210 research outputs found
Modern nucleon-nucleon interactions and charge-symmetry breaking in nuclei
Coulomb displacement energies, i.e., the differences between the energies of
corresponding nuclear states in mirror nuclei, are evaluated using recent
models for the nucleon-nucleon (NN) interaction. These modern NN potentials
account for breaking of isospin symmetry and reproduce and phase
shifts accurately. The predictions by these new potentials for the binding of
are calculated. A particular focus of our study are effects due to
nuclear correlations and charge-symmetry breaking (CSB). We find that the CSB
terms in the modern NN interactions substantially reduce the discrepancy
between theory and experiment for the Coulomb displacement energies; however,
our calculations do not completely explain the Nolen-Schiffer anomaly.
Potential sources for the remaining discrepancies are discussed.Comment: 10 pages RevTeX, no figure
Saposins (sap) A and C activate the degradation of galactosylceramide in living cells
AbstractIn loading tests using galactosylceramide which had been labelled with tritium in the ceramide moiety, living skin fibroblast lines derived from the original prosaposin-deficient patients had a markedly reduced capacity to degrade galactosylceramide. The hydrolysis of galactosylceramide could be partially restored in these cells, up to about half the normal rate, by adding pure saposin A, pure saposin C, or a mixture of these saposins to the culture medium. By contrast, saposins B and D had little effect on galactosylceramide hydrolysis in the prosaposin-deficient cells. Cells from β-galactocerebrosidase-deficient (Krabbe) patients had a relatively high residual galactosylceramide degradation, which was similar to the rate observed for prosaposin-deficient cells in the presence of saposin A or C. An SV40-transformed fibroblast line from the original saposin C-deficient patient, where saposin A is not affected, showed normal degradation of galactosylceramide. The findings support the hypothesis, which was deduced originally from in vitro experiments, that saposins A and C are the in vivo activators of galactosylceramide degradation. Although the results with saposin C-deficient fibroblasts suggest that the presence of only saposin A allows galactosylceramide breakdown to proceed at a normal rate in fibroblasts, it remains to be determined whether saposins A and C can substitute for each other with respect to their effects on galactosylceramide metabolism in the whole organism
Additional biochemical findings in a patient and fetal sibling with a genetic defect in the sphingolipid activator protein (SAP) precursor, prosaposin. Evidence for a deficiency in SAP-1 and for a normal lysosomal neuraminidase
The Sagnac Phase Shift suggested by the Aharonov-Bohm effect for relativistic matter beams
The phase shift due to the Sagnac Effect, for relativistic matter beams
counter-propagating in a rotating interferometer, is deduced on the bases of a
a formal analogy with the the Aharonov-Bohm effect. A procedure outlined by
Sakurai, in which non relativistic quantum mechanics and newtonian physics
appear together with some intrinsically relativistic elements, is generalized
to a fully relativistic context, using the Cattaneo's splitting technique. This
approach leads to an exact derivation, in a self-consistently relativistic way,
of the Sagnac effect. Sakurai's result is recovered in the first order
approximation.Comment: 18 pages, LaTeX, 2 EPS figures. To appear in General Relativity and
Gravitatio
The relativistic Sagnac Effect: two derivations
The phase shift due to the Sagnac Effect, for relativistic matter and
electromagnetic beams, counter-propagating in a rotating interferometer, is
deduced using two different approaches. From one hand, we show that the
relativistic law of velocity addition leads to the well known Sagnac time
difference, which is the same independently of the physical nature of the
interfering beams, evidencing in this way the universality of the effect.
Another derivation is based on a formal analogy with the phase shift induced by
the magnetic potential for charged particles travelling in a region where a
constant vector potential is present: this is the so called Aharonov-Bohm
effect. Both derivations are carried out in a fully relativistic context, using
a suitable 1+3 splitting that allows us to recognize and define the space where
electromagnetic and matter waves propagate: this is an extended 3-space, which
we call "relative space". It is recognized as the only space having an actual
physical meaning from an operational point of view, and it is identified as the
'physical space of the rotating platform': the geometry of this space turns out
to be non Euclidean, according to Einstein's early intuition.Comment: 49 pages, LaTeX, 3 EPS figures. Revised (final) version, minor
corrections; to appear in "Relativity in Rotating Frames", ed. G. Rizzi and
M.L. Ruggiero, Kluwer Academic Publishers, Dordrecht, (2003). See also
http://digilander.libero.it/solciclo
Absence of stable collinear configurations in Ni(001)ultrathin films: canted domain structure as ground state
Brillouin light scattering (BLS) measurements were performed for (17-120)
Angstrom thick Cu/Ni/Cu/Si(001) films. A monotonic dependence of the frequency
of the uniform mode on an in-plane magnetic field H was observed both on
increasing and on decreasing H in the range (2-14) kOe, suggesting the absence
of a metastable collinear perpendicular ground state. Further investigation by
magneto-optical vector magnetometry (MOKE-VM) in an unconventional canted-field
geometry provided evidence for a domain structure where the magnetization is
canted with respect to the perpendicular to the film. Spin wave calculations
confirm the absence of stable collinear configurations.Comment: 6 pages, 3 figures (text, appendix and 1 figure added
Influence of uncorrelated overlayers on the magnetism in thin itinerant-electron films
The influence of uncorrelated (nonmagnetic) overlayers on the magnetic
properties of thin itinerant-electron films is investigated within the
single-band Hubbard model. The Coulomb correlation between the electrons in the
ferromagnetic layers is treated by using the spectral density approach (SDA).
It is found that the presence of nonmagnetic layers has a strong effect on the
magnetic properties of thin films. The Curie temperatures of very thin films
are modified by the uncorrelated overlayers. The quasiparticle density of
states is used to analyze the results. In addition, the coupling between the
ferromagnetic layers and the nonmagnetic layers is discussed in detail. The
coupling depends on the band occupation of the nonmagnetic layers, while it is
almost independent of the number of the nonmagnetic layers. The induced
polarization in the nonmagnetic layers shows a long-range decreasing
oscillatory behavior and it depends on the coupling between ferromagnetic and
nonmagnetic layers.Comment: 9 pages, RevTex, 6 figures, for related work see:
http://orion.physik.hu-berlin.d
Stress and displacement pattern evaluation using two different palatal expanders in unilateral cleft lip and palate: a three-dimensional finite element analysis
Specific saposin C deficiency: CNS impairment and acid β-glucosidase effects in the mouse
Saposins A, B, C and D are derived from a common precursor, prosaposin (psap). The few patients with saposin C deficiency develop a Gaucher disease-like central nervous system (CNS) phenotype attributed to diminished glucosylceramide (GC) cleavage activity by acid β-glucosidase (GCase). The in vivo effects of saposin C were examined by creating mice with selective absence of saposin C (C−/−) using a knock-in point mutation (cysteine-to-proline) in exon 11 of the psap gene. In C−/− mice, prosaposin and saposins A, B and D proteins were present at near wild-type levels, but the saposin C protein was absent. By 1 year, the C−/− mice exhibited weakness of the hind limbs and progressive ataxia. Decreased neuromotor activity and impaired hippocampal long-term potentiation were evident. Foamy storage cells were observed in dorsal root ganglion and there was progressive loss of cerebellar Purkinje cells and atrophy of cerebellar granule cells. Ultrastructural analyses revealed inclusions in axonal processes in the spinal cord, sciatic nerve and brain, but no excess of multivesicular bodies. Activated microglial cells and astrocytes were present in thalamus, brain stem, cerebellum and spinal cord, indicating regional pro-inflammatory responses. No storage cells were found in visceral organs of these mice. The absence of saposin C led to moderate increases in GC and lactosylceramide (LacCer) and their deacylated analogues. These results support the view that saposin C has multiple roles in glycosphingolipid (GSL) catabolism as well as a prominent function in CNS and axonal integrity independent of its role as an optimizer/stabilizer of GCase
Neurological deficits and glycosphingolipid accumulation in saposin B deficient mice
Saposin B derives from the multi-functional precursor, prosaposin, and functions as an activity enhancer for several glycosphingolipid (GSL) hydrolases. Mutations in saposin B present in humans with phenotypes resembling metachromatic leukodystrophy. To gain insight into saposin B's physiological functions, a specific deficiency was created in mice by a knock-in mutation of an essential cysteine in exon 7 of the prosaposin locus. No saposin B protein was detected in the homozygotes (B−/−) mice, whereas prosaposin, and saposins A, C and D were at normal levels. B−/− mice exhibited slowly progressive neuromotor deterioration and minor head tremor by 15 months. Excess hydroxy and non-hydroxy fatty acid sulfatide levels were present in brain and kidney. Alcian blue positive (sulfatide) storage cells were found in the brain, spinal cord and kidney. Ultrastructural analyses showed lamellar inclusion material in the kidney, sciatic nerve, brain and spinal cord tissues. Lactosylceramide (LacCer) and globotriaosylceramide (TriCer) were increased in various tissues of B−/− mice supporting the in vivo role of saposin B in the degradation of these lipids. CD68 positive microglial cells and activated GFAP positive astrocytes showed a proinflammatory response in the brains of B−/− mice. These findings delineate the roles of saposin B for the in vivo degradation of several GSLs and its primary function in maintenance of CNS function. B−/− provide a useful model for understanding the contributions of this saposin to GSL metabolism and homeostasis
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