303 research outputs found

    Dopant-induced crossover from 1D to 3D charge transport in conjugated polymers

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    The interplay between inter- and intra-chain charge transport in bulk polythiophene in the hopping regime has been clarified by studying the conductivity as a function of frequency (up to 3 THz), temperature and doping level. We present a model which quantitatively explains the observed crossover from quasi-one-dimensional transport to three-dimensional hopping conduction with increasing doping level. At high frequencies the conductivity is dominated by charge transport on one-dimensional conducting chains.Comment: 4 pages, 2 figure

    Search for Millicharged Particles at SLAC

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    Particles with electric charge q < 10^(-3)e and masses in the range 1--100 MeV/c^2 are not excluded by present experiments. An experiment uniquely suited to the production and detection of such "millicharged" particles has been carried out at SLAC. This experiment is sensitive to the infrequent excitation and ionization of matter expected from the passage of such a particle. Analysis of the data rules out a region of mass and charge, establishing, for example, a 95%-confidence upper limit on electric charge of 4.1X10^(-5)e for millicharged particles of mass 1 MeV/c^2 and 5.8X10^(-4)e for mass 100 MeV/c^2.Comment: 4 pages, REVTeX, multicol, 3 figures. Minor typo corrected. Submitted to Physical Review Letter

    Ranking of Fuzzy Similar Faces Using Relevance Matrix and Aggregation Operators

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    AbstractIn perception based imaging, Sketching With Words (SWW) is a well-established methodology in which the objects of computation are fuzzy geometric objects (f-objects).The problem of facial imaging of criminal on the basis of onlooker statement is not lack of method and measures but the modeling of onlooker(s) mind set. Because the onlooker has to give statements about different human face parts like forehead, eyes, nose, and chin etc.The concept of fuzzy similarity (f-similarity) and proper aggregation of components of face may provide more flexibility to onlooker(s). In proposed work onlooker(s) statement is recorded. Thereafter it is compared with existing statements. The f-similarity with different faces in database is estimated by using ‘as many as possible’ linguistic quantifier. Three types of constraints over size of parts of face ‘small’, ‘medium’, and ‘large’ are considered. Possibilistic constraints with linguistic hedges and negation operator like ‘very long’, ‘not long’, ‘not very long’ etc. are used. Moreover we have generated ranking of alike faces in decreasing order by using the concepts of f-similarity and relevance matrix

    Novel tumor suppressive function of Smad4 in serum starvation-induced cell death through PAK1–PUMA pathway

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    DPC4 (deleted in pancreatic cancer 4)/Smad4 is an essential factor in transforming growth factor (TGF)-β signaling and is also known as a frequently mutated tumor suppressor gene in human pancreatic and colon cancer. However, considering the fact that TGF-β can contribute to cancer progression through transcriptional target genes, such as Snail, MMPs, and epithelial–mesenchymal transition (EMT)-related genes, loss of Smad4 in human cancer would be required for obtaining the TGF-β signaling-independent advantage, which should be essential for cancer cell survival. Here, we provide the evidences about novel role of Smad4, serum-deprivation-induced apoptosis. Elimination of serum can obviously increase the Smad4 expression and induces the cell death by p53-independent PUMA induction. Instead, Smad4-deficient cells show the resistance to serum starvation. Induced Smad4 suppresses the PAK1, which promotes the PUMA destabilization. We also found that Siah-1 and pVHL are involved in PAK1 destabilization and PUMA stabilization. In fact, Smad4-expressed cancer tissues not only show the elevated expression of PAK1, but also support our hypothesis that Smad4 induces PUMA-mediated cell death through PAK1 suppression. Our results strongly suggest that loss of Smad4 renders the resistance to serum-deprivation-induced cell death, which is the TGF-β-independent tumor suppressive role of Smad4

    Search for high-mass narrow resonances in virtual photon-photon interactions

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    LKB1 as the ghostwriter of crypt history

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    Familial cancer syndromes present rare insights into malignant tumor development. The molecular background of polyp formation and the cancer prone state in Peutz-Jeghers syndrome remain enigmatic to this day. Previously, we proposed that Peutz-Jeghers polyps are not pre-malignant lesions, but an epiphenomenon to the malignant condition. However, Peutz-Jeghers polyp formation and the cancer-prone state must both be accounted for by the same molecular mechanism. Our contribution focuses on the histopathology of the characteristic Peutz-Jeghers polyp and recent research on stem cell dynamics and how these concepts relate to Peutz-Jeghers polyposis. We discuss a protracted clonal evolution scenario in Peutz-Jeghers syndrome due to a germline LKB1 mutation. Peutz-Jeghers polyp formation and malignant transformation are separately mediated through the same molecular mechanism played out on different timescales. Thus, a single mechanism accounts for the development of benign Peutz-Jeghers polyps and for malignant transformation in Peutz-Jeghers syndrome
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