117 research outputs found
Two-Step Model of Fusion for Synthesis of Superheavy Elements
A new model is proposed for fusion mechanisms of massive nuclear systems
where so-called fusion hindrance exists. The model describes two-body collision
processes in an approaching phase and shape evolutions of an amalgamated system
into the compound nucleus formation. It is applied to Ca-induced
reactions and is found to reproduce the experimental fusion cross sections
extremely well, without any free parameter. Combined with the statistical decay
theory, residue cross sections for the superheavy elements can be readily
calculated. Examples are given.Comment: 4 pages, 4 figure
Classical Analysis of Phenomenological Potentials for Metallic Clusters
The classical trajectories of single particle motion in a Wodds-Saxon and a
modified Nilsson potential are studied for axial quadrupole deformation. Both
cases give rise to chaotic behaviour when the deformation in the Woods-Saxon
and the l**2 term in the modified Nilsson potential are turned on. Important
similarities, in particular with regard to the shortest periodic orbits, have
been found.Comment: 9 pages LaTex + 4 figures available via e-mail requests from the
authors, to appear in Phys.Rev.Let
Neutron-induced astrophysical reaction rates for translead nuclei
Neutron-induced reaction rates, including fission, are calculated in the
temperature range 1.d8 <T (K) < 1.d10 within the framework of the statistical
model for targets with atomic number 83 < Z < 119 (from Po to Uuo) from the
neutron to the proton drip-line. Four sets of rates have been calculated,
utilizing - where possible - consistent nuclear data for neutron separation
energies and fission barriers from Thomas-Fermi (TF), Extended Thomas-Fermi
plus Strutinsky Integral (ETFSI), Finite-Range Droplet Model (FRDM) and
Hartree-Fock-Bogolyubov (HFB) predictions. Tables of calculated values as well
as analytic seven parameter fits in the standard REACLIB format are supplied.
We also discuss the sensitivity of the rates to the input, aiming at a better
understanding of the uncertainties introduced by the nuclear input.Comment: 14 pages, 10 figures, 2 tables in paper, 2 in Annex and online tables
example
Nuclear fission: The "onset of dissipation" from a microscopic point of view
Semi-analytical expressions are suggested for the temperature dependence of
those combinations of transport coefficients which govern the fission process.
This is based on experience with numerical calculations within the linear
response approach and the locally harmonic approximation. A reduced version of
the latter is seen to comply with Kramers' simplified picture of fission. It is
argued that for variable inertia his formula has to be generalized, as already
required by the need that for overdamped motion the inertia must not appear at
all. This situation may already occur above T=2 MeV, where the rate is
determined by the Smoluchowski equation. Consequently, comparison with
experimental results do not give information on the effective damping rate, as
often claimed, but on a special combination of local stiffnesses and the
friction coefficient calculated at the barrier.Comment: 31 pages, LaTex, 9 postscript figures; final, more concise version,
accepted for publication in PRC, with new arguments about the T-dependence of
the inertia; e-mail: [email protected]
Quantum Tunneling in Nuclear Fusion
Recent theoretical advances in the study of heavy ion fusion reactions below
the Coulomb barrier are reviewed. Particular emphasis is given to new ways of
analyzing data, such as studying barrier distributions; new approaches to
channel coupling, such as the path integral and Green function formalisms; and
alternative methods to describe nuclear structure effects, such as those using
the Interacting Boson Model. The roles of nucleon transfer, asymmetry effects,
higher-order couplings, and shape-phase transitions are elucidated. The current
status of the fusion of unstable nuclei and very massive systems are briefly
discussed.Comment: To appear in the January 1998 issue of Reviews of Modern Physics. 13
Figures (postscript file for Figure 6 is not available; a hard copy can be
requested from the authors). Full text and figures are also available at
http://nucth.physics.wisc.edu/preprints
Unsaturated Fatty Acids Revert Diet-Induced Hypothalamic Inflammation in Obesity
Background: In experimental models, hypothalamic inflammation is an early and determining factor in the installation and progression of obesity. Pharmacological and gene-based approaches have proven efficient in restraining inflammation and correcting the obese phenotypes. However, the role of nutrients in the modulation of hypothalamic inflammation is unknown. Methodology/Principal Findings: Here we show that, in a mouse model of diet-induced obesity, partial substitution of the fatty acid component of the diet by flax seed oil (rich in C18:3) or olive oil (rich in C18:1) corrects hypothalamic inflammation, hypothalamic and whole body insulin resistance, and body adiposity. In addition, upon icv injection in obese rats, both v3 and v9 pure fatty acids reduce spontaneous food intake and body mass gain. These effects are accompanied by the reversal of functional and molecular hypothalamic resistance to leptin/insulin and increased POMC and CART expressions. In addition, both, v3 and v9 fatty acids inhibit the AMPK/ACC pathway and increase CPT1 and SCD1 expression in the hypothalamus. Finally, acute hypothalamic injection of v3 and v9 fatty acids activate signal transduction through the recently identified GPR120 unsaturated fatty acid receptor. Conclusions/Significance: Unsaturated fatty acids can act either as nutrients or directly in the hypothalamus, reverting dietinduced inflammation and reducing body adiposity. These data show that, in addition to pharmacological and geneti
Hyperleptinemia Is Required for the Development of Leptin Resistance
Leptin regulates body weight by signaling to the brain the availability of energy stored as fat. This negative feedback loop becomes disrupted in most obese individuals, resulting in a state known as leptin resistance. The physiological causes of leptin resistance remain poorly understood. Here we test the hypothesis that hyperleptinemia is required for the development of leptin resistance in diet-induced obese mice. We show that mice whose plasma leptin has been clamped to lean levels develop obesity in response to a high-fat diet, and the magnitude of this obesity is indistinguishable from wild-type controls. Yet these obese animals with constant low levels of plasma leptin remain highly sensitive to exogenous leptin even after long-term exposure to a high fat diet. This shows that dietary fats alone are insufficient to block the response to leptin. The data also suggest that hyperleptinemia itself can contribute to leptin resistance by downregulating cellular response to leptin as has been shown for other hormones
Substrate cycling between de novo lipogenesis and lipid oxidation: a thermogenic mechanism against skeletal muscle lipotoxicity and glucolipotoxicity
Life is a combustion, but how the major fuel substrates that sustain human life compete and interact with each other for combustion has been at the epicenter of research into the pathogenesis of insulin resistance ever since Randle proposed a 'glucose-fatty acid cycle' in 1963. Since then, several features of a mutual interaction that is characterized by both reciprocality and dependency between glucose and lipid metabolism have been unravelled, namely: 1. the inhibitory effects of elevated concentrations of fatty acids on glucose oxidation (via inactivation of mitochondrial pyruvate dehydrogenase or via desensitization of insulin-mediated glucose transport), 2. the inhibitory effects of elevated concentrations of glucose on fatty acid oxidation (via malonyl-CoA regulation of fatty acid entry into the mitochondria), and more recently 3. the stimulatory effects of elevated concentrations of glucose on de novo lipogenesis, that is, synthesis of lipids from glucose (via SREBP1c regulation of glycolytic and lipogenic enzymes). This paper first revisits the physiological significance of these mutual interactions between glucose and lipids in skeletal muscle pertaining to both blood glucose and intramyocellular lipid homeostasis. It then concentrates upon emerging evidence, from calorimetric studies investigating the direct effect of leptin on thermogenesis in intact skeletal muscle, of yet another feature of the mutual interaction between glucose and lipid oxidation: that of substrate cycling between de novo lipogenesis and lipid oxidation. It is proposed that this energy-dissipating substrate cycling that links glucose and lipid metabolism to thermogenesis could function as a 'fine-tuning' mechanism that regulates intramyocellular lipid homeostasis, and hence contributes to the protection of skeletal muscle against lipotoxicity
Differential aetiology and impact of phosphoinositide 3-kinase (PI3K) and Akt signalling in skeletal muscle on in vivo insulin action
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