Split isobaric analog state in 55Ni: case of strong isospin mixing.

Study of ß+ decay of the exotic Tz=-3/2 nucleus 55Cu, via delayed γ rays, has revealed a strongly isospin mixed doublet (4599-4579 keV) in 55Ni, which represents the fragmented and previously unknown isobaric analog of the ground state of 55Cu. The observed small log ft values to both states in the doublet confirm the superallowed Fermi ß decay. The near degeneracy of a pair of 3/2- levels in 55Ni results in the strong isospin mixing. The isospin mixing matrix element between the T=3/2 and T=1/2 levels is inferred from the experiment to be 9(1) keV, which agrees well with the matrix element of the charge symmetry breaking shell model Hamiltonian of Ormand and Brown. A precise value of the half-life of 55Cu at 57(3) ms was also obtained.

Intruder configurations in the A=33 isobars: 33Mg and 33Al.

The beta decay of 33Mg (N=21) presented in this Letter reveals intruder configurations in both the parent and the daughter nucleus. The lowest excited states in the N=20 daughter nucleus, 33Al, are found to have nearly 2p-2h intruder configuration, thus extending the "island of inversion" beyond Mg. The allowed direct beta-decay branch to the 5/2{+} ground state of the daughter nucleus 33Al implies positive parity for the ground state of the parent 33Mg, contrary to an earlier suggestion of negative parity from a g-factor measurement. An admixture of 1p-1h and 3p-3h configurations is proposed for the ground state of 33Mg to explain all of the experimental observables.

Determination of the N=16 shell closure at the oxygen drip line.

The neutron unbound ground state of (25)O (Z=8, N=17) was observed for the first time in a proton knockout reaction from a (26)F beam. A single resonance was found in the invariant mass spectrum corresponding to a neutron decay energy of 770_+20(-10) keV with a total width of 172(30) keV. The N=16 shell gap was established to be 4.86(13) MeV by the energy difference between the nu1s(1/2) and nu0d(3/2) orbitals. The neutron separation energies for (25)O agree with the calculations of the universal sd shell model interaction. This interaction incorrectly predicts an (26)O ground state that is bound to two-neutron decay by 1 MeV, leading to a discrepancy between the theoretical calculations and experiment as to the particle stability of (26)O. The observed decay width was found to be on the order of a factor of 2 larger than the calculated single-particle width using a Woods-Saxon potential.

Observation of proton radioactivity of the (21+) high-spin isomer in 94Ag.

We have observed direct one-proton decay of the (21+) isomer in the N=Z nuclide 94Ag into high-spin states in 93Pd by detecting protons in coincidence with gamma-gamma correlations and applying gamma gates based on known 93Pd levels. Two decay branches have been identified, with proton energies of 0.79(3) and 1.01(3) MeV and branching ratios of 1.9(5)% and 2.2(4)%, respectively. The corresponding partial half-life values are 21(6) and 18(4) s. The Q value of the direct proton decay of the (21+) isomer was found to be 5.78(3) MeV. The very small reduced widths of the observed proton decays might reflect dominating collective configurations in the (21+) isomer, and the fine structure of the proton spectrum might indicate a strong deformation of this state.

p-sd Shell gap reduction in neutron-rich systems and cross-shell excitations in 20 O.

Excited states in 20O were populated in the reaction 10Be(14C,alpha) at Florida State University (FSU). Charged particles were detected with a particle telescope consisting of 4 annularly segmented Si surface barrier detectors and gamma radiation was detected with the FSU gamma detector array. Five new states were observed below 6 MeV from the alpha-gamma and alpha-gamma-gamma coincidence data. Shell model calculations suggest that most of the newly observed states are core-excited 1p-1h excitations across the N=Z=8 shell gap. Comparisons between experimental data and calculations for the neutron-rich O and F isotopes imply a steady reduction of the p-sd shell gap as neutrons are added.

29Na: defining the edge of the island of inversion for Z=11.

The low-energy level structure of the exotic Na isotopes (28,29)Na has been investigated through beta-delayed gamma spectroscopy. The N=20 isotones for Z=10-12 are considered to belong to the "island of inversion" where intruder configurations dominate the ground state wave function. However, it is an open question as to where and how the transition from normal to intruder dominated configurations happens in an isotopic chain. The present work, which presents the first detailed spectroscopy of (28,29)Na, clearly demonstrates that such a transition in the Na isotopes occurs between 28Na (N=17) and 29Na (N=18), supporting the smaller N=20 shell gap in neutron-rich sd shell nuclei. The evidence for inverted shell structure is found in beta-decay branching ratios, intruder dominated spectroscopy of low-lying states, and shell model analysis.

Lowest excitations in 56Ti and the predicted N=34 shell closure.

Recent experimental characterization of the subshell closure at N=32 in the Ca, Ti, and Cr isotones has stimulated shell-model calculations that indicated the possibility that the N=34 isotones of these same elements could exhibit characteristics of a shell closure, namely, a high energy for the first excited 2(+) level. To that end, we have studied the decay of 56Sc produced in fragmentation reactions and identified new gamma rays in the daughter N=34 isotone 56Ti. The first 2(+) level is found at an energy of 1127 keV, well below the expected position that would indicate the presence of an N=34 shell closure in 56Ti.

Focal brain injury and its effects on cerebral mantle, neurons, and fiber tracks.

Following a mild cortical impact injury delivered by a piston to the right sensorimotor cortex of the anesthetized rat, we evaluated mantle loss, neuronal changes, and fiber track degeneration by deOlmos silver stains up to 8 weeks after injury. Darkened neurons indicating damage (chromatolysis) occurred widely throughout both hemispheres and were seen from 1 h to 8 weeks after injury. This effect might have occurred from pressure wave damage from piston impact, brain displacement or deafferentation. Cerebral mantle loss was variable but fiber track degeneration related to projection and corticofugal descending tracks associated with the right sensorimotor system was rather constant. Unexpectedly, considerable fiber track degeneration occurred within the cerebellum, especially the inferior vermis. Cells directly under the piston face were surprisingly well-preserved but axon degeneration studies showed that these apparently intact neuronal cell bodies were surrounded by a dense network of degenerating fiber tracks. The intact cells, therefore, may have been functionally cut off from the rest of the brain owing to interruption of their efferents and afferents. The increased susceptibility of axons compared to cell bodies seen with this focal injury is similar to that observed with diffuse brain injury. The early appearing, severe and widespread axon damage we observed suggests that amelioration of focal traumatic brain injury will have to be directed promptly to the preservation of axons as well as cell bodies.

Reference memory and allocentric spatial localization deficits after unilateral cortical brain injury in the rat.

Traumatic brain injury (TBI) produces learning and memory impairments in humans. This study investigated the effects of TBI on memory and spatial localization strategies in rats. Prior to TBI, separate groups of rats were trained in an 8-arm radial maze with either all 8 arms baited (Expt. 1) or only 4 of the 8 arms baited (Expt. 2). TBI was produced by a controlled pneumatic impactor striking the entire right sensorimotor cortex of the anesthetized rat. Rats used in Expt. 1 were selected because they did not use a stereotypic response strategy (going to adjacent arms) in performing the maze before injury. After TBI the rats were not different from control rats in the number of working memory (WM) errors made. They did, however, display a distinct propensity to go to adjacent arms, i.e., exhibit stereotypic behavior, with a right-handed (ipsiversive) bias (P < 0.005). After TBI, rats which were trained with only 4 of 8 arms baited committed more reference memory (RM) errors than control rats (P < 0.05). They did not differ from controls on WM errors. Injured rats took longer to re-attain criteria than controls (P < 0.0001). Injured rats also initially displayed a propensity to enter the adjacent arm sequentially before re-attaining criteria. Further analysis indicated that injured rats re-learned the maze with a right-hand bias (P < 0.0001). The results of both experiments suggest that after TBI, rats shifted from an allocentric to an egocentric strategy to re-learn the maze. It was suggested that damage to the parietal cortex may have been responsible for both RM errors and the shift away from an allocentric strategy to an egocentric strategy. Possibly, the ipsiversive (right-hand) bias may be the result of a behaviorally or injury-induced neurochemical asymmetry within the motor system.

Traumatic brain injury of the forelimb and hindlimb sensorimotor areas in the rat: physiological, histological and behavioral correlates.

This study characterizes physiological, histological and behavioral effects of traumatic brain injury (TBI) produced by a controlled pneumatic impactor striking the entire right sensorimotor cortex of the anesthetized rat. Damage to both the fore- and hindlimb sensorimotor areas resulted in a hemiparetic animal which allowed us to use four sensitive behavioral/neurological tests to track the recovery sequelae after injury. Initial experiments measured cardiovascular and respiratory effects after cortical impact which depressed the dura to varying depths. Both 0.5 mm and 1 mm cortical depressions produced a momentary decrease (P < 0.05) in mean arterial blood pressure (MABP) while cortical impacts to depths of 2 mm or 3 mm produced a momentary increase (P < 0.05) in MABP. Normotension was re-established within 30 s after the initial response at all injury levels. Respiratory rate was affected only following 3 mm cortical depressions. A 1 mm cortical depression appeared ideal in terms of minimal cardiorespiratory effects, low mortality and lasting behavioral effects. For behavioral and histologic studies, therefore, additional rats were injured by a 1 mm cortical impact and tested for 8 weeks after TBI using four behavioral tests. Injured rats displayed both fore- and hindlimb deficits up to 56 days while traversing a narrow beam (P < 0.001) and up to 28 days when crossing a pegged beam (P < 0.05). Forelimb deficits evaluated on a wire grid platform were evident for 28 days (P < 0.05). Forepaw preference measured in a non-test setting indicated a bias to use the unaffected forepaw for 35 days (P < 0.05). A biphasic pattern of functional recovery was seen on all tests. A period of rapid functional recovery lasting 7 to 10 days was followed by a slower period of functional recovery lasting many weeks. Possible meanings of this biphasic recovery are discussed as issues of behavioral compensation/adaptation versus true neural recovery. Eight weeks after TBI histological analyses indicated that axonal degeneration was present in the areas adjacent to the ipsilateral cortical injury site. Degenerating fibers also extended across the corpus callosum into the homologous area in the contralateral cortex and were seen in the ipsilateral striatum, somatosensory and motor thalamic nuclei and substantia nigra. Significant axonal degeneration occurred bilaterally around the deep cerebellar nuclei. Degenerating fibers extended into the folia and terminated in the cerebellar granule cell layer. Thus the entire sensorimotor control system appeared to have been affected by a cortical injury.