The effect of wave conditions and surfer ability on performance and the physiological response of recreational surfers.

This study investigated the effects of wave conditions on performance and the physiological responses of surfers. After institutional ethical approval 39 recreational surfers participated in 60 surfing sessions where performance and physiological response were measured using global positioning system (GPS) heart rate monitors. Using GPS, the percentage time spent in surfing activity categories was on average 41.6, 47.0, 8.1, and 3.1% for waiting, paddling, riding, and miscellaneous activities, respectively. Ability level of the surfers, wave size, and wave period are significantly associated with the physiological, ride, and performance parameters during surfing. As the ability level of the surfers increases there is a reduction in the relative exercise intensity (e.g., average heart rate as a percentage of laboratory maximum, rpartial = -0.412, p < 0.01) which is in contrast to increases in performance parameters (e.g., maximum ride speed (0.454, p < 0.01). As the wave size increased there were reductions in physiological demand (e.g., total energy expenditure rpartial = -0.351, p ≤ 0.05) but increases in ride speed and distance measures (e.g., the maximum ride speed, 0.454, p < 0.01). As the wave period increased there were increases in intensity (e.g., average heart rate as a percentage of laboratory maximum, rp = 0.490, p < 0.01) and increases in ride speed and distance measures (e.g., the maximum ride speed, rpartial = 0.371, p < 0.01). This original study is the first to show that wave parameters and surfer ability are significantly associated with the physiological response and performance characteristics of surfing

Rigorous constraints on the matrix elements of the energy-momentum tensor

The structure of the matrix elements of the energy-momentum tensor play an important role in determining the properties of the form factors $A(q^{2})$, $B(q^{2})$ and $C(q^{2})$ which appear in the Lorentz covariant decomposition of the matrix elements. In this paper we apply a rigorous frame-independent distributional-matching approach to the matrix elements of the Poincar\'{e} generators in order to derive constraints on these form factors as $q \rightarrow 0$. In contrast to the literature, we explicitly demonstrate that the vanishing of the anomalous gravitomagnetic moment $B(0)$ and the condition $A(0)=1$ are independent of one another, and that these constraints are not related to the specific properties or conservation of the individual Poincar\'{e} generators themselves, but are in fact a consequence of the physical on-shell requirement of the states in the matrix elements and the manner in which these states transform under Poincar\'{e} transformations.Comment: 11 pages; v2: additional comments added, matches published versio

The third international hackathon for applying insights into large-scale genomic composition to use cases in a wide range of organisms

In October 2021, 59 scientists from 14 countries and 13 U.S. states collaborated virtually in the Third Annual Baylor College of Medicine & DNANexus Structural Variation hackathon. The goal of the hackathon was to advance research on structural variants (SVs) by prototyping and iterating on open-source software. This led to nine hackathon projects focused on diverse genomics research interests, including various SV discovery and genotyping methods, SV sequence reconstruction, and clinically relevant structural variation, including SARS-CoV-2 variants. Repositories for the projects that participated in the hackathon are available at https://github.com/collaborativebioinformatics

Comparative DNA methylome analysis of endometrial carcinoma reveals complex and distinct deregulation of cancer promoters and enhancers

BACKGROUND: Aberrant DNA methylation is a hallmark of many cancers. Classically there are two types of endometrial cancer, endometrioid adenocarcinoma (EAC), or Type I, and uterine papillary serous carcinoma (UPSC), or Type II. However, the whole genome DNA methylation changes in these two classical types of endometrial cancer is still unknown. RESULTS: Here we described complete genome-wide DNA methylome maps of EAC, UPSC, and normal endometrium by applying a combined strategy of methylated DNA immunoprecipitation sequencing (MeDIP-seq) and methylation-sensitive restriction enzyme digestion sequencing (MRE-seq). We discovered distinct genome-wide DNA methylation patterns in EAC and UPSC: 27,009 and 15,676 recurrent differentially methylated regions (DMRs) were identified respectively, compared with normal endometrium. Over 80% of DMRs were in intergenic and intronic regions. The majority of these DMRs were not interrogated on the commonly used Infinium 450K array platform. Large-scale demethylation of chromosome X was detected in UPSC, accompanied by decreased XIST expression. Importantly, we discovered that the majority of the DMRs harbored promoter or enhancer functions and are specifically associated with genes related to uterine development and disease. Among these, abnormal methylation of transposable elements (TEs) may provide a novel mechanism to deregulate normal endometrium-specific enhancers derived from specific TEs. CONCLUSIONS: DNA methylation changes are an important signature of endometrial cancer and regulate gene expression by affecting not only proximal promoters but also distal enhancers. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/1471-2164-15-868) contains supplementary material, which is available to authorized users

Regulatory network decoded from epigenomes of surface ectoderm-derived cell types

Developmental history shapes the epigenome and biological function of differentiated cells. Epigenomic patterns have been broadly attributed to the three embryonic germ layers. Here we investigate how developmental origin influences epigenomes. We compare key epigenomes of cell types derived from surface ectoderm (SE), including keratinocytes and breast luminal and myoepithelial cells, against neural crest-derived melanocytes and mesoderm-derived dermal fibroblasts to identify SE differentially methylated regions (SE-DMRs). DNA methylomes of neonatal keratinocytes share many more DMRs with adult breast luminal and myoepithelial cells than with melanocytes and fibroblasts from the same neonatal skin. This suggests that SE origin contributes to DNA methylation patterning, while shared skin tissue environment has limited effect on epidermal keratinocytes. Hypomethylated SE-DMRs are in proximity to genes with SE relevant functions. They are also enriched for enhancer- and promoter-associated histone modifications in SE-derived cells, and for binding motifs of transcription factors important in keratinocyte and mammary gland biology. Thus, epigenomic analysis of cell types with common developmental origin reveals an epigenetic signature that underlies a shared gene regulatory network

Angular analysis of the B0→K∗0e+e−B^0 \rightarrow K^{*0} e^+ e^- decay in the low-q2q^2 region

An angular analysis of the $B^0 \rightarrow K^{*0} e^+ e^-$ decay is performed using a data sample, corresponding to an integrated luminosity of 3.0 {\mbox{fb}^{-1}}, collected by the LHCb experiment in $pp$ collisions at centre-of-mass energies of 7 and 8 TeV during 2011 and 2012. For the first time several observables are measured in the dielectron mass squared ($q^2$) interval between 0.002 and 1.120${\mathrm{\,Ge\kern -0.1em V^2\!/}c^4}$. The angular observables $F_{\mathrm{L}}$ and $A_{\mathrm{T}}^{\mathrm{Re}}$ which are related to the $K^{*0}$ polarisation and to the lepton forward-backward asymmetry, are measured to be $F_{\mathrm{L}}= 0.16 \pm 0.06 \pm0.03$ and $A_{\mathrm{T}}^{\mathrm{Re}} = 0.10 \pm 0.18 \pm 0.05$, where the first uncertainty is statistical and the second systematic. The angular observables $A_{\mathrm{T}}^{(2)}$ and $A_{\mathrm{T}}^{\mathrm{Im}}$ which are sensitive to the photon polarisation in this $q^2$ range, are found to be $A_{\mathrm{T}}^{(2)} = -0.23 \pm 0.23 \pm 0.05$ and $A_{\mathrm{T}}^{\mathrm{Im}} =0.14 \pm 0.22 \pm 0.05$. The results are consistent with Standard Model predictions

Measurement of CPCP asymmetries and polarisation fractions in Bs0→K∗0Kˉ∗0B_s^0 \rightarrow K^{*0}\bar{K}{}^{*0} decays

An angular analysis of the decay $B_s^0 \rightarrow K^{*0}\bar{K}{}^{*0}$ is performed using $pp$ collisions corresponding to an integrated luminosity of $1.0$ ${fb}^{-1}$ collected by the LHCb experiment at a centre-of-mass energy $\sqrt{s} = 7$ TeV. A combined angular and mass analysis separates six helicity amplitudes and allows the measurement of the longitudinal polarisation fraction $f_L = 0.201 \pm 0.057 {(stat.)} \pm 0.040{(syst.)}$ for the $B_s^0 \rightarrow K^*(892)^0 \bar{K}{}^*(892)^0$ decay. A large scalar contribution from the $K^{*}_{0}(1430)$ and $K^{*}_{0}(800)$ resonances is found, allowing the determination of additional $CP$ asymmetries. Triple product and direct $CP$ asymmetries are determined to be compatible with the Standard Model expectations. The branching fraction $\mathcal{B}(B_s^0 \rightarrow K^*(892)^0 \bar{K}{}^*(892)^0)$ is measured to be $(10.8 \pm 2.1 {\ \rm (stat.)} \pm 1.4 {\ \rm (syst.)} \pm 0.6 \ (f_d/f_s) ) \times 10^{-6}$

The Effect of Own Body Concerns on Judgments of Other Women’s Body Size

We investigated the relationships between healthy women’s estimates of their own body size, their body dissatisfaction, and how they subjectively judge the transition from normal to overweight in other women’s bodies (the “normal/overweight” boundary). We propose two complementary hypotheses. In the first, participants compare other women to an internalized Western “thin ideal,” whose size reflects the observer’s own body dissatisfaction. As dissatisfaction increases, so the size of their “thin ideal” reduces, predicting an inverse relationship between the “normal/overweight” boundary and participants’ body dissatisfaction. Alternatively, participants judge the size of other women relative to the body size they believe they have. For this implicit or explicit social comparison, the participant selects a “normal/overweight” boundary that minimizes the chance of her making an upward social comparison. So, the “normal/overweight” boundary matches or is larger than her own body size. In an online study of 129 healthy women, we found that both opposing factors explain where women place the “normal/overweight” boundary. Increasing body dissatisfaction leads to slimmer judgments for the position of the “normal/overweight” boundary in the body mass index (BMI) spectrum. Whereas, increasing overestimation by the observer of their own body size shifts the “normal/overweight” boundary toward higher BMIs