437 research outputs found
Spin-flip processes and ultrafast magnetization dynamics in Co - unifying the microscopic and macroscopic view of femtosecond magnetism
The femtosecond magnetization dynamics of a thin cobalt film excited with
ultrashort laser pulses has been studied using two complementary pump-probe
techniques, namely spin-, energy- and time-resolved photoemission and
time-resolved magneto-optical Kerr effect. Combining the two methods it is
possible to identify the microscopic electron spin-flip mechanisms responsible
for the ultrafast macroscopic magnetization dynamics of the cobalt film. In
particular, we show that electron-magnon excitation does not affect the overall
magnetization even though it is an efficient spin-flip channel on the sub-200
fs timescale. Instead we find experimental evidence for the relevance of
Elliott-Yafet type spin-flip processes for the ultrafast demagnetization taking
place on a time scale of 300 fs.Comment: 12 pages, 3 figures; accepted by Physical Review Letter
Shape of primary proton spectrum in multi-TeV region from data on vertical muon flux
It is shown, that primary proton spectrum, reconstructed from sea-level and
underground data on muon spectrum with the use of QGSJET 01, QGSJET II, NEXUS
3.97 and SIBYLL 2.1 interaction models, demonstrates not only model-dependent
intensity, but also model-dependent form. For correct reproduction of muon
spectrum shape primary proton flux should have non-constant power index for all
considered models, except SIBYLL 2.1, with break at energies around 10-15 TeV
and value of exponent before break close to that obtained in ATIC-2 experiment.
To validate presence of this break understanding of inclusive spectra behavior
in fragmentation region in p-air collisions should be improved, but we show,
that it is impossible to do on the basis of the existing experimental data on
primary nuclei, atmospheric muon and hadron fluxes.Comment: Submitted to Phys. Rev.
Inhibition of the mitochondrial pyruvate carrier protects from excitotoxic neuronal death.
Glutamate is the dominant excitatory neurotransmitter in the brain, but under conditions of metabolic stress it can accumulate to excitotoxic levels. Although pharmacologic modulation of excitatory amino acid receptors is well studied, minimal consideration has been given to targeting mitochondrial glutamate metabolism to control neurotransmitter levels. Here we demonstrate that chemical inhibition of the mitochondrial pyruvate carrier (MPC) protects primary cortical neurons from excitotoxic death. Reductions in mitochondrial pyruvate uptake do not compromise cellular energy metabolism, suggesting neuronal metabolic flexibility. Rather, MPC inhibition rewires mitochondrial substrate metabolism to preferentially increase reliance on glutamate to fuel energetics and anaplerosis. Mobilizing the neuronal glutamate pool for oxidation decreases the quantity of glutamate released upon depolarization and, in turn, limits the positive-feedback cascade of excitotoxic neuronal injury. The finding links mitochondrial pyruvate metabolism to glutamatergic neurotransmission and establishes the MPC as a therapeutic target to treat neurodegenerative diseases characterized by excitotoxicity
Mitochondrial dysfunction in an Opa1Q285STOP mouse model of dominant optic atrophy results from Opa1 haploinsufficiency
Mutations in the opa1 (optic atrophy 1) gene lead to autosomal dominant optic atrophy (ADOA), a hereditary eye disease. This gene encodes the Opa1 protein, a mitochondrial dynamin-related GTPase required for mitochondrial fusion and the maintenance of normal crista structure. The majority of opa1 mutations encode truncated forms of the protein, lacking a complete GTPase domain. It is unclear whether the phenotype results from haploinsufficiency or rather a deleterious effect of truncated Opa1 protein. We studied a heterozygous Opa1 mutant mouse carrying a defective allele with a stop codon in the beginning of the GTPase domain at residue 285, a mutation that mimics human pathological mutations. Using an antibody raised against an N-terminal portion of Opa1, we found that the level of wild-type protein was decreased in the mutant mice, as predicted. However, no truncated Opa1 protein was expressed. In embryonic fibroblasts isolated from the mutant mice, this partial loss of Opa1 caused mitochondrial respiratory deficiency and a selective loss of respiratory Complex IV subunits. Furthermore, partial Opa1 deficiency resulted in a substantial resistance to endoplasmic reticulum stress-induced death. On the other hand, the enforced expression of truncated Opa1 protein in cells containing normal levels of wild-type protein did not cause mitochondrial defects. Moreover, cells expressing the truncated Opa1 protein showed reduced Bax activation in response to apoptotic stimuli. Taken together, our results exclude deleterious dominant-negative or gain-of-function mechanisms for this type of Opa1 mutation and affirm haploinsufficiency as the mechanism underlying mitochondrial dysfunction in ADOA
Intruder bands and configuration mixing in the lead isotopes
A three-configuration mixing calculation is performed in the context of the
interacting boson model with the aim to describe recently observed collective
bands built on low-lying states in neutron-deficient lead isotopes. The
configurations that are included correspond to the regular, spherical states as
well as two-particle two-hole and four-particle four-hole excitations across
the Z=82 shell gap.Comment: 20 pages, 4 figures, accepted by PRC, reference added for section 1
in this revised versio
Large-Scale Sidereal Anisotropy of Galactic Cosmic-Ray Intensity Observed by the Tibet Air Shower Array
We present the large-scale sidereal anisotropy ofgalactic cosmic-ray
intensity in the multi-TeV region observed with the Tibet-IIIair shower array
during the period from 1999 through 2003. The sidereal daily variation of
cosmic rays observed in this experiment shows an excess of relative intensity
around hours local sidereal time, as well as a deficit around 12
hours local sidereal time. While the amplitude of the excess is not significant
when averaged over all declinations, the excess in individual declinaton bands
becomes larger and clearer as the viewing direction moves toward the south. The
maximum phase of the excess intensity changes from 7 at the northern
hemisphere to 4 hours at the equatorial region. We also show that both
the amplitude and the phase of the first harmonic vector of the daily variation
are remarkably independent of primary energy in the multi-TeV region. This is
the first result determining the energy and declination dependences of the full
24-hour profiles of the sidereal daily variation in the multi-TeV region with a
single air shower experiment.Comment: 13 pages, 3 figures, 1 table. Accepted for publication in ApJ
Beta-Delayed fission of 230Am
The exotic decay process of β-delayed fission (βDF) has been studied in the neutron-deficient isotope Am230. The Am230 nuclei were produced in the complete fusion reaction Pb207(Al27,4n)Am230 and separated by using the GARIS gas-filled recoil ion separator. A lower limit for the βDF probability PβDF(Am230)>0.30 was deduced, which so far is the highest value among all known βDF nuclei. The systematics of βDF in the region of Am230 will be discussed
A proposed reaction channel for the synthesis of the superheavy nucleus Z = 109
We apply a statistical-evaporation model (HIVAP) to calculate the cross
sections of superheavy elements, mainly about actinide targets and compare with
some available experimental data. A reaction channel Si + Am is
proposed for the synthesis of the element Z = 109 and the cross section is
estimated.Comment: 4 pages, 2 figures, 2 tables; two typos are corrected in Ref. [12]
and [19
Role of Multichance Fission in the Description of Fission-Fragment Mass Distributions at High Energies
Fission-fragment mass distributions were measured for U237-240, Np239-242, and Pu241-244 populated in the excitation-energy range from 10 to 60 MeV by multinucleon transfer channels in the reaction O18+U238 at the Japan Atomic Energy Agency tandem facility. Among them, the data for U240 and Np240,241,242 were observed for the first time. It was found that the mass distributions for all the studied nuclides maintain a double-humped shape up to the highest measured energy in contrast to expectations of predominantly symmetric fission due to the washing out of nuclear shell effects. From a comparison with the dynamical calculation based on the fluctuation-dissipation model, this behavior of the mass distributions was unambiguously attributed to the effect of multichance fission
A phase II study of S-1 monotherapy administered for 2 weeks of a 3-week cycle in advanced gastric cancer patients with poor performance status
Systemic chemotherapy for gastric cancer is often associated with treatment-related toxicity, which is particularly severe in patients with a poor performance status. In this paper, we describe the first study to evaluate S-1 monotherapy as an option for advanced gastric cancer patients who are not candidates for combination chemotherapy due to poor clinical condition. Fifty-two patients with Eastern Cooperative Oncology Group (ECOG) performance scale 2–3, whose general condition had made use of combination chemotherapy impossible, were enrolled. S-1 was administered to 30 patients as second- or third-line therapy. The initial dose of S-1 was 35 mg m−2, administered b.i.d for 14 days every 3 weeks. With a median follow-up period of 33 weeks, the median progression-free survival, and overall survival were 11 weeks (95% CI, 8–14) and 33 weeks (95% CI, 19–47), respectively. The overall 1-year survival rate was 29% by intent-to-treat analysis. The overall response rate was 12% (95% CI, 3–21), and the percentage of stable disease was 35%, resulting in the disease control rate of 47% (95% CI, 32–60). Significant drug-related toxicity included grade 3 diarrhoea (14%), anorexia (14%), fatigue (10%), neutropenia (10%), and leucopenia (6%). In conclusion, this study indicated the modest activity of S-1 in gastric cancer patients with poor performance status
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