Effect of nucleon exchange on projectile multifragmentation in the reactions of 28Si + 112Sn and 124Sn at 30 and 50 MeV/nucleon

Multifragmentation of quasiprojectiles was studied in reactions of 28Si beam with 112Sn and 124Sn targets at projectile energies 30 and 50 MeV/nucleon. The quasiprojectile observables were reconstructed using isotopically identified charged particles with Z_f <= 5 detected at forward angles. The nucleon exchange between projectile and target was investigated using isospin and excitation energy of reconstructed quasiprojectile. For events with total reconstructed charge equal to the charge of the beam (Z_tot = 14) the influence of beam energy and target isospin on neutron transfer was studied in detail. Simulations employing subsequently model of deep inelastic transfer, statistical model of multifragmentation and software replica of FAUST detector array were carried out. A concept of deep inelastic transfer provides good description of production of highly excited quasiprojectiles. The isospin and excitation energy of quasiprojectile were described with good overall agreement. The fragment multiplicity, charge and isospin were reproduced satisfactorily. The range of contributing impact parameters was determined using backtracing procedure.Comment: 11 pages, 8 Postscript figures, LaTeX, to appear in Phys. Rev. C ( Dec 2000

Introduction: looking beyond the walls

In its consideration of the remarkable extent and variety of non-university researchers, this book takes a broader view of ‘knowledge’ and ‘research’ than in the many hot debates about today’s knowledge society, ‘learning age’, or organisation of research. It goes beyond the commonly held image of ‘knowledge’ as something produced and owned by the full-time experts to take a look at those engaged in active knowledge building outside the university walls

Signals for a Transition from Surface to Bulk Emission in Thermal Multifragmentation

Excitation-energy-gated two-fragment correlation functions have been studied between 2 to 9A MeV of excitation energy for equilibrium-like sources formed in $\pi^-$ and p + $^{197}$Au reactions at beam momenta of 8,9.2 and 10.2 GeV/c. Comparison of the data to an N-body Coulomb-trajectory code shows a decrease of one order of magnitude in the fragment emission time in the excitation energy interval 2-5A MeV, followed by a nearly constant breakup time at higher excitation energy. The observed decrease in emission time is shown to be strongly correlated with the increase of the fragment emission probability, and the onset of thermally-induced radial expansion. This result is interpreted as evidence consistent with a transition from surface-dominated to bulk emission expected for spinodal decomposition.Comment: 11 pages including 3 postscript figures (1 color

Thermal excitation of heavy nuclei with 5-15 GeV/c antiproton, proton and pion beams

Excitation-energy distributions have been derived from measurements of 5.0-14.6 GeV/c antiproton, proton and pion reactions with $^{197}$Au target nuclei, using the ISiS 4$\pi$ detector array. The maximum probability for producing high excitation-energy events is found for the antiproton beam relative to other hadrons, $^3$He and $\bar{p}$ beams from LEAR. For protons and pions, the excitation-energy distributions are nearly independent of hadron type and beam momentum above about 8 GeV/c. The excitation energy enhancement for $\bar{p}$ beams and the saturation effect are qualitatively consistent with intranuclear cascade code predictions. For all systems studied, maximum cluster sizes are observed for residues with E*/A $\sim$ 6 MeV.Comment: 14 pages including 5 figures and 1 table. Accepted in Physics Letter B. also available at http://nuchem.iucf.indiana.edu

Increased SK3 expression in DM1 lens cells leads to impaired growth through a greater calcium-induced fragility

Although cataract is a characteristic feature of myotonic dystrophy type 1 (DM1), little is known of the underlying mechanisms. We generated four lens epithelial cell lines derived from DM1 cataracts and two from age-matched, non-DM cataracts. Small-pool PCR revealed typical large triplet repeat expansions in the DM1 cells. Furthermore, real-time PCR analysis showed reduced SIX5 expression and increased expression of the Ca2+-activated K+ channel SK3 in the DM1 cells. These cells also exhibited longer population doubling times which did not arise through reduced proliferation, but rather increased cell death as shown by increased release of lactate dehydrogenase (LDH). Using 86Rb+ as a tracer for K+, we found no difference in the resting K+ influx or efflux kinetics. In all cases, the ouabain sensitive component of the influx contributed ~50% of the total. However, stimulating internal Ca2+ by exposure to ionomycin not only caused greater stimulation of K+ (86Rb) efflux in the DM1 cells but also induced a higher rate of cell death (LDH assay). Since both the hyper-stimulation of K+ efflux and cell death were reduced by the highly specific SK inhibitor apamin, we suggest that increased expression of SK3 has a critical role in the increased Ca2+-induced fragility in DM1 cells. The present data, therefore, both help explain the lower epithelial cell density previously observed in DM1 cataracts and provide general insights into mechanisms underlying the fragility of other DM1-affected tissues