16 research outputs found

    Id1 Promotes Tumor Cell Migration in Nonsmall Cell Lung Cancers

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    Id1, which belongs to the Id family of helix-loop-helix transcription factors has been most associated with tumor progression and metastatsis; however, its significance in lung cancers has not been extensively explored. Here we seek to evaluate the expression of Id1 in a pilot study of nonsmall-cell lung cancers (NSCLCs) and determine its diagnostic and functional significance in these tumors. Paired normal and malignant lung tissues as well as a panel of NSCLC primary tumors and cell lines were evaluated for Id1 expression using Western blotting and quantitative RT-PCR. Functional assays were performed to evaluate the role of Id1 in tumor cell growth, migration and progression. We find Id1 expression is upregulated in squamous cell carcinoma when compared to adenocarcinoma of the lung and that expression of Id1 versus the normal control is variable in NSCLCs. We also note that Id1 expression in NSCLC cells is largely growth factor dependant and constitutive expression of Id1 in NSCLC cells significantly increases tumor cell migration without affecting cell proliferation. We conclude that Id1, as a mediator of tumor cell migration, may be an indicator of aggressive potential in nonsmall-cell lung cancers

    Strange Pulsar Hypothesis

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    It appears that there is a genuine shortage of radio pulsars with surface magnetic fields significantly smaller than 108\sim 10^8 Gauss. We propose that the pulsars with very low magnetic fields are actually strange stars locked in a state of minimum free energy and therefore at a limiting value of the magnetic field which can not be lowered by the system spontaneously.Comment: 4 pages, 1 figure, uses LaTeX2e(mn2e.cls) and astrobib(mnras.bst), accepted in MNRA

    The micro-glitch in PSR B1821-24 : A case for a strange pulsar?

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    The single glitch observed in PSR B1821-24, a millisecond pulsar in M28, is unusual on two counts. First, the magnitude of this glitch is at least an order of magnitude smaller (Δν/ν1011\Delta \nu / \nu \sim 10^{-11}) than the smallest glitch observed to date. Secondly, all other glitching pulsars have strong magnetic fields with B \gsim 10^{11} G and are young, whereas PSR B1821-24 is an old recycled pulsar with a field strength of 2.25×109G2.25\times10^9 G. We have suggested earlier that some of the recycled pulsars could actually be strange quark stars. In this work we argue that the crustal properties of such a {\em strange} pulsar are just right to give rise to a glitch of this magnitude, explaining the scarcity of larger glitches in millisecond pulsars.Comment: 5 pages, 5 figures, uses LaTeX2e(mn2e.cls) and astrobib(mn2e.bst): text substantially modified, to be published in MNRA

    Id1 Promotes Tumor Cell Migration in Nonsmall Cell Lung Cancers

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    Id1, which belongs to the Id family of helix-loop-helix transcription factors has been most associated with tumor progression and metastatsis; however, its significance in lung cancers has not been extensively explored. Here we seek to evaluate the expression of Id1 in a pilot study of nonsmall-cell lung cancers (NSCLCs) and determine its diagnostic and functional significance in these tumors. Paired normal and malignant lung tissues as well as a panel of NSCLC primary tumors and cell lines were evaluated for Id1 expression using Western blotting and quantitative RT-PCR. Functional assays were performed to evaluate the role of Id1 in tumor cell growth, migration and progression. We find Id1 expression is upregulated in squamous cell carcinoma when compared to adenocarcinoma of the lung and that expression of Id1 versus the normal control is variable in NSCLCs. We also note that Id1 expression in NSCLC cells is largely growth factor dependant and constitutive expression of Id1 in NSCLC cells significantly increases tumor cell migration without affecting cell proliferation. We conclude that Id1, as a mediator of tumor cell migration, may be an indicator of aggressive potential in nonsmall-cell lung cancers

    Familial hemophagocytic lymphohistiocytosis

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    The HMG-I

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