC can be seen as targets of potential new therapeutic schemes acting on lymphoma microenvironment, to redirect the stress immune response and avoid escape strategies, by inducing stress molecules, inhibiting sheddase activity, shifting cytokine production to Th1 pattern and blocking Treg differentiation.
    Frontiers in Bioscience 01/2014; 19:281-90.

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