178 research outputs found
Projectile fragmentation reactions and production of nuclei near the neutron drip-line
The reaction mechanism of projectile fragmentation at intermediate energies
has been investigated observing the target dependence of the production cross
sections of very neutron-rich nuclei. Measurement of longitudinal momentum
distributions of projectile-like fragments within a wide range of fragment mass
and its charge was performed using a hundred-MeV/n Ar beam incident on
Be and Ta targets. By measurement of fragment momentum distribution, a
parabolic mass dependence of momentum peak shift was observed in the results of
both targets, and a phenomenon of light-fragment acceleration was found only in
the Be-target data. The analysis of production cross sections revealed an
obvious enhancement of the target dependence except target size effect when the
neutron excess is increased. This result implies the breakdown of factorization
(BOF) of production cross sections for very neutron-rich nuclei near the drip
line.Comment: 16 pages, 18 figures, submitted to Phys. Rev.
Measurement of the spin and magnetic moment of 23Al
For the first time, we obtained the g factor for the ground state of 23Al by use of a -NMR measurement. 23Al has a small proton separation energy and is a potential proton-halo candidate. The obtained g factor, |g|=1.557Ā±0.088, clearly shows the spin and parity, J=5/2+, for 23Al, which is the same as that of its mirror partner, 23Ne. The possible nuclear structure of 23Al is also discussed
Dibucaine Mitigates Spreading Depolarization in Human Neocortical Slices and Prevents Acute Dendritic Injury in the Ischemic Rodent Neocortex
Spreading depolarizations that occur in patients with malignant stroke, subarachnoid/intracranial hemorrhage, and traumatic brain injury are known to facilitate neuronal damage in metabolically compromised brain tissue. The dramatic failure of brain ion homeostasis caused by propagating spreading depolarizations results in neuronal and astroglial swelling. In essence, swelling is the initial response and a sign of the acute neuronal injury that follows if energy deprivation is maintained. Choosing spreading depolarizations as a target for therapeutic intervention, we have used human brain slices and in vivo real-time two-photon laser scanning microscopy in the mouse neocortex to study potentially useful therapeutics against spreading depolarization-induced injury.We have shown that anoxic or terminal depolarization, a spreading depolarization wave ignited in the ischemic core where neurons cannot repolarize, can be evoked in human slices from pediatric brains during simulated ischemia induced by oxygen/glucose deprivation or by exposure to ouabain. Changes in light transmittance (LT) tracked terminal depolarization in time and space. Though spreading depolarizations are notoriously difficult to block, terminal depolarization onset was delayed by dibucaine, a local amide anesthetic and sodium channel blocker. Remarkably, the occurrence of ouabain-induced terminal depolarization was delayed at a concentration of 1 ĀµM that preserves synaptic function. Moreover, in vivo two-photon imaging in the penumbra revealed that, though spreading depolarizations did still occur, spreading depolarization-induced dendritic injury was inhibited by dibucaine administered intravenously at 2.5 mg/kg in a mouse stroke model.Dibucaine mitigated the effects of spreading depolarization at a concentration that could be well-tolerated therapeutically. Hence, dibucaine is a promising candidate to protect the brain from ischemic injury with an approach that does not rely on the complete abolishment of spreading depolarizations
Myc proteins in brain tumor development and maintenance
Myc proteins are often deregulated in human brain tumors, especially in embryonal tumors that affect children. Many observations have shown how alterations of these pleiotropic Myc transcription factors provide initiation, maintenance, or progression of tumors. This review will focus on the role of Myc family members (particularly c-myc and Mycn) in tumors like medulloblastoma and glioma and will further discuss how to target stabilization of these proteins for future brain tumor therapies
Basement Membrane Zone Collagens XV and XVIII/Proteoglycans Mediate Leukocyte Influx in Renal Ischemia/Reperfusion
Collagen type XV and XVIII are proteoglycans found in the basement membrane zones of endothelial and epithelial cells, and known for their cryptic anti-angiogenic domains named restin and endostatin, respectively. Mutations or deletions of these collagens are associated with eye, muscle and microvessel phenotypes. We now describe a novel role for these collagens, namely a supportive role in leukocyte recruitment. We subjected mice deficient in collagen XV or collagen XVIII, and their compound mutant, as well as the wild-type control mice to bilateral renal ischemia/reperfusion, and evaluated renal function, tubular injury, and neutrophil and macrophage influx at different time points after ischemia/reperfusion. Five days after ischemia/reperfusion, the collagen XV, collagen XVIII and the compound mutant mice showed diminished serum urea levels compared to wild-type mice (all
Endogenous fertility, endogenous lifetime and economic growth: the role of child policies
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