Determination of the η\eta and η′\eta' Mixing Angle from the Pseudoscalar Transition Form Factors

The possible range of $\eta-\eta'$ mixing angle is determined from the transition form factors $F_{\eta \gamma}(Q^2)$ and $F_{\eta' \gamma}(Q^2)$ with the help of the present experimental data. For such purpose, the quark-flavor mixing scheme is adopted and the pseudoscalar transition form factors are calculated under the light-cone pQCD framework, where the transverse momentum corrections and the contributions beyond the leading Fock state have been carefully taken into consideration. We construct a phenomenological expression to estimate the contributions to the form factors beyond the leading Fock state based on their asymptotic behavior at $Q^2\to 0$ and $Q^2\to\infty$. By taking the quark-flavor mixing scheme, our results lead to $\phi= 38.0^{\circ}\pm 1.0^{\circ}\pm 2.0^{\circ}$, where the first error coming from experimental uncertainty and the second error coming from the uncertainties of the wavefunction parameters. The possible intrinsic charm component in $\eta$ and $\eta'$ is discussed and our present analysis also disfavors a large portion of intrinsic charm component in $\eta$ and $\eta'$, e.g. $|f^c_{\eta'}|\le 50 {\rm MeV}$.Comment: 18 Pages, 3 figures. Several references added. To be published in EPJ

B→KB\to K Transition Form Factor up to O(1/mb2){\cal O}(1/m^2_b) within the kTk_T Factorization Approach

In the paper, we apply the $k_T$ factorization approach to deal with the $B\to K$ transition form factor $F^{B\to K}_{+,0}(q^2)$ in the large recoil regions. The B-meson wave functions $\Psi_B$ and $\bar\Psi_B$ that include the three-particle Fock states' contributions are adopted to give a consistent PQCD analysis of the form factor up to ${\cal O} (1/m^2_b)$. It has been found that both the wave functions $\Psi_B$ and $\bar\Psi_B$ can give sizable contributions to the form factor and should be kept for a better understanding of the $B$ meson decays. Then the contributions from different twist structures of the kaon wavefunction are discussed, including the $SU_f(3)$-breaking effects. A sizable contribution from the twist-3 wave function $\Psi_p$ is found, whose model dependence is discussed by taking two group of parameters that are determined by different distribution amplitude moments obtained in the literature. It is also shown that $F^{B\to K}_{+,0}(0)=0.30\pm0.04$ and $[F^{B\to K}_{+,0}(0)/F^{B\to \pi}_{+,0}(0)]=1.13\pm0.02$, which are more reasonable and consistent with the light-cone sum rule results in the large recoil regions.Comment: 22 pages and 6 figure

Collaborative multidisciplinary management and expertise of cT2-3 locally advanced operable esophageal squamous cell carcinoma:two case reports

Background: The accurate clinical staging of esophageal squamous cell carcinoma (ESCC) is pivotal for guiding treatment strategies. However, the current precision in staging for clinical T (cT)2 and cT3 stages remains unsatisfactory. This article discusses the role of multidisciplinary teams (MDTs) in the clinical staging and formulation of neoadjuvant treatment strategies for locally advanced operable ESCC. These challenges underscore the importance of precise staging in the decision-making process for appropriate therapeutic interventions.Case Description: Through the lens of two patient case studies with locally advanced resectable ESCC, the article showcases the intricate process of treatment planning undertaken by MDTs. It captures a range of expert perspectives from Japan, China, Hong Kong (China), Korea, the USA, and Europe, focusing on the challenges of differentiating between cT2 and cT3 stages of the disease, which is a critical determinant in the management and therapeutic approach for patients.Conclusions: The article concludes that the accurate staging of ESCC is a cornerstone in determining the most suitable treatment strategies. It underscores the vital role that MDTs play in both clinical staging and the decision-making process for treatment. Highlighting the limitations in current diagnostic methods, the article emphasizes the urgent need for advanced research and the refinement of diagnostic tools to improve the precision of staging, particularly between the cT2 and cT3 stages. It suggests that future research should consider whether a reclassification of these stages could be warranted to enhance treatment planning and outcomes for patients with ESCC.<br/

Optical properties of dust

http://arxiv.org/abs/0808.4123Except in a few cases cosmic dust can be studied in situ or in terrestrial laboratories, essentially all of our information concerning the nature of cosmic dust depends upon its interaction with electromagnetic radiation. This chapter presents the theoretical basis for describing the optical properties of dust -- how it absorbs and scatters starlight and reradiates the absorbed energy at longer wavelengths.Partial support by a Chandra Theory program and HST Theory Programs is gratefully acknowledged

FOXP3 Is an X-Linked Breast Cancer Suppressor Gene and an Important Repressor of the HER-2/ErbB2 Oncogene

The X-linked Foxp3 is a member of the forkhead/winged helix transcription factor family. Germ-line mutations cause lethal autoimmune diseases in males. Serendipitously, we observed that Foxp3sf/+ heterozygous mice developed cancer at a high rate. The majority of the cancers were mammary carcinomas in which the wild-type Foxp3 allele was inactivated and ErbB2 was over-expressed. Foxp3 bound and repressed the ErbB2 promoter. Deletion, functionally significant somatic mutations and down-regulation of the FOXP3 gene were commonly found in human breast cancer samples and correlated significantly with HER-2 over-expression, regardless of the status of HER-2 amplification. In toto, the data demonstrate that FOXP3 is an X-linked breast cancer suppressor gene and an important regulator of the HER-2/ErbB2 oncogene

The Pediatric Cell Atlas: defining the growth phase of human development at single-cell resolution

Single-cell gene expression analyses of mammalian tissues have uncovered profound stage-specific molecular regulatory phenomena that have changed the understanding of unique cell types and signaling pathways critical for lineage determination, morphogenesis, and growth. We discuss here the case for a Pediatric Cell Atlas as part of the Human Cell Atlas consortium to provide single-cell profiles and spatial characterization of gene expression across human tissues and organs. Such data will complement adult and developmentally focused HCA projects to provide a rich cytogenomic framework for understanding not only pediatric health and disease but also environmental and genetic impacts across the human lifespan

Dynamic response of Dam-Reservoir systems : review and a semi-analytical proposal

This paper presents a review of current techniques employed for dynamic analysis of concrete gravity dams under seismic action. Traditional procedures applied in design bureaus, such as the Pseudo-Static method, often neglect structural dynamic properties, as well as ground amplification effects. A practical alternative arises with the Pseudo-Dynamic method, which considers a simplified spectrum response in the fundamental mode. The authors propose a self-contained development and detailed examples of this latter method, including a comparison with finite element models using transient response of fluid-structure systems. It is verified that application of the traditional procedure should be done carefully and limited to extremely rigid dams. On the other hand, the proposed development is straightforward and in agreement with finite element results for general cases where dam flexibility plays an important role

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

Integrating sequence and array data to create an improved 1000 Genomes Project haplotype reference panel

A major use of the 1000 Genomes Project (1000GP) data is genotype imputation in genome-wide association studies (GWAS). Here we develop a method to estimate haplotypes from low-coverage sequencing data that can take advantage of single-nucleotide polymorphism (SNP) microarray genotypes on the same samples. First the SNP array data are phased to build a backbone (or 'scaffold') of haplotypes across each chromosome. We then phase the sequence data 'onto' this haplotype scaffold. This approach can take advantage of relatedness between sequenced and non-sequenced samples to improve accuracy. We use this method to create a new 1000GP haplotype reference set for use by the human genetic community. Using a set of validation genotypes at SNP and bi-allelic indels we show that these haplotypes have lower genotype discordance and improved imputation performance into downstream GWAS samples, especially at low-frequency variants. © 2014 Macmillan Publishers Limited. All rights reserved

Mapping and characterization of structural variation in 17,795 human genomes

A key goal of whole-genome sequencing for studies of human genetics is to interrogate all forms of variation, including single-nucleotide variants, small insertion or deletion (indel) variants and structural variants. However, tools and resources for the study of structural variants have lagged behind those for smaller variants. Here we used a scalable pipeline1 to map and characterize structural variants in 17,795 deeply sequenced human genomes. We publicly release site-frequency data to create the largest, to our knowledge, whole-genome-sequencing-based structural variant resource so far. On average, individuals carry 2.9 rare structural variants that alter coding regions; these variants affect the dosage or structure of 4.2 genes and account for 4.0–11.2% of rare high-impact coding alleles. Using a computational model, we estimate that structural variants account for 17.2% of rare alleles genome-wide, with predicted deleterious effects that are equivalent to loss-of-function coding alleles; approximately 90% of such structural variants are noncoding deletions (mean 19.1 per genome). We report 158,991 ultra-rare structural variants and show that 2% of individuals carry ultra-rare megabase-scale structural variants, nearly half of which are balanced or complex rearrangements. Finally, we infer the dosage sensitivity of genes and noncoding elements, and reveal trends that relate to element class and conservation. This work will help to guide the analysis and interpretation of structural variants in the era of whole-genome sequencing