317 research outputs found
Differential contribution of PB1-F2 to the virulence of highly pathogenic H5N1 influenza A virus in mammalian and avian species
Highly pathogenic avian influenza A viruses (HPAIV) of the H5N1 subtype occasionally transmit from birds to humans and can cause severe systemic infections in both hosts. PB1-F2 is an alternative translation product of the viral PB1 segment that was initially characterized as a pro-apoptotic mitochondrial viral pathogenicity factor. A full-length PB1-F2 has been present in all human influenza pandemic virus isolates of the 20(th) century, but appears to be lost evolutionarily over time as the new virus establishes itself and circulates in the human host. In contrast, the open reading frame (ORF) for PB1-F2 is exceptionally well-conserved in avian influenza virus isolates. Here we perform a comparative study to show for the first time that PB1-F2 is a pathogenicity determinant for HPAIV (A/Viet Nam/1203/2004, VN1203 (H5N1)) in both mammals and birds. In a mammalian host, the rare N66S polymorphism in PB1-F2 that was previously described to be associated with high lethality of the 1918 influenza A virus showed increased replication and virulence of a recombinant VN1203 H5N1 virus, while deletion of the entire PB1-F2 ORF had negligible effects. Interestingly, the N66S substituted virus efficiently invades the CNS and replicates in the brain of Mx+/+ mice. In ducks deletion of PB1-F2 clearly resulted in delayed onset of clinical symptoms and systemic spreading of virus, while variations at position 66 played only a minor role in pathogenesis. These data implicate PB1-F2 as an important pathogenicity factor in ducks independent of sequence variations at position 66. Our data could explain why PB1-F2 is conserved in avian influenza virus isolates and only impacts pathogenicity in mammals when containing certain amino acid motifs such as the rare N66S polymorphism
Angiotensin-(1-7) receptor Mas deficiency does not exacerbate cardiac atrophy following high-level spinal cord injury in mice
Experimental spinal cord injury (SCI) causes a morphological and functional deterioration of the heart, in which the renin–angiotensin system (RAS) might play a role. The recently discovered non-canonical axis of RAS with angiotensin-(1-7) and its receptor Mas, which is associated with cardioprotection could be essential to prevent damage to the heart following SCI. We investigated the cardiac consequences of SCI and the role of Mas in female wild-type (WT, n = 22) and mice deficient of Mas (Mas(-/-), n = 25) which underwent spinal cord transection at thoracic level T4 (T4-Tx) or sham-operation by echocardiography (0, 7, 21, and 28 days post-SCI), histology and gene expression analysis at 1 or 2 months post-SCI. We found left ventricular mass reduction with preserved ejection fraction (EF) and fractional shortening in WT as well as Mas(-/-) mice. Cardiac output was reduced in Mas(-/-) mice, whereas stroke volume (SV) was reduced in WT T4-Tx mice. Echocardiographic indices did not differ between the genotypes. Smaller heart weight (HW) and smaller cardiomyocyte diameter at 1 month post-SCI compared to sham mice was independent of genotype. The muscle-specific E3 ubiquitin ligases Atrogin-1/MAFbx and MuRF1 were upregulated or showed a trend for upregulation in WT mice at 2 months post-SCI, respectively. Angiotensinogen gene expression was upregulated at 1 month post-SCI and angiotensin II receptor type 2 downregulated at 2 month post-SCI in Mas(-/-) mice. Mas was downregulated post-SCI. Cardiac atrophy following SCI, not exacerbated by lack of Mas, is a physiological reaction as there were no signs of cardiac pathology and dysfunction
Scaling of the specific heat in superfluid films
We study the specific heat of the model on lattices with (i.e. on lattices representing a film geometry) using the
Cluster Monte--Carlo method. In the --direction we apply Dirichlet boundary
conditions so that the order parameter in the top and bottom layers is zero. We
find that our results for the specific heat of various thickness size
collapse on the same universal scaling function. The extracted scaling function
of the specific heat is in good agreement with the experimentally determined
universal scaling function using no free parameters.Comment: 4 pages, uuencoded compressed PostScrip
Angiotensin‐II receptor type Ia does not contribute to cardiac atrophy following high‐thoracic spinal cord injury in mice
NEW FINDINGS: What is the central question of this study? Spinal cord injury leads to cardiac atrophy and the role of the renin-angiotensin system with angiotensin II acting via its receptor AT1a in this effect has not been previously explored. What is the main finding and its importance? In mice undergone thoracic level 4 transection, we confirm cardiac atrophy. Knockout of AT1a does not protect mice from cardiac atrophy. We observed no histopathological signs but reduced load-dependent left ventricular function (lower stroke volume and cardiac output) with preserved ejection fraction. Further investigations are warranted to assess cardiac function under stress conditions. ABSTRACT: Spinal cord injury (SCI) leads to cardiac atrophy often accompanied by functional deficits. The renin-angiotensin system (RAS) with angiotensin II (AngII) signalling via its receptor AT1a might contribute to cardiac atrophy post-SCI. We performed spinal cord transection at thoracic level T4 (T4-Tx) or sham-operation in female wild type mice (WT, n = 27) and mice deficient of AT1a (Agtr1a(-/-), n = 27). Echocardiography (0, 7, 21 and 28 days post-SCI) as well as histology and gene expression analyses at 1 and 2 months post-SCI were performed. We found cardiac atrophy post-SCI: reduced heart weight, estimated left ventricular mass in Agtr1a(-/-), and cardiomyocyte diameter in WT mice. Although, the latter as well as stroke volume (SV) and cardiac output (CO) were reduced in Agtr1a(-/-) mice already at baseline, cardiomyocyte diameter was even smaller in injured Agtr1a(-/-) mice compared to injured WT mice. SV and CO were reduced in WT mice post-SCI. Ejection fraction and fractional shortening was preserved post-SCI in both genotypes. There were no histological signs of fibrosis and pathology in the cardiac sections of both genotypes post-SCI. Gene expression of Agtr1a showed a trend for upregulation at 2 months post-SCI, angiotensinogen was upregulated at 2 month post-SCI in both genotypes. AngII receptor type 2 (Agtr2) was up-and down-regulated at 1 and 2 months post-SCI in WT mice, respectively, and Ang-(1-7) receptor (Mas) at 1 and 2 months post-SCI. Atrogin-1/MAFbx and MuRF1, the atrophy markers were not significantly upregulated post-SCI. Our data shows that lack of AT1a does not protect from cardiac atrophy post-SCI
Scaling of thermal conductivity of helium confined in pores
We have studied the thermal conductivity of confined superfluids on a
bar-like geometry. We use the planar magnet lattice model on a lattice with . We have applied open boundary conditions on the bar
sides (the confined directions of length ) and periodic along the long
direction. We have adopted a hybrid Monte Carlo algorithm to efficiently deal
with the critical slowing down and in order to solve the dynamical equations of
motion we use a discretization technique which introduces errors only
in the time step . Our results demonstrate the
validity of scaling using known values of the critical exponents and we
obtained the scaling function of the thermal resistivity. We find that our
results for the thermal resistivity scaling function are in very good agreement
with the available experimental results for pores using the tempComment: 5 two-column pages, 3 figures, Revtex
Perturbative calculation of the scaled factorial moments in second-order quark-hadron phase transition within the Ginzburg-Landau description
The scaled factorial moments are studied for a second-order
quark-hadron phase transition within the Ginzburg-Landau description. The role
played by the ground state of the system under low temperature is emphasized.
After a local shift of the order parameter the fluctuations are around the
ground state, and a perturbative calculation for can be carried out.
Power scaling between 's is shown, and a universal scaling exponent
is given for the case with weak correlations and weak
self-interactions.Comment: 12 pages in RevTeX, 12 eps figure
The specific heat of thin films near the lambda-transition: A Monte Carlo study of an improved three-dimensional lattice model
We study the finite size scaling behaviour of the specific heat of thin films
in the neighbourhood of the lambda-transition. To this end we have simulated
the improved two-component phi^4 model on the simple cubic lattice. We employ
free boundary conditions in the short direction to mimic the vanishing order
parameter at the boundaries of a 4He film. Most of our simulations are
performed for the thicknesses L_0=8,16 and 32 of the film. It turns out that
one has to take into account corrections proportional 1/L_0 to obtain a good
collapse of the finite size scaling functions obtained from different L_0. Our
results are compared with those obtained from experiments on thin films of 4He
near the lambda-transition, from field theory and from previous Monte Carlo
simulations.Comment: 46 pages, 15 figure
Li14Ln5[Si11N19O5]O2F2 with Ln = Ce, Nd-Representatives of a Family of Potential Lithium Ion Conductors
The isotypic layered oxonitridosilicates Li14Ln5[Si11N19O5]O2F2 (Ln = Ce, Nd) have been synthesized using Li as fluxing agent and crystallize in the orthorhombic space group Pmmn (Z = 2, Li14Ce5[Si11N19O5]O2F2: a = 17.178(3), b = 7.6500(15), c = 10.116(2) Å, R1 = 0.0409, wR2 = 0.0896; Li14Nd5 Si11N19O5]O2F2: a = 17.126(2), b = 7.6155 15), c = 10.123(2) Å, R1 = 0.0419, wR2 = 0.0929). The silicate layers consist of dreier and sechser rings interconnected via common corners, yielding an unprecedented silicate substructure. A topostructural analysis indicates possible 1D ion migration pathways between five crystallographic independent Li positions. The specific Li-ionic conductivity and its temperature dependence were determined by impedance spectroscopy as well as DC polarization/depolarization measurements. The ionic conductivity is on the order of 5 ×
10−5 S/cm at 300°C, while the activation energy is 0.69 eV. Further adjustments of the defect chemistry (e.g., through doping)can make these compounds interesting candidates for novel oxonitridosilicate based ion conductors
The specific heat of superfluids near the transition temperature
The specific heat of the model is studied on cubic lattices of sizes and on lattices with (i.e.
on lattices representing a film geometry) using the Cluster Monte Carlo method.
Periodic boundary conditions were applied in all directions. In the cubic case
we obtained the ratio of the critical exponents from the size
dependence of the energy density at the critical temperature .
Using finite--size scaling theory, we find that while for both geometries our
results scale to universal functions, these functions differ for the different
geometries. We compare our findings to experimental results and results of
renormalization group calculations.Comment: self-unpacking uuencoded PostScript file (for instructions see the
beginning of the file), 18 pages
- …