2,556 research outputs found

    Vascular Flora of Hooper Branch Savanna Nature Preserve, Iroquois County, Illinois

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    INHS Technical Report prepared for Illinois Department of Natural Resources, Division of Natural Heritag

    Physical Activity Measures in the Healthy Communities Study

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    The risk of obesity is reduced when youth engage in recommended levels of physical activity (PA). For that reason, public health organizations in the U.S. have encouraged communities to implement programs and policies designed to increase PA in youth, and many communities have taken on that challenge. However, the long-term effects of those programs and policies on obesity are largely unknown. The Healthy Communities Study is a large-scale observational study of U.S. communities that is examining the characteristics of programs and policies designed to promote healthy behaviors (e.g., increase PA and improve diet) and determining their association with obesity-related outcomes. The purpose of this paper is to describe the methods used to measure PA in children and the personal and community factors that may influence it. The study used both self-reported and objective measures of PA, and measured personal, family, and home influences on PA via three constructs: (1) PA self-schema; (2) parental support; and (3) parental rules regarding PA. Neighborhood and community factors related to PA were assessed using three measures: (1) child perceptions of the neighborhood environment; (2) availability of PA equipment; and (3) attributes of the child’s street segment via direct observation. School influences on children’s PA were assessed via three constructs: (1) school PA policies; (2) child perceptions of the school PA environment; and (3) school outdoor PA environment. These measures will enable examination of the associations between characteristics of community PA programs and policies and obesity-related outcomes in children and youth

    Supersymmetric Noncommutative QED and Lorentz Violation

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    We consider Lorentz-violating operators induced at the loop level in softly-broken supersymmetric noncommutative QED. Dangerous operators forbidden in the supersymmetric limit are generated via finite corrections, with the scale of supersymmetry breaking serving as a gauge-invariant regulator. We compare the most dangerous loop effects to those obtained in noncommutative theories truncated by a momentum-space cutoff, and find significantly improved bounds.Comment: 11 pages LaTeX, 4 eps figure

    Coherent Electron Transport by Adiabatic Passage in an Imperfect Donor Chain

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    Coherent Tunneling Adiabatic Passage (CTAP) has been proposed as a long-range physical qubit transport mechanism in solid-state quantum computing architectures. Although the mechanism can be implemented in either a chain of quantum dots or donors, a 1D chain of donors in Si is of particular interest due to the natural confining potential of donors that can in principle help reduce the gate densities in solid-state quantum computing architectures. Using detailed atomistic modeling, we investigate CTAP in a more realistic triple donor system in the presence of inevitable fabrication imperfections. In particular, we investigate how an adiabatic pathway for CTAP is affected by donor misplacements, and propose schemes to correct for such errors. We also investigate the sensitivity of the adiabatic path to gate voltage fluctuations. The tight-binding based atomistic treatment of straggle used here may benefit understanding of other donor nanostructures, such as donor-based charge and spin qubits. Finally, we derive an effective 3 × 3 model of CTAP that accurately resembles the voltage tuned lowest energy states of the multi-million atom tight-binding simulations, and provides a translation between intensive atomistic Hamiltonians and simplified effective Hamiltonians while retaining the relevant atomic-scale information. This method can help characterize multi-donor experimental structures quickly and accurately even in the presence of imperfections, overcoming some of the numeric intractabilities of finding optimal eigenstates for non-ideal donor placements

    1976: Abilene Christian College Bible Lectures - Full Text

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    FREEDOM IN CHRIST Being the Abilene Christian College Annual Bible Lectures 1976 Published by ABILENE CHRISTIAN COLLEGE Book Store ACC Station Abilene, Texas 7960

    Characterization of Gastrin-Releasing Peptide and Its Receptor Aberrantly Expressed by Human Colon Cancer Cell Lines

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    ABSTRACT Gastrin-releasing peptide (GRP) is a mitogen and morphogen important in the development of human colon cancers. Although epithelial cells lining the colon do not normally express GRP or its receptor (GRP-R), most human tumors express GRP-R mRNA. Yet functional protein has only been detected in 24 to 40% of colon cancers. To elucidate the reason for the difference between the expression of GRP/GRP-R mRNA and protein, we studied nine human colon cancer cell lines. Quantitative polymerase chain reaction revealed that all colon cancer cell lines expressed similar amounts of mRNA for both GRP as well as GRP-R. Yet binding studies using 125 I-Tyr 4 -bombesin detected functional receptors on only five of the nine cell lines studied. Conformational fragment-length polymorphism analysis indicated that although mRNA for the ligand GRP was never mutated, mRNA for the GRP-R was always mutated. Sequencing revealed that the message for GRP-R contained between two and seven separate mutations at the nucleotide level. This resulted in 14 separate coding mutations, 2 of which were observed in more than one cell line. Each mutation was individually recreated by site-directed mutagenesis and studied in transiently transfected Chinese hamster ovary-K1 cells. Alteration of Pro 145 into a tyrosine, of Val 317 into a glutamic acid, and insertion of a 32-nucleotide segment resulting in a frameshift distal to Asp 137 all resulted in GRP receptors incapable of binding ligand. Thus, these data indicate that human colon cancers commonly express GRP and GRP-R mRNA but that receptor mutations account for the failure of functional protein to be generated
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