Entrance-channel Mass-asymmetry Dependence of Compound-nucleus Formation Time in Light Heavy-ion Reactions

The entrance-channel mass-asymmetry dependence of the compound nucleus formation time in light heavy-ion reactions has been investigated within the framework of semiclassical dissipative collision models. the model calculations have been succesfully applied to the formation of the $^{38}$Ar compound nucleus as populated via the $^{9}$Be+$^{29}$Si, $^{11}$B+$^{27}$Al, $^{12}$C+$^{26}$Mg and $^{19}$F+$^{19}$F entrance channels. The shape evolution of several other light composite systems appears to be consistent with the so-called "Fusion Inhibition Factor" which has been experimentally observed. As found previously in more massive systems for the fusion-evaporation process, the entrance-channel mass-asymmetry degree of freedom appears to determine the competition between the different mechanisms as well as the time scales involved.Comment: 12 pages, 3 Figures available upon request, Submitted at Phys. Rev.

Chaotic Scattering in Heavy--Ion Reactions

We discuss the relevance of chaotic scattering in heavy--ion reactions at energies around the Coulomb barrier. A model in two and three dimensions which takes into account rotational degrees of freedom is discussed both classically and quantum-mechanically. The typical chaotic features found in this description of heavy-ion collisions are connected with the anomalous behaviour of several experimental data.Comment: 35 pages in RevTex (version 3.0) plus 27 PostScript figures obtainable by anonymous ftp from VAXFCT.CT.INFN.IT in directory kaos. Fig. 1 upon request to the authors. To be published in the October Focus issue on chaotic scattering of CHAO

JA: A model of controlled acute hyperglycemia in rats: effects of insulin and glucagonlike peptide-1 analog

ABSTRACT A rodent model of controlled acute hyperglycemia that is sensitive to glucose-lowering agents insulin and glucagon-like peptide-1 (GLP-1) analog has been developed. The studies show that anesthesia could be induced in fasted rats with ketamine (100 mg/kg) plus a low dose of xylazine (5 mg/kg) without inducing the acute hyperglycemia typically associated with these agents. Under these conditions, continuous infusion of glucose (10 and 20%) via the jugular vein for 30 to 150 min induced hyperglycemia in a time-dependent fashion. Administration of "loading" boluses of glucose (0.2-0.6 ml of a 20% solution) prior to continuous infusion of 10% glucose produced more immediate and sustained hyperglycemia. Plasma levels of a variety of glucoregulatory and stress hormones such as insulin, growth hormone, glucagon, and corticosterone were determined. Only glucagon levels changed significantly during induction and maintenance of hyperglycemia. The infusion of insulin (0.1 U/kg/h) or GLP-1 analog (10 g/kg/h) effectively lowered blood glucose from its elevated levels. Insulin produced a significant increase in glucagon levels, and GLP-1 analog produced a significant increase in insulin levels without any change in other glucoregulatory and stress hormone levels. In conclusion, the present studies identified a novel approach for the induction of anesthesia and surgical manipulations without inducing hyperglycemia and further defined an approach for producing acute hyperglycemia in a controlled fashion in rodents. This model will be beneficial to study the influence of hyperglycemia in acute models of critical illness where hyperglycemia develops following the precipitating event. This model was responsive to insulin and GLP-1 analog, both of which were effective in ameliorating hyperglycemia