1,200 research outputs found

    M(atrix) Theory on an Orbifold and Twisted Membrane

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    M(atrix) theory on an orbifold and classical two-branes therein are studied with particular emphasis to heterotic M(atrix) theory on S1/Z2S_1/Z_2 relevant to strongly coupled heterotic and dual Type IA string theories. By analyzing orbifold condition on Chan-Paton factors, we show that three choice of gauge group are possible for heterotic M(atrix) theory: SO(2N), SO(2N+1) or USp(2N). By examining area-preserving diffeomorphism that underlies the M(atrix) theory, we find that each choices of gauge group restricts possible topologies of two-branes. The result suggests that only the choice of SO(2N) or SO(2N+1) groups allows open two-branes, hence, relevant to heterotic M(atrix) theory. We show that requirement of both local vacuum energy cancellation and of worldsheet anomaly cancellation of resulting heterotic string identifies supersymmetric twisted sector spectra with sixteen fundamental representation spinors from each of the two fixed points. Twisted open and closed two-brane configurations are obtained in the large N limit.Comment: latex, 23 pages, version to appear in Nuclear Physics

    A novel and efficient synthesis of the naturally occurring nucleoside doridosine

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    1-Methylisoguanosine was synthesized by a one-pot reaction involving a condensation of 5-amino-1-([beta]--ribofuranosyl)imidazole-4-carboxamide (1) with methyl isothiocyanate, treatment of the resulting thiourea derivative with DCC furnished 5-(3-methyl-1-ureido)-1-([beta]--ribofuranosyl)imidazole-4-carbonitrile (4) which was then annulated with ethanolic ammonia to furnish doridosine in a 68% yield from 1.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/25938/1/0000501.pd

    Direct numerical simulation of a 30R long turbulent pipe flow at Re=3008

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    A direct numerical simulation of a turbulent pipe flow at a high Reynolds number of Re-tau = 3008 over a long axial domain length (30R) was performed. The stream-wise mean velocity followed the power law in the overlap region (y(+) = 90-300; y/R = 0.03-0.1) based on the power law indicator function. The scale separation of the Reynolds shear stresses into two components of small-and large-scale motions (LSMs) revealed that the LSMs in the outer region played an important role in constructing the constant-stress layer and the mean velocity. In the pre-multiplied energy spectra of the streamwise velocity fluctuations, the bimodal distribution was observed at both short and long wavelengths. The k(x)(-1) region associated with the attached eddies appeared in lambda(x)/R = 2-5 and lambda(x)/y = 18-160 at y(+) = 90-300, where the power law was established in the same region. The k(z)(-1) region also appeared in lambda(z)/R = 0.3-0.6 at y(+) = 3 and 150. Linear growth of small-scale energy to large-scale energy induced the k(x)(-1) region at high Reynolds numbers, resulting in a large population of the LSMs. This result supported the origin of very-large-scale motions in the pseudo-streamwise alignment of the LSMs. In the pre-multiplied energy spectra of the Reynolds shear stress, the bimodal distribution was observed without the k(x)(-1) region.open

    Influence of ocean freshening on shelf phytoplankton dynamics

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    Author Posting. © American Geophysical Union, 2007. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Geophysical Research Letters 34 (2007): L24607, doi:10.1029/2007GL032010.Climate change-induced freshening of the ocean can enhance vertical stratification and alter circulation patterns in ways that influence phytoplankton dynamics. We examined the timing of spring phytoplankton blooms and the magnitude of net primary productivity in the Nova Scotian Shelf (NSS) - Gulf of Maine (GoM) region with respect to seasonal and interannual changes in surface water freshening from 1998 to 2006. The general pattern of temporal westward progression of the phytoplankton bloom corresponds with the gradient of increasing sea surface salinity from the NSS in the east to the western GoM. Increased freshening enhances the spatial gradients in bloom timing by stimulating earlier blooms upstream (NSS), but it has less impact downstream (the western GoM). Strong spatial gradients (increasing westward) of mean chlorophyll concentration and net primary productivity during post-bloom months (May–June) indicate that lower sea surface salinity upstream can likely impede nutrient fluxes from deep water and therefore affect overall productivity.We thank NSF grant OCE-0727033 and NOAA grant NA17RJ1223 to RJ, CSD and RCB, NSF grants OCE- 0606612 and OCE-0726577 to DWT, and NSF grants OCE-0606928 and OCE-0726851 to CC

    The seasonal nitrogen cycle in Wilkinson Basin, Gulf of Maine, as estimated by 1-D biological model optimization

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    Author Posting. © Elsevier B.V., 2009. This is the author's version of the work. It is posted here by permission of Elsevier B.V. for personal use, not for redistribution. The definitive version was published in Journal of Marine Systems 78 (2009): 77-93, doi:10.1016/j.jmarsys.2009.04.001.The objective of this study was to fit a simple ecosystem model to climatological nitrogen cycle data in the Gulf of Maine, in order to calibrate the biological model for use in future 3-D modelling studies. First depth-dependent monthly climatologies of nitrate, ammonium, chlorophyll, zooplankton, detritus and primary production data from Wilkinson Basin, Gulf of Maine, were created. A 6-box nitrogen-based ecosystem model was objectively fitted to the data through parameter optimization. Optimization was based on weighted least squares with model-data misfits nondi- mensionalized by assigned uncertainties in the monthly climatological estimates. These uncertainties were estimated as the standard deviations of the raw data from the 6-meter and monthly bin averages. On average the model fits the monthly means almost within their assigned uncertainties. Several statistics are examined to assess model-data misfit. Pattern statistics such as the correlation coefficient lack practical significance when data errors are large relative to the signal, as in this application. Thus Taylor diagrams were not found to be useful. The RMSE and model bias normalized by the data error were found to be the most useful skill metrics as they indicate whether the model fits the data within its estimated error. The optimal simulated nitrogen cycle budgets are presented, as an estimate of the seasonal nitrogen cycle in Wilkinson Basin, and discussed in context of the available data.Wilkinson Basin has spring and fall phytoplankton blooms, and strong summer stratification with a deep chlorophyll maximum near 21 m, just above the nitracline. The mean euphotic zone depth is estimated to be 25 m, relatively constant with season. The model estimates annual primary production as 176 g C m−2 yr−1, annual new production as 71 g C m−2 yr−1 and sinking PON fluxes of 9.7 and 4.7 g N m−2 yr−1 at 24 and 198 m respectively. Areas for improvement in the biological model, the model optimization method, and significant data gaps are identified.This work was supported by ONR, NSF, and NOAA grant to Dennis McGillicuddy

    Neurotensin Receptor 3/Sortilin Contributes to Tumorigenesis of Neuroendocrine Tumors Through Augmentation of Cell Adhesion and Migration

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    Neurotensin (NTS), a 13–amino acid peptide which is distributed predominantly along gastrointestinal tract, has multiple physiologic and pathologic functions, and its effects are mediated by three distinct NTS receptors (NTSRs). Overexpression and activation of NTS signaling components, especially NTS and/or NTSR1, are closely linked with cancer progression and metastasis in various types of cancers including neuroendocrine tumors (NETs). Although deregulation of NTSR3/sortilin has been implicated in a variety of human diseases, the expression and role of NTSR3/sortilin in NETs have not been elucidated. In this study, we investigated the expression and oncogenic effect of NTSR3/sortilin in NETs. Increased protein levels of NTSR3/sortilin were noted in the majority of human clinical NETs (n = 21) by immunohistochemical analyses compared with normal tissues (n = 12). Expression of NTS and NTSR3/sortilin was also noted in all tested NET cell lines. In addition, small interfering RNA–mediated knockdown of NTSR3/sortilin decreased cell number without alteration of cell cycle progression and apoptosis induction in NET cell lines BON and QGP-1. Moreover, silencing of NTSR3/sortilin significantly suppressed cell adhesion and cell migration with inhibition of focal adhesion kinase and Src phosphorylation in the NET cells. Our results demonstrate increased expression of NTSR3/sortilin in NET patient tissues and a critical role of NTSR3/sortilin on NET cell adhesion and migration suggesting that NTSR3/sortilin contributes to NET tumorigenesis

    Differential Expression and Tumorigenic Function of Neurotensin Receptor 1 in Neuroendocrine Tumor Cells

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    Neurotensin (NTS), localized predominantly to the small bowel, stimulates the growth of a variety of cancers, including neuroendocrine tumors (NETs), mainly through its interaction with the high-affinity NTS receptor 1 (NTSR1). Here, we observed increased expression of NTSR1 in almost all tested clinical NET samples, but not in normal tissues. Through RT-PCR analysis, we found that the expression of NTSR1 and NTSR2 was either variable (NTSR1) or absent (NTSR2) in human NET cell lines. In contrast, NTSR3 and NTS were expressed in all NET cells. Treatment with 5-aza-2\u27-deoxycytidine, a demethylating agent, increased levels of NTSR1 and NTSR2 suggesting that DNA methylation contributes to NTSR1/2 expression patterns, which was confirmed by methylation analyses. In addition, we found that knockdown of NTSR1 decreased proliferation, expression levels of growth-related proteins, and anchorage-independent growth of BON human carcinoid cells. Moreover, stable silencing of NTSR1 suppressed BON cell growth, adhesion, migration and invasion. Our results show that high expression of NTSR1 is found in clinical NETs and that promoter methylation is an important mechanism controlling the differential expression of NTSR1 and silencing of NTSR2 in NET cells. Furthermore, knockdown of NTSR1 in BON cells suppressed oncogenic functions suggesting that NTSR1 contributes to NET tumorigenesis

    Georges Bank : a leaky incubator of Alexandrium fundyense blooms

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    Author Posting. © The Author(s), 2012. This is the author's version of the work. It is posted here by permission of Elsevier B.V. for personal use, not for redistribution. The definitive version was published in Deep Sea Research Part II: Topical Studies in Oceanography 103 (2014): 163-173, doi:10.1016/j.dsr2.2012.11.002.A series of oceanographic surveys on Georges Bank document variability of populations of the toxic dinoflagellate Alexandrium fundyense on time scales ranging from synoptic to seasonal to interannual. Blooms of A. fundyense on Georges Bank can reach concentrations on the order of 104 cells l-1, and are generally bank-wide in extent. Georges Bank populations of A. fundyense appear to be quasi-independent of those in the adjacent coastal Gulf of Maine, insofar as they occupy a hydrographic niche that is colder and saltier than their coastal counterparts. In contrast to coastal populations that rely on abundant resting cysts for bloom initiation, very few cysts are present in the sediments on Georges Bank. Bloom dynamics must therefore be largely controlled by the balance between growth and mortality processes, which are at present largely unknown for this population. Based on correlations between cell abundance and nutrient distributions, ammonium appears to be an important source of nitrogen for A. fundyense blooms on Georges Bank.We appreciate financial support of the National Oceanic Atmospheric Administration (grant NA06NOS4780245 for the Gulf of Maine Toxicity (GOMTOX) program) and the Woods Hole Center for Oceans and Human Health through National Science Foundation grants OCE-0430724 and OCE-0911031 and National Institute of Environmental Health Sciences grant 1P50-ES01274201
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