266 research outputs found
Thermomagnetic detection of recrystallization in FeCoNbBCu nanocrystalline alloys
The recrystallization process in FeCoNbBCu nanocrystallinealloys is evidenced from thermomagnetic results as a significant decrease in magnetization at the second crystallization stage. The lowering in the volume fraction of α-FeCo crystals indicates that some of these crystals contribute to the boride phases formed. Electron microscopy images reveal that the final microstructure consists of large crystals (âŒ500 nm) of a fcc (FeCo)23B6(FeCo)23B6 phase and small crystals (âŒ20 nm) of bcc α-FeCo and of some boride phases as such (FeCo)2B
Trois cas graves de rickettsiose humaine à R. conori sans transmission entomologique avérée
Bertoye A., Royer J., Vincent P., Joubert L., Guillermet F. N., Garin J. P. Trois cas graves de Rickettsiose humaine à R. Conori, sans transmission entomologique avérée. In: Bulletin de l'Académie Vétérinaire de France tome 123 n°6, 1970. pp. 247-256
Bronchopulmonary Dysplasia
Hospitalizations for respiratory syncytial virus bronchioliti
Steam reforming on transition-metal carbides from density-functional theory
A screening study of the steam reforming reaction (CH_4 + H_2O -> CO + 3H_2)
on early transition-metal carbides (TMC's) is performed by means of
density-functional theory calculations. The set of considered surfaces includes
the alpha-Mo_2C(100) surfaces, the low-index (111) and (100) surfaces of TiC,
VC, and delta-MoC, and the oxygenated alpha-Mo_2C(100) and TMC(111) surfaces.
It is found that carbides provide a wide spectrum of reactivities towards the
steam reforming reaction, from too reactive via suitable to too inert. The
reactivity is discussed in terms of the electronic structure of the clean
surfaces. Two surfaces, the delta-MoC(100) and the oxygen passivated
alpha-Mo_2C(100) surfaces, are identified as promising steam reforming
catalysts. These findings suggest that carbides provide a playground for
reactivity tuning, comparable to the one for pure metals.Comment: 6 pages, 4 figure
A constant and similar assembly defect of mitochondrial respiratory chain complex I allows rapid identification of NDUFS4 mutations in patients with Leigh syndrome
AbstractIsolated complex I deficiency is a frequent cause of respiratory chain defects in childhood. In this study, we report our systematic approach with blue native PAGE (BN-PAGE) to study mitochondrial respiratory chain assembly in skin fibroblasts from patients with Leigh syndrome and CI deficiency. We describe five new NDUFS4 patients with a similar and constant abnormal BN-PAGE profile and present a meta-analysis of the literature. All NDUFS4 mutations that have been tested with BN-PAGE result in a constant and similar abnormal assembly profile with a complete loss of the fully assembled complex I usually due to a truncated protein and the loss of its canonical cAMP dependent protein kinase phosphorylation consensus site. We also report the association of abnormal brain MRI images with this characteristic BN-PAGE profile as the hallmarks of NDUFS4 mutations and the first founder NDUFS4 mutations in the North-African population
Saturation of electrical resistivity
Resistivity saturation is observed in many metallic systems with a large
resistivity, i.e., when the resistivity has reached a critical value, its
further increase with temperature is substantially reduced. This typically
happens when the apparent mean free path is comparable to the interatomic
separations - the Ioffe-Regel condition. Recently, several exceptions to this
rule have been found. Here, we review experimental results and early theories
of resistivity saturation. We then describe more recent theoretical work,
addressing cases both where the Ioffe-Regel condition is satisfied and where it
is violated. In particular we show how the (semiclassical) Ioffe-Regel
condition can be derived quantum-mechanically under certain assumptions about
the system and why these assumptions are violated for high-Tc cuprates and
alkali-doped fullerides.Comment: 16 pages, RevTeX, 15 eps figures, additional material available at
http://www.mpi-stuttgart.mpg.de/andersen/saturation
Effects of anharmonic strain on phase stability of epitaxial films and superlattices: applications to noble metals
Epitaxial strain energies of epitaxial films and bulk superlattices are
studied via first-principles total energy calculations using the local-density
approximation. Anharmonic effects due to large lattice mismatch, beyond the
reach of the harmonic elasticity theory, are found to be very important in
Cu/Au (lattice mismatch 12%), Cu/Ag (12%) and Ni/Au (15%). We find that
is the elastically soft direction for biaxial expansion of Cu and Ni, but it is
for large biaxial compression of Cu, Ag, and Au. The stability of
superlattices is discussed in terms of the coherency strain and interfacial
energies. We find that in phase-separating systems such as Cu-Ag the
superlattice formation energies decrease with superlattice period, and the
interfacial energy is positive. Superlattices are formed easiest on (001) and
hardest on (111) substrates. For ordering systems, such as Cu-Au and Ag-Au, the
formation energy of superlattices increases with period, and interfacial
energies are negative. These superlattices are formed easiest on (001) or (110)
and hardest on (111) substrates. For Ni-Au we find a hybrid behavior:
superlattices along and like in phase-separating systems, while for
they behave like in ordering systems. Finally, recent experimental
results on epitaxial stabilization of disordered Ni-Au and Cu-Ag alloys,
immiscible in the bulk form, are explained in terms of destabilization of the
phase separated state due to lattice mismatch between the substrate and
constituents.Comment: RevTeX galley format, 16 pages, includes 9 EPS figures, to appear in
Physical Review
Melting of tantalum at high pressure determined by angle dispersive x-ray diffraction in a double-sided laser-heated diamond-anvil cell
The high pressure and high temperature phase diagram of Ta has been studied
in a laser-heated diamond-anvil cell (DAC) using x-ray diffraction measurements
up to 52 GPa and 3800 K. The melting was observed at nine different pressures,
being the melting temperature in good agreement with previous laser-heated DAC
experiments, but in contradiction with several theoretical calculations and
previous piston-cylinder apparatus experiments. A small slope for the melting
curve of Ta is estimated (dTm/dP = 24 K/GPa at 1 bar) and a possible
explanation for this behaviour is given. Finally, a P-V-T equation of states is
obtained, being the temperature dependence of the thermal expansion coefficient
and the bulk modulus estimated.Comment: 31 pages, 8 figures, to appear in J.Phys.:Cond.Matte
Pancreatic cancer intrinsic PI3Kα activity accelerates metastasis and rewires macrophage component.
Pancreatic ductal adenocarcinoma (PDAC) patients frequently suffer from undetected micro-metastatic disease. This clinical situation would greatly benefit from additional investigation. Therefore, we set out to identify key signalling events that drive metastatic evolution from the pancreas. We searched for a gene signature that discriminate localised PDAC from confirmed metastatic PDAC and devised a preclinical protocol using circulating cell-free DNA (cfDNA) as an early biomarker of micro-metastatic disease to validate the identification of key signalling events. An unbiased approach identified, amongst actionable markers of disease progression, the PI3K pathway and a distinctive PI3Kα activation signature as predictive of PDAC aggressiveness and prognosis. Pharmacological or tumour-restricted genetic PI3Kα-selective inhibition prevented macro-metastatic evolution by hindering tumoural cell migratory behaviour independently of genetic alterations. We found that PI3Kα inhibition altered the quantity and the species composition of the produced lipid second messenger PIP3 , with a selective decrease of C36:2 PI-3,4,5-P3 . Tumoural PI3Kα inactivation prevented the accumulation of pro-tumoural CD206-positive macrophages in the tumour-adjacent tissue. Tumour cell-intrinsic PI3Kα promotes pro-metastatic features that could be pharmacologically targeted to delay macro-metastatic evolution
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