Mechanisms of limitation and nature of field dependence of critical current in HTS epitaxial YBaCuO films

Magnetic field and temperature dependencies of the critical current density, J/sub c/(H/spl par/c, T) were measured by SQUID-magnetometry, ac magnetic susceptibility, and dc transport current techniques in the single-crystalline epitaxially-grown by off-axis dc magnetron sputtering YBa/sub 2/Cu/sub 3/O/sub 7-/spl delta// (YBCO) films with J/sub c/(H/spl par/c, 77 K) /spl ges/ 2 /spl middot/ 10/sup 6/ A/cm/sup 2/. The mechanism of vortex depinning from growth-induced linear defects, i.e., out-of-plane edge dislocations in low-angle tilt domain boundaries, is shown to describe quantitatively measured J/sub c/(H/spl par/c, T). The developed model takes into account a statistical distribution of the dislocation domain boundaries ordered in a network as well as the interdislocation spacing within boundaries. Actual structural features of YBCO film known from HREM data turn out to be extracted from J/sub c/(H/spl par/c, T)-curves by a fitting procedure within the proposed model

The origin of paramagnetic magnetization in field-cooled YBa2Cu3O7 films

Temperature dependences of the magnetic moment have been measured in YBa_2Cu_3O_{7-\delta} thin films over a wide magnetic field range (5 <= H <= 10^4 Oe). In these films a paramagnetic signal known as the paramagnetic Meissner effect has been observed. The experimental data in the films, which have strong pinning and high critical current densities (J_c ~ 2 \times 10^6 A/cm^2 at 77 K), are quantitatively shown to be highly consistent with the theoretical model proposed by Koshelev and Larkin [Phys. Rev. B 52, 13559 (1995)]. This finding indicates that the origin of the paramagnetic effect is ultimately associated with nucleation and inhomogeneous spatial redistribution of magnetic vortices in a sample which is cooled down in a magnetic field. It is also shown that the distribution of vortices is extremely sensitive to the interplay of film properties and the real experimental conditions of the measurements.Comment: RevTex, 8 figure

High shock release in ultrafast laser irradiated metals: Scenario for material ejection

We present one-dimensional numerical simulations describing the behavior of solid matter exposed to subpicosecond near infrared pulsed laser radiation. We point out to the role of strong isochoric heating as a mechanism for producing highly non-equilibrium thermodynamic states. In the case of metals, the conditions of material ejection from the surface are discussed in a hydrodynamic context, allowing correlation of the thermodynamic features with ablation mechanisms. A convenient synthetic representation of the thermodynamic processes is presented, emphasizing different competitive pathways of material ejection. Based on the study of the relaxation and cooling processes which constrain the system to follow original thermodynamic paths, we establish that the metal surface can exhibit several kinds of phase evolution which can result in phase explosion or fragmentation. An estimation of the amount of material exceeding the specific energy required for melting is reported for copper and aluminum and a theoretical value of the limit-size of the recast material after ultrashort laser irradiation is determined. Ablation by mechanical fragmentation is also analysed and compared to experimental data for aluminum subjected to high tensile pressures and ultrafast loading rates. Spallation is expected to occur at the rear surface of the aluminum foils and a comparison with simulation results can determine a spall strength value related to high strain rates

Transient optical response of ultrafast nonequilibrium excited metals: Effects of electron-electron contribution to collisional absorption

Approaching energy coupling in laser-irradiated metals, we point out the role of electron-electron collision as an efficient control factor for ultrafast optical absorption. The high degree of laser-induced electron-ion nonequilibrium drives a complex absorption pattern with consequences on the transient optical properties. Consequently, high electronic temperatures determine largely the collision frequency and establish a transition between absorptive regimes in solid and plasma phases. In particular, taking into account umklapp electron-electron collisions, we performed hydrodynamic simulations of the laser-matter interaction to calculate laser energy deposition during the electron-ion nonequilibrium stage and subsequent matter transformation phases. We observe strong correlations between optical and thermodynamic properties according to the experimental situations. A suitable connection between solid and plasma regimes is chosen in accordance with models that describe the behavior in extreme, asymptotic regimes. The proposed approach describes as well situations encountered in pump-probe types of experiments, where the state of matter is probed after initial excitation. Comparison with experimental measurements shows simulation results which are sufficiently accurate to interpret the observed material behavior. A numerical probe is proposed to analyze the transient optical properties of matter exposed to ultrashort pulsed laser irradiation at moderate and high intensities. Various thermodynamic states are assigned to the observed optical variation. Qualitative indications of the amount of energy coupled in the irradiated targets are obtained. Keywords: ultrafast absorption ; umklapp electron-electron collision ; collisional absorption ; laser-matter interactio

Intragenic DNA methylation: implications of this epigenetic mechanism for cancer research

Epigenetics is the study of all mechanisms that regulate gene transcription and genome stability that are maintained throughout the cell division, but do not include the DNA sequence itself. The best-studied epigenetic mechanism to date is DNA methylation, where methyl groups are added to the cytosine base within cytosine–guanine dinucleotides (CpG sites). CpGs are frequently clustered in high density (CpG islands (CGIs)) at the promoter of over half of all genes. Current knowledge of transcriptional regulation by DNA methylation centres on its role at the promoter where unmethylated CGIs are present at most actively transcribed genes, whereas hypermethylation of the promoter results in gene repression. Over the last 5 years, research has gradually incorporated a broader understanding that methylation patterns across the gene (so-called intragenic or gene body methylation) may have a role in transcriptional regulation and efficiency. Numerous genome-wide DNA methylation profiling studies now support this notion, although whether DNA methylation patterns are a cause or consequence of other regulatory mechanisms is not yet clear. This review will examine the evidence for the function of intragenic methylation in gene transcription, and discuss the significance of this in carcinogenesis and for the future use of therapies targeted against DNA methylation

Genome-wide binding of the orphan nuclear receptor TR4 suggests its general role in fundamental biological processes

<p>Abstract</p> <p>Background</p> <p>The orphan nuclear receptor TR4 (human testicular receptor 4 or NR2C2) plays a pivotal role in a variety of biological and metabolic processes. With no known ligand and few known target genes, the mode of TR4 function was unclear.</p> <p>Results</p> <p>We report the first genome-wide identification and characterization of TR4 <it>in vivo </it>binding. Using chromatin immunoprecipitation followed by high throughput sequencing (ChIP-seq), we identified TR4 binding sites in 4 different human cell types and found that the majority of target genes were shared among different cells. TR4 target genes are involved in fundamental biological processes such as RNA metabolism and protein translation. In addition, we found that a subset of TR4 target genes exerts cell-type specific functions. Analysis of the TR4 binding sites revealed that less than 30% of the peaks from any of the cell types contained the DR1 motif previously derived from <it>in vitro </it>studies, suggesting that TR4 may be recruited to the genome via interaction with other proteins. A bioinformatics analysis of the TR4 binding sites predicted a <it>cis </it>regulatory module involving TR4 and ETS transcription factors. To test this prediction, we performed ChIP-seq for the ETS factor ELK4 and found that 30% of TR4 binding sites were also bound by ELK4. Motif analysis of the sites bound by both factors revealed a lack of the DR1 element, suggesting that TR4 binding at a subset of sites is facilitated through the ETS transcription factor ELK4. Further studies will be required to investigate the functional interdependence of these two factors.</p> <p>Conclusions</p> <p>Our data suggest that TR4 plays a pivotal role in fundamental biological processes across different cell types. In addition, the identification of cell type specific TR4 binding sites enables future studies of the pathways underlying TR4 action and its possible role in metabolic diseases.</p

Impact of DNA methylation on trophoblast function

The influence of epigenetics is evident in many fields of medicine today. This is also true in placentology, where versatile epigenetic mechanisms that regulate expression of genes have shown to have important influence on trophoblast implantation and placentation. Such gene regulation can be established in different ways and on different molecular levels, the most common being the DNA methylation. DNA methylation has been shown today as an important predictive component in assessing clinical prognosis of certain malignant tumors; in addition, it opens up new possibilities for non-invasive prenatal diagnosis utilizing cell-free fetal DNA methods. By using a well known demethylating agent 5-azacytidine in pregnant rat model, we have been able to change gene expression and, consequently, the processes of trophoblast differentiation and placental development. In this review, we describe how changes in gene methylation effect trophoblast development and placentation and offer our perspective on use of trophoblast epigenetic research for better understanding of not only placenta development but cancer cell growth and invasion as well

ZNF274 Recruits the Histone Methyltransferase SETDB1 to the 3′ Ends of ZNF Genes

Only a small percentage of human transcription factors (e.g. those associated with a specific differentiation program) are expressed in a given cell type. Thus, cell fate is mainly determined by cell type-specific silencing of transcription factors that drive different cellular lineages. Several histone modifications have been associated with gene silencing, including H3K27me3 and H3K9me3. We have previously shown that genes for the two largest classes of mammalian transcription factors are marked by distinct histone modifications; homeobox genes are marked by H3K27me3 and zinc finger genes are marked by H3K9me3. Several histone methyltransferases (e.g. G9a and SETDB1) may be involved in mediating the H3K9me3 silencing mark. We have used ChIP-chip and ChIP-seq to demonstrate that SETDB1, but not G9a, is associated with regions of the genome enriched for H3K9me3. One current model is that SETDB1 is recruited to specific genomic locations via interaction with the corepressor TRIM28 (KAP1), which is in turn recruited to the genome via interaction with zinc finger transcription factors that contain a Kruppel-associated box (KRAB) domain. However, specific KRAB-ZNFs that recruit TRIM28 (KAP1) and SETDB1 to the genome have not been identified. We now show that ZNF274 (a KRAB-ZNF that contains 5 C2H2 zinc finger domains), can interact with KAP1 both in vivo and in vitro and, using ChIP-seq, we show that ZNF274 binding sites co-localize with SETDB1, KAP1, and H3K9me3 at the 3′ ends of zinc finger genes. Knockdown of ZNF274 with siRNAs reduced the levels of KAP1 and SETDB1 recruitment to the binding sites. These studies provide the first identification of a KRAB domain-containing ZNF that is involved in recruitment of the KAP1 and SETDB1 to specific regions of the human genome