Nuclear Force Imprints Revealed on the Elastic Scattering of Protons with

How does nature hold together protons and neutrons to form the wide variety of complex nuclei in the Universe? Describing many-nucleon systems from the fundamental theory of quantum chromodynamics has been the greatest challenge in answering this question. The chiral effective field theory description of the nuclear force now makes this possible but requires certain parameters that are not uniquely determined. Defining the nuclear force needs identification of observables sensitive to the different parametrizations. From a measurement of proton elastic scattering on ^{10}C at TRIUMF and ab initio nuclear reaction calculations, we show that the shape and magnitude of the measured differential cross section is strongly sensitive to the nuclear force prescription.

Evidence of soft dipole resonance in

The first conclusive evidence of a dipole resonance in ^{11}Li having isoscalar character observed from inelastic scattering with a novel solid deuteron target is reported. The experiment was performed at the newly commissioned IRIS facility at TRIUMF. The results show a resonance peak at an excitation energy of 1.03±0.03 MeV with a width of 0.51±0.11 MeV (FWHM). The angular distribution is consistent with a dipole excitation in the distorted-wave Born approximation framework. The observed resonance energy together with shell model calculations show the first signature that the monopole tensor interaction is important in ^{11}Li. The first ab initio calculations in the coupled cluster framework are also presented.

Fusion reactions with the one-neutron halo nucleus (15)C.

The structure of (15)C, with an s(1/2) neutron weakly bound to a closed-neutron shell nucleus (14)C, makes it a prime candidate for a one-neutron halo nucleus. We have for the first time studied the cross section for the fusion-fission reaction (15)C+(232)Th at energies in the vicinity of the Coulomb barrier and compared it to the yield of the neighboring (14)C+(232)Th system measured in the same experiment. At sub-barrier energies, an enhancement of the fusion yield by factors of 2-5 was observed for (15)C, while the cross sections for (14)C match the trends measured for (12,13)C.

¹5C(d,p)¹6C reaction and exotic behavior in ¹6C.

We have studied the ¹5C(d,p)¹6C reaction in inverse kinematics using the Helical Orbit Spectrometer at Argonne National Laboratory. Prior studies of electromagnetic-transition rates in ¹6C suggested an exotic decoupling of the valence neutrons from the core in that nucleus. Neutron-adding spectroscopic factors give a different probe of the wave functions of the relevant states in ¹6C. Shell-model calculations reproduce both the present transfer data and the previously measured transition rates, suggesting that ¹6C may be described without invoking very exotic phenomena.

First experiment with HELIOS: the structure of 13B.

A first experiment is reported that makes use of a new kind of spectrometer uniquely suited to the study of reactions with radioactive beams in inverse kinematics, the helical orbit spectrometer, HELIOS. The properties of some low-lying states in the neutron-rich N=8 nucleus 13B were studied with good resolution. From the measured angular distributions of the (d,p) reaction and the relative spectroscopic factors, spin and configuration assignments of the first- and third-excited states of this nucleus can be constrained.

An HRP and autoradiographic study of the projection from the cerebellar cortex to the nucleus interpositus anterior and nucleus interpositus posterior of the cat.

The recently developed anatomical techniques of retrograde transport of the enzyme horseradish peroxidase (HRP), anterograde transport of tritiated amino acid, and intracellular injections of HRP were used to study the organization of the corticonuclear projection to the nucleus interpositus anterior (NIA) and the nucleus interpositus posterior (NIP) of the cat. Injections of HRP into the NIA and the NIP revealed that the major areas of the cortex which provided afferents to these two nuclei were the intermediate cortex of the anterior lobe (IAL) and the paramedian lobule (PML). There were, however, significant differences in the distribution of Purkinje (Pk) cells which projected to each nucleus. The NIA received afferents from all areas of the IAL while the NIP projection area was restricted to a band located at the medi-almost aspect of the lobe. All areas of the PML, in particular the intermediate folia, projected to the NIP, while the Pk cells which sent axons to the NIA were restricted to the rostral and caudal folia of this lobule. The projection from each area was somatotopically organized. The axons of intracellularly stained Pk cells were followed to their termination in the NIA and NIP confirming the results obtained with the two extracellular techniques. An attempt was made to examine the organization of the corticonuclear projection at the single cell level in the PML. Pk cells located in the same sagittal plane appeared to terminate in the same area of the same nucleus while Pk cells located not more than 500 micrometers medial or lateral to each other terminated in different nuclei. Basically, the organization of the corticonuclear projection from the IAL is longitudinally organized while the PML has a much more complex arrangement in which the Pk cells projecting to the NIA and NIP are interspersed.

Controlled cortical impact: a new experimental brain injury model.

A new experimental model of mechanical brain injury was produced in the laboratory ferret (Mustela putorius furo) using a stroke-constrained pneumatic impactor. Cortical impacts were made on vertex to the intact dura mater overlying the cerebral cortex with contact velocities ranging from 2.0 to 4.0 m/sec and with deformations of 2.0 to 5.0 mm. The dwell time of the impact and the stability of the skull during impact were verified with high speed (1000 to 3000 frames/sec) cineradiography. Systemic arterial blood pressure, heart rate, and respiration were monitored, and postinjury changes were recorded. Anatomic brain injury, including subdural hematoma, subarachnoid hemorrhage, tears or rents of the dura mater, and contusions of the cortex, brainstem, cervical spinal cord, and cerebellum was observed. Injury responses ranged from no apparent anatomic injury or alterations in the systemic physiology at low severity impact (2.0 m/sec, 2.0 mm) to immediate fatality in the highest severity impact groups (4.0 m/sec, 4.0 mm). The range of changes in systemic physiology and of pathology in the brain, brainstem, and spinal cord was a function of both contact velocity and the amount of brain deformation. In two cases where postinjury time was 8-10 h, diffuse axonal injury, indicated by beaded axons and retraction balls, was present in subcortical regions underlying the site of impact. The spectrum of anatomic injury and systemic physiologic responses closely resembled aspects of closed head injury seen clinically. This procedure complements and improves on existing techniques by allowing independent control of contact velocity and level of deformation of the brain to facilitate biomechanical and analytic modeling of brain trauma. Graded cortical contusions and subcortical injury are produced by precisely controlled brain deformations, thereby allowing questions to be addressed regarding the influence of contact velocity and level of deformation on the anatomic and functional severity of brain injury.

Experimental models of brain injury.

General categories of experimental brain injury models are reviewed regarding their clinical significance, and two new models are presented that use different methodology to produce injury. This report describes and characterizes the pathophysiologic changes produced by a novel fluid percussion (FP) method and a controlled cortical impact (CI) technique, both developed at the General Motors Research Laboratories (GMRL). The new models are compared to prior experimental brain injury techniques in relation to ongoing physical and analytical modeling used in automotive safety research by GMRL. Experimental results from our laboratory indicate that although the FP technique, currently the most widely used method for producing brain injury, is useful for producing graded injury responses systemically and centrally, it is not well-suited for detailed biomechanical analyses. This conclusion is based on high-speed cineradiographic studies where the physiologic saline in the FP cannula was substituted with a radiopaque contrast medium (Conray 1:1 dilution/saline). High speed x-ray movies (1000 fps) were taken of the fluid percussion pulse (1.5-3.4 atm/20 msec) in sagittal, dorsal, and frontal planes of orientation. When viewed together, the cineradiography revealed a complex, dynamic interaction between the injected fluid and the skull/cranial contents. Rapid lateral and anterior/posterior epidural fluid flow suggest that the pathology and dysfunction following FP brain injury reflects diffuse mechanical loading of the brain. Because fluid is used to transfer mechanical energy to brain tissue, and because fluid flow characteristics (i.e., direction, velocity, and displacement) are dependent on the brain geometry and species used, accurate analytical and biomechanical analyses of the resultant injury would be difficult at best. In contrast, the cortical impact model of experimental brain injury uses a known impact interface and a measurable, controllable impact velocity and cortical compression. These controlled variables enable the amount of deformation and the change in deformation over time to be accurately determined. In addition, the CI model produces graded, reproducible cortical contusion, prolonged functional coma, and extensive axonal injury, unlike the FP technique. The quantifiable nature of the single mechanical input used to produce the injury allows correlations to be made between the amount of deformation and the resultant pathology and functional changes.(ABSTRACT TRUNCATED AT 400 WORDS)

Characterization of axonal injury produced by controlled cortical impact.

Axonal injury and behavioral changes were evaluated 3-7 days after traumatic brain injury. Previous research from this laboratory demonstrated that clinical central nervous pathology is produced by dynamic brain compression using a stroke-constrained impactor. We wanted to determine if the technique also would produce diffuse axonal injury after recovery from the procedure. The experiments were performed at Wayne State University School of Medicine using aseptic techniques while assuring analgesic care. Impacts were performed at 4.3 m/sec or 8.0 m/sec, with congruent to 10% compression (2.5 mm). Extensive axonal injury was observed at 3 and 7 days postinjury using both velocity-compression combinations. Regions displaying axonal injury were the subcortical white matter, internal capsule, thalamic relay nuclei, midbrain, pons, and medulla. Axonal injury also was evident in the white matter of the cerebellar folia and the region of the deep cerebellar nuclei. Behavioral assessment showed functional coma lasting up to 36 h following 8.0 m/sec impacts, with impaired movement and control of the extremities over the duration of the postinjury monitoring time. These experiments confirm that the cortical impact model of traumatic brain injury mimics all aspects of traumatic brain injury in humans and can be used to investigate mechanisms of axonal damage and prolonged behavioral suppression.

Physiologic, histopathologic, and cineradiographic characterization of a new fluid-percussion model of experimental brain injury in the rat.

The fluid-percussion technique produces experimental brain injury by rapid injection of a fluid volume into the closed cranial cavity. The experiments reported here characterize a new, more controlled technique for fluid-percussion brain injury in the rat and systematically examine systemic physiologic, histopathologic, and electroencephalographic responses in the rat at two levels of injury severity. The new technique was developed to permit independent variation of the fluid pressure pulse parameters and, thus, more accurately define the brain loading conditions associated with fluid-percussion injury. The new technique produced changes in mean arterial blood pressure similar to previous techniques; however, bradycardia was not observed. Significant increases in heart rate were produced by both injury levels and were more prolonged at the high level of injury severity. Both magnitudes of injury produced significant decreases in EEG amplitude immediately postinjury, but high severity injury produced a greater decrease in delta frequency band (1-4 Hz) activity than did low severity injury. Both levels produced hemorrhage at the site of injury, thalamus, corpus callosum, hippocampus, and fimbria hippocampus similar to previous techniques. Higher levels of injury produced more extensive cerebral hemorrhage and greater spinal involvement. In a separate group of animals, cineradiographic images were made at coronal, sagittal, and dorsal orientations during the fluid pressure pulse. Intracranial fluid movement was characterized by rapid radial movement within the epidural space. The data suggest that the distributed nature of fluid-percussion induces pathology, and dysfunction may reflect a diffuse mechanical loading of the brain surface. The model appears to give repeatable effects useful in the study of closed head injury.

Development of tissue level brain injury criteria by finite element analysis.

A three-dimensional finite element model of the direct cortical impact experiment was built and a preliminary validation against mechanical response was completed. The motion of the impactor was enforced in the model by applying the same acceleration history as that of the experimental impactor. A nonlinear contact surface algorithm was used for impactor-brain interface with the ABAQUS general purpose finite element program. The resulting motion of the impactor and the contacting node in the brain model confirmed that the impactor moved realistically and contacted the brain surface. The pressure generated in the model compared favorably with that measured by a pressure transducer in the experiment. The pattern of high shear deformation generated at the impact site in the model was similar to the pattern of contusion hemorrhage seen in the experiment. The pressure generated at the impact site propagated to the skull-brain boundary, especially, at the posterior margin of the cerebellum. Analysis of experimental data using a biomechanically validated finite element model will enable determination of tissue-level injury criteria for application in human brain models to predict head injury potential in contact, noncontact, or side impact situations.

A controlled cortical impact model of traumatic brain injury in the rat.

Controlled cortical impact models produce brain injury by using a pneumatic impactor to impact exposed brain. This study systematically examined the effects of varying magnitudes of controlled cortical impact to the rat brain on neurological, cardiovascular, and histopathological variables. As the magnitude of injury increased, the duration of suppression of somatomotor reflexes and the duration of chronic vestibular motor deficits increased. The blood pressure response was observed to depend on injury levels; a moderate injury level produced a hypotensive response while a high injury level produced an immediate brief hypertensive response followed by hypotension. Low injury levels produced no significant macroscopic or microscopic change, but higher injury levels produced cortical contusion and intraparenchymal hemorrhage which, with increasing survival time, evolved into necrotic changes and cavitation underlying the injury site. Also with high levels of injury, axonal injury was found throughout the brain-stem with the greatest concentration of injured axons occurring in the cerebellar peduncles and pontomedullary junction. These data demonstrate that controlled cortical impact in the rat reproduces many of the features observed in other experimental animal models. This model allows independent control of many mechanical loading parameters associated with traumatic brain injury. The controlled cortical impact rat model should be an effective experimental tool to investigators of traumatic brain injury.

Recurrent inhibition in the rat neostriatum.

During intracellular recording, in the neostriatum of rats anesthetized with urethane, the triggering of an action potential in the recorded neuron by a depolarizing pulse of current resulted in inhibition in that same neuron. This inhibition was evident through its ability to reduce the amplitude of EPSPs evoked from stimulation of substantia nigra. The shunting of SN EPSPs was shown not to be due to action potential currents. The inhibition is antagonized by the GABA blocking agent bicuculline. Intracellular labeling of recorded neurons revealed them as medium spiny neurons. It is concluded that the extensive axon collaterals of spiny projection neurons mediate recurrent inhibition, a portion of which involves autaptic synapses of a neuron back onto itself.

Cerebral uric acid increases following experimental traumatic brain injury in rat.

Following traumatic brain injury (TBI), cortical and thalamic areas were analyzed histologically and by high-performance liquid chromatography with electrochemical detection for uric acid at various survival times. Following TBI, cortical uric acid was elevated by ten-fold at 24 and 48 h, but not at 1 h post-TBI. Histological evidence of neurodegeneration was found not only in cortex but also in the anteroventral thalamus. These data suggest that as in stroke, uric acid measurements may be a convenient and sensitive method for measuring peroxidative status in TBI.

A short duration GABAergic inhibition in identified neostriatal medium spiny neurons: in vitro slice study.

Inhibition in the neostriatum was investigated in rat in vitro slice preparation using intracellular recording and labeling technique. The initial response recorded following local stimulation is a monosynaptically activated EPSP. In 17% of the neurons tested, IPSPs were observed following EPSPs evoked by local stimulation. In paired shock experiments reduction of test EPSP amplitude or action potentials occurred over interstimulus intervals (ISIs) of 3-38 msec. In some neurons, a pulse injection of depolarizing current was used to trigger an action potential which was in a paired shock, used to condition a test monosynaptically induced EPSP. Test EPSPs were shunted over ISIs less than 45 msec. Paired shock performed on the slices perfused with the medium containing GABA antagonists (e.g., bicuculline methiodide, picrotoxin, or penicillin-G) resulted invariably in potentiation of test EPSPs. Inhibition in the neostriatum in vitro is demonstrated as reduction in test amplitude in paired shock tests, by the presence of IPSPs and by the shunting of EPSPs conditioned by an action potential triggered by direct depolarization. Neurons exhibiting these forms of inhibition were intracellularly labelled with HRP and identified as medium spiny neurons. These results indicate that striatal GABAergic medium spiny neurons which are known to have an extensive axon collateral plexus play in a role in a short lasting inhibition observed in the striatum.

Comparative electrophysiology of pyramidal and sparsely spiny stellate neurons of the neocortex.

Slices of sensorimotor and anterior cingulate cortex from guinea pigs were maintained in vitro and bathed in a normal physiological medium. Electrophysiological properties of neurons were assessed with intracellular recording techniques. Some neurons were identified morphologically by intracellular injection of the fluorescent dye Lucifer yellow CH. Three distinct neuronal classes of electrophysiological behavior were observed; these were termed regular spiking, bursting, and fast spiking. The physiological properties of neurons from sensorimotor and anterior cingulate areas did not differ significantly. Regular-spiking cells were characterized by action potentials with a mean duration of 0.80 ms at one-half amplitude, a ratio of maximum rate of spike rise to maximum rate of fall of 4.12, and a prominent afterhyperpolarization following a train of spikes. The primary slope of initial spike frequency versus injected current intensity was 241 Hz/nA. During prolonged suprathreshold current pulses the frequency of firing adapted strongly. When local synaptic pathways were activated, all cells were transiently excited and then strongly inhibited. Bursting cells were distinguished by their ability to generate endogenous, all-or-none bursts of three to five action potentials. Their properties were otherwise very similar to regular-spiking cells. The ability to generate a burst was eliminated when the membrane was depolarized to near the firing threshold with tonic current. By contrast, hyperpolarization of regular-spiking (i.e., nonbursting) cells did not uncover latent bursting tendencies. The action potentials of fast-spiking cells were much briefer (mean of 0.32 ms) than those of the other cell types.(ABSTRACT TRUNCATED AT 250 WORDS)