366 research outputs found
Colossal dielectric constants in transition-metal oxides
Many transition-metal oxides show very large ("colossal") magnitudes of the
dielectric constant and thus have immense potential for applications in modern
microelectronics and for the development of new capacitance-based
energy-storage devices. In the present work, we thoroughly discuss the
mechanisms that can lead to colossal values of the dielectric constant,
especially emphasising effects generated by external and internal interfaces,
including electronic phase separation. In addition, we provide a detailed
overview and discussion of the dielectric properties of CaCu3Ti4O12 and related
systems, which is today's most investigated material with colossal dielectric
constant. Also a variety of further transition-metal oxides with large
dielectric constants are treated in detail, among them the system La2-xSrxNiO4
where electronic phase separation may play a role in the generation of a
colossal dielectric constant.Comment: 31 pages, 18 figures, submitted to Eur. Phys. J. for publication in
the Special Topics volume "Cooperative Phenomena in Solids: Metal-Insulator
Transitions and Ordering of Microscopic Degrees of Freedom
X(3872) and Other Possible Heavy Molecular States
We perform a systematic study of the possible molecular states composed of a
pair of heavy mesons such as , , in
the framework of the meson exchange model. The exchanged mesons include the
pseudoscalar, scalar and vector mesons. Through our investigation, we find that
(1) the structure X(3764) is not a molecular state; (2) There exists strong
attraction in the range fm for the system with .
If future experiments confirm as a loosely bound molecular state,
its quantum number is probably . Its partner state may
be searched for in the channel; (3) The vector meson exchange
provides strong attraction in the channel together with the
pion exchange. A bound state solution exists with a reasonable cutoff parameter
GeV. X(3872) may be accommodated as a molecular state
dynamically although drawing a very definite conclusion needs further
investigation; (4) The molecular state exists.Comment: 21 pages, 17 tables, 11 figures. Typos correcte
On a free boundary problem for a two-species weak competition system
[[abstract]]We study a Lotka–Volterra type weak competition model with a free boundary in a one-dimensional habitat. The main objective is to understand the asymptotic behavior of two competing species spreading via a free boundary. We also provide some sufficient conditions for spreading success and spreading failure, respectively. Finally, when spreading successfully, we provide an estimate to show that the spreading speed (if exists) cannot be faster than the minimal speed of traveling wavefront solutions for the competition model on the whole real line without a free boundary.[[incitationindex]]SCI[[booktype]]紙本[[booktype]]電子
Is X(3872) {\sl Really} a Molecular State?
After taking into account both the pion and sigma meson exchange potential,
we have performed a dynamical calculation of the system.
The meson exchange potential is repulsive from heavy quark symmetry
and numerically important for a loosely bound system. Our analysis disfavors
the interpretation of X(3872) as a loosely bound molecular state if we use the
experimental coupling constant and a reasonable cutoff
around 1 GeV, which is the typical hadronic scale. Bound state solutions with
negative eigenvalues for the system exist only with either a
very large coupling constant (two times of the experimental value) or a large
cutoff ( GeV or GeV). In contrast, there
probably exists a loosely bound S-wave molecular state. Once
produced, such a molecular state would be rather stable since its dominant
decay mode is the radiative decay through . Experimental
search of these states will be very interesting.Comment: 11 pages, 7 figures, 9 tables. The version to appear in EPJ
Identification of New SRF Binding Sites in Genes Modulated by SRF Over-Expression in Mouse Hearts
Background To identify in vivo new cardiac binding sites of serum response factor (SRF) in genes and to study the response of these genes to mild over-expression of SRF, we employed a cardiac-specific, transgenic mouse model, with mild over-expression of SRF (Mild-O SRF Tg). Methodology Microarray experiments were performed on hearts of Mild-O-SRF Tg at 6 months of age. We identified 207 genes that are important for cardiac function that were differentially expressed in vivo. Among them the promoter region of 192 genes had SRF binding motifs, the classic CArG or CArG-like (CArG-L) elements. Fifty-one of the 56 genes with classic SRF binding sites had not been previously reported. These SRF-modulated genes were grouped into 12 categories based on their function. It was observed that genes associated with cardiac energy metabolism shifted toward that of carbohydrate metabolism and away from that of fatty acid metabolism. The expression of genes that are involved in transcription and ion regulation were decreased, but expression of cytoskeletal genes was significantly increased. Using public databases of mouse models of hemodynamic stress (GEO database), we also found that similar altered expression of the SRF-modulated genes occurred in these hearts with cardiac ischemia or aortic constriction as well. Conclusion and significance SRF-modulated genes are actively regulated under various physiological and pathological conditions. We have discovered that a large number of cardiac genes have classic SRF binding sites and were significantly modulated in the Mild-O-SRF Tg mouse hearts. Hence, the mild elevation of SRF protein in the heart that is observed during typical adult aging may have a major impact on many SRF-modulated genes, thereby affecting Cardiac structure and performance. The results from our study could help to enhance our understanding of SRF regulation of cellular processes in the aged heart
Genetic insights into resting heart rate and its role in cardiovascular disease.
Resting heart rate is associated with cardiovascular diseases and mortality in observational and Mendelian randomization studies. The aims of this study are to extend the number of resting heart rate associated genetic variants and to obtain further insights in resting heart rate biology and its clinical consequences. A genome-wide meta-analysis of 100 studies in up to 835,465 individuals reveals 493 independent genetic variants in 352 loci, including 68 genetic variants outside previously identified resting heart rate associated loci. We prioritize 670 genes and in silico annotations point to their enrichment in cardiomyocytes and provide insights in their ECG signature. Two-sample Mendelian randomization analyses indicate that higher genetically predicted resting heart rate increases risk of dilated cardiomyopathy, but decreases risk of developing atrial fibrillation, ischemic stroke, and cardio-embolic stroke. We do not find evidence for a linear or non-linear genetic association between resting heart rate and all-cause mortality in contrast to our previous Mendelian randomization study. Systematic alteration of key differences between the current and previous Mendelian randomization study indicates that the most likely cause of the discrepancy between these studies arises from false positive findings in previous one-sample MR analyses caused by weak-instrument bias at lower P-value thresholds. The results extend our understanding of resting heart rate biology and give additional insights in its role in cardiovascular disease development
The trans-ancestral genomic architecture of glycemic traits
Glycemic traits are used to diagnose and monitor type 2 diabetes and cardiometabolic health. To date, most genetic studies of glycemic traits have focused on individuals of European ancestry. Here we aggregated genome-wide association studies comprising up to 281,416 individuals without diabetes (30% non-European ancestry) for whom fasting glucose, 2-h glucose after an oral glucose challenge, glycated hemoglobin and fasting insulin data were available. Trans-ancestry and single-ancestry meta-analyses identified 242 loci (99 novel; P < 5 x 10(-8)), 80% of which had no significant evidence of between-ancestry heterogeneity. Analyses restricted to individuals of European ancestry with equivalent sample size would have led to 24 fewer new loci. Compared with single-ancestry analyses, equivalent-sized trans-ancestry fine-mapping reduced the number of estimated variants in 99% credible sets by a median of 37.5%. Genomic-feature, gene-expression and gene-set analyses revealed distinct biological signatures for each trait, highlighting different underlying biological pathways. Our results increase our understanding of diabetes pathophysiology by using trans-ancestry studies for improved power and resolution.A trans-ancestry meta-analysis of GWAS of glycemic traits in up to 281,416 individuals identifies 99 novel loci, of which one quarter was found due to the multi-ancestry approach, which also improves fine-mapping of credible variant sets.Diabetes mellitus: pathophysiological changes and therap
Permanence in periodic Kolmogorov competition models with diffusion and nonperiodic feedback control
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