The model of entropy for the Upper Carboniferous coal-bearing formations in the Upper Silesian Coal Basin and an attempt of its geological interpretation

The paper presents the model of entropy for the coal-bearing formations of the Upper Silesian Coal Basin. The coal-bearing formations include exclusively continental (fluvial) sediments in their upper parts and paralic sediments in the lower parts, the latter composed of partly continental, partly near-shore deposits laid down in broadly understood sea coast environment (shoreline, sand bars, beaches, etc.). For studies 18 boreholes were selected in which both the continental and the paralic successions were represented. For all lithofacies distinguished in all successions the normalized, pre- and post-depositional entropies were calculated. Then, successions were categorized on the basis of these calculations. The dendrogram shows three groups of successions from which the first corresponds almost exclusively to the Paralic Series and the second one - to the Mudstone Series. The third group differs distinctly from the first two groups and represents the sediments of the Krakow Sandstone Series

Modal sequences in lithological profiles analysis - methodological approach

The Markov chains theory is a tool commonly applied to sedimentological studies. Unfortunately, this method does not provide fully credible conclusions concerning the cyclicity of sedimentation. Such cyclicity is documented, among others, by the appearance of modal sequences, i.e., sequences many times repeated in the lithological profile and having unequivocal genetic interpretation. The paper proposes the statistical permutation test, which can verify the hypothesis of the randomness of layers succession in a given lithological profile. Applying the Monte Carlo simulation method, the probability is estimated that in a random sequence composed of the same layers as the studied profile the given number of particular sequences of layers will occur. Such attempt allows the researcher to distinguish the modal sequences, i.e., those indicating the important features of sedimentation process, from sequences whose frequent appearance results exclusively from the dominance of particular lithological varieties of rocks

Polish adaptation of the Dimensional Anhedonia Rating Scale (DARS) - validation in the clinical sample

BackgroundAnhedonia is the core symptom of depression. Its presence has been linked to worsened prognosis. The Dimensional Anhedonia Rating Scale (DARS) is a scale measuring desire, motivation, effort and consummatory pleasure across different domains. The aim of this paper was to confirm factor structure, assess reliability and validity of the Polish adaptation of the DARS in a clinical sample of patients with mood disorders and healthy controls (HC).MethodsThe study sample included 161 participants aged 18–65 years - 34 HC, 72 patients with bipolar disorder and 55 with major depressive disorder (in depressive episode or remission). Reliability of the Polish adaptation of the DARS was assessed using Cronbach’s α and the average inter-item correlation (AIC). Convergent and divergent validity was established by Pearson’s correlations between the DARS and the Snaith-Hamilton Pleasure Scale (SHAPS), the Quick Inventory of Depressive Symptomatology- self-report (QIDS-SR), the Hospital Anxiety and Depression Scale (HADS). The structure of the scale was examined by factor analysis.ResultsThe factor structure was consistent with the original scale. Strong internal consistency for the DARS total score (Cronbach’s α = 0.95) and all subscales (0.86–0.93) was observed. The DARS demonstrated good convergent (moderate to strong correlations with measures of anhedonia and depression) and divergent validity (weak correlations with anxiety level).ConclusionThe Polish DARS demonstrated excellent internal consistency and very good validity. The scale is a valuable contribution to the psychometrics of anhedonia measures in patients with mood disorders

Versatile approach for functional analysis of human proteins and efficient stable cell line generation using FLP-mediated recombination system

Deciphering a function of a given protein requires investigating various biological aspects. Usually, the protein of interest is expressed with a fusion tag that aids or allows subsequent analyses. Additionally, downregulation or inactivation of the studied gene enables functional studies. Development of the CRISPR/Cas9 methodology opened many possibilities but in many cases it is restricted to non-essential genes. Recombinase-dependent gene integration methods, like the Flp-In system, are very good alternatives. The system is widely used in different research areas, which calls for the existence of compatible vectors and efficient protocols that ensure straightforward DNA cloning and generation of stable cell lines. We have created and validated a robust series of 52 vectors for streamlined generation of stable mammalian cell lines using the FLP recombinase-based methodology. Using the sequence-independent DNA cloning method all constructs for a given coding-sequence can be made with just three universal PCR primers. Our collection allows tetracycline-inducible expression of proteins with various tags suitable for protein localization, FRET, bimolecular fluorescence complementation (BiFC), protein dynamics studies (FRAP), co-immunoprecipitation, the RNA tethering assay and cell sorting. Some of the vectors contain a bidirectional promoter for concomitant expression of miRNA and mRNA, so that a gene can be silenced and its product replaced by a mutated miRNA-insensitive version. Our toolkit and protocols have allowed us to create more than 500 constructs with ease. We demonstrate the efficacy of our vectors by creating stable cell lines with various tagged proteins (numatrin, fibrillarin, coilin, centrin, THOC5, PCNA). We have analysed transgene expression over time to provide a guideline for future experiments and compared the effectiveness of commonly used inducers for tetracycline-responsive promoters. As proof of concept we examined the role of the exoribonuclease XRN2 in transcription termination by RNAseq

Lepton anomalous magnetic moments - a theory update

Standard Model contributions to the electron, muon, and tau lepton anomalous magnetic moments, a_l=(g_l-2)/2, are reviewed and updated. The fine structure constant is obtained from the electron g_e-2 and used to refine the QED contribution to the muon g_mu-2. Recent advances in electroweak and hadronic effects on g_mu-2 are summarized. Examples of ``New Physics'' probed by the a_mu Brookhaven experiment E821 are outlined. The prediction for a_tau is also given.Comment: 8 pages; invited talk at the 5th International Workshop on Tau Lepton Physics (Tau'98), September 1998, Santander, Spai

The Muon Anomalous Magnetic Moment: A Harbinger For "New Physics"

QED, Hadronic, and Electroweak Standard Model contributions to the muon anomalous magnetic moment, a_mu = (g_mu-2)/2, and their theoretical uncertainties are scrutinized. The status and implications of the recently reported 2.6 sigma experiment vs.theory deviation a_mu^{exp}-a_mu^{SM} = 426(165) times 10^{-11} are discussed. Possible explanations due to supersymmetric loop effects with m_{SUSY} \simeq 55 sqrt{tan beta} GeV, radiative mass mechanisms at the 1--2 TeV scale and other ``New Physics'' scenarios are examined.Comment: 24 page

Identification of genetic variants associated with Huntington's disease progression: a genome-wide association study

Background Huntington's disease is caused by a CAG repeat expansion in the huntingtin gene, HTT. Age at onset has been used as a quantitative phenotype in genetic analysis looking for Huntington's disease modifiers, but is hard to define and not always available. Therefore, we aimed to generate a novel measure of disease progression and to identify genetic markers associated with this progression measure. Methods We generated a progression score on the basis of principal component analysis of prospectively acquired longitudinal changes in motor, cognitive, and imaging measures in the 218 indivduals in the TRACK-HD cohort of Huntington's disease gene mutation carriers (data collected 2008–11). We generated a parallel progression score using data from 1773 previously genotyped participants from the European Huntington's Disease Network REGISTRY study of Huntington's disease mutation carriers (data collected 2003–13). We did a genome-wide association analyses in terms of progression for 216 TRACK-HD participants and 1773 REGISTRY participants, then a meta-analysis of these results was undertaken. Findings Longitudinal motor, cognitive, and imaging scores were correlated with each other in TRACK-HD participants, justifying use of a single, cross-domain measure of disease progression in both studies. The TRACK-HD and REGISTRY progression measures were correlated with each other (r=0·674), and with age at onset (TRACK-HD, r=0·315; REGISTRY, r=0·234). The meta-analysis of progression in TRACK-HD and REGISTRY gave a genome-wide significant signal (p=1·12 × 10−10) on chromosome 5 spanning three genes: MSH3, DHFR, and MTRNR2L2. The genes in this locus were associated with progression in TRACK-HD (MSH3 p=2·94 × 10−8 DHFR p=8·37 × 10−7 MTRNR2L2 p=2·15 × 10−9) and to a lesser extent in REGISTRY (MSH3 p=9·36 × 10−4 DHFR p=8·45 × 10−4 MTRNR2L2 p=1·20 × 10−3). The lead single nucleotide polymorphism (SNP) in TRACK-HD (rs557874766) was genome-wide significant in the meta-analysis (p=1·58 × 10−8), and encodes an aminoacid change (Pro67Ala) in MSH3. In TRACK-HD, each copy of the minor allele at this SNP was associated with a 0·4 units per year (95% CI 0·16–0·66) reduction in the rate of change of the Unified Huntington's Disease Rating Scale (UHDRS) Total Motor Score, and a reduction of 0·12 units per year (95% CI 0·06–0·18) in the rate of change of UHDRS Total Functional Capacity score. These associations remained significant after adjusting for age of onset. Interpretation The multidomain progression measure in TRACK-HD was associated with a functional variant that was genome-wide significant in our meta-analysis. The association in only 216 participants implies that the progression measure is a sensitive reflection of disease burden, that the effect size at this locus is large, or both. Knockout of Msh3 reduces somatic expansion in Huntington's disease mouse models, suggesting this mechanism as an area for future therapeutic investigation