1,678 research outputs found
The Diversity and Evolution of Sex Chromosomes in Frogs
Frogs are ideal organisms for studying sex chromosome evolution because of their diversity in sex chromosome differentiation and sex-determination systems. We review 222 anuran frogs, spanning ~220 Myr of divergence, with characterized sex chromosomes, and discuss their evolution, phylogenetic distribution and transitions between homomorphic and heteromorphic states, as well as between sex-determination systems. Most (~75%) anurans have homomorphic sex chromosomes, with XY systems being three times more common than ZW systems. Most remaining anurans (~25%) have heteromorphic sex chromosomes, with XY and ZW systems almost equally represented. There are Y-autosome fusions in 11 species, and no W-/Z-/X-autosome fusions are known. The phylogeny represents at least 19 transitions between sex-determination systems and at least 16 cases of independent evolution of heteromorphic sex chromosomes from homomorphy, the likely ancestral state. Five lineages mostly have heteromorphic sex chromosomes, which might have evolved due to demographic and sexual selection attributes of those lineages. Males do not recombine over most of their genome, regardless of which is the heterogametic sex. Nevertheless, telomere-restricted recombination between ZW chromosomes has evolved at least once. More comparative genomic studies are needed to understand the evolutionary trajectories of sex chromosomes among frog lineages, especially in the ZW systems
Numerical Model on Sound-Solid Coupling in Human Ear and Study on Sound Pressure of Tympanic Membrane
Establishment of three-dimensional finite-element model of the whole auditory system includes external ear, middle ear, and inner ear. The sound-solid-liquid coupling frequency response analysis of the model was carried out. The correctness of the FE model was verified by comparing the vibration modes of tympanic membrane and stapes footplate with the experimental data. According to calculation results of the model, we make use of the least squares method to fit out the distribution of sound pressure of external auditory canal and obtain the sound pressure function on the tympanic membrane which varies with frequency. Using the sound pressure function, the pressure distribution on the tympanic membrane can be directly derived from the sound pressure at the external auditory canal opening. The sound pressure function can make the boundary conditions of the middle ear structure more accurate in the mechanical research and improve the previous boundary treatment which only applied uniform pressure acting to the tympanic membrane
Exact diagonalization for spin-1/2 chains and the first order quantum phase transitions of the XXX chain in a uniform transverse field
A simple Mathematica code based on the differential realization of hard-core boson operators for finding exact solutions of the periodic-N spin-1/2 systems with or beyond nearest neighbor interactions is proposed; it can easily be used to study general spin-1/2 interaction systems. As an example, the code is applied to study XXX spin-1/2 chains with nearest neighbor interaction in a uniform transverse field. It shows that there are [N/2] level-crossing points in the ground state, where N is the periodic number of the system and [x] stands for the integer part of x, when the interaction strength and magnitude of the magnetic field satisfy certain conditions. The quantum phase transitional behavior in the ground state of the system in the thermodynamic limit is also studied. © IOP Publishing Ltd
Next-to-leading order QCD predictions for the hadronic +jet production
We calculate the next-to-leading order(NLO) QCD corrections to the
production in association with a jet at hadron colliders. We study the impacts
of the complete NLO QCD radiative corrections to the integrated cross sections,
the scale dependence of the cross sections, and the differential cross sections
(, ) of the final -,
Higgs-boson and jet. We find that the corrections significantly modify the
physical observables, and reduce the scale uncertainty of the LO cross section.
Our results show that by applying the inclusive scheme with and taking , , the
K-factor is 1.15 for the process at the Tevatron,
while the K-factors for the processes and
at the LHC are 1.12 and 1.08 respectively. We conclude that to understand the
hadronic associated production, it is necessary to study the NLO QCD
corrections to production process which is part of the inclusive
production.Comment: 26 pages, 27 figures, accepted by Phys. Rev.
Bright nonblinking photoluminescence with blinking lifetime from a nanocavity-coupled quantum dot
Colloidal semiconductor quantum dots (QDs) are excellent luminescent
nanomaterials for a broad range of optoelectronic applications. Their
photoluminescence blinking, however, hinders their practical use in many
aspects. It has been shown that coupling QDs to plasmonic nanostructures may
provide a viable way to suppress blinking. Nevertheless, the underlying
mechanism of blinking suppression remains unclear and debated. Here, by
deterministically coupling a single QD to a plasmonic nanocavity, we clarify
the mechanism of blinking suppression, and demonstrate unprecedentedly bright
emission from a single colloidal QD. In particular, we report for the first
time that the coupled system exhibits nonblinking photoluminescence with
blinking lifetime, which shows that the elimination of photoluminescence
blinking originates from enhanced quantum yield of the charged states. We
identify that the radiative decay rate is boosted from (48 ns)-1 to (0.7 ns)-1,
which outcompetes Auger processes and enables similar quantum yields for
charged and neutral excitons. Moreover, we demonstrate ultrabright
photoluminescence of up to 17 million detected photons per second from a single
QD. This work sheds new light on the goal of achieving ultrabright nonblinking
QDs and may benefit a variety of QD-based applications.Comment: 17 pages; 3 figures
Poly[[diaqua(μ4-1H-benzimidazole-5,6-dicarboxylato)strontium] monohydrate]
Each of the carboxylate –CO2 fragments of the dianion ligand in the title compound, {[Sr(C9H4N2O4)(H2O)2]·H2O}n, chelates to a SrII atom and at the same time, one of the two O atoms coordinates to a third SrII atom. The μ4-bridging mode of the dianion generates a square-grid layer motif; adjacent layers are connected by O—H⋯O, O—H⋯N and N—H⋯O hydrogen bonds, forming a three-dimensional network. The eight-coordinate Sr atom exists in a distorted square-antiprismatic geometry. The crystal studied was a non-merohedral twin with a minor twin component of 24%
Heat Shock Protein 70 Protects the Heart from Ischemia/Reperfusion Injury through Inhibition of p38 MAPK Signaling.
BackgroundHeat shock protein 70 (Hsp70) has been shown to exert cardioprotection. Intracellular calcium ([Ca2+]i) overload induced by p38 mitogen-activated protein kinase (p38 MAPK) activation contributes to cardiac ischemia/reperfusion (I/R) injury. However, whether Hsp70 interacts with p38 MAPK signaling is unclear. Therefore, this study investigated the regulation of p38 MAPK by Hsp70 in I/R-induced cardiac injury.MethodsNeonatal rat cardiomyocytes were subjected to oxygen-glucose deprivation for 6 h followed by 2 h reoxygenation (OGD/R), and rats underwent left anterior artery ligation for 30 min followed by 30 min of reperfusion. The p38 MAPK inhibitor (SB203580), Hsp70 inhibitor (Quercetin), and Hsp70 short hairpin RNA (shRNA) were used prior to OGD/R or I/R. Cell viability, lactate dehydrogenase (LDH) release, serum cardiac troponin I (cTnI), [Ca2+]i levels, cell apoptosis, myocardial infarct size, mRNA level of IL-1β and IL-6, and protein expression of Hsp70, phosphorylated p38 MAPK (p-p38 MAPK), sarcoplasmic/endoplasmic reticulum Ca2+-ATPase2 (SERCA2), phosphorylated signal transducer and activator of transcription3 (p-STAT3), and cleaved caspase3 were assessed.ResultsPretreatment with a p38 MAPK inhibitor, SB203580, significantly attenuated OGD/R-induced cell injury or I/R-induced myocardial injury, as evidenced by improved cell viability and lower LDH release, resulted in lower serum cTnI and myocardial infarct size, alleviation of [Ca2+]i overload and cell apoptosis, inhibition of IL-1β and IL-6, and modulation of protein expressions of p-p38 MAPK, SERCA2, p-STAT3, and cleaved-caspase3. Knockdown of Hsp70 by shRNA exacerbated OGD/R-induced cell injury, which was effectively abolished by SB203580. Moreover, inhibition of Hsp70 by quercetin enhanced I/R-induced myocardial injury, while SB203580 pretreatment reversed the harmful effects caused by quercetin.ConclusionsInhibition of Hsp70 aggravates [Ca2+]i overload, inflammation, and apoptosis through regulating p38 MAPK signaling during cardiac I/R injury, which may help provide novel insight into cardioprotective strategies
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