714 research outputs found

    Diffraction of sound by a rigid screen with a soft or perfectly absorbing edge

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    A solution is obtained for the problem of the diffraction of a plane wave sound source by a semi-infinite plane. A finite region in the vicinity of the edge has a soft (pressure release) boundary condition; the remaining part of the semi-infinite plane is rigid. This solution is then used to derive an approximation for the behaviour of a rigid barrier with an absorbing edge. It is concluded ,that the absorbing material that comprises the edge need only be of the order of a wavelength long to have approximately the same effect, on the sound attenuation in the shadow side of the barrier, as a completely absorbent barrier

    Diffraction by an absorbing wedge

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    For the abstract of this paper, please see the PDF file

    Diffraction by a rigid barrier with a soft or perfectly absorbent end face

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    The reduction of noise levels in the shadow region of a rigid barrier of finite thickness is considered when the end face of the barrier is lined with either a soft or a perfectly absorbent material. Solutions, obtained by the method of matched asymptotic expansions, are given for both a semi-infinite barrier and for a finite length barrier placed on a rigid plane. Comparisons are made with existing solutions for barriers that have a rigid end face

    Harnessing the Heterogeneity of Prostate Cancer for Target Discovery Using Patient-Derived Explants

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    Prostate cancer is a complex and heterogeneous disease, but a small number of cell lines have dominated basic prostate cancer research, representing a major obstacle in the field of drug and biomarker discovery. A growing lack of confidence in cell lines has seen a shift toward more sophisticated pre-clinical cancer models that incorporate patient-derived tumors as xenografts or explants, to more accurately reflect clinical disease. Not only do these models retain critical features of the original tumor, and account for the molecular diversity and cellular heterogeneity of prostate cancer, but they provide a unique opportunity to conduct research in matched tumor samples. The challenge that accompanies these complex tissue models is increased complexity of analysis. With over 10 years of experience working with patient-derived explants (PDEs) of prostate cancer, this study provides guidance on the PDE method, its limitations, and considerations for addressing the heterogeneity of prostate cancer PDEs that are based on statistical modeling. Using inhibitors of the molecular chaperone heat shock protein 90 (Hsp90) as an example of a drug that induces robust proliferative response, we demonstrate how multi-omics analysis in prostate cancer PDEs is both feasible and essential for identification of key biological pathways, with significant potential for novel drug target and biomarker discovery.Margaret M. Centenera, Andrew D. Vincent, Max Moldovan, Hui-Ming Lin, David J. Lynn, Lisa G. Horvath, and Lisa M. Butle

    Quenched Lattice QCD with Domain Wall Fermions and the Chiral Limit

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    Quenched QCD simulations on three volumes, 83×8^3 \times, 123×12^3 \times and 163×3216^3 \times 32 and three couplings, ÎČ=5.7\beta=5.7, 5.85 and 6.0 using domain wall fermions provide a consistent picture of quenched QCD. We demonstrate that the small induced effects of chiral symmetry breaking inherent in this formulation can be described by a residual mass (\mres) whose size decreases as the separation between the domain walls (LsL_s) is increased. However, at stronger couplings much larger values of LsL_s are required to achieve a given physical value of \mres. For ÎČ=6.0\beta=6.0 and Ls=16L_s=16, we find \mres/m_s=0.033(3), while for ÎČ=5.7\beta=5.7, and Ls=48L_s=48, \mres/m_s=0.074(5), where msm_s is the strange quark mass. These values are significantly smaller than those obtained from a more naive determination in our earlier studies. Important effects of topological near zero modes which should afflict an accurate quenched calculation are easily visible in both the chiral condensate and the pion propagator. These effects can be controlled by working at an appropriately large volume. A non-linear behavior of mπ2m_\pi^2 in the limit of small quark mass suggests the presence of additional infrared subtlety in the quenched approximation. Good scaling is seen both in masses and in fπf_\pi over our entire range, with inverse lattice spacing varying between 1 and 2 GeV.Comment: 91 pages, 34 figure

    Historical separation and present-day structure of common dolphinfish (Coryphaena hippurus) populations in the Atlantic Ocean and Mediterranean Sea

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    The common dolphinfish (Coryphaena hippurus) is an epipelagic, mid-trophic level, highly migratory species distributed throughout the world’s tropical and subtropical oceans in waters greater than 20C. Life-history variables, migratory behaviour, and genetic markers have been used to define major stocks in the central Atlantic Ocean and Mediterranean Sea. Here, we used the mitochondrial DNA gene NADH subunit 1 (688 bp) to test for differences between population groups. A total of 103 haplotypes were detected among 203 fish. Gene diversities in samples were large and similar among populations (mean h ÂŒ 0.932; range 0.894–0.987), but nucleotide diversities varied widely among samples (range p ÂŒ 0.004–0.034) and appear to reflect population histories. Principal component analysis revealed two large populations groups, and the analysis of molecular variation and pairwise values of UST resolved population structure within these groups. Populations in the eastern Atlantic and Mediterranean showed the largest amounts of divergence from one another (UCT ÂŒ 0.331). Adult movement and biophysical barriers to larval dispersal may explain contemporary differences between stocks, but the divergent populations in the Mediterranean Sea are likely due to isolations by cold temperature barriers during Pleistocene glaciations. The geographically large stock groupings require international cooperation in the harvest management and conservation of local dolphinfish populations

    Measurements of Six-Body Hadronic Decays of the D^0 Charmed Meson

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    Using data collected by the FOCUS experiment at Fermilab, we report the discovery of the decay modes D^0 --> K- pi+ pi+ pi+ pi- pi- and D^0 --> pi+ pi+ pi+ pi- pi- pi-. With a sample of 48 +/- 10 reconstructed D^0 --> K- pi+ pi+ pi+ pi- pi- decays and 149 +/- 17 reconstructed D^0 --> pi+ pi+ pi+ pi- pi- pi- decays, we measure the following relative branching ratios: Γ(D0→K−π+π+π+π−π−)/Γ(D0→K−π+π+π−)=(2.70±0.58±0.38)×10−3{\Gamma (D^0 \to K^- \pi^+ \pi^+ \pi^+ \pi^- \pi^-) / \Gamma (D^0 \to K^- \pi^+ \pi^+ \pi^-)} = (2.70 \pm 0.58 \pm 0.38) \times 10^{-3} Γ(D0→π+π+π+π−π−π−)/Γ(D0→K−π+π+π−)=(5.23±0.59±1.35)×10−3{\Gamma (D^0 \to \pi^+ \pi^+ \pi^+ \pi^- \pi^- \pi^-) / \Gamma (D^0 \to K^- \pi^+ \pi^+ \pi^-)} = (5.23 \pm 0.59 \pm 1.35) \times 10^{-3} Γ(D0→π+π+π+π−π−π−)/Γ(D0→K−π+π+π+π−π−)=1.93±0.47±0.48{\Gamma (D^0 \to \pi^+ \pi^+ \pi^+ \pi^- \pi^- \pi^-) / \Gamma (D^0 \to K^- \pi^+ \pi^+ \pi^+ \pi^- \pi^-)} = 1.93 \pm 0.47 \pm 0.48 The first errors are statistical and the second are systematic. The branching fraction of the Cabibbo suppressed six-body decay mode is measured to be a factor of two higher than the branching fraction of the Cabibbo favored six-body decay mode.Comment: To be submitted to Phys. Lett.

    Measurement of the Ratio of the Vector to Pseudoscalar Charm Semileptonic Decay Rate \Gamma(D+ > ANTI-K*0 mu+ nu)/\Gamma(D+ > ANTI-K0 mu+ nu)

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    Using a high statistics sample of photo-produced charm particles from the FOCUS experiment at Fermilab, we report on the measurement of the ratio of semileptonic rates \Gamma(D+ > ANTI-K pi mu+ nu)/\Gamma(D+ > ANTI-K0 mu+ nu)= 0.625 +/- 0.045 +/- 0.034. Allowing for the K pi S-wave interference measured previously by FOCUS, we extract the vector to pseudoscalar ratio \Gamma(D+ > ANTI-K*0 mu+ nu)/\Gamma(D+ > ANTI-K0 mu+ nu)= 0.594 +/- 0.043 +/- 0.033 and the ratio \Gamma(D+ > ANTI-K0 mu+ nu)/\Gamma(D+ > K- pi+ pi+)= 1.019 +/- 0.076 +/- 0.065. Our results show a lower ratio for \Gamma(D > K* \ell nu})/\Gamma(D > K \ell nu) than has been reported recently and indicate the current world average branching fractions for the decays D+ >ANTI-K0(mu+, e+) nu are low. Using the PDG world average for B(D+ > K- pi+ pi+) we extract B(D+ > ANIT-K0 mu+ nu)=(9.27 +/- 0.69 +/- 0.59 +/- 0.61)%.Comment: 15 pages, 1 figur

    Melanocortin Receptor 4 Deficiency Affects Body Weight Regulation, Grooming Behavior, and Substrate Preference in the Rat

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    Obesity is caused by an imbalance between energy intake and expenditure and has become a major health-care problem in western society. The central melanocortin system plays a crucial role in the regulation of feeding and energy expenditure, and functional loss of melanocortin receptor 4 (MC4R) is the most common genetic cause of human obesity. In this study, we present the first functional Mc4r knockout model in the rat, resulting from an N-ethyl-N-nitrosourea mutagenesis–induced point mutation. In vitro observations revealed impaired membrane-binding and subsequent nonfunctionality of the receptor, whereas in vivo observations showed that functional loss of MC4R increased body weight, food intake, white adipose mass, and changed substrate preference. In addition, intracerebroventricular (ICV) administration of Agouti-Related Protein79–129 (AgRP79–129), an MC4R inverse agonist, or Melanotan-II (MTII), an MC4R agonist, did affect feeding behavior in wild-type rats but not in homozygous mutant rats, confirming complete loss of MC4R function in vivo. Finally, ICV administration of MTII induced excessive grooming behavior in wild-type rats, whereas this effect was absent in homozygous mutant rats, indicating that MTII-induced grooming behavior is exclusively regulated via MC4R pathways. Taken together, we expect that the MC4R rat model described here will be a valuable tool for studying monogenic obesity in humans. More specifically, the relative big size and increased cognitive capacity of rats as compared to mice will facilitate complex behavioral studies and detailed mechanistic studies regarding central function of MC4R, both of which ultimately may help to further understand the specific mechanisms that induce obesity during loss of MC4R function
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