766 research outputs found

    The frequency of wing damage in a migrating butterfly

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    The ability to fly is crucial for migratory insects. Consequently, the accumulation of damage on the wings over time can affect survival, especially for species that travel long distances. We examined the frequency of irreversible wing damage in the migratory butterfly Vanessa cardui to explore the effect of wing structure on wing damage frequency, as well as the mechanisms that might mitigate wing damage. An exceptionally high migration rate driven by high precipitation levels in their larval habitats in the winter of 2018–2019 provided us with an excellent opportunity to collect data on the frequency of naturally occurring wing damage associated with long-distance flights. Digital images of 135 individuals of V. cardui were collected and analyzed in Germany. The results show that the hindwings experienced a greater frequency of damage than the forewings. Moreover, forewings experienced more severe damage on the lateral margin, whereas hindwings experienced more damage on the trailing margin. The frequency of wing margin damage was higher in the painted lady butterfly than in the migrating monarch butterfly and in the butterfly Pontia occidentalis following artificially induced wing collisions. The results of this study could be used in future comparative studies of patterns of wing damage in butterflies and other insects. Additional studies are needed to clarify whether the strategies for coping with wing damage differ between migratory and non-migratory species

    Examination of Resistive Switching Energy of Some Nonlinear Dopant Drift Memristor Models

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    Radiative pion capture by a nucleon

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    The differential cross sections for πpγn\pi^- p \to \gamma n and π+nγp\pi^+ n \to \gamma p are computed up to O(p3)O(p^3) in heavy baryon chiral perturbation theory (HBChPT). The expressions at O(p)O(p) and O(p2)O(p^2) have no free parameters. There are three unknown parameters at O(p3)O(p^3), low energy constants of the HBChPT Lagrangian, which are determined by fitting to experimental data. Two acceptable fits are obtained, which can be separated by comparing with earlier dispersion relation calculations of the inverse process. Expressions for the multipoles, with emphasis on the p-wave multipoles, are obtained and evaluated at threshold. Generally the results obtained from the best of the two fits are in good agreement with the dispersion relation predictions.Comment: 24 pages, Latex, using RevTe

    Quasi-free Compton Scattering from the Deuteron and Nucleon Polarizabilities

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    Cross sections for quasi-free Compton scattering from the deuteron were measured for incident energies of 236--260 MeV at the laboratory angle -135 degrees. The recoil nucleons were detected in a liquid-scintillator array situated at 20 degrees. The measured differential cross sections were used, with the calculations of Levchuk et al., to determine the polarizabilities of the bound nucleons. For the bound proton, the extracted values were consistent with the accepted value for the free proton. Combining our results for the bound neutron with those from Rose et al., we obtain one-sigma constraints of alpha_n = 7.6-14.0 and beta_n = 1.2-7.6.Comment: 4 pages, 3 figures, accepted in PR

    Addition of vardenafil into storage solution protects the endothelium in a hypoxia-reoxygenation model

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    OBJECTIVE: Based upon the well known protective effect of intracellular cyclic guanosine monophosphate (cGMP) accumulation, we tested the hypothesis that storage solution enriched with optimal concentration of the phosphodiestherase-5 inhibitor vardenafil could provide better protection of vascular grafts against reperfusion injury after long-term cold ischaemic storage. METHODS: Isolated thoracic aorta obtained from rats underwent 24-h cold ischaemic preservation in physiological saline or vardenafil (10(-11) M)-supplemented saline solution. Reperfusion injury was simulated by hypochlorite (200 muM) exposure for 30 minutes. Endothelium-dependent vasorelaxation was assessed, and histopathological and molecular-biological examination of the aortic tissue were performed. RESULTS: Compared with the control group, the saline group showed significantly attenuated endothelium-dependent maximal relaxation (Rmax) to acetylcholine after hypoxia-reoxygenation, which was significantly improved by vardenafil supplementation (Rmax control: 98 +/- 1%; saline: 48 +/- 6%; vardenafil: 75 +/- 4%; p < .05). Vardenafil treatment significantly reduced DNA strand breaks (control: 10.6 +/- 6.2%; saline: 72.5 +/- 4.0%; vardenafil: 14.2 +/- 5.2%; p < .05) and increased cGMP score in the aortic wall (control: 8.2 +/- 0.6; saline: 4.5 +/- 0.3; vardenafil: 6.7 +/- 0.6; p < .05). CONCLUSIONS: Our results support the view that impairment of intracellular cGMP signalling plays a role in the pathogenesis of the endothelial dysfunction induced by cold storage warm reperfusion, which can be effectively reversed by pharmacological phosphodiesterase-5 inhibition

    Qweak: A Precision Measurement of the Proton's Weak Charge

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    The Qweak experiment at Jefferson Lab aims to make a 4% measurement of the parity-violating asymmetry in elastic scattering at very low Q2Q^2 of a longitudinally polarized electron beam on a proton target. The experiment will measure the weak charge of the proton, and thus the weak mixing angle at low energy scale, providing a precision test of the Standard Model. Since the value of the weak mixing angle is approximately 1/4, the weak charge of the proton Qwp=14sin2θwQ_w^p = 1-4 \sin^2 \theta_w is suppressed in the Standard Model, making it especially sensitive to the value of the mixing angle and also to possible new physics. The experiment is approved to run at JLab, and the construction plan calls for the hardware to be ready to install in Hall C in 2007. The theoretical context of the experiment and the status of its design are discussed.Comment: 5 pages, 2 figures, LaTeX2e, to be published in CIPANP 2003 proceeding

    Acute and delayed sulfur mustard toxicity; novel mechanisms and future studies

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    Sulfur mustard (SM), also known as mustard gas, has been the most widely used chemical weapon. The toxicity of SM as an incapacitating agent is of much greater importance than its ability to cause lethality. Acute toxicity of SM is related to reactive oxygen and nitrogen species, DNA damage, poly(ADP-ribose) polymerase activation and energy depletion within the affected cell. Therefore melatonin shows beneficial effects against acute SM toxicity in a variety of manner. It scavenges most of the oxygen- and nitrogen-based reactants, inhibits inducible nitric oxide synthase, repairs DNA damage and restores cellular energy depletion. The delayed toxicity of SM however, currently has no mechanistic explanation. We propose that epigenetic aberrations may be responsible for delayed detrimental effects of mustard poisoning. Epigenetic refers to the study of changes that influence the phenotype without causing alteration of the genotype. It involves changes in the properties of a cell that are inherited but do not involve a change in DNA sequence. It is now known that in addition to genetic mutations, epimutations can also involve in the pathogenesis of a variety of human diseases. Several actions of melatonin are now delineated by epigenetic actions including modulation of histone acetylation and DNA methylation. Future studies are warranted to clarify whether epigenetic mechanisms are involved in pathogenesis of delayed sulfur mustard toxicity and melatonin alleviates delayed toxicity of this warfare agent

    On the close to threshold meson production in neutron-neutron collisions

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    A method of measuring the close to threshold meson production in neutron-neutron collisions is described where the momenta of the colliding neutrons can be determined with the accuracy obtainable for the proton-proton reaction. The technique is based on the double quasi-free nn --> nn X^0 reaction, where deuterons are used as a source of neutronsComment: 6 pages, 2 figures, to be published in Phys. Lett.

    MIR376A is a regulator of starvation-induced autophagy

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    Background: Autophagy is a vesicular trafficking process responsible for the degradation of long-lived, misfolded or abnormal proteins, as well as damaged or surplus organelles. Abnormalities of the autophagic activity may result in the accumulation of protein aggregates, organelle dysfunction, and autophagy disorders were associated with various diseases. Hence, mechanisms of autophagy regulation are under exploration. Methods: Over-expression of hsa-miR-376a1 (shortly MIR376A) was performed to evaluate its effects on autophagy. Autophagy-related targets of the miRNA were predicted using Microcosm Targets and MIRanda bioinformatics tools and experimentally validated. Endogenous miRNA was blocked using antagomirs and the effects on target expression and autophagy were analyzed. Luciferase tests were performed to confirm that 3’ UTR sequences in target genes were functional. Differential expression of MIR376A and the related MIR376B was compared using TaqMan quantitative PCR. Results: Here, we demonstrated that, a microRNA (miRNA) from the DlkI/Gtl2 gene cluster, MIR376A, played an important role in autophagy regulation. We showed that, amino acid and serum starvation-induced autophagy was blocked by MIR376A overexpression in MCF-7 and Huh-7 cells. MIR376A shared the same seed sequence and had overlapping targets with MIR376B, and similarly blocked the expression of key autophagy proteins ATG4C and BECN1 (Beclin 1). Indeed, 3’ UTR sequences in the mRNA of these autophagy proteins were responsive to MIR376A in luciferase assays. Antagomir tests showed that, endogenous MIR376A was participating to the control of ATG4C and BECN1 transcript and protein levels. Moreover, blockage of endogenous MIR376A accelerated starvation-induced autophagic activity. Interestingly, MIR376A and MIR376B levels were increased with different kinetics in response to starvation stress and tissue-specific level differences were also observed, pointing out to an overlapping but miRNA-specific biological role. Conclusions: Our findings underline the importance of miRNAs encoded by the DlkI/Gtl2 gene cluster in stress-response control mechanisms, and introduce MIR376A as a new regulator of autophagy
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