Calculation of thermodynamic properties of liquid alkali metals by the first-principle-pseudopotential and Weeks-Chandler-Andersen methods

A study was conducted to demonstrate calculation of thermodynamic properties of liquid alkali metals by the first-principle-pseudo-potential and Weeks Chandler Andersen (WCA) methods. The pseudo-potential was used for calculating the thermodynamic properties of liquid alkali metals within the framework of the variational method. The use of the true wave functions of conduction electrons also enabled to take into account correctly the energy shifts for the core electrons caused by their interaction with the potential formed by the distribution of the conduction-electron charge. The results of calculations by the WCA method agreed well with the experimental data. This agreement for Li and Na was better than that in the case of using the variational method

Diffusion Processes in the Liquid Borosilicate with Nonequilibrium Structure

Abstract The influence of temperature relaxation of the liquid borosilicate structure for diffusion coefficients of nickel cations (DNi 2+ ) was investigated. On the termotime curves of the diffusion coefficients, obtained in the slow heating (equilibrium conditions) and rapid cooling hysteresis is observed. This demonstrates the slowness of the borosilicate complexes reconstruction. During isothermal exposure values DNi 2+ approached equilibrium for several dozens of minutes. Keywords: liquid borosilicate, structural relaxation, diffusion coefficients Establishing a relationship between the structure and transport properties of borosilicate melts is one of the fundamental problems of physical chemistry. The structure of oxide melts in many respects defines their physicochemical properties, the rate of interaction with metal alloys, service characteristics of enamel and glass. Investigation of the temperature and time dependences of the nickel ions' diffusion coefficients was carried out in the melt Na2OB2O32SiO2 with the addition of 0.5 wt. % NiO in equilibrium and non-equilibrium conditions by Faraday impedance. In the experiment, the frequency dependences of the electrode impedance's constituents at a particular selected temperature were obtained under equilibrium conditions. They were satisfactorily described by the model curves, obtained for the equivalent electrical circuit that contained the Warburg impedance, indicating that the inhibition of diffusion processes with th

Research on the Process of Al–Mo–Ti Master Alloy Dissolution in Titanium

This paper presents the results of studying the behavior of the components of the molybdenum-containing Al-(48-52)Mo-(6-9)Ti (wt. %) master alloy when it is dissolved in liquid titanium. The nature and characteristics of the dissolution of the master alloy in titanium were judged by the results of X-ray microanalysis of the matrix phases (titanium, master alloy) and transition zones (phase boundary). In order to bring the model closer to actual melting conditions, a vacuum arc melting of a titanium sample was used, in which a certain amount of master alloy was encapsulated. The samples were melted around the perimeter so that the liquid titanium only began to interact with the master alloy, after which the melting process was stopped. The obtained results suggest that the composition of the Al-Mo-Ti master alloy is changed by the diffusion transition of molybdenum and aluminum into the titanium melt and counter diffusion of titanium into the master alloy melt. At the same time, a decrease in the concentration of molybdenum in the master alloy is compensated by aluminum and titanium. For every 1.0 wt. % of Al converted into Ti about 2.0 wt. % of Ti dissolves in the master alloy melt. The revealed patterns of changes in the composition of the Al-Mo-Ti master alloy when interacting with liquid titanium suggest that under vacuum-arc melting of titanium alloys the dissolution of the master alloy should not lead to the formation of refractory phases. Keywords: titanium, molybdenum, aluminum, master alloys, dissolutio

The Evolution of Epigenetic Regulators CTCF and BORIS/CTCFL in Amniotes

CTCF is an essential, ubiquitously expressed DNA-binding protein responsible for insulator function, nuclear architecture, and transcriptional control within vertebrates. The gene CTCF was proposed to have duplicated in early mammals, giving rise to a paralogue called “brother of regulator of imprinted sites” (BORIS or CTCFL) with DNA binding capabilities similar to CTCF, but testis-specific expression in humans and mice. CTCF and BORIS have opposite regulatory effects on human cancer-testis genes, the anti-apoptotic BAG1 gene, the insulin-like growth factor 2/H19 imprint control region (IGF2/H19 ICR), and show mutually exclusive expression in humans and mice, suggesting that they are antagonistic epigenetic regulators. We discovered orthologues of BORIS in at least two reptilian species and found traces of its sequence in the chicken genome, implying that the duplication giving rise to BORIS occurred much earlier than previously thought. We analysed the expression of CTCF and BORIS in a range of amniotes by conventional and quantitative PCR. BORIS, as well as CTCF, was found widely expressed in monotremes (platypus) and reptiles (bearded dragon), suggesting redundancy or cooperation between these genes in a common amniote ancestor. However, we discovered that BORIS expression was gonad-specific in marsupials (tammar wallaby) and eutherians (cattle), implying that a functional change occurred in BORIS during the early evolution of therian mammals. Since therians show imprinting of IGF2 but other vertebrate taxa do not, we speculate that CTCF and BORIS evolved specialised functions along with the evolution of imprinting at this and other loci, coinciding with the restriction of BORIS expression to the germline and potential antagonism with CTCF

Evolutionary Diversification of SPANX-N Sperm Protein Gene Structure and Expression

The sperm protein associated with nucleus in the X chromosome (SPANX) genes cluster at Xq27 in two subfamilies, SPANX-A/D and SPANX-N. SPANX-A/D is specific for hominoids and is fairly well characterized. The SPANX-N gave rise to SPANX-A/D in the hominoid lineage ∼7 MYA. Given the proposed role of SPANX genes in spermatogenesis, we have extended studies to SPANX-N gene evolution, variation, regulation of expression, and intra-sperm localization. By immunofluorescence analysis, SPANX-N proteins are localized in post-meiotic spermatids exclusively, like SPANX-A/D. But in contrast to SPANX-A/D, SPANX-N are found in all ejaculated spermatozoa rather than only in a subpopulation, are localized in the acrosome rather than in the nuclear envelope, and are expressed at a low level in several nongametogenic adult tissues as well as many cancers. Presence of a binding site for CTCF and its testis-specific paralogue BORIS in the SPANX promoters suggests, by analogy to MAGE-A1 and NY-ESO-1, that their activation in spermatogenesis is mediated by the programmed replacement of CTCF by BORIS. Based on the relative density of CpG, the more extended expression of SPANX-N compared to SPANX-A/D in nongametogenic tissues is likely attributed to differences in promoter methylation. Our findings suggest that the recent duplication of SPANX genes in hominoids was accompanied by different localization of SPANX-N proteins in post-meiotic sperm and additional expression in several nongonadal tissues. This suggests a corresponding functional diversification of SPANX gene families in hominoids. SPANX proteins thus provide unique targets to investigate their roles in the function of spermatozoa, selected malignancies, and for SPANX-N, in other tissues as well

BORIS, a paralogue of the transcription factor, CTCF, is aberrantly expressed in breast tumours

BORIS (for brother of the regulator of imprinted sites), a paralogue of the transcription factor, CTCF, is a novel member of the cancer-testis antigen family. The aims of the present study were as follows: (1) to investigate BORIS expression in breast cells and tumours using immunohistochemical staining, western and real-time RT–PCR analyses and (2) assess potential correlation between BORIS levels in tumours with clinical/pathological parameters. BORIS was detected in all 18 inspected breast cell lines, but not in a primary normal breast cell culture. In 70.7% (41 of 58 cases) BORIS was observed in breast tumours. High levels of BORIS correlated with high levels of progesterone receptor (PR) and oestrogen receptor (ER). The link between BORIS and PR/ER was further confirmed by the ability of BORIS to activate the promoters of the PR and ER genes in the reporter assays. Detection of BORIS in a high proportion of breast cancer patients implies potential practical applications of BORIS as a molecular biomarker of breast cancer. This may be important for diagnosis of the condition and for the therapeutic use of BORIS. The ability of BORIS to activate promoters of the RP and ER genes points towards possible involvement of BORIS in the establishment, progression and maintenance of breast tumours

Coordinated Activation of Candidate Proto-Oncogenes and Cancer Testes Antigens via Promoter Demethylation in Head and Neck Cancer and Lung Cancer

Background: Epigenetic alterations have been implicated in the pathogenesis of solid tumors, however, proto-oncogenes activated by promoter demethylation have been sporadically reported. We used an integrative method to analyze expression in primary head and neck squamous cell carcinoma (HNSCC) and pharmacologically demethylated cell lines to identify aberrantly demethylated and expressed candidate proto-oncogenes and cancer testes antigens in HNSCC. Methodology/Principal Findings: We noted coordinated promoter demethylation and simultaneous transcriptional upregulation of proto-oncogene candidates with promoter homology, and phylogenetic footprinting of these promoters demonstrated potential recognition sites for the transcription factor BORIS. Aberrant BORIS expression correlated with upregulation of candidate proto-oncogenes in multiple human malignancies including primary non-small cell lung cancers and HNSCC, induced coordinated proto-oncogene specific promoter demethylation and expression in non-tumorigenic cells, and transformed NIH3T3 cells. Conclusions/Significance: Coordinated, epigenetic unmasking of multiple genes with growth promoting activity occurs i

CTCF cis-Regulates Trinucleotide Repeat Instability in an Epigenetic Manner: A Novel Basis for Mutational Hot Spot Determination

At least 25 inherited disorders in humans result from microsatellite repeat expansion. Dramatic variation in repeat instability occurs at different disease loci and between different tissues; however, cis-elements and trans-factors regulating the instability process remain undefined. Genomic fragments from the human spinocerebellar ataxia type 7 (SCA7) locus, containing a highly unstable CAG tract, were previously introduced into mice to localize cis-acting “instability elements,” and revealed that genomic context is required for repeat instability. The critical instability-inducing region contained binding sites for CTCF—a regulatory factor implicated in genomic imprinting, chromatin remodeling, and DNA conformation change. To evaluate the role of CTCF in repeat instability, we derived transgenic mice carrying SCA7 genomic fragments with CTCF binding-site mutations. We found that CTCF binding-site mutation promotes triplet repeat instability both in the germ line and in somatic tissues, and that CpG methylation of CTCF binding sites can further destabilize triplet repeat expansions. As CTCF binding sites are associated with a number of highly unstable repeat loci, our findings suggest a novel basis for demarcation and regulation of mutational hot spots and implicate CTCF in the modulation of genetic repeat instability