543 research outputs found

    Hamilton - Jacobi treatment of front-form Schwinger model

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    The Hamilton-Jacobi formalism was applied to quantize the front-form Schwinger model. The importance of the surface term is discussed in detail. The BRST-anti-BRST symmetry was analyzed within Hamilton-Jacobi formalism.Comment: 11 pages, to be published in Int. Journ. Mod. Phys.

    Geometrical dynamics of Born-Infeld objects

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    We present a geometrical inspired study of the dynamics of DpDp-branes. We focus on the usual nonpolynomial Dirac-Born-Infeld action for the worldvolume swept out by the brane in its evolution in general background spacetimes. We emphasize the form of the resulting equations of motion which are quite simple and resemble Newton's second law, complemented with a conservation law for a worldvolume bicurrent. We take a closer look at the classical Hamiltonian analysis which is supported by the ADM framework of general relativity. The constraints and their algebra are identified as well as the geometrical role they play in phase space. In order to illustrate our results, we review the dynamics of a D1D1-brane immersed in a AdS3×S3AdS_3 \times S^3 background spacetime. We exhibit the mechanical properties of Born-Infeld objects paving the way to a consistent quantum formulation.Comment: LaTex, 20 pages, no figure

    Essential role of MED1 in the transcriptional regulation of ER-dependent oncogenic miRNAs in breast cancer

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    Mediator complex has been extensively shown to regulate the levels of several protein-coding genes; however, its role in the regulation of miRNAs in humans remains unstudied so far. Here we show that MED1, a Mediator subunit in the Middle module of Mediator complex, is overexpressed in breast cancer and is a negative prognostic factor. The levels of several miRNAs (miR-100-5p, -191-5p, -193b-3p, -205-5p, -326, -422a and -425-5p) were found to be regulated by MED1. MED1 induces miR-191/425 cluster in an estrogen receptor-alpha (ER-\u3b1) dependent manner. Occupancy of MED1 on estrogen response elements (EREs) upstream of miR-191/425 cluster is estrogen and ER-\u3b1-dependent and ER-\u3b1-induced expression of these miRNAs is MED1-dependent. MED1 mediates induction of cell proliferation and migration and the genes associated with it (JUN, FOS, EGFR, VEGF, MMP1, and ERBB4) in breast cancer, which is abrogated when used together with miR-191-inhibition. Additionally, we show that MED1 also regulates the levels of direct miR-191 target genes such as SATB1, CDK6 and BDNF. Overall, the results show that MED1/ER-\u3b1/miR-191 axis promotes breast cancer cell proliferation and migration and may serve as a novel target for therapy

    Analysis of microRNA transcriptome by deep sequencing of small RNA libraries of peripheral blood

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    <p>Abstract</p> <p>Background</p> <p>MicroRNAs are a class of small non-coding RNAs that regulate mRNA expression at the post - transcriptional level and thereby many fundamental biological processes. A number of methods, such as multiplex polymerase chain reaction, microarrays have been developed for profiling levels of known miRNAs. These methods lack the ability to identify novel miRNAs and accurately determine expression at a range of concentrations. Deep or massively parallel sequencing methods are providing suitable platforms for genome wide transcriptome analysis and have the ability to identify novel transcripts.</p> <p>Results</p> <p>The results of analysis of small RNA sequences obtained by Solexa technology of normal peripheral blood mononuclear cells, tumor cell lines K562 and HL60 are presented. In general K562 cells displayed overall low level of miRNA population and also low levels of DICER. Some of the highly expressed miRNAs in the leukocytes include several members of the let-7 family, miR-21, 103, 185, 191 and 320a. Comparison of the miRNA profiles of normal versus K562 or HL60 cells revealed a specific set of differentially expressed molecules. Correlation of the miRNA with that of mRNA expression profiles, obtained by microarray, revealed a set of target genes showing inverse correlation with miRNA levels. Relative expression levels of individual miRNAs belonging to a cluster were found to be highly variable. Our computational pipeline also predicted a number of novel miRNAs. Some of the predictions were validated by Real-time RT-PCR and or RNase protection assay. Organization of some of the novel miRNAs in human genome suggests that these may also be part of existing clusters or form new clusters.</p> <p>Conclusions</p> <p>We conclude that about 904 miRNAs are expressed in human leukocytes. Out of these 370 are novel miRNAs. We have identified miRNAs that are differentially regulated in normal PBMC with respect to cancer cells, K562 and HL60. Our results suggest that post - transcriptional processes may play a significant role in regulating levels of miRNAs in tumor cells. The study also provides a customized automated computation pipeline for miRNA profiling and identification of novel miRNAs; even those that are missed out by other existing pipelines. The Computational Pipeline is available at the website: <url>http://mirna.jnu.ac.in/deep_sequencing/deep_sequencing.html</url></p

    Chiral Bosons Through Linear Constraints

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    We study in detail the quantization of a model which apparently describes chiral bosons. The model is based on the idea that the chiral condition could be implemented through a linear constraint. We show that the space of states is of indefinite metric. We cure this disease by introducing ghost fields in such a way that a BRST symmetry is generated. A quartet algebra is seen to emerge. The quartet mechanism, then, forces all physical states, but the vacuum, to have zero norm.Comment: 9 page

    Chiral bosons and improper constraints

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    We argue that a consistent quantization of the Floreanini-Jackiw model, as a constrained system, should start by recognizing the improper nature of the constraints. Then each boundary conditon defines a problem which must be treated sparately. The model is settled on a compact domain which allows for a discrete formulation of the dynamics; thus, avoiding the mixing of local with collective coordinates. For periodic boundary conditions the model turns out to be a gauge theory whose gauge invariant sector contains only chiral excitations. For antiperiodoc boundary conditions, the mode is a second-class theory where the excitations are also chiral. In both cases, the equal-time algebra of the quantum energy-momentum densities is a Virasoro algebra. The Poincar\'e symmetry holds for the finite as well as for the infinite domain.Comment: 13 pages, Revtex file, IF.UFRGS Preprin

    miR-22 regulates expression of oncogenic neuro-epithelial transforming gene 1, NET1

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    MicroRNAs control cellular processes by regulating expression of their target genes. Here we report that neuro-epithelial transforming gene 1 (NET1) is a target of tumor suppressor microRNA 22 (miR-22). miR-22 is downregulated in peripheral blood mononuclear cells derived from chronic myeloid leukemia (CML) patients and in CML cell line K562. NET1 was identified as one of the targets of miR-22 using both in vitro and in vivo experiments. Either mutations or naturally occurring single-nucleotide polymorphisms in NET1 3′-UTR that map at the miR-22 binding site were found to affect binding of miR-22 to NET1 mRNA. Over expression of NET1 in K562 cells resulted in increased proliferation. However decreased proliferation and alteration in cell cycle were observed on either overexpression of miR-22 or knockdown of NET1 expression respectively. We also found that overexpression of miR-22 or NET1 knockdown inhibits actin fiber formation, probably by downregulation of NET1 as NET1 knockdown also resulted in depletion of actin fiber formation. We suggest that the oncogenic properties of CML cells are probably due to deregulated expression of NET1 as a result of altered expression of miR-22
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