26 research outputs found
Tri-meson-mixing of -- and -- in the light-cone quark model
The radiative transition form factors of the pseudoscalar mesons {,
, } and the vector mesons {, , } are restudied
with -- and -- in tri-meson-mixing
pattern, which is described by tri-mixing matrices in the light-cone
constituent quark model. The experimental transition decay widths are better
reproduced with tri-meson-mixing than previous results in a two-mixing-angle
scenario of only two-meson - mixing and - mixing.Comment: 8 pages, 6 figures, final version to appear in EPJ
Horizontal Branch Stars: The Interplay between Observations and Theory, and Insights into the Formation of the Galaxy
We review HB stars in a broad astrophysical context, including both variable
and non-variable stars. A reassessment of the Oosterhoff dichotomy is
presented, which provides unprecedented detail regarding its origin and
systematics. We show that the Oosterhoff dichotomy and the distribution of
globular clusters (GCs) in the HB morphology-metallicity plane both exclude,
with high statistical significance, the possibility that the Galactic halo may
have formed from the accretion of dwarf galaxies resembling present-day Milky
Way satellites such as Fornax, Sagittarius, and the LMC. A rediscussion of the
second-parameter problem is presented. A technique is proposed to estimate the
HB types of extragalactic GCs on the basis of integrated far-UV photometry. The
relationship between the absolute V magnitude of the HB at the RR Lyrae level
and metallicity, as obtained on the basis of trigonometric parallax
measurements for the star RR Lyrae, is also revisited, giving a distance
modulus to the LMC of (m-M)_0 = 18.44+/-0.11. RR Lyrae period change rates are
studied. Finally, the conductive opacities used in evolutionary calculations of
low-mass stars are investigated. [ABRIDGED]Comment: 56 pages, 22 figures. Invited review, to appear in Astrophysics and
Space Scienc
Whole genome sequence association analysis of fasting glucose and fasting insulin levels in diverse cohorts from the NHLBI TOPMed program
The genetic determinants of fasting glucose (FG) and fasting insulin (FI) have been studied mostly through genome arrays, resulting in over 100 associated variants. We extended this work with high-coverage whole genome sequencing analyses from fifteen cohorts in NHLBI’s Trans-Omics for Precision Medicine (TOPMed) program. Over 23,000 non-diabetic individuals from five race-ethnicities/populations (African, Asian, European, Hispanic and Samoan) were included. Eight variants were significantly associated with FG or FI across previously identified regions MTNR1B, G6PC2, GCK, GCKR and FOXA2. We additionally characterize suggestive associations with FG or FI near previously identified SLC30A8, TCF7L2, and ADCY5 regions as well as APOB, PTPRT, and ROBO1. Functional annotation resources including the Diabetes Epigenome Atlas were compiled for each signal (chromatin states, annotation principal components, and others) to elucidate variant-to-function hypotheses. We provide a catalog of nucleotide-resolution genomic variation spanning intergenic and intronic regions creating a foundation for future sequencing-based investigations of glycemic traits
Whole-genome sequencing reveals host factors underlying critical COVID-19
Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
A marine origin for the late Mesoproterozoic Copper Harbor and Nonesuch Formations of the Midcontinent Rift of Laurentia
Experimental evidence for interplay of dynamic heterogeneity and finite-size effect in glassy polymers
Wnt5a Signaling — A New and Attractive Target for Specific Anticancer Therapy
Wnt signaling has been shown to engage a multifunctional pathway that is involved in the regulation of a wide variety of normal and pathologic processes, including embryogenesis, diff erentiation and tumorigenesis. Recent studies have demonstrated that Wnt5a expression is frequently seen in various human cancers. In contrast to the transforming members of the Wnt family, shown to be upregulated in many cancers, the role of Wnt5a is still controversial in its expression in different tumors. There is increasing evidence that Wnt5a has tumor suppressor function in some malignancies, and in addition, it elicits promigratory and proinvasive effects via the planar cell polarity pathway, which suggests that Wnt5a might be an effective marker for the progression and prognosis of tumors. Obviously, the outcome of Wnt5a signaling is dependent on a multitude of variables, ranging from receptors, downstream effectors and inhibitors, to external influences coming from the tumor microenvironment. This review will focus on the role of Wnt5a signaling and, as a consequence, provide an outline describing the expression and functions of Wnt5a in cancer progression