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Author |
Khushi, M.; Liddle, C.; Clarke, C.L.; Graham, J.D. |
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Title |
Binding sites analyser (BiSA): software for genomic binding sites archiving and overlap analysis |
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Journal Article |
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Year |
2014 |
Publication |
PloS one |
Abbreviated Journal |
PLoS One |
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Volume |
9 |
Issue |
2 |
Pages  |
e87301 |
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Abstract |
Genome-wide mapping of transcription factor binding and histone modification reveals complex patterns of interactions. Identifying overlaps in binding patterns by different factors is a major objective of genomic studies, but existing methods to archive large numbers of datasets in a personalised database lack sophistication and utility. Therefore we have developed transcription factor DNA binding site analyser software (BiSA), for archiving of binding regions and easy identification of overlap with or proximity to other regions of interest. Analysis results can be restricted by chromosome or base pair overlap between regions or maximum distance between binding peaks. BiSA is capable of reporting overlapping regions that share common base pairs; regions that are nearby; regions that are not overlapping; and average region sizes. BiSA can identify genes located near binding regions of interest, genomic features near a gene or locus of interest and statistical significance of overlapping regions can also be reported. Overlapping results can be visualized as Venn diagrams. A major strength of BiSA is that it is supported by a comprehensive database of publicly available transcription factor binding sites and histone modifications, which can be directly compared to user data. The documentation and source code are available on http://bisa.sourceforge.net. |
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Westmead Institute for Cancer Research, Sydney Medical School, University of Sydney and the Westmead Millennium Institute, Westmead, New South Wales, Australia |
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1932-6203 |
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PMID:24533055 |
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no |
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Call Number |
CBM.UAM @ ccobaleda @ |
Serial |
535 |
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Author |
Nie, Y.; Chen, Y.; Mou, Y.; Weng, L.; Xu, Z.; Du, Y.; Wang, W.; Hou, Y.; Wang, T. |
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Title |
Low frequency magnetic fields enhance antitumor immune response against mouse H22 hepatocellular carcinoma |
Type |
Journal Article |
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Year |
2013 |
Publication |
PloS one |
Abbreviated Journal |
PLoS One |
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Volume |
8 |
Issue |
11 |
Pages |
e72411 |
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Keywords |
Adaptive Immunity/physiology; Animals; Carcinoma, Hepatocellular/blood/*immunology/*therapy; Cell Line, Tumor; Cell Survival/physiology; Cytokines/blood; Female; Flow Cytometry; Immunity, Innate/physiology; Immunohistochemistry; Liver Neoplasms/blood/*immunology/*therapy; *Magnetic Fields; Mice; Mice, Inbred BALB C; Real-Time Polymerase Chain Reaction; T-Lymphocytes/immunology |
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Abstract |
OBJECTIVE: Many studies have shown that magnetic fields (MF) inhibit tumor growth and influence the function of immune system. However, the effect of MF on mechanism of immunological function in tumor-bearing mice is still unclear. METHODS: In this study, tumor-bearing mice were prepared by subcutaneously inoculating Balb/c mice with hepatocarcinoma cell line H22. The mice were then exposed to a low frequency MF (0.4 T, 7.5 Hz) for 30 days. Survival rate, tumor growth and the innate and adaptive immune parameters were measured. RESULTS: MF treatment could prolong survival time (n = 28, p<0.05) and inhibit tumor growth (n = 9, p<0.01) in tumor-bearing mice. Moreover, this MF suppressed tumor-induced production of cytokines including interleukin-6 (IL-6), granulocyte colony- stimulating factor (G-CSF) and keratinocyte-derived chemokine (KC) (n = 9-10, p<0.05 or 0.01). Furthermore, MF exposure was associated with activation of macrophages and dendritic cells, enhanced profiles of CD4(+) T and CD8(+) T lymphocytes, the balance of Th17/Treg and reduced inhibitory function of Treg cells (n = 9-10, p<0.05 or 0.01) in the mice model. CONCLUSION: The inhibitory effect of MF on tumor growth was related to the improvement of immune function in the tumor-bearing mice. |
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State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing, China |
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1932-6203 |
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PMID:24278103 |
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CBM.UAM @ ccobaleda @ |
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599 |
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Author |
Mo, W.-chuan; Zhang, Z.-jian; Liu, Y.; Bartlett, P.F.; He, R.-qiao |
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Title |
Magnetic shielding accelerates the proliferation of human neuroblastoma cell by promoting G1-phase progression |
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Journal Article |
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Year |
2013 |
Publication |
PloS one |
Abbreviated Journal |
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8 |
Issue |
1 |
Pages |
e54775-e54775 |
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Keywords |
Cell Division; Cell Line, Tumor; G1 Phase; G2 Phase; Humans; Magnetic Fields; Neuroblastoma; Neuroblastoma: metabolism; Neuroblastoma: pathology |
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Organisms have been exposed to the geomagnetic field (GMF) throughout evolutionary history. Exposure to the hypomagnetic field (HMF) by deep magnetic shielding has recently been suggested to have a negative effect on the structure and function of the central nervous system, particularly during early development. Although changes in cell growth and differentiation have been observed in the HMF, the effects of the HMF on cell cycle progression still remain unclear. Here we show that continuous HMF exposure significantly increases the proliferation of human neuroblastoma (SH-SY5Y) cells. The acceleration of proliferation results from a forward shift of the cell cycle in G1-phase. The G2/M-phase progression is not affected in the HMF. Our data is the first to demonstrate that the HMF can stimulate the proliferation of SH-SY5Y cells by promoting cell cycle progression in the G1-phase. This provides a novel way to study the mechanism of cells in response to changes of environmental magnetic field including the GMF. |
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WP5 In vitro |
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UNIBAS @ david.schuermann @ |
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565 |
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Author |
Walters, Z.B. |
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Title |
Quantum dynamics of the avian compass |
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Journal Article |
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Year |
2014 |
Publication |
Physical Review. E, Statistical, Nonlinear, and Soft Matter Physics |
Abbreviated Journal |
Phys Rev E Stat Nonlin Soft Matter Phys |
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90 |
Issue |
4 |
Pages |
042710 |
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Abstract |
The ability of migratory birds to orient relative to the Earth's magnetic field is believed to involve a coherent superposition of two spin states of a radical electron pair. However, the mechanism by which this coherence can be maintained in the face of strong interactions with the cellular environment has remained unclear. This paper addresses the problem of decoherence between two electron spins due to hyperfine interaction with a bath of spin-1/2 nuclei. Dynamics of the radical pair density matrix are derived and shown to yield a simple mechanism for sensing magnetic field orientation. Rates of dephasing and decoherence are calculated ab initio and found to yield millisecond coherence times, consistent with behavioral experiments. |
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Max Planck Institute for Physics of Complex Systems, Nothnitzer Strasse 38, D-01187 Dresden, Germany |
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1539-3755 |
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PMID:25375526 |
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no |
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Call Number |
CBM.UAM @ ccobaleda @ |
Serial |
537 |
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Author |
Vincenzi, F.; Targa, M.; Corciulo, C.; Gessi, S.; Merighi, S.; Setti, S.; Cadossi, R.; Borea, P.A.; Varani, K. |
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The anti-tumor effect of A3 adenosine receptors is potentiated by pulsed electromagnetic fields in cultured neural cancer cells |
Type |
Journal Article |
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Year |
2012 |
Publication |
PloS one |
Abbreviated Journal |
PLoS One |
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Volume |
7 |
Issue |
6 |
Pages |
e39317 |
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Keywords |
Animals; Apoptosis/genetics; Brain Neoplasms/*genetics/metabolism; Caspase 3/genetics/metabolism; Cell Line, Tumor; *Electromagnetic Fields; Humans; NF-kappa B/genetics/metabolism; Neurons/*metabolism; PC12 Cells; Rats; Receptor, Adenosine A2A/genetics/metabolism; Receptor, Adenosine A3/*genetics/metabolism; Tumor Cells, Cultured; Up-Regulation |
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Abstract |
A(3) adenosine receptors (ARs) play a pivotal role in the development of cancer and their activation is involved in the inhibition of tumor growth. The effects of pulsed electromagnetic fields (PEMFs) on cancer have been controversially discussed and the detailed mechanisms are not yet fully understood. In the past we have demonstrated that PEMFs increased A(2A) and A(3)AR density and functionality in human neutrophils, human and bovine synoviocytes, and bovine chondrocytes. In the same cells, PEMF exposure increased the anti-inflammatory effect mediated by A(2A) and/or A(3)ARs. The primary aim of the present study was to evaluate if PEMF exposure potentiated the anti-tumor effect of A(3)ARs in PC12 rat adrenal pheochromocytoma and U87MG human glioblastoma cell lines in comparison with rat cortical neurons. Saturation binding assays and mRNA analysis revealed that PEMF exposure up-regulated A(2A) and A(3)ARs that are well coupled to adenylate cyclase activity and cAMP production. The activation of A(2A) and A(3)ARs resulted in the decrease of nuclear factor-kappa B (NF-kB) levels in tumor cells, whilst only A(3)ARs are involved in the increase of p53 expression. A(3)AR stimulation mediated an inhibition of tumor cell proliferation evaluated by thymidine incorporation. An increase of cytotoxicity by lactate dehydrogenase (LDH) release and apoptosis by caspase-3 activation in PC12 and U87MG cells, but not in cortical neurons, was observed following A(3)AR activation. The effect of the A(3)AR agonist in tumor cells was enhanced in the presence of PEMFs and blocked by using a well-known selective antagonist. Together these results demonstrated that PEMF exposure significantly increases the anti-tumor effect modulated by A(3)ARs. |
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Department of Clinical and Experimental Medicine, Pharmacology Unit, University of Ferrara, Ferrara, Italy |
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1932-6203 |
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PMID:22761760 |
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Call Number |
IT'IS @ evaj @ |
Serial |
427 |
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