The interaction of 11Li with 208Pb

Background: 11Li is one of the most studied halo nuclei. The fusion of 11Li with 208Pb has been the subject of a number of theoretical studies with widely differing predictions, ranging over four orders of magnitude, for the fusion excitation function. Purpose: To measure the excitation function for the 11Li + 208Pb reaction. Methods: A stacked foil/degrader assembly of 208Pb targets was irradiated with a 11Li beam producing center of target beam energies from above barrier to near barrier energies (40 to 29 MeV). The intensity of the 11Li beam (chopped) was 1250 p/s and the beam on-target time was 34 hours. The alpha-decay of the stopped evaporation residues was detected in a alpha-detector array at each beam energy in the beam-off period (the beam was on for <= 5 ns and then off for 170 ns). Results: The 215At evaporation residues were associated with the fusion of 11Li with 208Pb. The 213,214At evaporation residues were formed by the breakup of 11Li into 9Li + 2n, with the 9Li fusing with 208Pb. The 214At evaporation residue appears to result from a "quasi-breakup" process. Conclusions: Most of 11Li + 208Pb interactions lead to breakup with a small fraction (<= 11%) leading to complete fusion.Comment: 25 pages, 11 figure

Diffusion over a saddle with a Langevin equation

The diffusion problem over a saddle is studied using a multi-dimensional Langevin equation. An analytical solution is derived for a quadratic potential and the probability to pass over the barrier deduced. A very simple solution is given for the one dimension problem and a general scheme is shown for higher dimensions.Comment: 13 pages, use revTeX, to appear in Phys. Rev. E6

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

Observation of Supershell Structure in Alkali Metal Nanowires

Nanowires are formed by indenting and subsequently retracting two pieces of sodium metal. Their cross-section gradually reduces upon retraction and the diameters can be obtained from the conductance. In previous work we have demonstrated that when one constructs a histogram of diameters from large numbers of indentation-retraction cycles, such histograms show a periodic pattern of stable nanowire diameters due to shell structure in the conductance modes. Here, we report the observation of a modulation of this periodic pattern, in agreement with predictions of a supershell structure.Comment: Phys. Rev. Lett., in prin

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 $^{48}$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

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]

Constitutively Active CaMKKα Stimulates Skeletal Muscle Glucose Uptake in Insulin-Resistant Mice In Vivo

In insulin-sensitive skeletal muscle, the expression of constitutively active Ca(2+)/calmodulin-dependent protein kinase kinase α (caCaMKKα) stimulates glucose uptake independent of insulin signaling (i.e., Akt and Akt-dependent TBC1D1/TBC1D4 phosphorylation). Our objectives were to determine whether caCaMKKα could stimulate glucose uptake additively with insulin in insulin-sensitive muscle, in the basal state in insulin-resistant muscle, and if so, to determine whether the effects were associated with altered TBC1D1/TBC1D4 phosphorylation. Mice were fed a control or high-fat diet (60% kcal) for 12 weeks to induce insulin resistance. Muscles were transfected with empty vector or caCaMKKα plasmids using in vivo electroporation. After 2 weeks, caCaMKKα protein was robustly expressed. In insulin-sensitive muscle, caCaMKKα increased basal in vivo [(3)H]-2-deoxyglucose uptake approximately twofold, insulin increased glucose uptake approximately twofold, and caCaMKKα plus insulin increased glucose uptake approximately fourfold. caCaMKKα did not increase basal TBC1D1 (Ser(237), Thr(590), Ser(660), pan-Thr/Ser) or TBC1D4 (Ser(588), Thr(642), pan-Thr/Ser) phosphorylation. In insulin-resistant muscle, caCaMKKα increased basal glucose uptake approximately twofold, and attenuated high-fat diet–induced basal TBC1D1 (Thr(590), pan-Thr/Ser) and TBC1D4 (Ser(588), Thr(642), pan-Thr/Ser) phosphorylation. In cell-free assays, CaMKKα increased TBC1D1 (Thr(590), pan-Thr/Ser) and TBC1D4 (Ser(588), pan-Thr/Ser) phosphorylation. Collectively, these results demonstrate that caCaMKKα stimulates glucose uptake additively with insulin, and in insulin-resistant muscle, and alters the phosphorylation of TBC1D1/TBC1D4

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

Gene Expression in Skeletal Muscle Biopsies from People with Type 2 Diabetes and Relatives: Differential Regulation of Insulin Signaling Pathways

BACKGROUND:Gene expression alterations have previously been associated with type 2 diabetes, however whether these changes are primary causes or secondary effects of type 2 diabetes is not known. As healthy first degree relatives of people with type 2 diabetes have an increased risk of developing type 2 diabetes, they provide a good model in the search for primary causes of the disease. METHODS/PRINCIPAL FINDINGS:We determined gene expression profiles in skeletal muscle biopsies from Caucasian males with type 2 diabetes, healthy first degree relatives, and healthy controls. Gene expression was measured using Affymetrix Human Genome U133 Plus 2.0 Arrays covering the entire human genome. These arrays have not previously been used for this type of study. We show for the first time that genes involved in insulin signaling are significantly upregulated in first degree relatives and significantly downregulated in people with type 2 diabetes. On the individual gene level, 11 genes showed altered expression levels in first degree relatives compared to controls, among others KIF1B and GDF8 (myostatin). LDHB was found to have a decreased expression in both groups compared to controls. CONCLUSIONS/SIGNIFICANCE:We hypothesize that increased expression of insulin signaling molecules in first degree relatives of people with type 2 diabetes, work in concert with increased levels of insulin as a compensatory mechanism, counter-acting otherwise reduced insulin signaling activity, protecting these individuals from severe insulin resistance. This compensation is lost in people with type 2 diabetes where expression of insulin signaling molecules is reduced

Ras Inhibition Induces Insulin Sensitivity and Glucose Uptake

BACKGROUND: Reduced glucose uptake due to insulin resistance is a pivotal mechanism in the pathogenesis of type 2 diabetes. It is also associated with increased inflammation. Ras inhibition downregulates inflammation in various experimental models. The aim of this study was to examine the effect of Ras inhibition on insulin sensitivity and glucose uptake, as well as its influence on type 2 diabetes development. METHODS AND FINDINGS: The effect of Ras inhibition on glucose uptake was examined both in vitro and in vivo. Ras was inhibited in cells transfected with a dominant-negative form of Ras or by 5-fluoro-farnesylthiosalicylic acid (F-FTS), a small-molecule Ras inhibitor. The involvement of IκB and NF-κB in Ras-inhibited glucose uptake was investigated by immunoblotting. High fat (HF)-induced diabetic mice were treated with F-FTS to test the effect of Ras inhibition on induction of hyperglycemia. Each of the Ras-inhibitory modes resulted in increased glucose uptake, whether in insulin-resistant C2C12 myotubes in vitro or in HF-induced diabetic mice in vivo. Ras inhibition also caused increased IκB expression accompanied by decreased expression of NF-κB . In fat-induced diabetic mice treated daily with F-FTS, both the incidence of hyperglycemia and the levels of serum insulin were significantly decreased. CONCLUSIONS: Inhibition of Ras apparently induces a state of heightened insulin sensitization both in vitro and in vivo. Ras inhibition should therefore be considered as an approach worth testing for the treatment of type 2 diabetes