A reappraisal of the problematic European, Late Cretaceous brachiopod <i>Leptothyrellopsis polonicus</i> Bitner & Pisera, 1979

This short note presents an emended description of Leptothyrellopsis polonicus BITNER & PISERA, 1979 based on new and well-preserved materia] from Cuesmes and Ciply (Mons Basin, Hainaut, Belgium), as well as re-examination of type and additional material from Mielnik, eastern Poland. The stratigraphic range of L. polonicus is defined as from Lower Campanian to Upper Maastrichtian. On the basis of comparisons between Leptothyrellopsis polonicus and various other similar-looking brachiopods, including the Recent Leptothyrella MUIR-WOOD, Leptothyrellopsis polonicus is retained, meantime, in Incertae sedis

Abelian Magnetic Monopole Dominance in Quark Confinement

We prove Abelian magnetic monopole dominance in the string tension of QCD. Abelian and monopole dominance in low energy physics of QCD has been confirmed for various quantities by recent Monte Carlo simulations of lattice gauge theory. In order to prove this dominance, we use the reformulation of continuum Yang-Mills theory in the maximal Abelian gauge as a deformation of a topological field theory of magnetic monopoles, which was proposed in the previous article by the author. This reformulation provides an efficient way for incorporating the magnetic monopole configuration as a topological non-trivial configuration in the functional integral. We derive a version of the non-Abelian Stokes theorem and use it to estimate the expectation value of the Wilson loop. This clearly exhibits the role played by the magnetic monopole as an origin of the Berry phase in the calculation of the Wilson loop in the manifestly gauge invariant manner. We show that the string tension derived from the diagonal (abelian) Wilson loop in the topological field theory (studied in the previous article) converges to that of the full non-Abelian Wilson loop in the limit of large Wilson loop. Therefore, within the above reformulation of QCD, this result (together with the previous result) completes the proof of quark confinement in QCD based on the criterion of the area law of the full non-Abelian Wilson loop.Comment: 33 pages, Latex, no figures, version accepted for publication in Phys. Rev. D (additions of sec. 4.5 and references, and minor changes

An Integrated TCGA Pan-Cancer Clinical Data Resource to Drive High-Quality Survival Outcome Analytics

For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale. Analysis of clinicopathologic annotations for over 11,000 cancer patients in the TCGA program leads to the generation of TCGA Clinical Data Resource, which provides recommendations of clinical outcome endpoint usage for 33 cancer types

Heritability estimates for 361 blood metabolites across 40 genome-wide association studies

Metabolomics examines the small molecules involved in cellular metabolism. Approximately 50% of total phenotypic differences in metabolite levels is due to genetic variance, but heritability estimates differ across metabolite classes. We perform a review of all genome-wide association and (exome-) sequencing studies published between November 2008 and October 2018, and identify >800 class-specific metabolite loci associated with metabolite levels. In a twin-family cohort (N = 5117), these metabolite loci are leveraged to simultaneously estimate total heritability (h2 total), and the proportion of heritability captured by known metabolite loci (h2 Metabolite-hits) for 309 lipids and

Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure

Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies

Novel genetic loci associated with hippocampal volume

The hippocampal formation is a brain structure integrally involved in episodic memory, spatial navigation, cognition and stress responsiveness. Structural abnormalities in hippocampal volume and shape are found in several common neuropsychiatric disorders. To identify the genetic underpinnings of hippocampal structure here we perform a genome-wide association study (GWAS) of 33,536 individuals and discover six independent loci significantly associated with hippocampal volume, four of them novel. Of the novel loci, three lie within genes (ASTN2, DPP4 and MAST4) and one is found 200 kb upstream of SHH. A hippocampal subfield analysis shows that a locus within the MSRB3 gene shows evidence of a localized effect along the dentate gyrus, subiculum, CA1 and fissure. Further, we show that genetic variants associated with decreased hippocampal volume are also associated with increased risk for Alzheimer's disease (rg =-0.155). Our findings suggest novel biological pathways through which human genetic variation influences hippocampal volume and risk for neuropsychiatric illness