962 research outputs found
High resolution Compton scattering as a Probe of the Fermi surface in the Iron-based superconductor
We have carried out first principles all-electron calculations of the
(001)-projected 2D electron momentum density and the directional Compton
profiles along the [100], [001] and [110] directions in the Fe-based
superconductor LaOFeAs within the framework of the local density approximation.
We identify Fermi surface features in the 2D electron momentum density and the
directional Compton profiles, and discuss issues related to the observation of
these features via Compton scattering experiments.Comment: 4 pages, 3 figure
White dwarf spins from low mass stellar evolution models
The prediction of the spins of the compact remnants is a fundamental goal of
the theory of stellar evolution. Here, we confront the predictions for white
dwarf spins from evolutionary models including rotation with observational
constraints. We perform stellar evolution calculations for stars in the mass
range 1... 3\mso, including the physics of rotation, from the zero age main
sequence into the TP-AGB stage. We calculate two sets of model sequences, with
and without inclusion of magnetic fields. From the final computed models of
each sequence, we deduce the angular momenta and rotational velocities of the
emerging white dwarfs. While models including magnetic torques predict white
dwarf rotational velocities between 2 and 10 km s, those from the
non-magnetic sequences are found to be one to two orders of magnitude larger,
well above empirical upper limits. We find the situation analogous to that in
the neutron star progenitor mass range, and conclude that magnetic torques may
be required in order to understand the slow rotation of compact stellar
remnants in general.Comment: Accepted for A&A Letter
Effect of the distal histidine on the peroxidatic activity of monomeric cytoglobin
The reaction of hydrogen peroxide with ferric human cytoglobin and a number of distal histidine variants were studied. The peroxidase activity of the monomeric wildtype protein with an internal disulfide bond, likely to be the form of the protein in vivo, exhibits a high peroxidase-like activity above that of other globins such as myoglobin. Furthermore, the peroxidatic activity of wildtype cytoglobin shows increased resistance to radical-based degradation compared to myoglobin. The ferryl form of wildtype cytoglobin is unstable, but is able to readily oxidize substrates such as guaiacol. In contrast distal histidine mutants of cytoglobin (H81Y and H81V) show very low peroxidase activity but enhanced radical-induced degradation. Therefore, the weakly bound distal histidine appears to modulate ferryl stability and limit haem degradation. These data are consistent with a role of a peroxidase activity of cytoglobin in cell stress response mechanisms.</ns4:p
Endocytic delivery of lipocalin-siderophore-iron complex rescues the kidney from ischemia-reperfusion injury
Neutrophil gelatinase-associated lipocalin (Ngal), also known as siderocalin, forms a complex with iron-binding siderophores (Ngal:siderophore:Fe). This complex converts renal progenitors into epithelial tubules. In this study, we tested the hypothesis that Ngal:siderophore:Fe protects adult kidney epithelial cells or accelerates their recovery from damage. Using a mouse model of severe renal failure, ischemia-reperfusion injury, we show that a single dose of Ngal (10 microg), introduced during the initial phase of the disease, dramatically protects the kidney and mitigates azotemia. Ngal activity depends on delivery of the protein and its siderophore to the proximal tubule. Iron must also be delivered, since blockade of the siderophore with gallium inhibits the rescue from ischemia. The Ngal:siderophore:Fe complex upregulates heme oxygenase-1, a protective enzyme, preserves proximal tubule N-cadherin, and inhibits cell death. Because mouse urine contains an Ngal-dependent siderophore-like activity, endogenous Ngal might also play a protective role. Indeed, Ngal is highly accumulated in the human kidney cortical tubules and in the blood and urine after nephrotoxic and ischemic injury. We reveal what we believe to be a novel pathway of iron traffic that is activated in human and mouse renal diseases, and it provides a unique method for their treatment
Evolution of Robustness to Noise and Mutation in Gene Expression Dynamics
Phenotype of biological systems needs to be robust against mutation in order
to sustain themselves between generations. On the other hand, phenotype of an
individual also needs to be robust against fluctuations of both internal and
external origins that are encountered during growth and development. Is there a
relationship between these two types of robustness, one during a single
generation and the other during evolution? Could stochasticity in gene
expression have any relevance to the evolution of these robustness? Robustness
can be defined by the sharpness of the distribution of phenotype; the variance
of phenotype distribution due to genetic variation gives a measure of `genetic
robustness' while that of isogenic individuals gives a measure of
`developmental robustness'. Through simulations of a simple stochastic gene
expression network that undergoes mutation and selection, we show that in order
for the network to acquire both types of robustness, the phenotypic variance
induced by mutations must be smaller than that observed in an isogenic
population. As the latter originates from noise in gene expression, this
signifies that the genetic robustness evolves only when the noise strength in
gene expression is larger than some threshold. In such a case, the two
variances decrease throughout the evolutionary time course, indicating increase
in robustness. The results reveal how noise that cells encounter during growth
and development shapes networks' robustness to stochasticity in gene
expression, which in turn shapes networks' robustness to mutation. The
condition for evolution of robustness as well as relationship between genetic
and developmental robustness is derived through the variance of phenotypic
fluctuations, which are measurable experimentally.Comment: 25 page
The MRN complex is transcriptionally regulated by MYCN during neural cell proliferation to control replication stress
The MRE11/RAD50/NBS1 (MRN) complex is a major sensor of DNA double strand breaks, whose role in controlling faithful DNA replication and preventing replication stress is also emerging. Inactivation of the MRN complex invariably leads to developmental and/or degenerative neuronal defects, the pathogenesis of which still remains poorly understood. In particular, NBS1 gene mutations are associated with microcephaly and strongly impaired cerebellar development, both in humans and in the mouse model. These phenotypes strikingly overlap those induced by inactivation of MYCN, an essential promoter of the expansion of neuronal stem and progenitor cells, suggesting that MYCN and the MRN complex might be connected on a unique pathway essential for the safe expansion of neuronal cells. Here, we show that MYCN transcriptionally controls the expression of each component of the MRN complex. By genetic and pharmacological inhibition of the MRN complex in a MYCN overexpression model and in the more physiological context of the Hedgehog-dependent expansion of primary cerebellar granule progenitor cells, we also show that the MRN complex is required for MYCN-dependent proliferation. Indeed, its inhibition resulted in DNA damage, activation of a DNA damage response, and cell death in a MYCN- and replication-dependent manner. Our data indicate the MRN complex is essential to restrain MYCN-induced replication stress during neural cell proliferation and support the hypothesis that replication-born DNA damage is responsible for the neuronal defects associated with MRN dysfunctions.Cell Death and Differentiation advance online publication, 12 June 2015; doi:10.1038/cdd.2015.81
General relativistic simulations of pasive-magneto-rotational core collapse with microphysics
This paper presents results from axisymmetric simulations of
magneto-rotational stellar core collapse to neutron stars in general relativity
using the passive field approximation for the magnetic field. These simulations
are performed using a new general relativistic numerical code specifically
designed to study this astrophysical scenario. The code is based on the
conformally-flat approximation of Einstein's field equations and conservative
formulations of the magneto-hydrodynamics equations. The code has been recently
upgraded to incorporate a tabulated, microphysical equation of state and an
approximate deleptonization scheme. This allows us to perform the most
realistic simulations of magneto-rotational core collapse to date, which are
compared with simulations employing a simplified (hybrid) equation of state,
widely used in the relativistic core collapse community. Furthermore,
state-of-the-art (unmagnetized) initial models from stellar evolution are used.
In general, stellar evolution models predict weak magnetic fields in the
progenitors, which justifies our simplification of performing the computations
under the approach that we call the passive field approximation for the
magnetic field. Our results show that for the core collapse models with
microphysics the saturation of the magnetic field cannot be reached within
dynamical time scales by winding up the poloidal magnetic field into a toroidal
one. We estimate the effect of other amplification mechanisms including the
magneto-rotational instability (MRI) and several types of dynamos.Comment: 25 pages, 15 figures, accepted for publication in Astronomy &
Astrophysics July 31, 2007. Added 1 figure and a new subsectio
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