453 research outputs found

    Neutrons from multiplicity-selected Au-Au collisions at 150, 250, 400, and 650 AMeV

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    We measured neutron triple-differential cross sections from multiplicity-selected Au-Au collisions at 150, 250, 400, and 650 \AMeV. The reaction plane for each collision was estimated from the summed transverse velocity vector of the charged fragments emitted in the collision. We examined the azimuthal distribution of the triple-differential cross sections as a function of the polar angle and the neutron rapidity. We extracted the average in--plane transverse momentum Px\langle P_x\rangle and the normalized observable Px/P\langle P_x/P_\perp\rangle, where PP_\perp is the neutron transverse momentum, as a function of the neutron center-of-mass rapidity, and we examined the dependence of these observables on beam energy. These collective flow observables for neutrons, which are consistent with those of protons plus bound nucleons from the Plastic Ball Group, agree with the Boltzmann--Uehling--Uhlenbeck (BUU) calculations with a momentum--dependent interaction. Also, we calculated the polar-angle-integrated maximum azimuthal anisotropy ratio R from the value of Px/P\langle P_x/P_\perp\rangle.Comment: 20 LaTeX pages. 11 figures to be faxed on request, send email to sender's addres

    Fragment Flow and the Nuclear Equation of State

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    We use the Boltzmann-Uehling-Uhlenbeck model with a momentum-dependent nuclear mean field to simulate the dynamical evolution of heavy ion collisions. We re-examine the azimuthal anisotropy observable, proposed as sensitive to the equation of state of nuclear matter. We obtain that this sensitivity is maximal when the azimuthal anisotropy is calculated for nuclear composite fragments, in agreement with some previous calculations. As a test case we concentrate on semi-central 197Au + 197Au^{197}{\rm Au}\ +\ ^{197}{\rm Au} collisions at 400 AA MeV.Comment: 12 pages, ReVTeX 3.0. 12 Postscript figures, uuencoded and appende

    Effects of Compression and Collective Expansion on Particle Emission from Central Heavy-Ion Reactions

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    Conditions under which compression occurs and collective expansion develops in energetic reactions of heavy nuclei, are analyzed, together with their effects on emitted light baryons and pions. Within transport simulations, it is shown that shock fronts perpendicular to beam axis form in head-on reactions. The fronts separate hot compressed matter from normal. As impact parameter increases, the angle of inclination of the fronts relative to beam axis decreases, and in-between the fronts a weak tangential discontinuity develops. Hot matter exposed to the vacuum in directions perpendicular to shock motion (and parallel to fronts), starts to expand sideways, early within reactions. Expansion in the direction of shock motion follows after the shocks propagate through nuclei, but due to the delay does not acquire same strength. Expansion affects angular distributions, mean-energy components, shapes of spectra and mean energies of different particles emitted into any one direction, and further particle yields. Both the expansion and a collective motion associated with the weak discontinuity, affect the magnitude of sideward flow within reaction plane. Differences in mean particle energy components in and out of the reaction plane in semicentral collisions, depend sensitively on the relative magnitude of shock speed in normal matter and speed of sound in hot matter.Comment: 71 pages, 33 figures (available on request), report MSUCL-94

    Effective Dark Matter Model: Relic density, CDMS II, Fermi LAT and LHC

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    The Cryogenic Dark Matter Search recently announced the observation of two signal events with a 77% confidence level. Although statistically inconclusive, it is nevertheless suggestive. In this work we present a model-independent analysis on the implication of a positive signal in dark matter scattering off nuclei. Assuming the interaction between (scalar, fermion or vector) dark matter and the standard model induced by unknown new physics at the scale Λ\Lambda, we examine various dimension-6 tree-level induced operators and constrain them using the current experimental data, e.g. the WMAP data of the relic abundance, CDMS II direct detection of the spin-independent scattering, and indirect detection data (Fermi LAT cosmic gamma-ray), etc. Finally, the LHC reach is also explored

    IGF-1 Induction by Acylated Steryl β-Glucosides Found in a Pre-Germinated Brown Rice Diet Reduces Oxidative Stress in Streptozotocin-Induced Diabetes

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    BACKGROUND: The pathology of diabetic neuropathy involves oxidative stress on pancreatic β-cells, and is related to decreased levels of Insulin-like growth factor 1 (IGF-1). Acylated steryl β-glucoside (PR-ASG) found in pre-germiated brown rice is a bioactive substance exhibiting properties that enhance activity of homocysteine-thiolactonase (HTase), reducing oxidative stress in diabetic neuropathy. The biological importance of PR-ASG in pancreatic β-cells remains unknown. Here we examined the effects of PR-ASG on IGF-1 and glucose metabolism in β-cells exposed to oxidative stress. METHODOLOGY/PRINCIPAL FINDINGS: In the present study, a pre-germinated brown rice (PR)-diet was tested in streptozotocin (STZ)-induced diabetic rats. Compared with diabetic rats fed control diets, the PR-diet fed rats showed an improvement of serum metabolic and neurophysiological parameters. In addition, IGF-1 levels were found to be increased in the serum, liver, and pancreas of diabetic rats fed the PR-diet. The increased IGF-1 level in the pancreas led us to hypothesize that PR-ASG is protective for islet β-cells against the extensive injury of advanced or severe diabetes. Thus we examined PR-ASG to determine whether it showed anti-apoptotic, pro-proliferative effects on the insulin-secreting β-cells line, INS-1; and additionally, whether PR-ASG stimulated IGF-1 autocrine secretion/IGF-1-dependent glucose metabolism. We have demonstrated for the first time that PR-ASG increases IGF-1 production and secretion from pancreatic β-cells. CONCLUSION/SIGNIFICANCE: These findings suggest that PR-ASG may affect pancreatic β-cells through the activation of an IGF-1-dependent mechanism in the diabetic condition. Thus, intake of pre-germinated brown rice may have a beneficial effect in the treatment of diabetes, in particular diabetic neuropathy

    Hypercholesterolemia downregulates autophagy in the rat heart

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    Background: We have previously shown that efficiency of ischemic conditioning is diminished in hypercholesterolemia and that autophagy is necessary for cardioprotection. However, it is unknown whether isolated hypercholesterolemia disturbs autophagy or the mammalian target of rapamycin (mTOR) pathways. Therefore, we investigated whether isolated hypercholesterolemia modulates cardiac autophagy-related pathways or programmed cell death mechanisms such as apoptosis and necroptosis in rat heart. Methods: Male Wistar rats were fed either normal chow (NORM; n=9) or with 2% cholesterol and 0.25% cholic acid-enriched diet (CHOL; n=9) for 12 weeks. CHOL rats exhibited a 41% increase in plasma total cholesterol level over that of NORM rats (4.09mmol/L vs. 2.89mmol/L) at the end of diet period. Animals were sacrificed, hearts were excised and briefly washed out. Left ventricles were snap-frozen for determination of markers of autophagy, mTOR pathway, apoptosis, and necroptosis by Western blot. Results: Isolated hypercholesterolemia was associated with a significant reduction in expression of cardiac autophagy markers such as LC3-II, Beclin-1, Rubicon and RAB7 as compared to controls. Phosphorylation of ribosomal S6, a surrogate marker for mTOR activity, was increased in CHOL samples. Cleaved caspase-3, a marker of apoptosis, increased in CHOL hearts, while no difference in the expression of necroptotic marker RIP1, RIP3 and MLKL was detected between treatments. Conclusions: This is the first comprehensive analysis of autophagy and programmed cell death pathways of apoptosis and necroptosis in hearts of hypercholesterolemic rats. Our data show that isolated hypercholesterolemia suppresses basal cardiac autophagy and that the decrease in autophagy may be a result of an activated mTOR pathway. Reduced autophagy was accompanied by increased apoptosis, while cardiac necroptosis was not modulated by isolated hypercholesterolemia. Decreased basal autophagy and elevated apoptosis may be responsible for the loss of cardioprotection reported in hypercholesterolemic animals

    Neonatal Androgenization Exacerbates Alcohol-Induced Liver Injury in Adult Rats, an Effect Abrogated by Estrogen

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    Alcoholic liver disease (ALD) affects millions of people worldwide and is a major cause of morbidity and mortality. However, fewer than 10% of heavy drinkers progress to later stages of injury, suggesting other factors in ALD development, including environmental exposures and genetics. Females display greater susceptibility to the early damaging effects of ethanol. Estrogen (E2) and ethanol metabolizing enzymes (cytochrome P450, CYP450) are implicated in sex differences of ALD. Sex steroid hormones are developmentally regulated by the hypothalamic-pituitary-gonadal (HPG) axis, which controls sex-specific cycling of gonadal steroid production and expression of hepatic enzymes. The aim of this study was to determine if early postnatal inhibition of adult cyclic E2 alters ethanol metabolizing enzyme expression contributing to the development of ALD in adulthood. An androgenized rat model was used to inhibit cyclic E2 production. Control females (Ctrl), androgenized females (Andro) and Andro females with E2 implants were administered either an ethanol or isocalorically-matched control Lieber-DeCarli diet for four weeks and liver injury and CYP450 expression assessed. Androgenization exacerbated the deleterious effects of ethanol demonstrated by increased steatosis, lipid peroxidation, profibrotic gene expression and decreased antioxidant defenses compared to Ctrl. Additionally, CYP2E1 expression was down-regulated in Andro animals on both diets. No change was observed in CYP1A2 protein expression. Further, continuous exogenous administration of E2 to Andro in adulthood attenuated these effects, suggesting that E2 has protective effects in the androgenized animal. Therefore, early postnatal inhibition of cyclic E2 modulates development and progression of ALD in adulthood
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